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This certified CME activity will be designed for retina specialists and general ophthalmologists involved in the management of patients with retinal disease.
Jointly sponsored by the Dulaney Foundation and Retina Today. Supported by an educational grant from ThromboGenics.
This continuing medical educational activity is supported by an unrestricted educational grant from ThromboGenics.
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Participants should read the CME activity in its entirety. After reviewing the material, please complete the self-assessment test, which consists of a series of multiple-choice questions. To answer these questions online and receive real-time results, please visit http://www.dulaneyfoundation.org and click “Online Courses.” Upon completing the activity and achieving a passing score of over 70% on the self-assessment test, you may print out a CME credit letter awarding 1 AMA PRA Category 1 Credit.™ The estimated time to complete this activity is 1 hour.
Symptomatic vitreomacular adhesion (VMA) is a condition when the vitreous gel adheres in an abnormally strong manner to the retina. VMA can lead to vitreomacular traction (VMT) and subsequent loss or distortion of visual acuity. Anomalous posterior vitreous detachment (PVD) is linked to several retinal disorders including macular pucker, macular hole, age-related macular generation (AMD), macular edema, and retinal tears and detachment. The incidence of VMA has been reported to be as high as 84% in cases of macular hole; 74% in VMT syndrome; and 56% in idiopathic epimacular membrane.1 The incidence of VMA in macular edema appears to depend on the severity of the underlying condition.2,3 In AMD, the rates vary3-12 but have been reported to be as high as 59% in exudative AMD.12 Currently, pars plana vitrectomy (PPV) is used to surgically induce PVD and release the traction on the retina for selected cases. A vitrectomy procedure, however, is not without risk. Complications with standard PPV12-15 and more recently with small-gauge PPV16-20 have been reported and include retinal detachment, retinal tears, endophthalmitis, and postoperative cataract formation. Additionally, PPV may result in incomplete separation and it may potentially leave a nidus for vasoactive and vasoproliferative substances or it may induce development of fibrovascular membranes. Further, as is with any invasive surgical procedure, PPV introduces more trauma to the vitreous and surrounding tissues.21,22 There are data showing that nonsurgical induction of PVD using ocriplasmin, a vitreolysis agent, can offer the benefits of successful PVD while eliminating the risks associated with a surgical procedure. Pharmacologic vitreolysis has the following advantages over PPV: It induces complete separation, creates a more physiologic state of the vitreomacular interface, prevents the development of fibrovascular membranes, is less traumatic to the vitreous, and is potentially prophylactic.21,22 Additionally, vitreolysis obviates the costs associated with surgery and allows for earlier intervention, whereas surgery is reserved for more advanced cases. In 2 phase 3 studies, a single injection of ocriplasmin was shown to be safe and effective for PVD induction,23 providing further evidence that pharmacologic vitreolysis with ocriplasmin may provide a safe and effective alternative to PPV for inducing PVD. To address these gaps, retina specialists and other ophthalmologists must master insights on the pathogenesis of VMA, the role that VMA plays in various retinal pathologies, and the benefits of induced PVD vs anomalous PVD. Mastery includes knowledge of the clinical implications of VMA and the results of recent clinical trials on both surgical and pharmacologic PVD induction, an understanding of vitreolysis agents and their differences, and the ability to identify patients who may benefit from PVD induction. 1. Koerner F, Garweg J. [Diseases of the vitreo-macular interface]. Klin Monbl Augenheilkd. 1999;214(5):305-310. 2. Takahashi MK, Hikichi T, Akiba J, Yoshida A, Trempe CL. Role of the vitreous and macular edema in branch retinal vein occlusion. Ophthalmic Surg Lasers. 1997;28(4):294-299. 3. Kado M, Jalkh AE, Yoshida A, et al. Vitreous changes and macular edema in central retinal vein occlusion. Ophthalmic Surg. 1990;21(8):544-549. 4. Lambert HM, Capone A, Jr., Aaberg TM, et al. Surgical excision of subfoveal neovascular membranes in agerelated macular degeneration. Am J Ophthalmol. 1992;113(3):257-262 5. Weber-Krause B, Eckardt U. [Incidence of posterior vitreous detachment in eyes with and without age-related macular degeneration. An ultrasonic study]. i 1996;93(6):660-665. 6. Ondes F, Yilmaz G, Acar MA, et al. Role of the vitreous in age-related macular degeneration. Jpn J Ophthalmol. 2000;44(1):91-93. 7. Krebs I, Brannath W, Glittenberg C, et al. Posterior vitreomacular adhesion: a potential risk factor for exudative age-related macular degeneration? Am J Ophthalmol. 2007;144(5):741-746. 8. Lee SJ, Lee CS, Koh HJ. Posterior vitreomacular adhesion and risk of exudative age-related macular degeneration: paired eye study. Am J Ophthalmol. 2009;147(4):621-626 e1. 9. Robison CD, Krebs I, Binder S, et al. Vitreomacular adhesion in active and end-stage age-related macular degeneration. Am J Ophthalmol .2009;148(1):79-82. 10. Wheatley HM. Posterior vitreomacular adhesion and exudative age-related macular degeneration. Am J Ophthalmol. 2008;145(4):765; author reply -6. 11. Schmidt JC, Mennel S, Meyer CH, Kroll P. Posterior vitreomacular adhesion: a potential risk factor for exudative age-related macular degeneration. Am J Ophthalmol. 2008;145(6):1107; author reply -8. 12. Mojana F, Cheng L, Bartsch DU, et al. The role of abnormal vitreomacular adhesion in age-related macular degeneration: spectral optical coherence tomography and surgical results. Am J Ophthalmol. 2008;146(2):218-227. 13. Doft BH, Wisniewski SR, Kelsey SF, Groer-Fitzgerald S; Endophthalmitis Vitrectomy Study Group. Diabetes and postcataract extraction endophthalmitis. Curr Opin Ophthalmol. 2002;13(3):147-151. 14. Doft BM, Kelsey SF, Wisniewski SR. Retinal detachment in the endophthalmitis vitrectomy study. Arch Ophthalmol. 2000;118(12):1661-1665. 15. Wisniewski SR, Capone A, Kelsey SF, et al. Characteristics after cataract extraction or secondary lens implantation among patients screened for the Endophthalmitis Vitrectomy Study. Ophthalmology. 2000;107(7):1274-1282. 16. Gupta OP, Weichel ED, Regillo CD, et al. Postoperative complications associated with 25-gauge pars plana vitrectomy. Ophthalmic Surg Lasers Imaging. 2007;38(4):270–275. 17. Liu DT, Chan CK, Fan DS, Lam SW, Lam DS, Chan WM. Choroidal folds after 25 gauge transconjunctival sutureless vitrectomy. Eye. 2005;19(7):825–827. 18. Scott IU, Flynn HW Jr, Dev S, et al. Endophthalmitis after 25-gauge and 20-gauge pars plana vitrectomy: incidence and outcomes. Retina. 2008;28(1):138–142. 19. Kunimoto DY, Kaiser RS; Wills Eye Retina Service. Incidence of endophthalmitis after 20- and 25-gauge vitrectomy. Ophthalmology. 2007;114(12):2133–2137. 20. Kaiser RS. Complications of sutureless vitrectomy and the findings of the Micro-Surgical Safety Task Force. Paper presented at: Retina Subspecialty Day, Annual Meeting of the American Academy of Ophthalmology; November 7-8, 2008; Atlanta, GA. 21. de Smet MD, Gandorfer A, Stalmans P, et al. Microplasmin intravitreal administration in patients with vitreomacular traction scheduled for vitrectomy: the MIVI I trial. Ophthalmology. 2009;116(7):1349-1355. 22. Goldenberg DT, Trese MT. Pharmacologic vitreodynamics and molecular flux. Dev Ophthalmol. 2009;44:31-36. 23. Stalmans P, Benz MS, Gandorfer A, et al; MIVI-TRUST Study Group. Enzymatic vitreolysis with ocriplasmin for vitreomacular traction and macular holes. N Engl J Med. 2012;367(7):606-615.
Carl D. Regillo, MD, is the Director of the Retina Service of Wills Eye Institute and a Professor of Ophthalmology at Thomas Jefferson University in Philadelphia. He is a member of the Retina Today Editorial Board. He may be reached at email@example.com.
Peter K. Kaiser, MD, is a Professor of Ophthalmology at the Cleveland Clinic Lerner College of Medicine and a staff surgeon in the Vitreoretinal Department at the Cole Eye Institute, Cleveland Clinic. He is a Retina Today Editorial Board member. Dr. Kaiser may be reached at firstname.lastname@example.org.
Faculty/Staff Disclosure Declarations Dr. Regillo states that he receives grant research support from Alimera, Allergan, Genentech, Glaxo Smith Kline, Ophthotech, Regeneron, ThromboGenics, Advanced Cell Technology, Johnson and Johnson, QLT, and Alcon Laboratories, Inc. He is a consultant and speaker for Alimera, Alcon, Genentech, GlaxoSmithKline, and Regeneron. Dr. Kaiser states that he has received research funding from Acucela, Alimera, Allergan, National Institutes of Health, Novartis, LPath, Research to Prevent Blindness, National Eye Institute, Genentech, Pfizer, Potentia, and Regeneron. He is a consultant to Alcon, Alimera, Allegro Ophthalmics, Arctic Dx, Bausch + Lomb, Bayer, Carl Zeiss Meditec, Genentech, GlaxoSmithKline, InSitu Therapeutics, Kanghong Biotech, LPath, Novartis, Ophthotec, Oraya, and Regeneron. All of those involved in the planning, editing, and peer review of this educational activity report no financial relationships.
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