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Glaucoma 2016 Innovations in Glaucoma Care— Evolution and Revolution Under Pressure® Program Directors Joel S Schuman MD and Jody R Piltz-Seymour MD In conjunction with the American Glaucoma Society McCormick Place Chicago, Illinois Saturday, Oct. 15, 2016 Presented by: The American Academy of Ophthalmology Supported in part by an unrestricted educational grant from Aerie Pharmaceuticals 2016 Glaucoma Planning Group Joel S Schuman MD Program Director 2009 Jody R Piltz-Seymour MD Program Director 2008 Meenakshi Chaku MD Andrew CS Crichton MD FRCS David S Greenfield MD Gregg A Heatley MD Shan C Lin MD Nils A Loewen MD PhD Cynthia Mattox MD FACS Kelly W Muir MD Lucy Q Shen MD Arthur J Sit MS MD Former Program Directors 2015 James D Brandt MD Joel S Schuman MD 2014 David S Friedman MD MPH PhD James D Brandt MD 2013 Thomas W Samuelson MD David S Friedman MD MPH PhD 2012 Wallace L M Alward MD Thomas W Samuelson MD 2011 Leon W Herndon MD Wallace LM Alward MD 2010 2007 2006 2005 2004 2003 2002 2001 2000 1999 1998 1997 Rohit Varma MD MPH Leon W Herndon MD Donald L Budenz MD MPH Rohit Varma MD MPH Henry D Jampel MD MHS Donald L Budenz MD MPH Anne Louise Coleman MD PhD Henry D Jampel MD MHS Christopher A Girkin MD Anne Louise Coleman MD PhD Claude F Burgoyne MD Christopher A Girkin MD David S Greenfield MD Claude F Burgoyne MD Kuldev Singh MD MPH David S Greenfield MD Theodore Krupin MD Kuldev Singh MD MPH Robert D Fechtner MD Theodore Krupin MD Jeffrey M Liebmann MD Robert D Fechtner MD Robert N Weinreb MD Jeffrey M Liebmann MD George A Cioffi MD Robert N Weinreb MD Richard A Lewis MD George A Cioffi MD 1996 1995 1994 M Bruce Shields MD E Michael Van Buskirk MD Reay H Brown MD Mary Gerard Lynch MD Richard A Lewis MD Subspecialty Day Advisory Committee Daniel S Durrie MD Associate Secretary Julia A Haller MD Francis S Mah MD R Michael Siatkowski MD Kuldev Singh MD MPH Nicolas J Volpe MD Jonathan B Rubenstein MD Secretary for Annual Meeting Staff Ann L’Estrange, Scientific Meetings Specialist Melanie R Rafaty CMP DES, Director, Scientific Meetings Lisa Romero, Presenter Coordinator Debra Rosencrance CMP CAE, Vice President, Meetings & Exhibits Patricia Heinicke Jr, Copy Editor Mark Ong, Designer Gina Comaduran, Cover Design ©2016 American Academy of Ophthalmology. All rights reserved. No portion may be reproduced without express written consent of the American Academy of Ophthalmology. ii Planning Group 2016 Subspecialty Day | Glaucoma 2016 Glaucoma Subspecialty Day Planning Group On behalf of the American Academy of Ophthalmology and the American Glaucoma Society (AGS), it is our pleasure to welcome you to Chicago and Glaucoma 2016: Innovations in Glaucoma Care—Evolution and Revolution. Joel S Schuman MD Jody R Piltz-Seymour MD Aerie Pharmaceuticals Inc.: C,S Alcon Laboratories Inc.: C Carl Zeiss Meditec: P DSM Inc.: C Glaukos Corporation: C,S Ocugenix: O,P Opticient: C Pfizer Inc.: C,L SLACK Incorporated: C Aerie Pharaceuticals: S Alcon Laboratories Inc.: L Allergan: C Forsight: C Program Director Program Director No photo available Meenakshi Chaku MD Andrew Crichton MD FRCS David S Greenfield MD None Alcon Laboratories Inc.: C,L Allergan: C,L Aerie: C Alcon Laboratories Inc.: C Allergan: C Bausch+Lomb: C Biometric Imaging: C Glaukos Corporation: C Quark: C Planning Group 2016 Subspecialty Day | Glaucoma Gregg A Heatley MD Cynthia Mattox MD FACS Arthur J Sit MS MD None Aerie: C Alcon Laboratories Inc.: C Alimera Sciences Inc.: L Allergan: C,S National Eye Institute: S Ocular Therapeutix: C Transcend: S Aerie Pharmaceuticals Inc.: S Allergan: C Glaukos Corporation: S Shan C Lin MD Allergan: C Iridex: C Kelly Walton Muir MD None Lucy Q Shen MD L.E.K. Consulting: C Nils A Loewen MD PhD NeoMedix Corporation: L iii iv Planning Group 2016 Subspecialty Day Advisory Committee Daniel S Durrie MD, Chair (Refractive Surgery) Abbott Medical Optics: L,S AcuFocus Inc.: C,L,O,S Alcon Laboratories Inc.: S Allergan: S | Alphaeon: C,L,O Avedro: L,O,S Hoopes Durrie Rivera Research Center: C Strathspey Crown LLC: C,L,O Wavetec: O Julia A Haller MD (Retina) Celgene: O | Janssen: C KalVista: C | Merck & Co. Inc.: C ThromboGenics Inc.: S Francis S Mah MD (Cornea) Abbott Medical Optics Inc.: S,L,C Aerie: C Alcon Laboratories Inc.: L,S,C Allergan: S,L,C Bausch+Lomb: C,L CoDa: C | ForeSight: C NovaBay: C | Ocular Science: O,C Ocular Therapeutix: C,S PolyActiva: C | Shire: C Slack Publishing: C Sun Pharma: C Sydnexis: C | TearLab: C 2016 Subspecialty Day | Glaucoma R Michael Siatkowski MD (Pediatric Ophthalmology) National Eye Institute: S Kuldev Singh MD MPH (Glaucoma) Abbott Medical Optics Inc.: C Aerie: C Alcon Laboratories Inc.: C Allergan: C Carl Zeiss Meditec: C ForSight Vision 5: C InnFocus: C | Ivantis: C Mynosys: C National Eye Institute: S National Space Biomedical Research Institute: C Santen Inc.: C | Shire: C Thieme Medical Publishers: C Transcend: C U.S. Food and Drug Administration: C Nicholas J Volpe MD (Neuro-Ophthalmology) Opticent Inc.: O AAO Staff Ann L’Estrange None Melanie Rafaty None Lisa Romero None Debra Rosencrance None Beth Wilson None 2016 Subspecialty Day | Glaucoma Glaucoma 2016 Contents Planning Group ii CME vi The American Glaucoma Society Subspecialty Day Lecturer viii Faculty Listing ix How to Ask a Question Using the Mobile Meeting Guide xvi Program Schedule xvii Section I: Is It Progression? Is It Glaucoma? 1 Section II: Controversies 17 Advocating for Patients 28 Section III: Glaucoma—It’s Not Just About IOP 30 The American Glaucoma Society (AGS) Subspecialty Day Lecture: Primary Open-Angle Glaucoma Redefined 41 Section IV: The “New Patient” in Your Clinic—Treatment Options 42 Section V: Past, Present, and Future of Surgical Techniques 49 Section VI: The Intersection of Glaucoma and Retina 56 Section VII: Video Surgical Nightmares 60 Faculty Financial Disclosure 65 Presenter Index 69 Contents v vi CME Credit 2016 Subspecialty Day | Glaucoma CME Credit Academy’s CME Mission Statement The purpose of the American Academy of Ophthalmology’s Continuing Medical Education (CME) program is to present ophthalmologists with the highest quality lifelong learning opportunities that promote improvement and change in physician practices, performance, or competence, thus enabling such physicians to maintain or improve the competence and professional performance needed to provide the best possible eye care for their patients. 2016 Glaucoma Subspecialty Day Meeting Learning Objectives Upon completion of this activity, participants should be able to: ■ ■ ■ ■ ■ Describe innovations in the diagnosis and management of glaucoma within their historical context Manage complex cases of glaucoma when other eye diseases are present Evaluate the current status of optic disc and retinal nerve fiber layer imaging and its role in diagnosing and managing glaucoma Demonstrate familiarity with current issues in medical and surgical therapy for glaucoma, both open-angle and angle-closure variants Identify and manage glaucoma surgical complications 2016 Glaucoma Subspecialty Day Meeting Target Audience This activity has been designed to meet the educational needs of general ophthalmologists, glaucoma specialists and other ophthalmologic subspecialists, and allied health personnel who are involved in the management of glaucoma patients. 2016 Glaucoma Subspecialty Day CME Credit ments is available at http://abop.org/maintain-certification/ part-2-lifelong-learning-self-assessment/sacme/. NOTE: Credit designated as “self-assessment” is AMA PRA Category 1 Credit™ and is also preapproved by the ABO for the Maintenance of Certification (MOC) Part II CME requirements. Teaching at a Live Activity Teaching instruction courses or delivering a scientific paper or poster is not an AMA PRA Category 1 Credit™ activity and should not be included when calculating your total AMA PRA Category 1 Credits™. Presenters may claim AMA PRA Category 1 Credits™ through the American Medical Association. To obtain an application form please contact the AMA at www.ama-assn.org. Scientific Integrity and Disclosure of Financial Interest The American Academy of Ophthalmology is committed to ensuring that all CME information is based on the application of research findings and the implementation of evidence-based medicine. It seeks to promote balance, objectivity, and absence of commercial bias in its content. All persons in a position to control the content of this activity must disclose any and all financial interests. The Academy has mechanisms in place to resolve all conflicts of interest prior to an educational activity being delivered to the learners. The Academy requires all presenters to disclose on their first slide whether they have any financial interests from the past 12 months. Presenters are required to verbally disclose any financial interests that specifically pertain to their presentation. Control of Content The American Academy of Ophthalmology is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. The American Academy of Ophthalmology designates this live activity for a maximum of 7 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity. The Academy considers presenting authors, not co-authors, to be in control of the educational content. It is Academy policy and traditional scientific publishing and professional courtesy to acknowledge all people contributing to the research, regardless of CME control of the live presentation of that content. This acknowledgement is made in a similar way in other Academy CME activities. Though they are acknowledged, co-authors do not have control of the CME content and their disclosures are not published or resolved. Self-Assessment Credit Attendance Verification for CME Reporting This activity meets the Self-Assessment CME requirements defined by the American Board of Ophthalmology (ABO). Please be advised that the ABO is not an accrediting body for purposes of any CME program. The ABO does not sponsor this or any outside activity, and the ABO does not endorse any particular CME activity. Complete information regarding the ABO Self-Assessment CME Maintenance of Certification require- Before processing your requests for CME credit, the Academy must verify your attendance at Subspecialty Day and/or AAO 2016. In order to be verified for CME or auditing purposes, you must either: ■ Register in advance, receive materials in the mail, and turn in the Subspecialty Day Syllabi exchange voucher(s) onsite; CME Credit 2016 Subspecialty Day | Glaucoma ■ ■ ■ Register in advance and pick up your badge onsite if materials did not arrive before you traveled to the meeting; Register onsite; or Scan the barcode on your badge as you enter an AAO 2016 course or session room. CME Credit Reporting Academy Resource Center, Booth 508 and South Level 2.5 Attendees whose attendance has been verified (see above) at AAO 2016 can claim their CME credit online during the meeting. Registrants will receive an email during the meeting with the link and instructions on how to claim credit. Onsite, you may report credits earned during Subspecialty Day and/or AAO 2016 at the CME Credit Reporting booth. Academy Members: The CME credit reporting receipt is not a CME transcript. CME transcripts that include AAO 2016 credits entered onsite will be available to Academy members on the Academy’s website beginning Nov. 10, 2016. After AAO 2016, credits can be claimed at www.aao.org/ cme. vii The Academy transcript cannot list individual course attendance. It will list only the overall credits spent in educational activities at Subspecialty Day and/or AAO 2016. Nonmembers: The Academy will provide nonmembers with verification of credits earned and reported for a single Academy-sponsored CME activity. Proof of Attendance The following types of attendance verification will be available during AAO 2016 and Subspecialty Day for those who need it for reimbursement or hospital privileges, or for nonmembers who need it to report CME credit: ■ ■ ■ CME credit reporting/proof-of-attendance letters Onsite registration receipt Instruction course and session verification Visit www.aao.org/cme for detailed CME reporting information. viii AGS Subspecialty Day Lecture 2016 Subspecialty Day | Glaucoma The American Glaucoma Society (AGS) Subspecialty Day Lecture Primary Open-Angle Glaucoma Redefined Saturday, Oct. 15, 2016 11:45 AM – 12:15 PM Louis R Pasquale MD FARVO Louis R Pasquale MD is professor of ophthalmology and Distinguished Scholar in Ophthalmology at Harvard Medical School. In addition to directing the Glaucoma Service at Massachusetts Eye and Ear Infirmary (MEEI), he directs the Glaucoma Fellowship Program and the MEEI Teleretinal Program and codirects Harvard’s Glaucoma Center of Excellence. Dr. Pasquale received his medical degree with distinction in research from the State University of New York, Stony Brook. He completed an internal medicine internship at Bronx Municipal Hospital affiliated with the Albert Einstein School of Medicine. After completing an ophthalmology residency at Temple University School of Medicine, he completed a 2-year glaucoma fellowship at the Wilmer Ophthalmological Institute. Dr. Pasquale is a member of the editorial boards for PLoS One and American Journal of Ophthalmology. He currently serves as chair of the American Glaucoma Society Research Committee and was chair of the Glaucoma Section, ARVO Meeting Program Committee for 2016. He currently serves on the National Eye Institute Advisory Council. Dr. Pasquale was awarded the 2006 American Academy of Ophthalmology Achievement Award and the 2009 Physician Scientist Award by Research to Prevent Blindness. Dr. Pasquale has received numerous awards for scientific achievement, including Sigma Xi from Manhattan College and a Distinguished Research Award when he was an ophthalmology resident at Temple University Hospital. He was recognized as an Irving H Leopold honoree, and he received a Physician Scientist Award from Research to Prevent Blindness in 2009. He is recognized for his dedication to teaching, having been nominated twice by Harvard Medical School for excellence in mentoring and once by the Harvard ophthalmology residents for Outstanding Teaching. He was acknowledged for service to ARVO and the Academy with a Silver Fellow award and Secretariat Award, respectively. Dr. Pasquale has dedicated himself to serving as a physician scientist who seeks opportunities to translate basic science discoveries into better treatments for glaucoma patients. He is an NIH Principal Investigator, with continuous support since 2006. His research, which leverages the rich resources available in the Nurses’ Health Study, the Health Professional Follow-up Study, and the Women’s Genome Health Study, focuses on the discovery of primary prevention strategies in the open-angle glaucomas. He has published over 160 peer-reviewed articles in scientific journals and 68 reviews / book chapters / editorials. He has delivered numerous named lectures and has given many talks and courses around the world. Faculty Listing 2016 Subspecialty Day | Glaucoma Faculty Iqbal K Ahmed MD Claude F Burgoyne MD Robert T Chang MD Mississauga, ON, Canada Assistant Professor University of Toronto Clinical Professor, University of Utah Portland, OR Senior Scientist and Director Optic Nerve Head Research Laboratory Devers Eye Institute Clinical Professor of Ophthalmology Oregon Health Sciences University Palo Alto, CA Assistant Professor Byers Eye Institute at Stanford University No photo available R Rand Allingham MD Durham, NC Professor of Ophthalmology Duke University Eye Center Professor and Senior Consultant Duke – National University of Singapore Balwantray C Chauhan PhD Joseph Caprioli MD FACS Los Angeles, CA Professor of Ophthalmology David Geffen School of Medicine University of California, Los Angeles Chief, Glaucoma Division Jules Stein Eye Institute Halifax, NS, Canada Professor and Research Director Department of Ophthalmology and Visual Sciences No photo available Vikas Chopra MD Husam Ansari MD PhD Needham, MA Glaucoma Service Ophthalmic Consultants of Boston Meenakshi Chaku MD Chicago, IL Director, Glaucoma Service Assistant Professor of Ophthalmology Loyola University, Chicago Santa Monica, CA Associate Clinical Professor David Geffen School of Medicine at UCLA Medical Director – Pasadena Doheny Eye Centers UCLA ix x Faculty Listing 2016 Subspecialty Day | Glaucoma E Randy Craven MD JoAnn A Giaconi MD David S Greenfield MD Baltimore, MD Chief of Glaucoma King Khaled Eye Specialist Hospital, Saudi Arabia Associate Professor Wilmer Eye Institute Johns Hopkins University Los Angeles, CA Health Sciences Associate Professor of Ophthalmology Jules Stein Eye Institute University of California, Los Angeles Chief of Ophthalmology Veterans Administration of Greater Los Angeles Palm Beach Gardens, FL Professor of Ophthalmology Bascom Palmer Eye Institute University of Miami Miller School of Medicine Michael Greenwood MD Andrew Crichton MD Calgary, AB, Canada Clinical Professor University of Calgary Christopher A Girkin MD Birmingham, AL Chairman and Professor Department of Ophthalmology University of Alabama at Birmingham School of Medicine Chief Medical Officer Callahan Eye Hospital Fargo, ND Cataract, Refractive, Glaucoma, Cornea Surgeon Vance Thompson Vision No photo available Alon Harris PhD Nancy L Flattem MD MS Colorado Springs, CO Ophthalmologist / Glaucoma Specialist Colorado Permanente Medical Group Jeffrey L Goldberg MD PhD Palo Alto, CA Professor and Chair Byers Eye Institute Stanford University Indianapolis, IN Letzter Endowed Professor of Ophthalmology Indiana University School of Medicine Professor of Cellular & Integrative Physiology Director of Clinical Research Indiana University School of Medicine Faculty Listing 2016 Subspecialty Day | Glaucoma xi Gregg A Heatley MD Malik Y Kahook MD Madison, WI Associate Professor of Ophthalmology Vice Chair, Clinical University of Wisconsin-Madison Denver, CO Professor of Ophthalmology University of Colorado School of Medicine Dale K Heuer MD L Jay Katz MD Richard A Lewis MD Milwaukee, WI Professor & Chair of Ophthalmology & Visual Sciences Medical College of Wisconsin Director, Froedtert & The Medical College of Wisconsin Eye Institute Philadelphia, PA Professor of Ophthalmology Thomas Jefferson University Director of Glaucoma Service Wills Eye Hospital Sacramento, CA Past President, American Glaucoma Society Past President, American Society of Cataract and Refractive Surgery Simon K Law MD Paul R Lichter MD Los Angeles, CA Professor, Stein Eye Institute Ann Arbor, MI Professor of Ophthalmology and Visual Sciences W K Kellogg Eye Center University of Michigan Chris A Johnson PhD Iowa City, IA Professor, Department of Ophthalmology and Visual Sciences University of Iowa Christopher Kai-shun Leung MD MBChB Ho Man Tin, Hong Kong Professor, The Chinese University of Hong Kong xii Faculty Listing 2016 Subspecialty Day | Glaucoma No photo available Shan C Lin MD Jeff S Maltzman MD Stuart J McKinnon MD PhD San Francisco, CA Professor of Clinical Ophthalmology University of California, San Francisco Director, Glaucoma Service San Francisco General Hospital Tucson, AZ Durham, NC Associate Professor of Ophthalmology and Neurobiology Duke University Medical Center Staff Ophthalmologist VA Medical Center Kaweh Mansouri MD Lausanne, Switzerland Yao Liu MD Felipe A Medeiros MD Madison, WI Assistant Professor of Ophthalmology University of Wisconsin School of Medicine and Public Health San Diego, CA Professor of Ophthalmology University of California, San Diego Cynthia Mattox MD FACS Nils A Loewen MD Pittsburgh, PA Associate Professor of Ophthalmology University of Pittsburgh Director, Glaucoma and Cataract Service University of Pittsburgh Medical Center Boston, MA Associate Professor of Ophthalmology Tufts University School of Medicine Director, Glaucoma and Cataract Service New England Eye Center No photo available M Lisa McHam MD Quincy, MA Partner, Eye Health Services No photo available Daniel B Moore MD Lexington, KY Assistant Professor Department of Ophthalmology and Visual Sciences University of Kentucky Faculty Listing 2016 Subspecialty Day | Glaucoma xiii Marlene R Moster MD Kouros Nouri-Mahdavi MD Louis R Pasquale MD Bala Cynwyd, PA Professor of Ophthalmology Thomas Jefferson University School of Medicine Attending Surgeon Glaucoma Service Wills Eye Hospital Los Angeles, CA Associate Professor of Ophthalmology Stein Eye Institute University of California, Los Angeles Boston, MA Professor of Ophthalmology Harvard Medical School Director, Glaucoma Service Massachusetts Eye and Ear Infirmary Mildred M G Olivier MD Jody R Piltz-Seymour MD Charlottesville, VA Vernah Scott Moyston Professor and Chair University of Virginia School of Medicine Hoffman Estates, IL Professor of Surgery Department of Ophthalmology Rosalind Franklin University of Medicine and Science at Chicago Medical School Associate Professor of Ophthalmology Midwestern University Robert J Noecker MD Richard K Parrish II MD Harry A Quigley MD Fairfield, CT Director of Glaucoma Ophthalmic Consultants of Connecticut Assistant Clinical Professor of Ophthalmology Yale School of Medicine Miami, FL Professor and Director, Glaucoma Service Bascom Palmer Eye Institute University of Miami Miller School of Medicine Associate Dean for Graduate Medical Education University of Miami Miller School of Medicine, Jackson Health System Baltimore, MD A Edward Maumenee Professor of Ophthalmology Glaucoma Center of Excellence Wilmer Eye Institute Johns Hopkins University Peter Andreas Netland MD PhD Huntingdon Valley, PA Clinical Professor of Ophthalmology Perelman School of Medicine University of Pennsylvania Glaucoma Specialist Valley Eye Professionals and Wills Eye Hospital xiv Faculty Listing 2016 Subspecialty Day | Glaucoma Douglas J Rhee MD Adrienne Williams Scott MD Kuldev Singh MD MPH Cleveland, OH Professor & Chair Case Western Reserve University School of Medicine Director, University Hospitals Eye Institute Baltimore, MD Assistant Professor of Ophthalmology Wilmer Eye Institute Johns Hopkins University School of Medicine Palo Alto, CA Professor of Ophthalmology Stanford University Director, Glaucoma Service Stanford University Shakeel R Shareef MD Arthur J Sit MD Rochester, NY Associate Professor Flame Eye Institute University of Rochester School of Medicine Rochester, MN Associate Professor of Ophthalmology Mayo Clinic College of Medicine Consultant, Mayo Clinic, Rochester Thomas W Samuelson MD Minneapolis, MN Consultant, Glaucoma and Anterior Segment Surgery Minnesota Eye Consultants Adjunct Associate Professor of Ophthalmology University of Minnesota Lucy Q Shen MD Joel S Schuman MD New York, NY Professor and Chairman of Ophthalmology NYU Langone Medical Center NYU School of Medicine Boston, MA Assistant Professor of Ophthalmology Harvard Medical School Massachusetts Eye and Ear Infirmary George L Spaeth MD FACS Philadelphia, PA Esposito Research Professor of Ophthalmology Wills Eye Hospital / Jefferson Medical College Faculty Listing 2016 Subspecialty Day | Glaucoma Tak Yee Tania Tai MD Steven D Vold MD Joanne C Wen MD New York, NY Assistant Professor of Ophthalmology Icahn School of Medicine of Mt. Sinai Adjunct Attending New York Eye and Ear Infirmary Fayetteville, AR Cataract & Glaucoma Surgery Consultant Vold Vision, PLLC Seattle, WA Assistant Professor University of Washington Clement C Y Tham FRCS MBBS FCOPHTHHK Kowloon, Hong Kong Professor, The Chinese University of Hong Kong Honorary Chief of Service Hong Kong Eye Hospital Kelly Walton Muir MD Durham, NC Associate Professor of Ophthalmology Duke Eye Center Career Development Awardee VA Health Services Research and Development xv xvi Mobile Meeting Guide Ask a Question Live During the Meeting Using the Mobile Meeting Guide To ask a question during the meeting, follow the directions below. Access at www.aao.org/mobile ■ Search Educational Sessions ■ Select Program Search ■ Filter by Meeting – Glaucoma Meeting ■ Select Current Session ■ Select “Ask the presenter a question (live)” Link ■ Click Submit Question ■ 2016 Subspecialty Day | Glaucoma Program Schedule 2016 Subspecialty Day | Glaucoma xvii Glaucoma Subspecialty Day 2016: Innovations in Glaucoma Care—Evolution and Revolution In conjunction with the American Glaucoma Society SATURDAY, OCT. 15 7:00 AM CONTINENTAL BREAKFAST 8:00 AM Welcome and Introductions Joel S Schuman MD* 8:02 AM American Glaucoma Society Introduction David S Greenfield MD* 8:04 AM Announcements Jody R Piltz-Seymour MD* Section I: Is It Progression? Is It Glaucoma? Moderators: Shan C Lin MD* and Christopher Kai-shun Leung MD MBChB* Virtual Moderator: Cynthia Mattox MD FACS* 8:06 AM Introduction Shan C Lin MD* 8:07 AM Case Presentation #1: OCT Changes in a Glaucoma Suspect With a Normal Visual Field Shan C Lin MD* 1 8:10 AM Audience Response 8:11 AM What Do These OCT Changes Mean? Balwantray C Chauhan PhD* 4 8:18 AM Point – Counterpoint: Do You Make Treatment Decisions on OCT Changes Alone? Yes, I Do! Felipe A Medeiros MD* 6 8:22 AM Point – Counterpoint: Do You Make Treatment Decisions on OCT Changes Alone? No, I Don’t! Kuldev Singh MD MPH* 8 8:26 AM Rebuttal Felipe A Medeiros MD* 8:27 AM Rebuttal Kuldev Singh MD MPH* 8:28 AM Audience Response 8:29 AM Case Presentation #2: Mild Progression of Visual Field Loss in Patient With Primary Open-Angle Glaucoma 8:32 AM Audience Response 8:33 AM How to Best Assess Visual Field Progression Chris A Johnson PhD* 10 8:40 AM Point – Counterpoint: Do You Advance Treatment Whenever There Is Visual Field Progression? Yes, I Do! Kouros Nouri-Mahdavi MD* 12 8:44 AM Point – Counterpoint: Do You Advance Treatment Whenever There Is Visual Field Progression? No, I Don’t! Harry A Quigley MD* 13 8:48 AM Rebuttal Kouros Nouri-Mahdavi MD* 8:49 AM Rebuttal Harry A Quigley MD* 8:50 AM Audience Response 8:51 AM It’s Not Always Glaucoma: Visual Field Loss due to Neurological Causes Christopher A Girkin MD 8:56 AM New and Future Technologies: mERG, mfVEP, Ganglion Cell Markers Stuart J McKinnon MD PhD* 15 9:01 AM Discussion * Indicates that the presenter has financial interest. No asterisk indicates that the presenter has no financial interest. Christopher Kai-shun Leung MD MBChB* 9 14 xviii Program Schedule 2016 Subspecialty Day | Glaucoma Section II: Controversies Moderators: Meenakshi Chaku MD and Nils A Loewen MD* 9:05 AM Controversy #1: Should Surgery Be Performed in Both Eyes at the Same Time? Pro Nancy L Flattem MD MS 17 9:10 AM Controversy #1: Should Surgery Be Performed in Both Eyes at the Same Time? Con M Lisa McHam MD 18 9:15 AM Rebuttal Nancy L Flattem MD MS 9:16 AM Rebuttal M Lisa McHam MD 9:17 AM Audience Vote 9:18 AM Discussion 9:22 AM Controversy #2: Glaucoma Surgery in the Elderly— Are We Preserving Quality of Life? Pro Steven D Vold MD* 19 9:27 AM Controversy #2: Glaucoma Surgery in the Elderly— Are We Preserving Quality of Life? Con George L Spaeth MD FACS 21 9:32 AM Rebuttal Steven D Vold MD* 9:33 AM Rebuttal George L Spaeth MD FACS 9:34 AM Audience Vote 9:35 AM Discussion 9:39 AM Controversy #3: Should We Adopt New Surgical Techniques Early On? Pro 9:44 AM Controversy #3: Should We Adopt New Surgical Techniques Early On? Con Paul R Lichter MD 9:49 AM Rebuttal Thomas W Samuelson MD* 9:50 AM Rebuttal Paul R Lichter MD 9:51 AM Audience Vote 9:52 AM Discussion 9:56 AM Controversy #4: Combining Glaucoma Surgeries— Does It Add Benefit? Pro Richard A Lewis MD* 26 10:01 AM Controversy #4: Combining Glaucoma Surgeries— Does It Add Benefit? Con Richard K Parrish II MD* 27 10:06 AM Rebuttal Richard A Lewis MD* 10:07 AM Rebuttal Richard K Parrish II MD* 10:08 AM Audience Vote 10:09 AM Discussion 10:13 AM Advocating for Patients 10:18 AM REFRESHMENT BREAK and AAO 2016 EXHIBITS Thomas W Samuelson MD* Jeff S Maltzman MD 22 25 28 Section III: Glaucoma—It’s Not Just About IOP Moderators: Arthur J Sit MD* and Kaweh Mansouri MD* 10:43 AM Introduction Arthur J Sit MD* 10:44 AM Case Presentation: Glaucomatous Visual Field and Optic Nerve Progression at “Low” IOP—What’s Going On? Arthur J Sit MD* 30 10:46 AM Is IOP Fluctuation Important? Joseph Caprioli MD FACS* 31 10:53 AM Does Ocular Biomechanics Define Tissue Damage? Claude F Burgoyne MD* 33 * Indicates that the presenter has financial interest. No asterisk indicates that the presenter has no financial interest. 2016 Subspecialty Day | Glaucoma Program Schedule xix 11:00 AM How Does Ocular Blood Flow Influence the Course of Glaucoma? Alon Harris PhD* 35 11:07 AM CSF Pressure: Is It an Important Part of Glaucoma? R Rand Allingham MD* 37 11:14 AM Novel Treatment Options for IOP: Independent Factors Cynthia Mattox MD FACS* 39 11:21 AM Innovations in Neuroprotection Jeffrey L Goldberg MD PhD* 40 11:28 AM Discussion The American Glaucoma Society Subspecialty Day Lecture 11:43 AM Introduction of the Lecturer David S Greenfield MD* 11:45 AM Primary Open-Angle Glaucoma Redefined Louis R Pasquale MD* 12:15 PM Presentation of the Award David S Greenfield MD* 12:16 PM LUNCH and AAO 2016 EXHIBITS 41 Section IV: The “New Patient” in Your Clinic—Treatment Options Moderators: Lucy Q Shen MD* and Simon K Law MD 1:30 PM Case #1: Appositional Angle Closure After Laser Peripheral Iridotomy 1:35 PM Audience Vote 1:36 PM Panel Discussion 1:42 PM Case #2: High IOP in Microphthalmia 1:47 PM Audience Vote 1:48 PM Panel Discussion 1:54 PM Case #3: Pseudopigmentary Glaucoma From One-Piece IOL 1:59 PM Audience Vote 2:00 PM Panel Discussion 2:06 PM Case #4: Pseudoexfoliation With Subluxed Lens and High IOP 2:11 PM Audience Vote 2:12 PM Panel Discussion 2:18 PM Case #5: Cataract and Glaucoma in a Myope 2:23 PM Audience Vote 2:24 PM Panel Discussion Clement C Y Tham FRCS MBBS FCOphthHK* 42 Vikas Chopra MD* 44 Douglas J Rhee MD* 46 Mildred M G Olivier MD* 47 Tak Yee Tania Tai MD 48 Section V: Past, Present, and Future of Surgical Techniques Moderators: Andrew Crichton MD* and L Jay Katz MD* 2:30 PM Evolution of Filtration Surgery Robert J Noecker MD* 49 2:37 PM Evolution of Tubes Peter Andreas Netland MD PhD* 50 2:44 PM Evolution of CPC Marlene R Moster MD* 52 2:51 PM Evolution of MIGS Iqbal K Ahmed MD* 54 2:58 PM Graveyard of Innovation E Randy Craven MD* 55 3:05 PM Discussion 3:15 PM REFRESHMENT BREAK and AAO 2016 EXHIBITS * Indicates that the presenter has financial interest. No asterisk indicates that the presenter has no financial interest. xx Program Schedule 2016 Subspecialty Day | Glaucoma Section VI: The Intersection of Glaucoma and Retina Moderators: Gregg A Heatley MD and Kelly Walton Muir MD Panelists: Robert T Chang MD*, Malik Y Kahook MD*, Daniel B Moore MD, Adrienne Williams Scott MD*, Joanne C Wen MD 3:45 PM Case #1: Anti-VEGF Agents and Glaucoma 3:48 PM Panel Discussion 3:53 PM Evidence Presentation Malik Y Kahook MD* 3:58 PM Case Follow-up Malik Y Kahook MD* 4:00 PM Case #2: Diagnostic and Therapeutic Challenges in High Myopia Robert T Chang MD* 4:03 PM Panel Discussion 4:08 PM Evidence Presentation Robert T Chang MD* 4:13 PM Case Follow-up Robert T Chang MD* 4:15 PM Case #3: Managing Neovascular Glaucoma Daniel B Moore MD 4:18 PM Panel Discussion 4:23 PM Evidence Presentation Daniel B Moore MD 4:28 PM Case Follow-up Daniel B Moore MD 4:30 PM Case #4: High IOP After Retina Surgery Joanne C Wen MD 4:33 PM Panel Discussion 4:38 PM Evidence Presentation Joanne C Wen MD 4:43 PM Case Follow-up Joanne C Wen MD Malik Y Kahook MD* 56 57 58 59 Section VII: Video Surgical Nightmares Moderators: Dale K Heuer MD* and JoAnn A Giaconi MD 4:45 PM The Fighting Iris or the Battle of the Bulge Husam Ansari MD PhD* 60 4:51 PM The Hyphemia That Keeps on Giving JoAnn A Giaconi MD 61 4:57 PM “I See Red” Michael Greenwood MD* 62 5:03 PM Training for Angle Surgery: No Good Deed Goes Unpunished Shakeel R Shareef MD 63 5:09 PM A Divining Rod for Angle Blood Yao Liu MD 64 5:15 PM Closing Remarks Joel S Schuman MD* * Indicates that the presenter has financial interest. No asterisk indicates that the presenter has no financial interest. Section I: Is It Progression? Is It Glaucoma? 2016 Subspecialty Day | Glaucoma Case Presentation #1: OCT Changes in a Glaucoma Suspect With a Normal Visual Field Shan Lin MD Clinical Data ■ ■ ■ ■ 43-year-old white male physician at UC, San Francisco CC: treated by in past for glaucoma and then followed as suspect Family history: no glaucoma Medical history: otherwise healthy, normal BP, no DM, no sleep apnea, no migraines, no Raynaud’s Exam Data ■ ■ ■ ■ ■ VA with correction: 20/20 O.U. Manifest refraction: Plano O.U. IOP: mid-high teens O.U. Central corneal thickness: 611 μm O.D., 623 μm O.S. Gonio: Open to SS 360° O.U. Figure 1. Figure 2. 1 2 Section I: Is It Progression? Is It Glaucoma? 2016 Subspecialty Day | Glaucoma Figure 3. Figure 4. 2016 Subspecialty Day | Glaucoma Section I: Is It Progression? Is It Glaucoma? Figure 5. Figure 6. 3 4 Section I: Is It Progression? Is It Glaucoma? 2016 Subspecialty Day | Glaucoma What Do These OCT Changes Mean? Balwantray C Chauhan PhD Introduction Optical coherence tomography (OCT) is transforming diagnostics and measurement of treatment efficacy in many areas in ophthalmology. In glaucoma, OCT is becoming the most common mode of imaging for evaluating the optic nerve head (ONH), retinal nerve fiber layer (RNFL), and macular thickness. Proving the Value of OCT As with any new technology in glaucoma, the most obvious question is whether it offers improvement over our currently accepted standards. This perennial question has posed a significant challenge in our field with the development of each new imaging or perimetric modality, as their merit is compared to the “accepted” standard of sound clinical observation of the optic disc and RNFL, or analysis of standard automated peri metry. When a new test has fewer positive results than the currently accepted standards, the test is deemed to be insensitive; when it yields more positive results, then it is either more sensitive or has more false-positive results. Investigators thus conduct longitudinal studies to determine whether changes found previously with the new techniques are predictive of changes that we accept today as clinical standards, assuming that the biological progressive “event” is the same in both cases. Unfortunately, proving the clinical value of changes observed with OCT requires numerous years of observation. This is because the relative infrequency of examinations carried out by most clinicians (1 or 2 per year) is probably statistically inadequate given that glaucoma usually develops and progresses slowly and that measurement noise represents a challenge. Ultimately, the value of OCT will be proven when clinical decisions made on the basis of OCT observations lead to improved outcomes, such as better visual preservation and quality of life. Several centers globally have made meaningful progress in these issues. Current Evidence That OCT Changes Are Clinically Meaningful Evidence that baseline measurements of RNFL thickness are predictive of visual field change emerged as early as 2002;1 however, it was recognized that the high false-positive rate with the older time domain–based instruments required better resolution. More recent evidence that spectral domain–based OCT devices are predictive of visual field loss has emerged from numerous groups.2-4 Of relevance to clinical outcomes, RNFL changes with OCT have been associated with a decreased quality of life.5 Importance of Changes due to Aging Most studies on rates of glaucomatous changes in the ONH, RNFL, and visual field do not contain parallel control subjects. Hence, the change observed in the patients is attributed to glaucoma alone. However, recent evidence shows that aging is an important contributor to the changes observed in glaucoma,6,7 with the pattern of topographical changes being similar. The ability to separate normal aging (which has significant interindividual variability) from glaucomatous change adds another layer of complexity to determining clinically meaningful progression. Other Signs From OCT Most of the evidence to date on the merit of OCT relates to changes in the RNFL. However, OCT also images the neuroretinal rim with anatomically accurate landmarks,8 the anterior laminar surface,9 choroid,10 and even sclera.11 It is plausible that changes in these structures, especially in the ONH, precede RNFL changes.12,13 Future research on the role of laminar changes, such as disinsertion or migration from the sclera, and changes in scleral shape or canal opening will provide clinicians with other markers of disease progression. References 1. Williams ZY, Schuman JS, Gamell L, et al. Optical coherence tomography measurement of nerve fiber layer thickness and the likelihood of a visual field defect. Am J Ophthalmol. 2002; 134:538-546. 2. Kuang TM, Zhang C, Zangwill LM, et al. Estimating lead time gained by optical coherence tomography in detecting glaucoma before development of visual field defects. Ophthalmology 2015; 122:2002-2009. 3. Miki A, Medeiros FA, Weinreb RN, et al. Rates of retinal nerve fiber layer thinning in glaucoma suspect eyes. Ophthalmology 2014; 121:1350-1358. 4. Zhang X, Loewen N, Tan O, et al. Predicting development of glaucomatous visual field conversion using baseline Fourierdomain optical coherence tomography. Am J Ophthalmol. 2016; 163:29-37. 5. Gracitelli CP, Abe RY, Tatham AJ, et al. Association between progressive retinal nerve fiber layer loss and longitudinal change in quality of life in glaucoma. JAMA Ophthalmol. 2015; 133:384390. 6. Leung CK, Ye C, Weinreb RN, et al. Impact of age-related change of retinal nerve fiber layer and macular thicknesses on evaluation of glaucoma progression. Ophthalmology 2013; 120:2485-2492. 7. Vianna JR, Danthurebandara VM, Sharpe GP, et al. Importance of normal aging in estimating the rate of glaucomatous neuroretinal rim and retinal nerve fiber layer loss. Ophthalmology 2015; 122:2392-2398. 8. Reis AS, O’Leary N, Yang H, et al. Influence of clinically invisible, but optical coherence tomography detected, optic disc margin anatomy on neuroretinal rim evaluation. Invest Ophthalmol Vis Sci. 2012; 53:1852-1860. 2016 Subspecialty Day | Glaucoma 9. Park SC, De Moraes CG, Teng CC, et al. Enhanced depth imaging optical coherence tomography of deep optic nerve complex structures in glaucoma. Ophthalmology 2012; 119:3-9. 10. Maul EA, Friedman DS, Chang DS, et al. Choroidal thickness measured by spectral domain optical coherence tomography: factors affecting thickness in glaucoma patients. Ophthalmology 2011; 118:1571-1579. 11. Lopilly Park HY, Lee NY, Choi JA, Park CK. Measurement of scleral thickness using swept-source optical coherence tomography in patients with open-angle glaucoma and myopia. Am J Ophthalmol. 2014; 157:876-884. 12. Fortune B, Reynaud J, Wang L, Burgoyne CF. Does optic nerve head surface topography change prior to loss of retinal nerve fiber layer thickness: a test of the site of injury hypothesis in experimental glaucoma. PLoS One 2013; 8:e77831. 13. He L, Yang H, Gardiner SK, et al. Longitudinal detection of optic nerve head changes by spectral domain optical coherence tomography in early experimental glaucoma. Invest Ophthalmol Vis Sci. 2014; 55:574-586. Section I: Is It Progression? Is It Glaucoma? 5 6 Section I: Is It Progression? Is It Glaucoma? 2016 Subspecialty Day | Glaucoma Point–Counterpoint: Do You Make Treatment Decisions on OCT Changes Alone? Yes, I Do! Felipe A Medeiros MD Glaucoma is a neurodegenerative disease caused by progressive retinal ganglion cell (RGC) loss associated with characteristic structural changes in the optic nerve and retinal nerve fiber layer. The neural insult can result in functional losses and decrease in vision-related quality of life. Detection of progression and estimation of rates of disease deterioration are essential in order to evaluate risk of functional impairment and establish treatment strategies. Even though standard automated perimetry (SAP) has been used as the gold standard for diagnosis and assessment of progression in glaucoma, there is substantial evidence indicating that many patients may show substantial structural changes despite absence of detectable or statistically significant changes on SAP.1-4 These structural changes may be detected by tests such as OCT assessment of the retinal nerve fiber layer (RNFL), macula, and optic disc. Contrary to long-standing teachings in glaucoma that prescribe that one should always search for a correlation between structural and functional losses when evaluating progression, evidence has shown that with currently available testing methods, agreement seems to be the exception rather than the rule. In most eyes, progressive structural changes are seen in the absence of visual field loss and vice versa. Therefore, requiring that functional changes must be present in order to confirm clinically significant structural findings is counterproductive. Even though the disagreement between structural and functional changes may seem puzzling, it can be easily understood when considering the properties of the tests available to measure structure and function, such as their different scales, variability, and dynamic range.5 If methods for assessing structural and functional progression were to agree perfectly, there would be no need to use both in monitoring progression. One test would suffice. Importantly, in order to justify decision making based on results of OCT only, these results need to be of demonstrable clinical relevance and predictive of outcomes that are clinically relevant for patients. It is crucial to demonstrate that progressive structural changes are actually predictive of outcomes that are clinically relevant for patients. Several studies have shown consistent data in this regard.6-8 OCT abnormalities have been identified up to 8 years before field loss in some patients.4 Using spectral domain OCT, rates of RNFL thinning were shown to be significantly faster in eyes that eventually developed a visual field defect compared to those that did not, with each 1-μm per year faster RNFL loss associated with a greater than 2 times higher risk of developing a future field defect. Measurement of progressive structural change has also been shown to be predictive of further visual field progression in eyes with established perimetric defects, at least in early to moderate disease. Progressive RNFL thinning has also been shown to be associated with quality of life outcomes in patients with glaucoma, as measured by the National Eye Institute Visual Function Questionnaire (NEI VFQ-25).9 Studies of the structure-function relationship in glaucoma have also attempted to identify when to use one vs. another test during the course of the disease. Imaging measurements seem to have most utility for detecting change in early stages of the disease, while perimetry seems to perform better when visual field losses are already present.5 The disagreement between the tests can be used to our advantage, by improving the chances of detecting progressive changes over time. However, the difficulty lies in how best to integrate their results without increasing the chance of false-positives. Several methods of combining structural and functional measurements have been proposed, including using sophisticated statistics10-12 and by a single combined structure function index.12 These combined measurements have been shown to outperform isolated measurements of structure and function for diagnosis and assessment of disease progression and are finding their way into clinical practice. References 1. Kass MA, Heuer DK, Higginbotham EJ, et al. The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002; 120:701713. 2. Medeiros FA, Alencar LM, Zangwill LM, et al. Prediction of functional loss in glaucoma from progressive optic disc damage. Arch Ophthalmol. 2009; 127:1250-1256. 3. Liu T, Tatham AJ, Gracitelli CP, Zangwill LM, Weinreb RN, Medeiros FA. Rates of retinal nerve fiber layer loss in contralateral eyes of glaucoma patients with unilateral progression by conventional methods. Ophthalmology 2015; 122:2243-2251. 4. Kuang TM, Zhang C, Zangwill LM, Weinreb RN, Medeiros FA. Estimating lead time gained by optical coherence tomography in detecting glaucoma before development of visual field defects. Ophthalmology 2015; 122(10):2002-2009. 5. Medeiros FA, Zangwill LM, Bowd C, et al. The structure and function relationship in glaucoma: implications for detection of progression and measurement of rates of change. Invest Ophthalmol Vis Sci. 2012; 53:6939-6946. 6. Medeiros FA, Lisboa R, Zangwill LM, et al. Evaluation of progressive neuroretinal rim loss as a surrogate end point for development of visual field loss in glaucoma. Ophthalmology 2014; 121:100-109. 7. Miki A, Medeiros FA, Weinreb RN, et al. Rates of retinal nerve fiber layer thinning in glaucoma suspect eyes. Ophthalmology 2014; 121:1350-1358. 8. Chauhan BC, Nicolela MT, Artes PH. Incidence and rates of visual field progression after longitudinally measured optic disc change in glaucoma. Ophthalmology 2009; 116:2110-2118. 9. Gracitelli CP, Abe RY, Tatham AJ, et al. Association between progressive retinal nerve fiber layer loss and longitudinal change in quality of life in glaucoma. JAMA Ophthalmol. 2015; 133:384390. 2016 Subspecialty Day | Glaucoma 10. Medeiros FA, Leite MT, Zangwill LM, Weinreb RN. Combining structural and functional measurements to improve detection of glaucoma progression using Bayesian hierarchical models. Invest Ophthalmol Vis Sci. 2011; 52:5794-5803. 11. Russell RA, Malik R, Chauhan BC, et al. Improved estimates of visual field progression using Bayesian linear regression to integrate structural information in patients with ocular hypertension. Invest Ophthalmol Vis Sci. 2012; 53:2760-2769. 12. Medeiros FA, Lisboa R, Weinreb RN, et al. A combined index of structure and function for staging glaucomatous damage. Arch Ophthalmol. 2012; 130:1107-1116. Section I: Is It Progression? Is It Glaucoma? 7 8 Section I: Is It Progression? Is It Glaucoma? 2016 Subspecialty Day | Glaucoma Point – Counterpoint: Do You Make Treatment Decisions on OCT Changes Alone? No, I Don’t! Kuldev Singh MD MPH The comments below represent an assigned position for the purpose of a debate. The goal of glaucoma management is to preserve vision. While there is often good correlation between structural and functional measures of optic nerve damage in glaucoma populations, there is tremendous interpatient variability with regard to such correlation using currently available tools to assess these parameters. While OCT is undoubtedly helpful in categorizing patients as having or not having glaucomatous disease, particularly in circumstances when visual field testing cannot be performed, the incremental benefit of such structural measures beyond visual field testing in determining when to begin or advance treatment for glaucoma has remained controversial. Some have advocated that OCT is most helpful in assessing ocular hypertensives and glaucoma suspects relative to those with moderate to severe glaucoma who already have reproducible visual field abnormalities. It is difficult to argue against the benefit of knowing that one has glaucoma sooner rather than later and OCT can help towards that end. Nevertheless, there are some potential pitfalls related to glaucoma therapy in patients with normal visual function as confirmed by modern automated perimetry. Not all patients with apparent structural optic nerve damage will go on to develop visual abnormalities and there is little evidence to suggest that waiting to see early mild visual field defects prior to starting or advancing therapy will generally result in greater lifetime glaucoma related visual disability than treating based solely on apparent structural progression. Despite the significant advances in assessing structural damage to the optic nerve over the past two decades, the diagnosis of glaucoma is not always clear cut, with many patients suspected of having the disease based on OCT testing not showing the natural history one would expect with such a diagnosis, even without treatment. The ever increasing resolution of imaging devices to compare structural optic nerve parameters of “glaucoma suspects” with age matched “normal” individuals has undoubtedly led to increased utilization of such devices, but the impact of these advances on the positive and negative predictive value of making definitive cross-sectional diagnoses of glaucomatous disease have been modest. Such increased resolution of imaging tools has created a clinical phenomenon where patients with average intraocular pressures, normal visual fields and normal appearing optic nerves as determined by ophthalmoscopy, who are found to have below average retinal nerve fiber layer thickness on imaging tests, may be told that they have glaucoma and prescribed IOP lowering treatment. The rate of false positives with OCT testing may be unacceptably high for us to solely use this technology to diagnose and treat glaucoma and glaucoma progression. Longitudinal assessment of the rate of structural optic nerve change remains critical in distinguishing between one patient who is classified as having glaucomatous disease from another who continues to be labeled a “glaucoma suspect.” The rapid advances in imaging technology, with less than optimal backward compatibility, have made it difficult to longitudinally assess structural change. Classifying a patient as having “glaucoma” and committing them to a lifetime of IOP lowering therapy, which may or may not be necessary or effective, should not be taken lightly in individuals who demonstrate no measurable visual abnormality from the disease. Similarly, advancing therapy in glaucoma patients who show changes in retinal nerve fiber layer thickness on OCT testing without measurable changes on perimetric measures of visual function can also be problematic, particularly given that it may be difficult to accurately distinguish structural progression related to aging versus disease. While the advent of OCT has undoubtedly improved our understanding of glaucomatous disease, an incremental benefit in terms of visual preservation beyond previously existing structural and functional parameters, including stereoscopic examination of the optic nerve and automated perimetry, has not been proven with this technology. Similarly, composite structural and functional measurements have not been proven to be better in terms of increasing the likelihood of visual preservation relative to functional measurements alone. Not surprisingly, the best measure of the glaucoma patient’s present visual function, and predictor of future visual function, is testing that measures visual function. Reference Singh K, Van Buskirk EM and Spaeth G. A Blink at Diagnosing Glaucoma Suggests that More May Be Less. Ophthalmology 114(7): 12391240. July, 2007. 2016 Subspecialty Day | Glaucoma Section I: Is It Progression? Is It Glaucoma? Case Presentation #2: Mild Progression of Visual Field Loss in Patient With Primary Open-Angle Glaucoma Christopher Kai-shun Leung MD MBChB A 37-year-old primary open-angle glaucoma patient (visual field mean deviation −1.5 dB O.D. −2.22 dB O.S.) with evidence of left visual field progression (“likely progression” by the Early Manifest Glaucoma Trial) and progressive retinal nerve fiber layer thinning (detected by OCT) will be presented for discussion on management approaches. 9 10 Section I: Is It Progression? Is It Glaucoma? 2016 Subspecialty Day | Glaucoma How to Best Assess Visual Field Progression Chris A Johnson PhD to classify groups (eg, normal vs. glaucoma, progressors vs. nonprogressors). It is a forecasting model. I. Key Points There are difficulties with assessing glaucomatous visual field progression: A. More than just one visual impairment (cataract or corneal problems, retinal disease, other optic neuropathies, chiasm, optic tract, optic radiations, cortical pathways) or systemic condition (diabetes, inflammatory, infiltrative, or compressive lesions) can also be involved. B. Visual field testing usually involves subjective responses, and reliability can be compromised. C. There can be considerable variability from one test to the next. D. Medical or surgical management of the patient may change over time. II. Methods of Determining Progression A. Clinical evaluation Determination of improvement, progression, or stability by experienced practitioners B. Classification systems Divide the range of visual field stages from normal to blind into discrete segments Determines the change in visual field properties for the current visual field in comparison to baseline values Determines the best fit of visual field sensitivity over time (regression). In most instances this is a linear fit, but exponential Tobit, polynomial, and spline fits have also been employed. 3. Classification and regression trees (CART) A decision tree procedure that uses recursive partitioning of numerical and categorical data Performs linear regression of visual field sensitivity values that are contained in various sectors of the visual field. It is used as a method of determining visual field progression for various local regions of the visual field, and as a simple means of comparing functional visual field changes with structural variations produced by glaucoma. 8. Permutation analysis Permutation of pointwise linear regression (PoPLR) is a linear regression procedure that performs a random permutation of the order of visual fields to find the best estimate of visual field progression 9. Least absolute shrinkage and selection operator (LASSO) 2. Support vector machine A heuristic method of using a machine classifier that develops a model based on a small learning set to classify different groups using a variety of mathematical techniques (eg, quadratic discriminant analysis, Gaussian kernels) 6. Polar trend analysis A linear regression model that incorporates the nonstationary variability at different levels of visual field sensitivity determined as mixtures of Weibull functions, and that also includes the spatial correlation measurements obtained at neighboring locations 1. Bayesian procedures Forecasting techniques that use prior probabilities and other useful information that are modified by the responses of the individual being tested This procedure uses clusters of points in the visual field that correspond to the arcuate nerve fiber bundle patterns that are characteristic of the distribution of optic nerve fiber patterns that enter the optic disc. E. New methods 5. Cluster analysis 7. ANSWERS (Analysis with Non-Stationary Weibull Error Regression and Spatial Enhancement) D. Trend analysis A dynamic model that continually updates knowledge about an individual’s visual field status and clinical findings to forecast future outcomes C. Event analysis 4. Kalman filters Uses robust regression and several other methods to provide the best prediction of future visual field status 10. Visual field index (VFI) A scale from 0 to 100 that classifies glaucomatous visual fields on the basis of mean deviation (MD) neighboring points, provides more weight to central points, and includes other information. It has a ceiling and a floor effect, which limits its use for early or advanced glaucomatous visual field loss. Section I: Is It Progression? Is It Glaucoma? 2016 Subspecialty Day | Glaucoma III. What Methods Have Been Used for Multicenter Clinical Trials? Clinical evaluation of Goldmann kinetic visual fields was used in the Collaborative Normal Glaucoma Tension Study (CIGTS). To achieve good sensitivity and specificity, progression was determined by 2 out of 3 visual fields within 6 months demonstrating progression followed by 2 out of 3 showing progression in the following 6 months. B.Classification In the Advanced Glaucoma Intervention Study (AGIS) and CIGTS multicenter trials, a 20-point glaucoma visual field severity scale was used, and a 4-point deterioration was an endpoint. Advantages: quantitative. Disadvantages: Not sure whether differences from one point to another are the same across the whole scale. C.Event The Early Manifest Glaucoma Trial (EMGT) used event analysis, which consisted of determination of a change in the current visual field from baseline (average of 2 visual fields). To improve specificity, confirmation of a minimum number of abnormal points were required on 2 subsequent tests. This formed the basis for the Glaucoma Progression Analysis (GPA). IV. How Do the Methods Compare? A. Clinical assessment E.ANSWERS By analyzing several large visual field datasets, ANSWERS demonstrated superior performance when compared to linear regression and permutation analysis (PoPLR). A. Clinical vs. trend Trend analysis performs better than highly trained clinicians’ evaluations. B. Event vs. trend Event analysis usually detects progression earlier (sensitivity), but trend analysis has higher specificity. C. Criteria for identifying progression Depending on what criteria are used for any of the analysis procedures, there are large differences in sensitivity to detect change, specificity for distinguishing stable from changing visual fields, and the time required to detect change. Agreement among the various methods occurs only about 50%-60% of the time. D. Continuous vs. discrete functions Continuous functions contain more information that discrete functions (eg, classification systems). V. Pearls to Remember A. When in doubt, repeat the test, and compare with other structural and clinical information. B. Individual changes are better than comparison to population-based information. C. Progression procedures should be simple and easy to interpret in a clinical setting. D. Asking the right questions, being a good listener, and interaction with the patient are vital. E. One test or examination is usually not sufficient to provide a complete answer to progression. D.Trend Linear regression analysis (the Progressor program) was used in the Primary Treatment Trial (Moorfields Eye Hospital). Progressor performs linear regression analysis of individual test locations and has procedures for minimizing the influence of “outliers” (measures that are inconsistent with the remainder of the data). 11 12 Section I: Is It Progression? Is It Glaucoma? 2016 Subspecialty Day | Glaucoma Point – Counterpoint: Do You Advance Treatment Whenever There Is Visual Field Progression? Yes, I Do Kouros Nouri-Mahdavi MD The main goal of glaucoma treatment is to preserve patients’ visual function. Measurement of visual fields (VFs) with standard achromatic perimetry remains the gold standard for estimating the functional adverse effects of glaucoma in individual patients. Given the large functional reserve or redundancy in retinal ganglion cells (RGCs), a significant number of these cells can die before evidence of VF damage manifests. Appearance of the earliest signs of VF loss is what distinguishes glaucoma suspects or eyes with “preperimetric” glaucoma from eyes with “established” glaucoma and is considered to be an important event in the course of glaucoma. Beyond this point, continuing loss of RGCs directly translates to varying degrees of VF loss or progression. Also, a history of prior visual field progression is one of the strongest predictors of future VF progression. Therefore, I would argue that even small amounts of VF progression need to be addressed and treated, taking into account the patient’s longevity so that progression to visual disability or blindness can be prevented during the patient’s lifetime. 2016 Subspecialty Day | Glaucoma Section I: Is It Progression? Is It Glaucoma? Point – Counterpoint: Do You Advance Treatment Whenever There Is Visual Field Progression? No, I Don’t! Harry A Quigley MD There are a number of important reasons why apparent visual field progression should not lead to an advancement of glaucoma treatment. While these arguments should have been obvious to my opponent prior to his acceptance of this assignment, I’m sure he will agree once he thinks it over during the debate. 13 14 Section I: Is It Progression? Is It Glaucoma? 2016 Subspecialty Day | Glaucoma It’s Not Always Glaucoma: Visual Field Loss due to Neurological Causes Clinical Characteristics of Nonglaucomatous Optic Neuropathy Christopher A Girkin MD I.History III. Neuro-Ophthalmic Glaucoma Imitators A. Neurologic symptoms A. Inflammatory optic neuropathy B. Endocrine symptoms B. Ischemic optic neuropathy C. Speed of progression of visual field/symptoms C. Compressive optic neuropathy D. Family history D. Traumatic optic neuropathy E.Diet E. Hereditary optic neuropathy F. History of blood loss G.Age F. Congenital disc abnormalities (pits, tilted discs, etc.) H.Headache G. Toxic optic neuropathy H. Neurodegenerative disease II.Examination A. The optic nerve head 1. Rim pallor 2. Rim volume preservation 3. Less connective tissue remodeling B. Visual field 1. Vertical midline respect 2. Central loss 3. Inconsistent with optic nerve contour changes C. Pupillary function D. Color vision/perception E. Other neurologic signs I. Retrochiasmal disease IV. Glaucomatous Neuro-Ophthalmic Imitators A. Old pressure elevation (eg, “burned out” pigmentary glaucoma) B. The small optic disc C. IOP variation D. Senile sclerotic glaucoma (rim pallor) E. Acquired optic nerve pits (paracentral loss common) Section I: Is It Progression? Is It Glaucoma? 2016 Subspecialty Day | Glaucoma 15 New and Future Technologies: mERG, mfVEP, Ganglion Cell Markers Electrophysiology: Not Just for Retina Anymore! Stuart J McKinnon MD PhD Description Review of acceptance and clinical application of visual electrophysiology in glaucoma management 3. Basic Clinical Science Courses: “Alternative” to visual field testing 4. American Board of Ophthalmology 5. Preferred Practice Patterns: “Additional test” Objective ■ ■ ■ ■ To learn about the Academy’s inclusion of visual electrophysiological tests To understand the subclinical nature of glaucoma To recognize the need for clinical application of visual electrophysiology To incorporate comparative data for medical decision making and glaucoma care plan Course Outline I.Introduction B. International Society for Clinical Electrophysiology of Vision (ISCEV) 1. Technical standards 2. Clinical indications C. American Optometric Association Clinical Practice Guidelines: “Supplemental” testing defined III. Clinical Applications A. Electroretinography (ERG) – dysfunction of retina: stimuli A. Diagnostic tests for glaucoma a. Fundus photos b. Heidelberg Retina Tomography c.OCT 1.Structure a. Visual acuity b. Central visual fields c. Automated perimetry d. Color vision e.Pupils 1. Patient limitations 2. Neuro-ophthalmic/subclinical nature of glaucoma a. Detection of early disease b. Management of early disease and known pathology II. Historical Acceptance of Visual Electrophysiology Technology 3. Subjective vs. objective: advantages of objective testing A. The Academy and visual electrophysiology 1. Residents Content Outline 2. Core Knowledge i. Early detection ii. Ganglion cell recovery b.AMD i. Early detection ii. Macular function recovery B. Limitations of current technologies a.Glaucoma 2.Function 1. Pattern ERG: ganglion cells c.Plaquenil i. Early detection ii. Appropriate testing timeframe d. Diabetic retinopathy/diabetic macular edema 2. Full field flash ERG: photoreceptors a. Inherited retinal dystrophies b. Opacities (cataracts+retina concerns): comorbidities c.Flicker B. VEP: electrical activity from retina, through optic nerve, pathway to visual cortex 1.Stimuli a. Pattern visual evoked potentials (VEP) b. Flash VEP: poor acuity / opacities 16 Section I: Is It Progression? Is It Glaucoma? 2016 Subspecialty Day | Glaucoma 2. VEP applications E. Discuss the results and implications of the examination with the patient F. Initiate an appropriate management plan, including determination of the frequency of future visits, further diagnostic tests, referral, or treatment a. Optic nerve function (eg, glaucoma) b. Multiple sclerosis c. Ischemic optic neuropathy d. Traumatic brain injury e.Malingering A. Historically proven and accepted ancillary testing f.Amblyopia B. Sensitive and specific for subclinical concerns on the rise C. Objective vs. subjective alternative for equivocal, differential diagnostic circumstances or patient limitations D. Provides quantitative data to aid in initial diagnosis and subsequent treatment, “to treat, or not to treat” V.Conclusions IV. Clinical Objectives A. Detect and diagnose ocular abnormalities and diseases B. Identify risk factors for ocular disease C. Identify risk factors for systemic disease based on ocular findings D. Establish the presence or absence of ocular signs or symptoms of systemic disease 2016 Subspecialty Day | Glaucoma Section II: Controversies Controversy #1: Should Surgery Be Performed in Both Eyes at the Same Time? Pro Nancy Flattem MD MS I. Bilateral Same-Day Cataract Surgery in All Individuals A. Every effort made to replicate separate day surgery 1. Separate packs 2. Solutions and medications of different lot numbers whenever possible 3. Use of disposables as much as possible to minimize risk for toxic anterior segment syndrome B. Proven very safe in our experience C. If any doubt, the expectation is that the second eye surgery will be postponed. D. Benefits to patients II. Bilateral Same-Day Cataract Surgery in Glaucomatous Patients A. An excellent choice for some patients B. Some patients may not be ideal candidates for same-day surgery. C. Benefits specific to glaucoma patients 17 18 Section II: Controversies 2016 Subspecialty Day | Glaucoma Controversy #1: Should Surgery Be Performed in Both Eyes at the Same Time? Con M Lisa McHam MD Today there are good reasons why simultaneous bilateral cataract surgery (SBCS) is being considered as an efficient strategy for delivering cataract care. When following stringent antisepsis guidelines, it appears that the risk of bilateral endophthalmitis is extremely low. Although some surgeons argue that refractive outcome in the first eye may guide adjustments for the second eye, current biometry technology has reached a level of accuracy that this advantage may be of minimal or no clinical significance for eyes with typical measurements. In normal, healthy eyes, the benefits of SBCS in terms of faster visual rehabilitation, patient convenience, and decreased postoperative visits are compelling. When it comes to glaucoma patients, however, the riskbenefit equation changes. On average, phacoemulsification results in modest improvements in long-term IOP control in open-angle glaucoma patients, but IOP can be highly variable in the early postoperative period. The lessons of the first eye with regard to IOP behavior can be very useful in planning appropriate surgery for the second eye. The risk of causing significant bilateral progression of glaucomatous damage is just too great for simultaneous bilateral cataract surgery to be appropriate in glaucoma patients. Selected Readings 1. Arshinoff S, Bastianelli P. Incidence of postoperative endophthalmitis after immediate sequential bilateral cataract surgery. J Cataract Refract Surg. 2011; 37:2105-2114. 2. Chen PP, Lin SC, Junk, et al. The effect of phacoemulsification on intraocular pressure in glaucoma patients: a report by the American Academy of Ophthalmology. Ophthalmology 2015; 122:1294-1307. 3. Slabaugh MA, Bojikian KD, Moore DB, Chen PP. Risk factors for acute postoperative intraocular pressure elevation after phacoemulsification in glaucoma patients. J Cataract Refract Surg. 2014; 40:538-544. Section II: Controversies 2016 Subspecialty Day | Glaucoma 19 Controversy #2: Glaucoma Surgery in the Elderly— Are We Preserving Quality of Life? Pro Steven D Vold MD I. Glaucoma Laser Surgery A. Laser iridotomy (used for narrow angles / angleclosure glaucoma) a.Cataract b. Other visual symptoms (glare, monocular diplopia) c. Iridotomy closure d. IOP elevation e. Chronic inflammation 2.Benefits a. Alleviates relative pupillary block in patients with angle closure b. Rapid postoperative recovery a. Inadequate response b. Early failure c. IOP elevation a. Excellent safety profile b. May reduce patient dependency on glaucoma medication 1.Risks a. Chronic inflammation b.Hypotony c. Phthisis bulbi d. Sympathetic ophthalmia c. Postoperative infection 2.Benefits a. Efficacious in lowering IOP into mid-high teens b. Easily combined with cataract surgery c. Excellent safety profile d. Rapid postoperative recovery 1.Risks a.Hyphema b. Device failure c. Postoperative infection 2.Benefits a. Efficacious in lowering IOP into mid-high teens b. Easily combined with cataract surgery c. Excellent safety profile d. Rapid postoperative recovery A. Newer subconjunctival devices (Ex-Press, XEN, InnFocus) a. May be done from both transscleral and endoscopic approaches b. Micropulse technology has dramatically improved safety and postoperative recovery profiles. b. Cleft or stent closure / failure III. Filtration Surgery 2.Benefits C. Cyclophotocoagulation (used for angle-closure and open-angle glaucomas) a.Hyphema 2.Benefits B. Suprachoroidal microstents (CyPass, iStent Supra, iStar) 1.Risks 1.Risks B. Laser trabeculoplasty (used for open-angle glaucoma) A. Trabecular bypass procedures (eg, Trabectome, gonioscopy assisted transluminal trabeculotomy (GATT), Visco360, Trab360, iStent, Hydrus) 1.Risks II. Microinvasive (Minimally Invasive) Glaucoma Surgery (MIGS) 1.Risks a. Bleb failure b.Hypotony c. Postoperative infection 2.Benefits a. Efficacious in lowering IOPs into low-mid teens b. Excellent safety profile c. More rapid recovery when compared to standard filtration surgery 20 Section II: Controversies B. Classic trabeculectomy / tube shunt surgery 1.Risks a. Bleb failure b.Hypotony c. Blebitis / endophthalmitis d. Bleb dysethesia (trabeculectomy) e. Diplopia, device erosion (tube shunts) f. Longer postoperative recovery 2.Benefits a. Efficacious in lowering IOPs into low-mid teens b. Good option for advanced glaucomas c. Generally used as last resort glaucoma therapeutic option 2016 Subspecialty Day | Glaucoma 2016 Subspecialty Day | Glaucoma Section II: Controversies Controversy #2: Glaucoma Surgery in the Elderly— Are We Preserving Quality of Life? Con George L Spaeth MD FACS The con side of this discussion relates to advice regarding diagnosis or treatment that is based on “risk factors, most especially age.” It is routine to hear recommendations based on chronological age; these are rarely appropriate. “Elderly” is a such a generic label; it means “past one’s prime,” that is, frail, fragile, unable to cope, unable to heal well, and likely to die soon. It is also used to mean “old.” “Elderly” is a dangerous generic term because people’s chronological age is poorly related to their biological and emotional ages. It is essential to determine what characteristics are present in a person being considered for surgery, such as estimated years remaining. However, a person’s chronological age is not a guide to that determination. If a person’s age is mentioned, it should never be done in isolation, as is presently routine. It must always be followed by a modifier, such as “with an estimated years remaining of x.” If that modifier is not included, the age should not be mentioned at all. 21 22 Section II: Controversies 2016 Subspecialty Day | Glaucoma Controversy #3: Should We Adopt New Surgical Techniques Early On? Pro Thomas W Samuelson MD Introduction As with most “point-counterpoint” discussions, the truth is likely somewhere in the middle, reminding me of what Dwight Eisenhower allegedly said about politics: “Politics is like a country road …, the far right and far left is the gutter and the only drivable road is in the middle.” Similarly, the somewhere near the middle is where the majority of surgeons rightly reside on this topic. Of course we should not all be early adopters. Nor should none of us be early adopters. Absolutely someone needs to pioneer and adopt innovative procedures, or all progress stops. That said, who should adopt new surgical procedures early, and who should wait to adopt? And on which patients? Further, some things perceived as innovations eventually fail to pass the ultimate test, evidence-based validation, and therefore don’t deserve to be adopted by the masses. This is Glaucoma Subspecialty Day, and I will frame my discussion to the adoption of glaucoma surgeries. First a few basic comments concerning the innovative process and diffusion of innovations. majority.” Moore reasons that “trying to convince the mass of a new idea is useless. It is better to convince innovators and early adopters first” (see Figure 2). Innovation and Glaucoma Surgery Progress in any field requires thoughtful assessment of the status quo, critical analysis of established methods, and incremental modification. The safer and more efficacious the current standard, the higher the bar for the next innovation (think prostaglandins). Diffusion of Innovation In his book Diffusion of Innovation,1 now in its fifth edition, EM Rogers describes a model that classifies individuals according to their adoption of innovation (see Figure 1). Geoffrey A Moore’s book Crossing the Chasm2 further characterizes the diffusion process of innovation. The chasm specifically refers to the difficult step during which innovations are transferred from “early adopters” to pragmatists, or the “early Figure 1. The Rogers Innovation Curve. Figure 2. From Crossing the Chasm by GA Moore. Section II: Controversies 2016 Subspecialty Day | Glaucoma Traditional glaucoma surgery has significant risk, and in my opinion that risk and a surgeon’s understandable reluctance to perform marginally safe surgery often result in unrealistic medication regimens, often to the point of surface toxicity. Few if any could objectively read the literature concerning the safety of trabeculectomy and tube shunts and not recognize the significant need for innovation in glaucoma surgical strategies for mild to moderate glaucoma. That we need innovation is simply without question. Consider trabeculectomy, which is highly efficacious but far from safe. There are many uncontrollable variables. For example, despite perfect surgery the success of the procedure is predicated on the healing whim of the conjunctiva, which is generally out of the surgeon’s control. Even if the perioperative period is navigated without incident, late hypotony or bleb leaks may ensue 5-10 years later. Perhaps most concerning is the fact that late bleb-related endophthalmitis, a devastating complication, remains a possibility as long as the bleb remains functional. These complications are completely unrelated to the disease process and are a direct consequence of the surgical treatment itself. Such risk is unacceptable with mild to moderate glaucoma at relatively low risk of functional impairment, by far the largest population of patients afflicted with glaucoma. Safer surgical options are welcomed, even if they are only modestly efficacious. In my opinion, the high-risk situations that we routinely put patients in with trabeculectomy and tube shunts mandate innovation. We have been too accepting of the poor safety profile of some of our glaucoma interventions. Early Adopters That said, who should be an early adopter? In order to justify the risks inherent in the adoption of innovation, someone must benefit from each specific innovation, preferably more than one party. In order of priority, these are: 1.Patients 2. Society at large a. Cost savings b. Healthier society 3.Surgeons a.Efficiency b. Capacity to serve more patients c. Safer surgery makes it easier to sleep at night! I consider myself an early adopter, but in order for me to champion a new surgical procedure I must be convinced that it will benefit patients. There have been several new technologies that I became certified to perform but have never adopted. Two examples are holmium laser sclerostomy and transscleral / subconjunctival placement of the Ex-Press mini-shunt (without the overlying scleral flap). In fact, although I became certified early, I never performed a single case of either procedure, as they simply didn’t pass my “gut check” threshold. I declined the early adopter option in those instances. Likewise, I am certified on 2 femtolaser cataract platforms but rarely use either. I am hesitant because I remain uncertain about who benefits with this technology. I don’t believe that it benefits me as a surgeon, at least for routine cataract surgery. I remain unconvinced it benefits my patients just yet. 23 Of the “out of pocket” surgical options I can offer, such as LASIK, toric or multifocal IOLs, or excimer enhancement after cataract surgery, etc., I feel that femto cataract surgery brings the least value to patients. Therefore I have not yet adopted it for routine use. Even so, I am pleased that other surgeons have been early adopters, so that the technology will continue to improve. It is quite likely that it will evolve so that one day I will find it beneficial. Who Should Be an Early Adopter? Early adoption of new technology isn’t for all surgeons. While most surgeons may eventually adopt certain technologies (think phacoemulsification), the first surgeons to adopt should be those that are most facile with current surgical options. For example, when lecturing on the intricacies of canal-based surgery and the inherent learning curve, I tell surgeons that if they are above-average phaco surgeons and above-average glaucoma surgeons, they will be able to adopt canal-based surgery. Most surgeons know if they are a “better than average” surgeon or not. It is not a crime to be average, and such surgeons might not be best served by paving the way and adopting new technologies. Early adoption requires critical self-assessment of the surgical skills required for each procedure. Patient-First Mentality As with all of medicine, innovation must have a patient-first mentality. Other considerations such as financial motivations are subordinate to the care of the patient. It is a misconception that surgeons pioneer new technologies out of financial motivations. With rare exception, physicians who spend time in the innovative process do so at a financial loss rather than a gain. Without question, a surgeon generally does better financially by spending time in clinic or the operating room serving patients than spending time in wet labs, advisory board meetings, and clinical trial meetings. Adopting new technology is very labor intensive and time consuming, although it is rewarding when it leads to safer procedures that benefit patients. Informed consent is mandatory when adopting new procedures. I actually prefer to think of the process as “informed choice,” a phrase that I first heard from my fellowship mentor, George Spaeth. In my experience, many patients enjoy participating in clinical trials and make an informed choice to do so. Other patients prefer time-tested, traditional interventions. Informed patient choice is mandatory, and basic clinical research principles disallow employing unproven technologies on vulnerable populations. Summary Innovation is necessary for quality medical care. Whether or not to become an early adopter is a complex decision best made by individual surgeons. Each situation is different and multifactorial. Patient-related considerations are paramount. Societal and surgeon considerations are subordinate to the needs and care of the patient. 24 Section II: Controversies References and Selected Readings 1. Rogers EM. Diffusion of Innovation. New York: The Free Press; 2003 (reprint). 2. Moore GA. Crossing the Chasm. New York: HarperCollins; 2002. 3. Gedde SJ, Herndon LW, Brandt JD, Budenz DL, Feuer WJ, Schiffman JC; the Tube Versus Trabeculectomy Study Group. Surgical complications in the Tube Versus Trabeculectomy Study during the first year of follow-up. Am J Ophthalmol. 2007; 143:23-31. 4. Gedde SJ, Schiffman JC, Feuer WJ, Herndon LW, Brandt JD, Budenz DL; on behalf of the Tube Versus Trabeculectomy Study Group. Three-year follow-up of the Tube Versus Trabeculectomy Study. Am J Ophthalmol. 2009; 148:670-684. 5. Gedde SJ, Herndon LW, Brandt JD, Budenz DL, Feuer WJ, Schiffman JC; on behalf of the Tube Versus Trabeculectomy Study Group. Postoperative complications in the Tube Versus Trabeculectomy (TVT) study during five years of follow-up. Am J Ophthalmol. 2012; 153:804-814. 6. Samuelson TW. Microinvasive glaucoma surgery: coming of age. J Cataract Refract Surg. 2014; 40:1253-1254. 2016 Subspecialty Day | Glaucoma 2016 Subspecialty Day | Glaucoma Section II: Controversies Controversy #3: Should We Adopt New Surgical Techniques Early On? Con Paul R Lichter MD MS While there are surely pros and cons to early adoption of new surgical techniques, the preponderance of evidence strongly favors those opposed to such an approach. “All that glitters is not gold” applies to the temptation to be an early adopter. There will be ample time to utilize newer surgical techniques without being a pioneer and going through troubling learning curves. 25 26 Section II: Controversies 2016 Subspecialty Day | Glaucoma Controversy #4: Combining Glaucoma Surgeries— Does It Add Benefit? Pro Richard A Lewis MD I. Defining the Term “Benefit” Reduced risk, enhanced efficacy, less cost, most expeditious II. Defining the Term “Combined” Usually means cataract plus … III. Cataract surgery is glaucoma’s safest, most predictable, and most appreciated procedures. IV.Traditional Traditional combined phaco/trab or phaco/drainage device procedures were lengthy and complicated and compromised the anticipated excellent postop visual acuity. V. Microinvasive Glaucoma Surgery (MIGS) MIGS in conjunction with phaco is safe and effective (see clinical trials and FDA submission documents which were never completed under FDA standards). 2016 Subspecialty Day | Glaucoma Section II: Controversies Controversy #4: Combining Glaucoma Surgeries— Does It Add Benefit? Con Richard K Parrish II MD When does 1 + 1 = 1? (a + b) (b + d) When b has no clinically meaningful IOP-lowering effect and a and/or d have some IOP-lowering effect. When does 1 + 1 = 2? (b + c) (b + d) When b has some IOPlowering effect and c or d have some IOP-lowering effect. When does 1 + 1 = 0? (a + c) When both a or c have comparable moderate IOP-lowering effects. When does 1 + 1 = −1? (a + d) When both a and d have substantial IOP-lowering effects. a = trabeculectomy b = FDA-approved minimally invasive glaucoma surgery (MIGS) procedure(s) c = cyclodestructive procedure d = tube shunt surgery Discussing the “benefit” of combination of glaucoma surgeries is meaningless in the absence of considering the individual risks of each procedure alone and in combination. Ultimately, the decision depends on considering both the benefits and the risks. Understanding the mechanism of IOP lowering is critical to predicting the additivity of the IOP-lowering effects. Successful translimbal filtration with formation of a bleb trumps any other single procedure when the goal is substantial IOP lowering. 27 28 Advocating for Patients 2016 Subspecialty Day | Glaucoma 2016 Advocating for Patients Jeff S Maltzman MD Ophthalmology’s goal to protect sight and empower lives requires active participation with and commitment to advocacy efforts. Contributions to the following three critical funds by all ophthalmologists is part of that commitment: 1.OPHTHPAC® Fund 2. Surgical Scope Fund (SSF) 3. State Eye PAC Your ophthalmologist colleagues serving on Academy committees—the Surgical Scope Fund Committee, the Secretariat for State Affairs, and the OPHTHPAC Committee—are dedicating significant time to advocating for patients and the profession. The OPHTHPAC Committee is identifying congressional advocates in each state to maintain close relationships with federal legislators in order to advance ophthalmology and patient causes. The Secretariat for State Affairs is collaborating closely with state ophthalmology society leaders to protect Surgery by Surgeons at the state level. Both groups require robust funds from both the Surgical Scope Fund and the OPHTHPAC Fund in order to protect quality patient care. These committed ophthalmologists serving on your behalf have a simple message to convey: “It takes the entire community of ophthalmologists” to be effective. ■ ■ ■ We need each member of the ophthalmology community to contribute to each of these 3 funds. We need each member of the ophthalmology community to establish relationships with state and federal legislators. We need each member of the ophthalmology community to make a commitment to protect quality patient eye care and the profession. OPHTHPAC® Fund OPHTHPAC is a crucial part of the Academy’s strategy to protect and advance ophthalmology’s interests in key areas, including physician payments from Medicare as well as protecting ophthalmology from federal scope of practice threats. Established in 1985, OPHTHPAC is one of the oldest, largest, and most successful political action committees in the physician community. We are very successful in representing your profession to the U.S. Congress. As one election cycle ends, a new one starts. OPHTHPAC is always under financial pressure to support our incumbent friends as well as to make new friends with candidates. These relationships allow us to have a seat at the table and legislators willing to work on issues important to us and our patients. For the past year, the media and the country have focused on the U.S. presidential primaries. But the races most important to ophthalmology involve seats in Congress. The entire House of Representatives and one-third of the Senate is up for election. Several physicians need our help—and we have many new friends to make. In order for ophthalmology to remain seated at the table, we need to be heavily invested in this year’s election. That takes investment by each member of the ophthalmology community, whether with time or money. Currently, only a minority of ophthalmologists have realized the vital importance of contributing to OPHTHPAC and the other funds. Right now, major transformations are taking place in health care and we need participation from the majority of ophthalmologists so that we have the resources to better our profession and ensure quality eye care for our patients. Among the significant impacts made by OPHTHPAC are the following: ■ ■ ■ ■ ■ ■ ■ Repealed the flawed Sustainable Growth Rate (SGR) formula Blocked the unbundling of Medicare global surgery payments Removed a provision in Medicare fraud and abuse legislation that targeted eyelid surgery Working to reduce the burdens from Medicare’s existing quality improvement programs, such as the EHR Meaningful Use program Working in collaboration with subspecialty societies to preserve access to compounded and repackaged drugs such as Avastin Working to get the Centers for Medicare and Medicaid Services to revisit drastic Medicare fee cuts to glaucoma and retinal detachment surgeries Working to protect your ability to perform in-office ancillary services in your office Contributions to OPHTHPAC can be made here at AAO 2016 or online at www.aao.org/ophthpac. Leaders of the American Glaucoma Society (AGS) are part of the American Academy of Ophthalmology’s Ophthalmic Advocacy Leadership Group (OALG), which has met for the past nine years in January in the Washington, DC, area to provide critical input and to discuss and collaborate on the Academy’s advocacy agenda. The topics discussed in the 2016 OALG agenda included the impact of the Medicare Access and the CHIP Reauthorization Act (MACRA); the IRISTM Registry and quality reporting under Medicare; data transparency and public reporting, and a roundtable to discuss challenges for surgical specialties. At Mid-Year Forum 2016, the Academy and the AGS ensured a strong presence of glaucoma specialists to support ophthalmology’s priorities, and a record number of ophthalmologists visited members of Congress and their key health staff to discuss ophthalmology priorities as part of Congressional Advocacy Day. The AGS remains a crucial partner with the Academy in its ongoing federal and state advocacy initiatives. Surgical Scope Fund (SSF) The Surgical Scope Fund (SSF) provides grants to state ophthalmology societies to support their legislative, regulatory, and public education efforts to derail optometric surgery proposals that pose a threat to patient safety, quality of surgical care, and surgical standards. Since its inception, the Surgery by Surgeons campaign—in partnership with state ophthalmology societies and with support from the SSF—has helped 32 state / territo- Advocating for Patients 2016 Subspecialty Day | Glaucoma 29 Surgical Scope Fund OPHTHPAC® Fund State EyePAC To derail optometric surgical scope of practice initiatives that threaten patient eye safety and quality of surgical care Ophthalmology’s interests at the federal level / support for candidates for U.S. Congress Support for candidates for State House and Senate Political grassroots activities, lobbyists, and media; No funds may be used for candidates or PACs Campaign contributions, legislative education Campaign contributions, legislative education Contributions: Unlimited Contributions: Limited to $5,000 Contribution limits vary based on state regulations. Contributions above $200 are on the public record. Contributions are on the public record depending upon state statutes. Individual, practice, and organization Contributions are 100% confidential. rial ophthalmology societies reject optometric scope of practice expansion into surgery. In 2016, thanks to Surgical Scope Fund support by Academy members and tireless advocacy by state ophthalmology society leaders, ophthalmology continues to champion surgical safety at state capitols across the country. State ophthalmological societies and the Academy’s Secretariat for State Affairs faced eight concurrent Surgery by Surgeons battles, in Alaska, California, Delaware, Illinois, Iowa, Massachusetts, Pennsylvania, and Puerto Rico. In each of these legislative battles, the benefits from Surgical Scope Fund distributions are crystal clear. The fund has allowed for successful implementation of patient safety advocacy campaigns, which result in defeating attempts by optometry to expand their scope of practice to include surgery. The Academy relies not only on the financial contributions to the Surgical Scope Fund from individual ophthalmologists and their practices, but also on the contributions made by ophthalmic state, subspecialty, and specialized interest societies. The AGS contributed to the Surgical Scope Fund in 2015, and the Academy counts on its contribution in 2016. Contributions to the SSF can be made here at AAO 2016 or online at www.aao.org/ssf. State Eye PAC It is also important for all ophthalmologists to support their respective State Eye PACs because PAC contributions to legislators at the state level must come from individual ophthalmologists and cannot come from the Academy, OPHTHPAC, or the Surgical Scope Fund. The presence of a strong State Eye PAC, providing financial support for campaign contributions and legislative education to elect ophthalmology-friendly candidates to the state legislature, is critical as scope of practice battles and many regulatory issues are all fought on the state level. Action Requested: ADVOCATE FOR YOUR PATIENTS Academy Surgical Scope Fund contributions are used to support the infrastructure necessary in state legislative / regulatory battles and for public education. PAC contributions are necessary at the state and federal level to help elect officials who will support the interests of our patients. Contributions to each of these three funds are necessary and help us protect sight and empower lives. Surgical Scope Fund contributions are completely confidential and may be made with corporate checks or credit cards, unlike PAC contributions, which must be made by individuals and are subject to reporting requirements. Please respond to your Academy colleagues and be part of the community that contributes to OPHTHPAC, the Surgical Scope Fund, and your State Eye PAC. Please be part of the community advocating for your patients now. *OPHTHPAC Committee Donald J Cinotti MD (NJ) – Chair Janet A Betchkal MD (FL) William S Clifford MD (KS) Sidney K Gicheru MD (TX) Michael L Gilbert MD (WA) Gary S Hirshfield MD (NY) David W Johnson MD (CO) Jeff Maltzman MD (AZ) Lisa Nijm MD JD (IL) John D Roarty MD (MI) Diana R Shiba MD (CA) Woodford S Van Meter MD (KY) John (“Jack”) A Wells III MD (SC) Charles M Zacks MD (ME) Ex Officio Members Daniel J Briceland MD (AZ) David W Parke II MD (CA) Michael X Repka MD (MD) William L Rich III MD FACS (VA) George A Williams MD (MI) **Surgical Scope Fund Committee Kenneth P Cheng MD (PA) – Chair Matthew F Appenzeller MD (NC) Ronald A Braswell MD (MS) John P Holds MD (MO) Cecily A Lesko MD FACS (NJ) C Blake Myers MD (SC) William (“Chip”) W Richardson II MD (KY) David E Vollman MD MBA (MO) Ex Officio Members: Daniel J Briceland MD (AZ) Kurt F Heitman MD (SC) 30 Section III: Glaucoma—It’s Not Just About IOP 2016 Subspecialty Day | Glaucoma Case Presentation: Glaucomatous Visual Field and Optic Nerve Progression at “Low” IOP— What’s Going On? Arthur J Sit MD This case involves a 71-year-old woman, first diagnosed with glaucoma 11 years ago. At the time of her diagnosis, her IOP was 21 mmHg in the right eye and 20 mmHg in the left eye. She was pseudophakic in the left eye. Her family history was significant for a sibling also diagnosed with glaucoma. Her central corneal thickness was 590 µm in the right eye and 580 µm in the left eye. Past medical history was not significant. She was started on medical therapy in both eyes with latanoprost and timolol and had a good response. Over the next 9 years, her IOP was apparently well controlled between 11 and 14 mmHg. Her visual fields and optic nerve remained stable until 2 years ago, when she started developing an inferior arcuate defect in the right eye, which progressed to encroach upon fixation. An MRI of the head and orbits was unremarkable. She underwent a combined cataract extraction and trabeculectomy with mitomycin C in the right eye, with a good outcome, and IOP remained between 7 and 9 mmHg over the next 2 years. Soon afterward, however, she developed a superior arcuate defect in the left eye with split fixation. She underwent a trabeculectomy with mitomycin C in the left eye and had a postoperative IOP of 6 to 9 mmHg. Despite apparently wellcontrolled IOP, her visual fields have continued to decline in both eyes. Reduction of IOP, even to low therapeutic levels, is not sufficient to stop glaucoma progression in all patients. This session will explore how IOP of any magnitude may contribute to glaucoma progression, and what factors beyond IOP may contribute to the disease. Treatment options for glaucoma other than reduction of IOP will be discussed as well. Section III: Glaucoma—It’s Not Just About IOP 2016 Subspecialty Day | Glaucoma 31 Is IOP Fluctuation Important? Joseph Caprioli MD FACS of AGIS data shows association of IOP fluctuation with progression in eyes with low mean IOPs. I. IOP Fluctuation: Definitions A. Instantaneous: caused by saccades, blinks, rubbing, etc. B. Diurnal-nocturnal (nyctohemeral) 1.Circadian 2. Central, humoral C. Short term: days–weeks D. Long term 1.Months–years 2. Intervisit in-office IOP measurements b. Collaborative Initial Glaucoma Treatment Study (CIGTS) data showed that peak IOP, SD of IOP, and range of IOP are all more important than mean IOP in visual field worsening. c. Other retrospective and prospective studies have implicated IOP fluctuation as an important risk factor in glaucoma progression. See CIGTS data cited below. d. Some studies have found no influence of IOP fluctuation and glaucoma progression (eg, Ocular Hypertension Treatment Study, Early Manifest Glaucoma Trial, European Glaucoma Prevention Study EGPS, and OHT in the Diagnostic Innovations in Glaucoma Study). These have in common: II. Evidence for Effect of IOP Fluctuation on Glaucoma Progression A.Instantaneous 1. No evidence 2. Interesting to speculate about effects of brief high peaks in susceptible eyes and high strain from IOP stress B. Diurnal-nocturnal (nyctoheneral) 1. No evidence 2. Speculation about why these may not be important: a. Higher nocturnal IOP in humans largely due to supine position b. Increased perfusion pressure in supine position may counteract IOP effects on susceptible tissues. c. Increased CSF pressure may counteract stresses caused by IOP on nerve head. d. Homeostatic mechanisms exist to compensate for regular rhythms. e. Difficult to measure nocturnal IOP without disturbing the IOP: Heisenberg-like uncertainty C. Short term: no evidence D. Long term (intervisit IOP measurements) 1. Evidence exists that larger long-term IOP fluctuations are important in the progression of glaucoma: a. IOP fluctuation is an independent and stronger predictor than mean IOP for visual field progression in the Advanced Glaucoma Intervention Study (AGIS). Post hoc analysis i. Higher IOP ii. Earlier glaucoma damage iii. Modest treatment or no treatment e. These varied findings are not contradictory, but rather complementary. 2. Causes for faster rates of progression with higher IOP fluctuation are unknown. Speculation: a. Lack of steady state b. Long-term uncompensated loading / unloading of stresses may break down homeostatic mechanisms. c. Irregular and uncompensated excursions into IOP levels that are damaging III.Relevance Consider IOP “modulation” rather than “reduction”: A. Quantity and quality of IOP control B. Target for progressing primary open-angle glaucoma at high risk 1. Low IOP (low mean, area under curve) 2. Constant IOP (reduce fluctuation and peaks), especially in patients who progress at low mean IOPs 32 Section III: Glaucoma—It’s Not Just About IOP 2016 Subspecialty Day | Glaucoma References 1. Mahdavi K, Hoffman D, Coleman AL, Liu G, Li G, Gaasterland D, Caprioli J. Predictive factors for glaucomatous visual field progression in the Advanced Glaucoma Intervention Study. Ophthalmology 2004; 111:1627-1635. 4. Hong S, Seong GJ, Hong YJ. Long-term intraocular pressure fluctuation and progressive visual field deterioration in patients with glaucoma and low intraocular pressures after a triple procedure. Arch Ophthalmol. 2007; 125:1010-1013. 2. Caprioli J, Coleman AL. Intraocular pressure fluctuation a risk factor for visual field progression at low intraocular pressures in the Advanced Glaucoma Intervention Study. Ophthalmology 2008; 115(7):1123-1129. 5. Lee PP, Walt JW, Rosenblatt LC, et al. Association between intraocular pressure variation and glaucoma progression: data from a United States chart review. Am J Ophthalmol. 2009; 144(6):901907. 3. Bengtsson B, Leske MC, Hyman L, et al. Fluctuation of intraocular pressure and glaucoma progression in the Early Manifest Glaucoma Trial. Ophthalmology 2007; 114:205-209. 6. Musch DC, Gillespie BW, Niziol LM, et al. Intraocular pressure control and long-term visual field loss in the Collaborative Initial Glaucoma Treatment Study. Ophthalmology 2011; 118:17661773. Section III: Glaucoma—It’s Not Just About IOP 2016 Subspecialty Day | Glaucoma 33 Does Ocular Biomechanics Define Tissue Damage? Claude F Burgoyne MD I. Alternative Titles/Questions A. Does biomechanics underlie or explain optic nerve head (ONH) tissue damage in glaucoma? B. Can eye-specific ONH biomechanics predict where a given ONH will become damaged from glaucoma and the IOP at which that damage will occur? C. Will eye-specific ONH biomechanics tell us how to “strengthen” an ONH or make it less susceptible? D. Answer to all of the above: Yes, these are all goals/ working hypotheses of ONH biomechanics. A. Retinal ganglion cell (RGC) / non-RGC retina? B. Retinal RGC axon? C. Orbital RGC axon? D. Lateral geniculate? E. Visual cortex? F. Answer: Maybe, but most data to date suggest ONH is the primary site of damage. G. Primary insults to all other sites of damage have not been shown to cause a glaucomatous optic neuropathy. A. IOP magnitude / fluctuation B. Orbital (atmospheric) pressure C. CSF pressure / fluctuation D. Blood pressure / fluctuation E. Extraocular muscle (EOM) / dural insertion anatomy F. ONH geometry / architecture G. ONH material properties C. Ocular cellular “senescence” (regardless of age or at any age) D. All non-ocular systemic factors A. ONH biomechanics 1. IOP magnitude / fluctuation 2. Orbital (atmospheric) pressure 3. CSF pressure / fluctuation 4. Blood: pressure / fluctuation / flow / autoregulation 5. EOM / dural insertion anatomy 1. Immune / inflammatory 2.Genetic V.IOP A. IOP is not the only thing that contributes to ONH biomechanics – see above. B. IOP contributes to ONH biomechanics at all levels of IOP. C. All IOP-related and non-IOP-related determinants of ONH physiology are likely influential at all levels of IOP. D. The magnitude of non-IOP related determinants of ONH physiology should be independent of the level of IOP (or we would identify them as IOP-related); this is not the same as saying that they are more important at low levels of IOP or less important when IOP is high. 1. We should look for them and treat them at all levels of IOP. 2. Systemic BP, CSF pressure, cellular senescence, EOM insertion and ocular movement effects … VI. How Do IOP-Related and Non-IOP Related Risk Factors Interact? Working prediction: The presence and magnitude of non-IOP related risk factors likely influence the level of IOP at which the ONH tissue will be “stable” or change the least. VII. Important Next Steps in ONH Biomechanics A. Build clinical tools to predict where a given ONH will be damaged regardless of the level of IOP at which that damage will occur B. Predict the level of IOP at which protective remodeling will occur and where C. Predict the level of IOP at which RGC axon damage and loss will occur D. Construct a strategy for staging the optic neuropathy of glaucoma that is separate from the magnitude of axon loss IV. Ocular, Orbital, and Systemic Determinants of ONH Physiology 7. ONH material properties B. Ocular / ONH local tissue immunity III. Ocular and Orbital Determinants of ONH Biomechanics 6. ONH geometry / architecture II. Why the ONH? Does Biomechanics (Ocular or Otherwise) Apply to Other Sites of Damage? 34 Section III: Glaucoma—It’s Not Just About IOP 2016 Subspecialty Day | Glaucoma E. Construct experimental models of the optic neuropathy of glaucoma that do not require IOP elevation 2. Burgoyne CF, Downs JC. Premise and prediction: how optic nerve head biomechanics underlies the susceptibility and clinical behavior of the aged optic nerve head. J Glaucoma. 2008; 17:318-328. F. Understand how and why the ONH becomes more susceptible to axonal injury with age 3. Burgoyne CF. A biomechanical paradigm for axonal insult within the optic nerve head in aging and glaucoma. Exp Eye Res. 2011; 93:120-132. G. Determine if those same processes contribute to glaucoma susceptibility at all ages H. Generate ONH-targeted, non-IOP lowering neuroprotective interventions Selected Readings 1. Burgoyne CF, Downs JC, Bellezza AJ, Suh JK, Hart RT. The optic nerve head as a biomechanical structure: a new paradigm for understanding the role of IOP-related stress and strain in the pathophysiology of glaucomatous optic nerve head damage. Prog Retin Eye Res. 2005; 24:39-73. 4. Sigal IA, Flanagan JG, Ethier CR. Factors influencing optic nerve head biomechanics. Invest Ophthalmol Vis Sci. 2005; 46:41894199. 5. Norman RE, Flanagan JG, Sigal IA, et al. Finite element modeling of the human sclera: influence on optic nerve head biomechanics and connections with glaucoma. Exp Eye Res. 2011; 93:4-12. 2016 Subspecialty Day | Glaucoma Section III: Glaucoma—It’s Not Just About IOP 35 How Does Ocular Blood Flow Influence the Course of Glaucoma? Alon Harris PhD, Giovanna Guidoboni PhD, Josh C Gross MD, Brent A Siesky PhD Awareness that vascular factors, jointly with the mechanical action of IOP, are involved in the pathophysiology of glaucoma dates back more than a century. The last decades have witnessed significant advancements of imaging technologies utilized to visualize and quantify hemodynamic and vascular parameters within the eye. These technologies have generated large amounts of varied data but have also led to many new questions on the appropriate interpretation of this data from the clinical viewpoint, such as whether vascular changes are primary or secondary to the disease process and what is the relationship between vascular, structural, and functional changes. Many population-based studies have identified decreased ocular perfusion pressure, calculated as differences between blood and intraocular pressures, to be associated with increased prevalence and incidence and the progression of glaucoma. The development of imaging modalities has allowed for many direct vascular tissue defects in glaucoma to be identified, including disturbances in vascular autoregulation and comparatively lower blood flow measures in retinal, choroidal, and retrobulbar tissues. Several studies have also found these vascular biomarkers to be associated with visual field and structural glaucomatous damage. Retinal oximetry has demonstrated metabolic disturbances, including lower extraction of oxygen, in glaucoma patients, while very recent advances in angiography OCT have produced pilot data on optic nerve capillary loss and perfusion deficits. The ocular circulation is complex and influenced by many factors that combine to give rise to what is actually measured in each specific patient. These factors may be local to the eye (eg, IOP, axial length, optic disc structure) or non-local (eg, blood pressure, cerebrospinal fluid pressure, vascular regulation, body mass index), and it is extremely difficult to disentangle and quantify their individual effect when analyzing the combined data. Indeed, all these factors coexist in each patient, but not always with the same relevance. For example, many glaucoma patients continue to experience disease progression despite significant reduction of IOP via medical and/or surgical intervention. Additionally, vascular factors seem to be more pronounced in some patient subgroups, including those of African descent and those suffering from diabetes. In order to advance the current understanding of vascular risk factors in glaucoma, long-term studies that comprehensively assess all risk factors across patient subgroups are indeed necessary. However, the implementation of such research has historically been arrested by several limitations. For example, clinical studies provide data on humans, but they are limited in the type of measurements and procedures that can be performed. Animal studies allow more invasive measurements and procedures, but they are limited in the translation of the results to humans. Biological studies provide data on cell functions and activities, but they are limited in the integration of the results with all other ocular and systemic risk factors. Further, even advancements in imaging of ocular vascular tissue often assess only few selected aspects of total perfusion. So how can all this data be rationalized, interpreted, and utilized to better serve each individual patient coming to the clinic? Novel interdisciplinary approaches are needed to build an integrated view of the diverse data coming from experimental and clinical studies, in order to provide attending physicians with effective tools to assess the relative weight of the various glaucoma risk factors in a given patient and to better tailor treatment and management strategies. Recent results obtained by analyzing experimental and clinical studies using a novel synergistic combination of statistical and biophysical approaches show great promise for advancing individualized glaucoma care. The main rationale of the combined approach is that statistical methods can unveil correlations among risk factors, and that biophysical methods, based on, for example, the laws of mass transport, fluid and tissue mechanics, and biochemistry, can elucidate cause-effect relationships among factors. For example, many studies have identified high IOP, low blood pressure, low ocular perfusion pressure, and low intracranial pressure as glaucoma risk factors. While the sole statistical analysis of data has not been able to explain how these factors combine to determine disease status and progression in a given patient, a combined statistical and biophysical approach can help us solve the riddle. By combining statistical and biophysical methods, we have shown that (1) patients with low blood pressure may be more susceptible to glaucomatous damage even at relatively low IOPs due to the reduced effectiveness of vascular regulatory compensatory mechanisms and the increased venous collapsibility, (2) an elevation in IOP or a decrease in intracranial pressure may have similar implications in terms of optic nerve head biomechanics, but very different consequences on retrobulbar and retinal blood flow, and (3) the clinically observed increase in retinal venous oxygen saturation may be due to a decrease in oxygen demand in patients with elevated IOP and to an impairment of vascular regulation in normal-tension glaucoma patients. As the advancement of ocular imaging modalities produces an ever-increasing number of biomarkers, including vascular parameters, the investigation, integration, and comprehensive understanding of their importance becomes paramount. Interdisciplinary approaches combining clinical research studies and biophysical modeling of outcomes, in combination with other clinical, diagnostic, and demographic factors, will likely be required to reveal their importance in glaucoma management and to devise effective tools to better tailor management and therapeutic strategies to each individual patient. Selected Readings 1. Weinreb RN, Harris A. World Glaucoma Association Consensus Series, no. 6: Ocular blood flow in glaucoma. Amsterdam: Kugler Publications; 2012. 2. Chen CL, Bojikian KD, Gupta D, et al. Optic nerve head perfusion in normal eyes and eyes with glaucoma using optical coherence tomography-based microangiography. Quant Imaging Med Surg. 2016; 6(2):125-133. 36 Section III: Glaucoma—It’s Not Just About IOP 3. Gross JC, Harris A, Siesky BA, Sacco R, Shah A, Guidoboni G. Mathematical modeling for novel treatment approaches to openangle glaucoma. Expert Rev Ophthalmol. In press. 4. Guglielmi A, Guidoboni G, Harris A. Role of ocular perfusion pressure in glaucoma: the issue of multicollinearity in statistical regression models. J Modeling Ophthalmol. In press. 5. Prada D, Harris A, Guidoboni G, Siesky B, Huang AM, Arciero J. Autoregulation in the optic nerve head. Surv Ophthalmol. 2016; 61(2):164-186. 6. Carichino L, Harris A, Guidoboni G, et al. A theoretical investigation of the increase in venous oxygen saturation levels in advanced glaucoma patients. J Modeling Ophthalmol. 2016; 1(1):64-87. 2016 Subspecialty Day | Glaucoma 7. Guidoboni G, Harris A, Cassani S, et al. Intraocular pressure, blood pressure and retinal blood flow autoregulation: a mathematical model to clarify their relationship and clinical relevance. Invest Ophthalmol Vis Sci. 2014; 55(7):4105-4118. 8. Guidoboni G, Harris A, Arciero JC, et al. Mathematical modeling approaches in the study of glaucoma disparities among people of African and European descents. J Coupled Syst Multiscale Dyn. 2013; 1(1):1-21. 9. Arciero J, Harris A, Siesky B, et al. Theoretical analysis of vascular regulatory mechanisms contributing to retinal blood flow autoregulation. Invest Ophthalmol Vis Sci. 2013; 54(8):55845593. 2016 Subspecialty Day | Glaucoma Section III: Glaucoma—It’s Not Just About IOP 37 CSF Pressure: Is It an Important Part of Glaucoma? R Rand Allingham MD Introduction Biological processes essential to life invariably utilize, mitigate, or confront forces, one of which is pressure. Glaucoma is a disease intimately related to the stress and strain produced by various pressures on the optic nerve. Does CSF Pressure Play a Role in Glaucoma? The damaging effects of elevated IOP and damage on the optic nerve observed in patients with glaucoma have been known since the mid-19th century. In the early 20th century, the first questions arose about the role of cerebrospinal fluid pressure, or CSFp, as a counterbalance to IOP. More specifically, does the pressure difference between IOP and CSFp at the lamina cribrosa (the translaminar pressure [TLP]) contribute to optic nerve damage in glaucoma? (See Figure 1.) and that the CSFp is even lower in patients with normal-tension glaucoma (NTG). In addition, both groups have shown that ocular hypertensive patients without glaucoma have a higher CSFp than controls, which suggests that higher CSFp may be protective for glaucoma. What Biological Factors Alter CSFp, and Are These Associated With POAG? Ren and co-workers reported that blood pressure and IOP are positively associated with CSFp in normal individuals but not in people with POAG. Body mass index (BMI) is positively associated with CSFp, so in general, patients with lower BMI have a lower CSFp. Consistent with these findings, Pasquale et al reported that higher BMI was associated with reduced risk of POAG in women. Asrani et al found that NTG patients have lower BMI than POAG patients with elevated IOP. These studies suggest that lower BMI may be a risk factor for POAG. Aging also affects CSFp. After age 50, mean CSFp drops over 30% through late life (see Figure 2). The timing for CSFp reduction is remarkably similar to that observed for increasing prevalence of POAG. Figure 1. The lamina cribrosa is the location where IOP comes in contact with the CSF pressure that surrounds the optic nerve. Does Altering CSFp (and TLP Difference) Affect the Optic Nerve? Altering CSFp in an animal model was first shown to cause an optic neuropathy similar to glaucoma by Yablonski and coworkers in a cat model. Morgan et al showed that the mechanical movement of the lamina cribrosa caused by altering CSFp was equivalent to that caused by changing IOP in a dog model. More recently, Wang and co-workers found that chronically reduced CSFp produces retinal nerve fiber thinning that resembles glaucoma in a monkey model. What Is the Evidence that CSFp Affects Risk for Glaucoma in Our Patients? In retrospective studies by Berdahl et al and prospective studies by Ren and co-workers, it has been shown that patients with primary open-angle glaucoma (POAG) have a lower CSFp, measured by lumbar puncture, than patients without glaucoma, Figure 2. CSFp progressively decreases in people after age 50, very similar to the age when POAG prevalence rises. CSFp and Its Implications for Clinical Practice There is growing evidence that lower CSFp (and higher TLP difference) increases risk of POAG and NTG and that higher CSFp reduces glaucoma risk. Other biological factors that are associated with lower CSFp, including age, lower blood pressure, and BMI, are also associated with increased risk of POAG and should be considered during assessment of patients with POAG. The ability to measure CSFp noninvasively and then calculate TLP difference could provide a potentially powerful approach to treating our patients with POAG and NTG. 38 Section III: Glaucoma—It’s Not Just About IOP References 1. Marek B, Harris A, Kanakamedala P, et al. Cerebrospinal fluid pressure and glaucoma: regulation of trans-lamina cribrosa pressure [review]. Br J Ophthalmol. 2014; 98(6):721-725. 2. Yang D, Fu J, Hou R, et al. Optic neuropathy induced by experimentally reduced cerebrospinal fluid pressure in monkeys. Invest Ophthalmol Vis Sci. 2014; 55(5):3067-3073. 3. Berdahl JP, Allingham RR, Johnson DH. Cerebrospinal fluid pressure is decreased in primary open-angle glaucoma. Ophthalmology 2008; 115(5):763-768. 4. Berdahl JP, Fautsch MP, Stinnett SS, Allingham RR. Intracranial pressure in primary open angle glaucoma, normal tension glaucoma, and ocular hypertension: a case-control study. Invest Ophthalmol Vis Sci. 2008; 49(12):5412-5418. 5. Ren R, Jonas JB, Tian G, et al. Cerebrospinal fluid pressure in glaucoma: a prospective study. Ophthalmology 2010; 117(2):259266. 6. Fleischman D, Berdahl JP, Zaydlarova J, Stinnett SS, Fautsch MP, Allingham RR. Cerebrospinal fluid pressure decreases with older age. PLOS ONE. 2012; 7(12). 2016 Subspecialty Day | Glaucoma Section III: Glaucoma—It’s Not Just About IOP 2016 Subspecialty Day | Glaucoma 39 Novel Treatment Options for IOP: Independent Factors Cynthia Mattox MD FACS I. Targets for IOP: Independent Factors on Optic Nerve, Retinal Ganglion Cells A. Ischemia, blood flow autoregulation B. Deprivation of growth factors, trophic factors, nourishment C.Excitotoxicity D. Oxidative stress E. Current drugs, or drugs in development A.Diet1-3 B. Body mass C. Exercise: Likely IOP effects, but blood flow, perfusion pressure also affected 1. Aerobic exercise 2. Isometric exercise, weight lifting 3. Yoga, inversion vs. flow5 instruments6 D. Wind or other resistance E. Eye rubbing, Valsalva maneuvers III. Concurrent Systemic Factors A.Estrogen7 B.Smoking8,9 C. Systemic hypertension control, nocturnal hypotension IV. Body Position A.Sleep10 B. Neck flexion, hyperextension11 V. Complementary and Alternative Treatments12 4. Passo MS, Goldberg L, Elliot DL, et al. Exercise training reduces intraocular pressure among subjects suspected of having glaucoma. Arch Ophthalmol. 1991; 109:1096-1098. 5. Baskaran M, Raman K, Ramani KK, Roy J, Vijaya L, Badrinath SS. Intraocular pressure changes and ocular biometry during sirsasana (headstand posture) in yoga practitioners. Ophthalmology 2006; 113:1327-1332. 6. Schuman JS, Massicotte EC, Connolly S, Hertzmark E, Mukherji B, Kunen MZ. Increased intraocular pressure and visual field defects in high resistance wind instrument players. Ophthalmology 2000; 107:127-133. II.Lifestyle 3. Kang JH, Pasquale LR, Willett WC, et al. Dietary fat consumption and primary open-angle glaucoma. Am J Clin Nutr. 2004; 79(5):755-764. A. Acupuncture, acupressure13,14 B. Herbals and supplements15-17 C.Meditation References 1. Kang JH, Willett WC, Rosner BA, Buys E, Wiggs JL, Pasquale LR. Association of dietary nitrate intake with primary open-angle glaucoma: a prospective analysis from the Nurses’ Health Study and Health Professionals Follow-up Study. JAMA Ophthalmol. 2016; 134(3):294-303. 2. Giaconi J, Yu F, Stone KL, et al; Study of Osteoporotic Fractures Research Group. The association of consumption of fruits/vegetables with decreased risk of glaucoma among older AfricanAmerican women in the study of osteoporotic fractures. Am J Ophthalmol. 2012; 154: 635-644. 7. Dewundara SS, Wiggs JL, Sullivan DA, Pasquale LR. Is estrogen a therapeutic target for glaucoma? Sem Ophthalmol. 2016; 31(12):140-146. 8. Kang JH, Pasquale LR, Rosner BA, et al. Prospective study of cigarette smoking and the risk of primary open-angle glaucoma. Arch Ophthalmol. 2003; 121:1762-1768. 9. Wise LA, Rosenberg L, Radin RG, et al. A prospective study of diabetes, lifestyle factors, and glaucoma among African-American women. Ann Epidemiol. 2011; 21(6):430-439. 10. Kim KN, Jeoung JW, Park KH, Kim DM, Ritch R. Relationship between preferred sleeping position and asymmetric visual field loss in open-angle glaucoma patients. Am J Ophthalmol. 2014; 157:739-745. 11. Malihi M, Sit AJ. Effect of head and body position on intraocular pressure. Ophthalmology 2012; 119:987-991. 12. Gunasekera V, Ernst E, Ezra DG. Systematic internet-based review of complementary and alternative medicine for glaucoma. Ophthalmology 2008; 115(3):435-439.e2. 13. Law SK, Lowe S, Law SM, Giaconi JA, Coleman AL, Caprioli J. Prospective evaluation of acupuncture as treatment for glaucoma. Am J Ophthalmol. 2015; 160(2):256-265. 14. Her JS, Liu PL, Cheng NC, et al. Intraocular pressure-lowering effect of auricular acupressure in patients with glaucoma: a prospective, single-blinded, randomized controlled trial. J Altern Complement Med. 2010; 16(11):1177-1184. 15. Anand A, Modgil S, Sharma VL, Shri R, Kaushik S. Preserving neural retina through re-emerging herbal interventions. J Cell Biochem. 2014; 115:1659-1668. 16. Lee J, Sohn SW, Kee C. Effect of ginkgo biloba extract on visual field progression in normal tension glaucoma. J Glaucoma. 2013; 22:780-784. 17. Wang SY, Singh K, Lin SC. Glaucoma prevalence and the intake of iron and calcium in a population-based study. Curr Eye Res. 2013; 38(10):1049-1056. 40 Section III: Glaucoma—It’s Not Just About IOP 2016 Subspecialty Day | Glaucoma Innovations in Neuroprotection Jeffrey L Goldberg MD PhD ■ ■ ■ ■ ■ ■ ■ Glaucoma is a neurodegenerative disease. In glaucoma, retinal ganglion cells (RGCs) and their axons in the optic nerve degenerate. Progressive optic nerve degeneration leads to progressive vision loss and blindness. Typically, treatment includes reducing IOP. However, not all patients with glaucoma have elevated IOP, and lowering IOP is not sufficient to completely block progression in many patients. Current glaucoma research aims to find complimentary therapies to decreasing IOP to promote neuroprotection, regeneration, and neuroenhancement of RGCs and their axons in the optic nerve. ●● “Neuroprotection” refers to keeping retinal ganglion cells alive. ●● “Regeneration” refers to promoting the regrowth of axons from damaged RGCs down the optic nerve. ●● “Neuroenhancement” refers to augmenting or enhancing the function of residual RGCs. Some therapeutics may promote more than one of these. ■ ■ ■ ■ ■ ■ ■ Advances in clinical trial design, patient selection, and outcome measures support the premise that clinical trials for neuroprotection can be designed and implemented. Ciliary neurotrophic factor (CNTF) is a protein normally expressed at low levels in the visual system. CNTF has been shown in preclinical research to improve survival and regeneration of RGCs in a variety of optic neuropathies. CNTF has been tested in human patients with retinitis pigmentosa, macular degeneration, and, in two Phase 1 open label trials, nonarteritic ischemic optic neuropathy and glaucoma. Data from human patients suggest that CNTF can increase retinal thickness and may stabilize or reverse visual dysfunction. Based on Phase 1 data, CNTF is hypothesized to prevent loss of vision (neuroprotection) and/or improve visual function (neuroenhancement) in patients with diagnosed glaucoma. A clinical trial has been designed to test this hypothesis in a sham controlled, randomized, masked Phase 2 trial. The AGS Subspecialty Day Lecture 2016 Subspecialty Day | Glaucoma 41 Primary Open-Angle Glaucoma Redefined Louis R Pasquale MD I. Ground Rules A. Primary open-angle glaucoma (POAG) ≠ “hightension glaucoma” (HTG) B. POAG = “HTG” + “NTG” (normal-tension glaucoma). C. “Low pressure glaucoma” (LPG) is a confusing term that should be discarded. D. POAG ≠ glaucoma II.POAG POAG is a heterogeneous group of IOP-related progressive optic nerve diseases in which multiple mechanisms of neuronal degeneration are implicated. It is not an idiopathic condition. Rejection of the notion that the cause of the disease is unknown will lead to more rational treatments that prevent and/or slow disease progression. III. Strategy for Redefining POAG Identify the upstream causes of POAG so that more rational drug targets are identified. Upstream factors that simultaneously contribute to variable outflow impairment and increased optic nerve vulnerability to degeneration are particularly attractive candidates. IV. Tools Used to Redefine POAG A.Genetics/genomics National Eye Institute Human Glaucoma Human Genetics Collaboration Heritable Overall Operational Database / International Glaucoma Genetics Collaboration1,2 B. Population-based studies with incident POAG 1. 20-year Ocular Hypertension Treatment Study cohort 2. Nurses Health Study 3. Health Professionals Follow-up Study3 C. Carefully performed clinical studies4 D. Animal models with relevance to the human disease mouse5 1. Nitric oxide synthase 3 knockout 2. Soluble guanylate cyclase knockout mouse6 V. Putative Upstream Causes of POAG A. Alteration in sex hormones7 B. Endothelial (outflow + vascular) dysfunction C. Mitochondrial dysfunction D. Oxidative stress E. Neuroinflammation (excess TNF alpha) F. Impaired glucose metabolism8 G. Pro-apoptotic genetic environment (p53) VI. Selected POAG Cases Redefined VII.Conclusion Current treatments for POAG are inadequate in that side effects are more prominent than the disease early on and halting neuronal progression when the disease is advanced does not seem possible. In the future we will have a better understanding of the natural history of POAG, and we will avert iatrogenic injury induced by our treatments. POAG is really several diseases, some of which are best defined by declining sex hormones; others described by impaired nitric oxide signaling; and still others, by insulin resistance. There are other disease mechanisms in POAG that remain undefined. Ultimately the terms “NTG,” “HTG,” and “POAG” will be replaced by biochemical pathway and molecular profiles that will lead to precision medicine solutions. Armed with such information we may be able to predict who will develop POAG and draw up pre-emptive strategies to avert visual field loss. References 1. Bailey JN, Loomis SJ, Kang JH, et al. Genome-wide association analysis identifies TXNRD2, ATXN2 and FOXC1 as susceptibility loci for primary open-angle glaucoma. Nat Genet. 2016; 48:189-194. 2. Hysi PG, Cheng CY, Springelkamp H, et al. Genome-wide analysis of multi-ancestry cohorts identifies new loci influencing intraocular pressure and susceptibility to glaucoma. Nat Genet. 2014; 46:1126-1130. 3. Kang JH, Willett WC, Rosner BA, Buys E, Wiggs JL, Pasquale LR. Association of dietary nitrate intake with primary open-angle glaucoma: a prospective analysis from the Nurses’ Health Study and Health Professionals Follow-up Study. JAMA Ophthalmol. 2016; 134:294-303. 4. Kim DW, Jeoung JW, Kim YW, et al. Prelamina and lamina cribrosa in glaucoma patients with unilateral visual field loss. Invest Ophthalmol Vis Sci. 2016; 57:1662-1670. 5. Lei Y, Zhang X, Song M, Wu J, Sun X. Aqueous humor outflow physiology in NOS3 knockout mice. Invest Ophthalmol Vis Sci. 2015; 56:4891-4898. 6. Buys ES, Ko YC, Alt C, et al. Soluble guanylate cyclase alpha1deficient mice: a novel murine model for primary open angle glaucoma. PLOS ONE 2013; 8, e60156. 7. Vajaranant TS, Pasquale LR. Estrogen deficiency accelerates aging of the optic nerve. Menopause 2012; 19:942-947. 8. Shen L, Walter S, Melles RB, Glymour MM, Jorgenson E. Diabetes pathology and risk of primary open-angle glaucoma: evaluating causal mechanisms by using genetic information. Am J Epidemiol. 2016; 183:147-155. 42 Section IV: The “New Patient” in Your Clinic—Treatment Options 2016 Subspecialty Day | Glaucoma Case #1: Appositional Angle Closure After Laser Peripheral Iridotomy Clement C Tham FRCS MBBS FCOphthHK I. Key Features of Clinical Case A. 51-year-old Asian woman with normal visual acuity and IOP in clinic now, without medications B. 180-degree appositional angle closure on darkroom gonioscopy despite patent laser peripheral iridotomy (LPI). No peripheral anterior synechiae (PAS). C. LPI performed previously elsewhere, for ocular hypertension (OHT) (O.D.: 32 mmHg; O.S.: 28 mmHg), “angle closure,” and iris bombé. D. No functional or structural evidence of glaucomatous optic neuropathy E. History suggestive of 1 to 2 episodes of possible acute OHT since LPI F. Imaging suggestive of plateau iris configuration (or even syndrome if episodes of raised IOP confirmed) a. As episodes of acute OHT are not yet confirmed, this may merely be a case of primary angle closure suspect (PACS) with plateau iris configuration. b. Least risk of adverse effects or complications arising from the treatment, among the options listed here 3. Comment: Observation may be one possible approach, especially if patient is able and willing to seek prompt ophthalmic attention if APAC occurs and will likely comply with regular follow-up arrangements. a. Long-term drug application is required to keep angle open, with both short- and longterm adverse drug effects. b. Drug compliance may be an issue, especially with adverse effects such as compromised night vision, accommodative change, headache and brow-ache, and ocular irritation. c. May make subsequent lens / cataract surgery more difficult 3. Comment: Patients of this active age group are unlikely to be able to tolerate regular drug administration and adverse effects in the long term. C. Laser peripheral iridoplasty 1.Advantages a. Noninvasive office procedure b. Effectively opens up appositionally closed angle in one setting, with no patient compliance issue. Effect can be maintained in long term.1,2 c. Lower risk of surgical complications compared to lens extraction a. Risk of acute primary angle closure (APAC) attack, which may result in irreversible structural damage or even visual loss if not promptly diagnosed and treated b. Risk of progression to PAC, or even PACG, in the long term, especially if patient lost from follow-up subsequently 2.Disadvantages 2.Disadvantages 1.Advantages Constricts pupil and widens angle pharmacologically, without risk of laser or surgical interventions A.Observation 1.Advantage II. Treatment Options B. Topical pilocarpine Episodic “acute blurring” in the evenings, with halo (?). Not sure whether affecting one eye or both. Occasional headache. No obvious redness, nausea, or vomiting. 2.Disadvantage Risk of laser complications (eg, iris atrophy, damage to corneal endothelium, etc.), especially if not properly applied2 3. Comment: May be a suitable approach, especially if recent episodic OHT likely. Even better justified if OHT is confirmed, or glaucomatous optic neuropathy is documented. D. Lens extraction 1.Advantages a. Most effective means to deepen anterior chamber and widen drainage angle3 b. Decreases IOP and need for glaucoma drugs4 c. Eliminates future need for cataract surgery 2016 Subspecialty Day | Glaucoma Section IV: The “New Patient” in Your Clinic—Treatment Options 2.Disadvantages a. Major surgery and risk of compared to more conservative options above b. May introduce presbyopia if not already present, though this can be partially alleviated with monovision or multifocal IOL 3. Comment: Clear lens extraction probably not justified in the absence of documented OHT or glaucomatous optic neuropathy. Lower threshold for cataract extraction may be considered. E. Alternative potential treatment option: Photocoagulation and shrinkage of prominent ciliary processes using endoscopic approach 1. Partially reversing plateau iris configuration 2. Experimental and not evidence-based yet 3. Best to combine with lens extraction 4. Comment: Not recommended for routine clinical practice, due to lack of evidence III.Conclusions B. With either approach, regular follow-up is necessary, in particular to monitor angle status, IOP, and signs of glaucoma. C. Patient should be educated about symptoms of acute OHT and advised to seek prompt ophthalmic attention should any of these arise. complications4 A. Depending on how likely it is that those were episodes of OHT, presenter is inclined toward offering observation or laser peripheral iridoplasty, with the aim of minimizing adverse effects, risk of complications, and need for patient compliance in the long term. 43 References 1. Ritch R, Tham CC, Lam DS. Long-term success of argon laser peripheral iridoplasty in the management of plateau iris syndrome. Ophthalmology 2004; 111(1):104-108. 2. Ritch R, Tham CC, Lam DS. Argon laser peripheral iridoplasty (ALPI): an update. Surv Ophthalmol. 2007; 52(3):279-288. 3. Tham CC, Leung DY, Kwong YY, Li FC, Lai JS, Lam DS. Effects of phacoemulsification versus combined phaco-trabeculectomy on drainage angle status in primary angle closure glaucoma (PACG). J Glaucoma. 2010; 19(2):119-123. 4. Tham CC, Kwong YY, Baig N, Leung DY, Li FC, Lam DS. Phacoemulsification versus trabeculectomy in medically uncontrolled chronic angle-closure glaucoma without cataract. Ophthalmology 2013; 120(1):62-67. 44 Section IV: The “New Patient” in Your Clinic—Treatment Options 2016 Subspecialty Day | Glaucoma Case #2: High IOP in Microphthalmia Vikas Chopra MD, Brian A Francis MD The patient is a 54-year-old monocular female with microphthalmia, aniridia, and aphakia. The IOP is 52 mmHg on maximum glaucoma medications including oral acetazolamide. There is advanced visual field loss with split fixation in the superior quadrant and severe glaucomatous optic nerve damage (0.9–0.95). C. Very high IOP: Risk of decompression D.Aphakia I. Key Features of the Clinical Case A. Patient has glaucoma with multiple mechanisms: 1. Aniridia – secondary angle closure 2.Aphakia 3. Microphthalmia – primary and secondary angle closure B. Patient is monocular. What was the cause of vision loss in the fellow eye? This will help guide surgical approach. 1. Unicameral eye 2.Vitreous 3. Refractive issues III. Surgical Options A. Microinvasive glaucoma surgery, angle based, and suprachoroidal shunt procedures B.Trabeculectomy C. Tube shunt: Ahmed D. Tube shunt: Baerveldt E. Transscleral cyclophotocoagulation (CPC) or micropulse diode CPC 1. Choroidal hemorrhage? F. Endoscopic cyclophotocoagulation (ECP) 2. Uncontrolled IOP and glaucoma damage? G. Secondary IOL implantation 3.Endophthalmitis? 4. Hypotony and phthisis? H. Glaucoma surgery combined with pars plana vitrectomy C. Extent of optic nerve damage and target IOP D. Prior surgeries in the operative eye and fellow eye? 1. Glaucoma surgeries 2. Retinal procedure (vitrectomy) E. Aphakia: Can patient see with contact lens, or is a secondary IOL needed? 1. This greatly increases the complexity of the case. 2. Scleral IOL fixation II. Management Issues A.Microphthalmia IV.Conclusions A. Clinical case management B. Follow-up for clinical case C. Management is individualized, depending on history of prior treatment and response, stage of disease, visual potential, and other factors. Selected Readings 1. Nelson LB, Spaeth GL, Nowinski TS, et al. Aniridia: a review. Surv Ophthalmol. 1984; 28:621-642. 2. Grant WM, Walton DS. Progressive changes in the angle in congenital aniridia, with development of glaucoma. Am J Ophthalmol. 1974; 78:842-847. 1. Axial length: 21 mm or less 2. Autosomal dominant, autosomal recessive and sporadic 3. Isolated vs. syndromic 4. Walton DS. Aniridic glaucoma: the results of goniosurgery to prevent and treat this problem. Trans Am Ophthalmol Soc. 1986; 84:59-70. 4.Microphthalmia–anophthalmia–coloboma spectrum (genetic testing) 5. Chen TC, Walton DS. Goniosurgery for prevention of aniridic glaucoma. Arch Ophthalmol. 1999; 117(9):1144-1148. 5. High risk for choroidal hemorrhage or effusion (intraoperatively and postoperatively) 6. Adachi M, Dickens CJ, Hetherington J, et al. Clinical experience of trabeculotomy for the surgical treatment of aniridic glaucoma. Ophthalmology 1997; 104:2121-2125. B.Aniridia 1. Angle anatomy 2. Compromised outflow pathways (both trabecular and suprachoroidal) 3. Wiggins RE, Tomey KF. The results of glaucoma surgery in aniridia. Arch Ophthalmol. 1992; 110:503-505. 7. Molteno ACB, Ancker E, Van Biljon G. Surgical technique for advanced juvenile glaucoma. Arch Ophthalmol. 1984; 102:51-57. 2016 Subspecialty Day | Glaucoma Section IV: The “New Patient” in Your Clinic—Treatment Options 8. Billson F, Thomas R, Aylward W. The use of two-stage Molteno implants in developmental glaucoma. J Pediatr Ophthalmol Strabismus. 1989; 26:3-8. 9. Arroyave CP, Scott IU, Gedde SJ, et al. Use of glaucoma drainage devices in the management of glaucoma associated with aniridia. Am J Ophthalmol. 2003; 135:155-159. 10. Wagle NS, Freedman SF, Buckley EG, et al. Long-term outcome of cyclocryotherapy for refractory pediatric glaucoma. Ophthalmology 1998; 105:1921-1927. 11. Kirwan JF, Shah P, Khaw PT. Diode laser cyclophotocoagulation: role in the management of refractory pediatric glaucomas. Ophthalmology 2002; 109:316-323. 45 46 Section IV: The “New Patient” in Your Clinic—Treatment Options 2016 Subspecialty Day | Glaucoma Case #3: Pseudopigmentary Glaucoma From One-Piece IOL Douglas J Rhee MD I. Key Features of Clinical Case A. Clinical history of intermittent spiking IOPs B. Patient has presence of inflammation. C. Clinically had appearance of IOL very close to pupillary margin D. External sutures are close to the limbus. E. Plateau iris appearance in only one eye F. Ultrasound biomicroscopy is diagnostic. G. Others possible findings but not seen in this case: pigment dispersion, iris transillumination defects, microhyphema B. Laser: Argon laser cautery if neovascularization of the angle or iris is seen C.Surgery 1. Pilocarpine to decrease IOL chaffing 2. Palliative care a. Usual antiglaucoma medications to lower IOP and blunt the IOP spikes b. Stop aspirin, NSAIDs, warfarin (ie, anticoagulation) if microhyphema is a significant component. 2. If condition has been present for > 6-12 months, will likely need IOP-lowering procedure along with IOL removal. A. IOL rotation if there is iris entrapment with an anterior chamber IOL (AC-IOL) B. IOL exchange A.Medical 1. If caught early, simple removal of IOL can be curative. III. Surgical Options II. Management Issues 1. Remove the offending IOL 2. Options for replacement include: AC-IOL, sutured (scleral or iris) or glued posterior chamber IOL IV.Conclusions A. Most important aspect is recognition, as this condition is potentially reversible. B. Surgical intervention is most often needed. 2016 Subspecialty Day | Glaucoma Section IV: The “New Patient” in Your Clinic—Treatment Options 47 Case #4: Pseudoexfoliation With Subluxed Lens and High IOP Mildred MG Olivier MD I. Pseudoexfoliation (PXF) C. IOL choice A. Worldwide incidence D. Late subluxation of IOL B. Systemic manifestations E. Approach to repair of IOL C. Causes of the disease 1.Iris D. Family history E. Mechanism of action 2. Transscleral: Video presentation, compliments of Brock Blakewell MD II. Key Features of Clinical Case A. Poor vision O.S. B. Uncontrolled IOP O.S. of 31 mmHg C. On maximum tolerated medical therapy (MTMT) D. Subluxated IOL O.S. E. Gonioscopic evaluation O.S. open-angle glaucoma / narrow angle O.D. F. Progressing visual fields III. Other Clinical Features A. Unilateral vs. bilateral B. Frequency of evaluations IV. Genetic / Environmental Influences A. Affected populations: Scandinavian / Bantu B.Alleles 1. LOXL 1 2.CACNA1A 3.Clusterin C. Environmental factors 1. Light exposure 2. Latitudes (northern) 3.Caffeine V. Cataract Challenges A. Capsular tension rings B. Zonular dehiscence / laxity VI. Surgical Options A. Laser trabeculoplasty B. Trabeculectomy or Ex-Press shunt C.Trabectome D. Glaucoma drainage device E. Micropulse G probe F.Cyclophotocoagulation G. Endoscopic cyclophotocoagulation H. Minimally invasive glaucoma surgery VII.Conclusions A. Patient expectations regarding visual rehabilitation B. Uncontrolled left eye pressure on MTMT C. Pseudoexfoliation of the lens O.D. with narrowing chamber D. Instability/subluxation of the IOL in the left eye E.Language/culture References 1. Kim KE, Kim MJ, Park KH, et al; Epidemiologic Survey Committee of the Korean Ophthalmological Society. Prevalence, awareness, and risk factors of primary open-angle glaucoma: Korea National Health and Nutrition Examination Survey 2008-2011. Ophthalmology 2016; 123(3):532-541. 2. Lam D, Lee J, Jonas J, et al. Glaucoma: today and tomorrow. Asia Pac J Ophthalmol (Phila). 2016; 5(1):2-4. 3. Wiggs JL. Association between LOXL1 and pseudoexfoliation. Arch Ophthalmol. 2008; 126(3):420-421. 48 Section IV: The “New Patient” in Your Clinic—Treatment Options 2016 Subspecialty Day | Glaucoma Case #5: Cataract and Glaucoma in a Myope Tak Yee Tania Tai MD I. Case Features A. Patient referred for glaucoma evaluation; cataract surgery planned, but referring ophthalmologist questions possible need for a combined procedure. B. Exam shows cataract. C. High myopia D. Gonioscopy shows angle open to ciliary body band. E. IOP elevated despite multiple medications. F. Advanced disc cupping II. Management Considerations A. Cataract is visually significant. B. IOP is higher than optimal. C. High myopia is associated with increased risks and challenges for cataract extraction. 1. Posterior capsule tear 2. Zonular dehiscence 3. Anterior capsule tear 4. Reverse pupillary block 5. Retinal detachment 6. Refractive error D. High myopia is associated with increased risks and challenges for glaucoma filtration surgery. 1. Thinner, more flexible sclera 2. Intraoperative suprachoroidal hemorrhage 3. Hypotony maculopathy 4. Delayed suprachoroidal hemorrhage III. Surgical Options A. Cataract surgery alone 1. Pro: IOP-lowering effect of cataract surgery 2. Con: Risk for IOP spike following cataract surgery 3. Con: IOP-lowering effect of cataract surgery may not be significant and may not last long. B. Glaucoma surgery first 1. Pro: Possibly better success for trabeculectomy later 2. Pro: Can revise filtration surgery during cataract extraction 3. Con: Likely inevitable second surgery 4. Con: Patient and referring physician less happy C. Combined cataract with glaucoma filtration surgery 1. Pro: Can achieve low pressures 2. Pro: Patient may not need another surgery. 3. Con: Possible lower success rate for filtration surgery 4. Con: Bigger surgery and longer surgical time for a complex eye may lead to even higher chance of complications. D. Combined cataract with microinvasive glaucoma surgery (MIGS) procedure 1. Pro: Options for future filtration surgery 2. Pro: Little additional surgical time compared to phacoemulsification alone 3. Pro: Low risk of hypotony / choroidal hemorrhage 4. Con: May not achieve the necessary IOP lowering References 1. Zuberbuhler B, Seyedian M, Tuft S. Phacoemulsification in eyes with extreme axial myopia. J Cataract Refract Surg. 2009; 35(2):335-340. 2. Dodick JM, Kahn JB. Special considerations for cataract surgery in the face of pathologic myopia. In: Spaide RF, Ohno-Matsui K, Yannuzzi LA, eds. Pathologic Myopia. New York: Springer Science and Business Media; 2014:313-314. 3. Sergienko NM, Shargorogska I. The scleral rigidity of eyes with different refractions. Graefes Arch Clin Exp Ophthalmol. 2012; 250:1009-1012. 4. Matsumoto Y, Fujihara M, Kanomori A, Yamada Y, Nakamura M. Effect of axial length reduction after trabeculectomy on the development of hypotony maculopathy. Jpn J Ophthalmol. 2014; 58:267-275. 5. Jeganathan VSE, Ghosh S, Ruddle JB, Gupta V, Coote MA, Crowston JG. Risk factors for delayed suprachoroidal hemorrhage following glaucoma surgery. Br J Ophthalmol. 2008; 92:13931396. 6. Vijaya L, Manish P, Ronnie G, Shantha B. Indian J Ophthalmol. 2011; 59(suppl 1):S131-S140. 7. Lochhead J, Casson RJ, Salmon JF. Long term effect on intraocular pressure of phacotrabeculectomy compared to trabeculectomy. Br J Ophthalmol. 2003; 87:850-852. 8. Chen PP, Lin SC, Junk AK, Radhakrishnan S, Singh K, Chen TC. The effect of phacoemulsification on the intraocular pressure in glaucoma patients: a report by the American Academy of Ophthalmology. Ophthalmology 2015; 122(7):1294-1307. 9. Rebolleda G, Muñoz-Negrete, FJ. Phacoemulsification in eyes with functioning filtering blebs: a prospective study. Ophthalmology 2001; 109:2248-2255. 2016 Subspecialty Day | Glaucoma Section V: Past, Present, and Future of Surgical Techniques 49 Evolution of Filtering Surgery Robert Noecker MD Filtration surgery has historically been the gold standard procedure for the surgical treatment of glaucoma. Historically, the common denominator of filtration surgery has been the creation of a hole through the sclera into the anterior chamber so that aqueous flow can occur into the subconjunctival space, thus lowering IOP. In the short term, the sclera and its ostium control outflow, while in the longer term, aqueous flow is controlled by the resistance of the conjunctiva. The earlier forms of filtration surgery involved scleral drainage sites that were full thickness through the sclera. While these procedures were effective in lowering IOP in the longer term, the short-term postoperative period typically involved significant hypotony, which caused significant morbidity and required intense management in an in-patient setting. The unregulated early flow was managed by full-time patching of the eye and the use of devices, such as the Simmons shell, that would apply pressure to the ostium and slow flow temporarily. The recognition of the difficulties in the early postop period associated with full-thickness filtration surgery led to the introduction of guarded filtration techniques. These techniques involved the creation of half-thickness scleral flaps that are sutured to mitigate the flow of aqueous from the eye. Sutures are lysed selectively to lower IOP further when the initial postoperative period, with its high risk of hypotony and associated complications, has passed. This technique is the still the basis of modern trabeculectomy and is used today. In an effort to minimize early hypotony even more, techniques such as deep sclerectomy have been introduced that leave a thin layer or window of the Descemet membrane in place. This layer of tissue provides more resistance to outflow and therefore has a lower rate of flow. The downside of this technique is that completing the procedure in an optimal manner requires optimal ocular tissue and exacting tissue dissection. Also, in some cases, the flow is not vigorous enough to lower IOP adequately in the longer term. Recently, devices have been introduced that attempt to standardize and regulate flow from the anterior chamber opening in the early postoperative period. These devices make the creation of an opening through the sclera more standardized intraoperatively, and restrict flow so that there is less early inflammation and hypotony. The most common cause of failure in filtering surgery is subconjunctival fibrosis. Recognition that certain population groups (patients of African American descent, younger patients, or those who have been using glaucoma medications for prolonged periods) are prone to inflammation and scarring postoperatively has been an important facet of filtration surgery management. Therefore anti-inflammatory therapy has played an important role in the management of filtration surgery. Corticosteroids, both systemic and topical, have always been the mainstay of anti-inflammatory therapy. Antimetabolites were initially introduced in the form of 5-fluorouracil and were typically administered postoperatively twice a day via subconjunctival injections after surgery. While this regimen was effective, it was uncomfortable for the patient and for the glaucoma fellow assigned to give the injections. Intraoperative administration of mitomycin C, a more potent antimetabolite, was introduced in the mid 1980s. This major step forward improved the success rate of filtration surgery through controlling subconjunctival fibrosis. The mitomycin is typically administered on top of the sclera and underneath the conjunctiva on sponges soaked in a predetermined concentration of solution for a predetermined amount of time and then washed away. The exposure is dictated by surgeon experience and patient risk profile. A newer commercial product has been introduced to standardize the solution and application materials. While mitomycin C use has become standard in filtration surgery, it has introduced new problems in the longer term. Late bleb leaks and prolonged hypotony occur in patients in which the subconjunctival healing has been retarded too much. Filtration surgery remains the standard for glaucoma surgery, owing to its ability to deliver efficacy in terms of prolonged IOP lowering at significant levels. The technique has evolved over time and may be enjoying a renaissance as newer devices are introduced that may enhance the safety profile of the procedure. 50 Section V: Past, Present, and Future of Surgical Techniques 2016 Subspecialty Day | Glaucoma Evolution of Tubes Peter A Netland MD PhD I.Introduction A. Use of setons to “wick” aqueous from the anterior chamber dates back to 1906, with the use of horsehair to drain aqueous through a paracentesis. Various materials, including suture, glass, metals, plastic, and biologic material, were used and ultimately failed due to problems with inflammation, fibrosis, and infection. B. In the 1970s, Molteno pioneered development of a posterior tube shunt implant, with a plate implanted posterior to the limbus connected to the anterior chamber by a long silicone tube, thereby initiating the modern glaucoma drainage implant era. B. An implant with a pressure-sensitive slit opening was described in 1976 by Krupin. 1. The slit “valve” was prone to variability of efficacy and obstruction by debris. 2. The Krupin (Eagle Vision) implant is no longer commercially available. C. Various other flow-restrictive implants, including the Joseph, White, and Optimed implants, were developed but did not remain commercially available. D. Ahmed Glaucoma Valve was introduced in 1993. 1. The valve is comprised of 2 thin silicone elastomer membranes positioned in a Venturi-shaped chamber. 2. Different models include polypropylene plates (single-, double-plate, and pediatric), silicone plates (single-, double-plate, and pediatric), and a porous polyethylene plate. II. Development of Nonrestrictive Implants A. Molteno implant variations 1. Polypropylene plates, including single-plate (133 mm2), double-plate, pressure ridge, and pediatric 2. Molteno3 implant is a flexible, larger, singleplate design (175 mm2 or 230 mm2 plates) B. Baerveldt implant introduced in 1990 1. Larger (250 mm 2 and 350 mm2) silicone plates 2. Intraluminal occlusion sutures and external ligation of the tube avoided postop hypotony. A. Flow-restrictive implants were developed in order to avoid problems associated with early postoperative hypotony after drainage implants. a. The silicone single-plate model (FP-7) has been popular among clinicians. b. The Ahmed Glaucoma Valve is the only available resistance glaucoma drainage device. IV. Clinical Experience A. Various factors associated with success and failure have been identified, which have clarified the role of glaucoma drainage implants in the clinical management of glaucoma patients and prompted modifications of the procedure to improve clinical outcomes (see Table 1). B. Reduction of complications C. While the Schocket implant is not commercially available, clinicians have attached tubes to previously implanted encircling bands to treat patients with elevated IOP after scleral buckle. III. Development of Flow-Restrictive Implants 1. Avoidance of hypotony during the early postoperative period 2. Prevention and treatment of other complications Table 1. Variables Influencing Success or Failure of Glaucoma Drainage Implant Surgery6 Patient-related Influence on Success or Failure Little or No Effect on Success or Failure Race Age Previous surgery Diagnosis Implant-related Diagnosis Silicone oil endotamponade Controlled uveitis Neovascular glaucoma Severe ocular surface disease Implant plate size Adjunctive antifibrosis drugs Implant plate material Location of implant: Superior versus inferior 2016 Subspecialty Day | Glaucoma Section V: Past, Present, and Future of Surgical Techniques C. Improved outcomes for refractory glaucomas 1. Ocular surface disease 2. Silicone oil endotamponade 3. Uveitic glaucoma 4. Neovascular glaucoma 5. Pediatric glaucoma V. Present Situation A. Available glaucoma drainage implants 1. Molteno implant (non–flow restrictive) 2. Baerveldt implant (non–flow restrictive) 3. Ahmed Glaucoma Valve (flow restrictive) B.Indications 1. Failure of primary glaucoma surgery 2. Extensive limbal-conjunctival fibrosis / scarring 3. Failure of other primary glaucoma surgery likely 4. Primary surgery VI. The Future A. Improved materials / nanomaterials B. Improved modulation of biological response C. Improved technology (valves, pumps, sensors) D. Alternative techniques 51 VII.Conclusions A. Several effective glaucoma drainage implants have been developed. B. Use of drainage implants has improved the prognosis for success for refractory glaucomas. C. Complications may be prevented or corrected. D. Glaucoma drainage implants have a wellestablished role in the surgical treatment of glaucoma. References 1. Rollett M, Moreau M. Traitement de le hypopyon par le drainage capillaire de la chamber anterieure. Rev Gen Ophthalmol. 1906; 25:481. 2. Molteno ACB, Luntz MH. The use of plastics in glaucoma surgery. Proceedings of the First South African International Ophthalmological Symposium. London: Butterworths; 1969. 3. Molteno AC, Straughan JL, Ancker E. Long tube implants in the management of glaucoma. S Afr Med J. 1976; 50:1062-1066. 4. Lloyd MA, Baerveldt G, Heuer DK, Minckler DS, Martone JF. Initial clinical experience with the Baerveldt implant in complicated glaucomas. Ophthalmology 1994; 101:640-650. 5. Ahmed AM. Ahmed valve surgery. In: Chen TC, ed. Surgical Techniques in Ophthalmology: Glaucoma Surgery (vol. 4). New York: Elsevier; 2008:55-73. 6. Netland PA. The Ahmed Glaucoma Valve in neovascular glaucoma. Trans Am Ophthalmol Soc. 2009; 107:325-342. 52 Section V: Past, Present, and Future of Surgical Techniques 2016 Subspecialty Day | Glaucoma Evolution of CPC Cyclodestructive Procedures: From Past to Present Marlene R Moster MD I. It All Began: Cyclocryotherapy A. 1950 Bietti: Freezing the ciliary body resulted in lower IOP. B. Quigley demonstrated histologically that cryo destroyed the epithelial cells and capillaries of the ciliary body, resulting in a decrease in aqueous production and a breakdown of the blood–aqueous barrier. C. Complications: pain, uveitis, extensive posterior synechiae, pupillary block, cataract, chronic flare, choroidal detachment, 52% decreased vision, phthisis 12% overall, with neovascular glaucoma, 22% II. Fast Forward: Cyclophotocoagulation (CPC) A. 1961 Weekers, first to use light energy as a means of cyclo destruction. Trans scleral xenon arc photocoagulation over ciliary body lowered IOP. B. 1985 Beckman used ruby laser than Nd:Yag which ushered in the present era of cyclophotocoagulation (CPC) C. Nd:Yag CPC is 1064 nm in the infrared spectrum (2-6 joules) D. Placed 2 to 3 mm from the limbus with 30 to 40 applications E. Pulsed mode: produces mechanical photodisruption of the ciliary processes with homogeneous lesions F. Continuous mode: energy 1000 times greater than for YAG iridectomy; full thickness burn to ciliary body and a mild thermal effect in the sclera. IOP decreases 44%-68%. A contact lens delivers the energy for 360°. III. Transscleral Cyclophotocoagulation (TSCPC) E. TSCPC is designed to target the melanin in the pigmented ciliary body epithelium, thereby decreasing the rate of aqueous production. F. Traditionally, this has been performed using a continuous delivery of laser energy. G. The diode continuous mode has been shown to cause significant collateral tissue damage to adjacent nonpigmented structures, including the ciliary stroma and ciliary muscle. H. The nonselective targeting feature of cyclodestruction is thought to contribute to higher rates of postoperative complications, including prolonged inflammation and hypotony. I. Traditional TSCPC may be associated with serious complications including uveitis, vision loss, chronic hypotony, and rarely phthisis bulbi and sympathetic ophthalmia. J. Newer studies recommend using TSCP for eyes that have better visual potential. IV. Endocyclophotocoagulation (ECP) A. 1991: ECP first available by Endo Optiks B. 2005: ECP has own CPT code; 2 units available in the United States A. Due to the risks of serious complications, TSCPC is typically reserved for the treatment of refractory glaucoma or palliation of painful eyes with a very poor prognosis. B. There has been debate over whether there is a direct correlation between the amount of laser energy used and the rate of complications. C. Concerns regarding postoperative complications must be balanced with concerns for overall efficacy, as studies have shown that mean IOP reduction is strongly correlated with the number of delivered laser burns. D. Diode laser cyclophotocoagulation emits light near the infrared spectrum at 810 nm, which is strongly absorbed by melanin. K. Rotchford et al published the results of a study that evaluated the effects of diode CPC in patients with good (≥ 20/60) visual acuity. The results showed that 73.5% of patients had a final IOP of 16 mmHg or less and that only 30.6% lost 2 or more Snellen lines. To compare, in the Tube Versus Trabeculectomy (TVT) study, 63.9% of patients in the tube shunt group and 63.5% of patients in the trabeculectomy group had an IOP of 14 mmHg or less. Forty-six percent of the tube shunt patients and 43% of the trabeculectomy patients lost 2 or more lines of Snellen visual acuity. 1. E2: endoscope + diode laser (pulsed continuouswave energy 810-nm laser, video camera, helium-neon laser aiming beam, and xenon light) 2. E4: Endoscope only (video and xenon light) for vitrectomy 3. Uses a 1.5- to 2.0-mm incision. Expand posterior chamber with ophthalmic viscosurgical device C. Laser settings: Treat 180 to 360 degrees (make a second incision 1.5-2 mm, 120 degrees away) 1. Continuous settings, about 3 seconds for slow whitening 2016 Subspecialty Day | Glaucoma Section V: Past, Present, and Future of Surgical Techniques 2. 250-900 mW (up to a maximum of 2.0 W) Selected Readings 3. No popping, gas bubbles, or pigment dispersion 1. Quigley HA, Broman AT. The number of people with glaucoma worldwide in 2010 and 2020. Br J Ophthalmol. 2006; 90(3):262267. D. Uses of ECP: phaco/ECP for mild to moderate glaucoma; target mid-teens E. Advanced refractory glaucoma with prior trabs/ tube shunts F. Eyes that cannot undergo a filtering procedure (chronic ocular surface disease or high risk of complications [history of pars plana vitrectomy, aphakia, suprachoroidal]) G. Can use at same time or after other angle surgeries (Trabectome, iStent) as it lowers IOP via a decrease in inflow H. Good for anterior segment disease where view is poor or in plateau iris as the ECP causes the ciliary processes to shrink and deepen the angle V. Micropulse Transscleral Cyclophotocoagulation (Micropulse TSCPC, MP-TSCPC, IRIDEX IQ810 Laser Systems; Mountain View, CA) A. Micropulse transscleral diode laser CPC uses micropulse technology to denature the target tissue while further minimizing collateral tissue damage. B. The device applies a series of short (microsecond), repetitive bursts of energy that effectively confines the thermal effect to the absorbing tissue. C. The micropulse delivery mode includes on and off cycles, allowing energy to build up in the targeted pigmented tissues, eventually reaching the coagulative threshold. D. The adjacent nonpigmented structures have time to cool off during the off cycle, thus never reaching the coagulative threshold, which minimizes collateral tissue damage. E. Only a few studies have described the outcomes of this novel treatment for glaucoma. They showed micropulse transscleral cyclophotocoagulation (MP-TSCPC) to have comparable efficacy with fewer side effects when compared with traditional continuous wave mode diode laser delivery. 53 F. This more favorable side effect profile has the potential to make MP-TSCPC an earlier therapeutic option instead of reserving it for end-stage refractory eyes. 2. Tham YC, Li X, Wong TY, Quigley HA, Aung T, Cheng CY. Global prevalence of glaucoma and projections of glaucoma burden through 2040: a systematic review and meta-analysis. Ophthalmology 2014; 121(11):2081-2090. 3. Bloom PA, Tsai JC, Sharma K, et al. “Cyclodiode.” Trans-scleral diode laser cyclophotocoagulation in the treatment of advanced refractory glaucoma. Ophthalmology 1997; 104(9):1508-1519, discussion 1519-1520. 4. Kosoko O, Gaasterland DE, Pollack IP, Enger CL; the Diode Laser Ciliary Ablation Study Group. Long-term outcome of initial ciliary ablation with contact diode laser transscleral cyclophotocoagulation for severe glaucoma. Ophthalmology 1996; 103(8):12941302. 5. Mistlberger A, Liebmann JM, Tschiderer H, Ritch R, Ruckhofer J, Grabner G. Diode laser transscleral cyclophotocoagulation for refractory glaucoma. J Glaucoma. 2001; 10(4):288-293. 6. Oguri A, Takahashi E, Tomita G, Yamamoto T, Jikihara S, Kitazawa Y. Transscleral cyclophotocoagulation with the diode laser for neovascular glaucoma. Ophthalmic Surg Lasers. 1998; 29(9):722-727. 7. Schlote T, Derse M, Rassmann K, Nicaeus T, Dietz K, Thiel HJ. Efficacy and safety of contact transscleral diode laser cyclophotocoagulation for advanced glaucoma. J Glaucoma. 2001; 10(4):294-301. 8. Pantcheva MB, Kahook MY, Schuman JS, Rubin MW, Noecker RJ. Comparison of acute structural and histopathological changes of the porcine ciliary processes after endoscopic cyclophotocoagulation and transscleral cyclophotocoagulation. Clin Exp Ophthalmol. 2007; 35(3):270-274. 9. Tan AM, Chockalingam M, Aquino MC, Lim ZI, See JL, Chew PT. Micropulse transscleral diode laser cyclophotocoagulation in the treatment of refractory glaucoma. Clin Exp Ophthalmol. 2010; 38(3):266-272. 10. Aquino MC, Barton K, Tan AM, Sng C, Li X, Loon SC, Chew PT. Micropulse versus continuous wave transscleral diode cyclophotocoagulation in refractory glaucoma: a randomized exploratory study. Clin Exp Ophthalmol. 2015; 43(1):40-46. 11. Rotchford AP, Jayasawal R, Madhusudhan S, Ho S, King AJ, Vernon SA. Transscleral diode laser cycloablation in patients with good vision. Br J Ophthalmol. 2010; 94(9):1180-1183. 12. Egbert PR, Fiadoyor S, Budenz DL, et al. Diode laser transscleral cyclophotocoagulation as a primary surgical treatment for primary open-angle glaucoma. Arch Ophthalmol. 2001; 119:345350. 54 Section V: Past, Present, and Future of Surgical Techniques Evolution of MIGS Iqbal K Ahmed MD N OTE S 2016 Subspecialty Day | Glaucoma 2016 Subspecialty Day | Glaucoma Section V: Past, Present, and Future of Surgical Techniques 55 Graveyard of Innovation E Randy Craven MD FACS I. Filtration Techniques A. Full-thickness procedures: sclerostomies with bleb 1.Laser C. Valve implants 1. Schocket and modifications of 2. Krupin valve a.Holmium 3. White shunt b.Erbium 4. Susanna implant c.Nd:YAG i.Contact ii.Noncontact II.Cyclodialysis A. With implant, tissue, or space-occupying substance 1. Gel film d.Excimer 2.Viscoelastics e.Diode 3. Scleral wick f.“Picosecond” B. Surgical variations of cyclodialysis 2. Automated trephine 1.Endoscopic 3. Shell to control flow 2. With posterior trephination B. Partial thickness: less bleb III.Cyclodestructive 1.Viscocanalostomy IV. Implications for Today 2. Gel implants 3. Trabecular removal, incision and puncture a. Yag “goniopuncture” b.CO2 laser c. Enzymes and acid ablation of tissue 56 Section VI: The Intersection of Glaucoma and Retina 2016 Subspecialty Day | Glaucoma Case #1: Anti-VEGF Agents and Glaucoma Malik Y Kahook MD Transient elevation in IOP is common after intravitreal injection of anti-VEGF agents. Sustained IOP elevation is less commonly seen but can require medical and/or surgical intervention. The mechanism for sustained IOP elevation is not well understood but has been attributed to trabecular meshwork injury from repeated injections, a potential toxic or inflammatory reaction after exposure to the biologic agents and/or vehicle, or mechanical blockade of the trabecular meshwork by protein aggregates or contaminant particles associated with packaging and injection techniques, among other potential causes. Intravitreal anti-VEGF injections are commonly used to treat neovascular diseases of the eye. Although they have a favorable side-effect profile, their use can be associated with both transient and sustained elevation in IOP. Further research is necessary to determine the cause of these findings. Evidence High-molecular-weight aggregates in repackaged bevacizumab (Kahook et al.). Purpose The anti-VEGF agents ranibizumab and bevacizumab are used to treat ocular neovascular diseases. There have been recent reports of sustained elevation of IOP after use of either agent, which we hypothesize could be because of high-molecularweight aggregates. Methods Enzyme-linked immunosorbent assay, size exclusion chromatography, and polyacrylamide gel electrophoresis were used to analyze repackaged bevacizumab syringes obtained from three outside compounding pharmacies and samples obtained directly from the original vial. Microflow imaging was used to examine particulate material within samples. Results All syringes contained statistically similar amounts of protein, consisting of immunoglobulin (IgG) heavy and light chains (polyacrylamide gel electrophoresis). However, two of the three compounding pharmacies’ batches had significantly less functional IgG in the solution (enzyme-linked immunosorbent assay). Additionally, the compounding pharmacies with the lowest IgG ( approximately 50%) also contained 10-fold the number of micron-sized particulate matter as measured by microflow imaging. Conclusion There are significant differences in IgG concentration measured from repackaged bevacizumab syringes. A trend exists for an increase in micron-sized protein aggregates with the decrease in IgG concentration. Large particulate matter within some samples may lead to obstruction of aqueous outflow and subsequent elevation in IOP. Additional studies are warranted to explore these findings. 2016 Subspecialty Day | Glaucoma Section VI: The Intersection of Glaucoma and Retina Case #2: Diagnostic and Therapeutic Challenges in High Myopia Detecting and Treating Glaucoma in a Myopic Patient Without High IOP Robert T Chang MD Several population-based studies have shown an association between myopia and glaucoma. High myopia often makes detecting glaucoma difficult because optic nerve features may confound glaucomatous changes. In addition, pathologic myopia may cause visual field defects and retinal nerve fiber layer thinning that are indistinguishable from those found in glaucoma patients. Deciding whether or not to treat a glaucoma suspect with these characteristics, particularly when the IOP is not elevated, may be considered a tradeoff between the risks of therapy and the benefits of reducing the likelihood of irreversible progressive optic nerve damage, if indeed that is a component. 57 58 Section VI: The Intersection of Glaucoma and Retina 2016 Subspecialty Day | Glaucoma Case #3: Managing Neovascular Glaucoma Daniel B Moore MD Case Presentation A 42-year-old woman with poorly controlled diabetes mellitus presents for evaluation and management of neovascular glaucoma (NVG) of the left eye. Her referring provider performed a combined cataract extraction and trabeculectomy in the left eye two months ago, but the trabeculectomy has failed and her IOP is elevated on maximum therapy. She has also undergone panretinal photocoagulation for her proliferative diabetic retinopathy, but no intravitreal injections. She is relatively monocular, with light perception vision in the right eye as a result of NVG. The right eye had a similar presentation roughly one year ago, with severely elevated IOP after cataract extraction and trabeculectomy, and she underwent an Ahmed Valve FP7 placement in the supratemporal quadrant at that time. She lives 2 hours away, is just above the federal poverty level, and is the primary caregiver for her 2 school-aged children. On examination, her vision is 20/400 in the left eye. Her IOP is 31 and 45 mmHg in the right and left eye, respectively, on 4 glaucoma medications, including oral acetazolamide. Slitlamp examination of the left eye reveals a focal, vascularized bleb at 12:00, 2+ diffuse injection of the conjunctiva, mildly edematous cornea, deep central anterior chamber, active neovascularization of the iris, and a centered posterior chamber IOL. Gonio scopy demonstrated active neovascularization of the angle with near circumferential peripheral anterior synechiae rising above the pigmented trabecular meshwork. Dilated fundus examination revealed moderate cupping of a slightly pale optic nerve, macular edema, and dense peripheral panretinal coagulation. Questions to Consider ■ ■ ■ How would you surgically manage this patient? Does the current state of the fellow eye influence your decision? Would your approach change if she had not previously undergone trabeculectomy or cataract surgery? Would you provide an intravitreal anti-VEGF injection? Does the timing of this injection make a difference for surgical planning? Does the patient’s social and financial status play a role in surgical decision making? 2016 Subspecialty Day | Glaucoma Section VI: The Intersection of Glaucoma and Retina 59 Case #4: High IOP After Retina Surgery Joanne C Wen MD Case Presentation A 46-year-old African American male with poorly controlled diabetes underwent a pars plana vitrectomy with silicone oil for extensive tractional retinal detachment secondary to severe proliferative diabetic retinopathy in the left eye. The patient is referred for a glaucoma evaluation when he presents on postoperative week 2 with an elevated IOP. On exam, visual acuity of the left eye is count fingers at 1 ft with an IOP of 39 mmHg. Slitlamp exam is significant for corneal edema, formed anterior chamber, iris with an overlying glistening sheen, and a posterior chamber IOL. A peripheral iridotomy (PI) was not seen. Gonioscopy is hazy but reveals 360 degrees of mostly open angles that have patchy peripheral anterior synechiae (PAS) inferiorly. Funduscopic exam reveals a pale, moderately cupped nerve with overlying fibrosis and dense panretinal photocoagulation scars with scattered fibrosis. The retina appears flat under oil. The elevated IOP is felt to be secondary to silicone oil in the anterior chamber, and an inferior PI is placed. The patient is advised to assume face-down positioning. Over the next 2 weeks, the IOP decreases to 15 and the oil migrates back to the posterior segment of the eye. In spite of the patent PI and oil remaining in the posterior segment, the IOP again increases at subsequent follow-ups and by postoperative month 3, the IOP is 31 mmHg on 4 glaucoma drops and oral acetazolamide. The retina surgeon decides to remove the oil to see if this will improve the IOP. Although the IOP initially improves, the patient is ultimately referred back at postoperative week 4 from silicone oil removal, when the vision is found to be 20/200 O.S. and the IOP 32 mmHg. The patient complains of headaches and is on all 4 glaucoma medications. He is no longer able to tolerate acetazolamide. Slitlamp exam reveals trace corneal edema, deep anterior chamber with trace pigmented cells, and no obvious oil droplets in the anterior chamber. Gonioscopy reveals 360 degrees of mostly open angles with few scattered PAS inferiorly and scant “fish egg” oil droplets superiorly. The decision is made to proceed with placement of a glaucoma drainage device (GDD) into the left eye. While the patient is supine on the operating table at the beginning of the case, we note a significant amount of emulsified oil droplets accumulating in the anterior chamber. We began the case by performing a thorough anterior chamber washout. Given the amount of occult emulsified oil droplets, the GDD is placed in the inferonasal quadrant to minimize risk of occlusion by silicone oil. The patient does well, and at postoperative year 1 his visually acuity is 20/100 and IOP is 15 mmHg on dorzolamide-timolol twice daily. Conclusion In patients with high IOP following retina surgery, identifying the underlying mechanism causing the IOP elevation is essential for guiding management. 60 Section VII: Video Surgical Nightmares 2016 Subspecialty Day | Glaucoma The Fighting Iris or the Battle of the Bulge Husam Ansari MD PhD A 71-year-old man with primary open-angle glaucoma presented with uncontrolled IOP in his right eye after selective laser trabeculoplasty and on maximum medical therapy. He had coronary artery disease, had required bypass grafting in the past, and was maintained on daily oral aspirin and clopidogrel. He underwent trabeculectomy with mitomycin C in his right eye. This video highlights the complications of iris prolapse and intraoperative hyphema that occurred during this patient’s surgery. 2016 Subspecialty Day | Glaucoma Section VII: Video Surgical Nightmares The Hyphema That Keeps on Giving JoAnn Giaconi MD A 74-year-old man presented with elevated pressures and recurrent hyphema after an initial anterior chamber washout for hyphema performed by the retina service. The patient has a history of metastatic renal cell carcinoma with a metastasis to the iris and neovascular glaucoma, previously treated surgically with an Ahmed tube and a Baerveldt shunt. This video highlights the difficulty in removing an 8-ball hyphema. 61 62 Section VII: Video Surgical Nightmares “I See Red” Michael Greenwood MD Suprachoroidal hemorrhage is a rare but devastating complication of intraocular surgery. A middle-aged female presented to our clinic with decreased vision and pain in her right eye. She had previously undergone multiple surgeries following trauma to that eye, including a pars plana vitrectomy with endolaser, sclerally fixated aniridia implants, and a Descemet-stripping automated endothelial keratoplasty. After diagnosing her with uncontrolled glaucoma and failing medical management, the decision was made to place an iStent and perform endocyclophotocoagulation to better control her IOPs. Although there were no difficulties during the surgical procedure, the patient developed a suprachoroidal hemorrhage. This video highlights the case and how it was managed intraoperatively. 2016 Subspecialty Day | Glaucoma 2016 Subspecialty Day | Glaucoma Section VII: Video Surgical Nightmares 63 Training for Angle Surgery: No Good Deed Goes Unpunished Shakeel R Shareef MD Brief Synopsis of Video Presentation The rate-limiting step in angle surgery is visualization of angle structures. The video demonstrates an intraocular complication following uncomplicated cataract surgery—iridodialysis—that resulted during angle surgery training from a Sinskey hook and highlights the differences between phacoemulsification (PE) and angle surgery: (1) PE is a bimanual intraocular surgery allowing for globe control with a second instrument, whereas angle surgery is a simultaneous extra- and intraocular surgery, making it a one-handed surgery. (2) There is minimal stimulation of the ocular surface with creation of a keratome and sideport incision during PE, whereas there is maximal stimulation of nerve endings on the entire corneal surface by docking of the surgical goniolens onto the cornea. (3) The entire corneal surface is accessible during PE, whereas it is limited with head tilt. (4) PE is performed posterior to the iris sphincter, whereas angle surgery is performed anterior to the iris in a confined space of 0.7 mm. Recommendations will be made to prevent intraoperative complications, including (1) use of modified goniolenses for better globe control, (2) use of lidocaine jelly not only as a coupling medium but also as a topical analgesic, providing a decreased sensation of tissue manipulation during angle surgery, and (3) performance of angle surgery prior to PE when patient is maximally anesthetized with IV sedation and preoperative lidocaine jelly. 64 Section VII: Video Surgical Nightmares 2016 Subspecialty Day | Glaucoma A Divining Rod for Angle Blood Yao Liu MD and Michele C Lim MD Minimally invasive glaucoma surgeries (MIGSs) are generally considered to have low-risk safety profiles relative to their traditional glaucoma surgical counterparts (ie, trabeculectomy and tube shunts). Thus they are often selected for surgical management in higher-risk glaucoma surgical patients, such as those who are elderly or monocular, use anticoagulants, or have a pre-existing bleeding diathesis. In this surgical video, we present a case in which a combined cataract and Glaukos iStent trabecular microbypass surgery (Glaukos Corp.; Laguna Hills, CA, USA) was performed in an elderly, monocular patient with a prior history of resolved idiopathic vitreous hemorrhage. Preoperatively, he had a visually significant cataract and his IOPs were well controlled medically. He elected to have iStent combined with cataract surgery to reduce his dependence on glaucoma medications. After unremarkable cataract surgery, two attempts were made to place the iStent in the trabecular meshwork. An intraoperative hyphema developed that was not cleared at the time of surgery. Postoperatively, the hyphema was vision limiting in this monocular patient, and it caused an intractable elevation in IOP despite maximal medical therapy. Due to his poor vision and need for assistance in instilling IOP-lowering medications, the patient was admitted to the hospital for treatment. Six days later, he underwent a second procedure to clear the hyphema, which resulted in improved vision and IOP control. He was then discharged home upon regaining his independence. This was an unusual case given that the safety profile of combined iStent with cataract surgery has been shown to be comparable to that of cataract surgery alone in multiple published studies.1,2 Hyphema has been reported to occur in 2.3%-70% of cases, depending on how it is defined.3,4 Some studies have reported occlusion of the iStent with blood clots that either spontaneously resolved or resolved following the use of recombinant tissue plasminogen activator.1,4 Donnenfeld et al reported 1 case of a hyphema at postoperative week 2 in a phakic patient following implantation of 2 iStents, which required surgical irrigation of the anterior chamber.5 This video presentation illustrates that as with all surgical procedures, caution should be taken in performing MIGS in high-risk glaucoma patients. Although MIGSs have a more favorable risk profile compared to traditional glaucoma surgeries, the resulting complications can have a significant impact on patient outcomes. An awareness of vision-threatening hyphema as a potential serious complication following MIGS procedures can aid in preoperative patient selection and counseling to reduce the risk of adverse outcomes. References 1. Wellik SR, Dale EA. A review of the iStent® trabecular microbypass stent: safety and efficacy. Clin Ophthalmol. 2015; 9:677684. 2. Craven ER, Katz LJ, Wells JM, et al. Cataract surgery with trabecular micro-bypass stent implantation in patients with mild-tomoderate open-angle glaucoma and cataract: two-year follow-up. J Cataract Refract Surg. 2012; 38(8):1339-1345. 3. Patel I, de Klerk TA, Au L. Manchester iStent study: early results from a prospective UK case series. Clin Experiment Ophthalmol. 2013; 41(7);648-652. 4. Buchacra O, Duch S, Milla E, et al. One-year analysis of the iStent trabecular microbypass in secondary glaucoma. Clin Ophthalmol. 2011; 5:321-326. 5. Donnenfeld ED, Solomon KD, Voskanyan L, et al. A prospective 3-year follow-up trial of implantation of two trabecular microbypass stents in open-angle glaucoma. Clin Ophthalmol. 2015; 9:2057-2065. Financial Disclosure 2016 Subspecialty Day | Glaucoma 65 Financial Disclosure The Academy has a profound duty to its members, the larger medical community and the public to ensure the integrity of all of its scientific, educational, advocacy and consumer information activities and materials. Thus each Academy Trustee, Secretary, committee Chair, committee member, taskforce chair, taskforce member, councilor, and representative to other organizations (“Academy Leader”), as well as the Academy staff and those responsible for organizing and presenting CME activities must disclose interactions with Companies and manage conflicts of interest or the appearance of conflicts of interest that affect this integrity. Where such conflicts or perceived conflicts exist, they must be appropriately and fully disclosed and resolved. All contributors to Academy educational and leadership activities must disclose all financial relationships (defined below) to the Academy annually. The ACCME requires the Academy to disclose the following to participants prior to the activity: ■ ■ All financial relationships with Commercial Companies that contributors and their immediate family have had within the previous 12 months. 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Financial Relationship Disclosure For purposes of this disclosure, a known financial relationship is defined as any financial gain or expectancy of financial gain brought to the Contributor or the Contributor’s immediate family (defined as spouse, domestic partner, parent, child or spouse of child, or sibling or spouse of sibling of the Contributor) by: ■ ■ ■ ■ ■ Direct or indirect compensation; Ownership of stock in the producing company; Stock options and/or warrants in the producing company, even if they have not been exercised or they are not currently exercisable; Financial support or funding to the investigator, including research support from government agencies (e.g., NIH), device manufacturers, and/or pharmaceutical companies; or Involvement with any for-profit corporation that is likely to become involved in activities directly impacting the Academy where the Contributor or the Contributor’s family is a director or recipient Description of Financial Interests Category Code Description Consultant / Advisor C Consultant fee, paid advisory boards or fees for attending a meeting Employee E Employed by a commercial company Lecture Fees L Lecture and speakers bureau fees (honoraria), travel fees or reimbursements when speaking at the invitation of a commercial company Equity Owner O Equity ownership/stock options (publicly or privately traded firms, excluding mutual funds) Patents / Royalty P Patents and/or royalties that might be viewed as creating a potential conflict of interest Grant Support S Grant support from all sources 66 Financial Disclosure 2016 Subspecialty Day | Glaucoma Faculty Financial Disclosure Control of Content The Academy considers presenting authors, not co-authors, to be in control of the educational content. It is Academy policy and traditional scientific publishing and professional courtesy to acknowledge all people contributing to the research, regardless of CME control of the live presentation of that content. This acknowledgement is made in a similar way in other Academy CME activities. Though they are acknowledged, co-authors do not have control of the CME content and their disclosures are not published or resolved. Iqbal K Ahmed MD Joseph Caprioli MD FACS JoAnn A Giaconi MD Abbott Medical Optics: C,L,S Aerie Pharmaceuticals: C Alcon Laboratories Inc.: C,L,S Allergan Inc.: C,L,S Bausch+Lomb: C Carl Zeiss Meditec: C,L,S Centervue: C Clarity: C,S Envisia: C Equinox: C Eyelight: C ForSight Labs: C Glaukos Corp.: C,O,S Iantech: C InjectSense: C InnFocus: C Iridex: C Ivantis: C,L,S LayerBio: C Leica: C New World Medical Inc.: C,S Oculus Inc.: C Omega Ophthalmics: C Ono Pharma: C PolyActiva: C Sanoculis: C ScienceBased Health: C Stroma: C Transcend Medical: C TrueVision: C Alcon Laboratories Inc.: S Allergan: S National Eye Institute: S New World Medical Inc.: S RPB: S None Meenakshi Chaku MD Alcon Laboratories Inc.: C Allergan: C NIH, DOD, GRF: S None Robert T Chang MD Christopher A Girkin MD None Jeffrey L Goldberg MD PhD Alcon Laboratories Inc.: C Allergan: C Carl Zeiss Inc.: S Healgoo: C Kali Care: C Paxos Scope: P Santen Inc.: C Transcend Medical: C Unity Biotechnology: C David S Greenfield MD Balwantray C Chauhan PhD Alcon Laboratories Inc.: L Imprimis Pharmaceuticals: C Allergan: C,L Heidelberg Engineering: S,C Topcon Medical Systems Inc.: S Aerie: C Alcon Laboratories Inc.: C Allergan: C Bausch+Lomb: C Biometric Imaging: C Glaukos Corp.: C Quark: C Michael Greenwood MD Alon Harris PhD Camras Vision: C NIH: S Allergan Inc.: C,L Ivantis: C,S King Khaled Eye Specialist Hospital: E Pfizer Inc.: C Transcend Medical: C AdOM: C,O BioLight: C Cipla: C Isarna Therapeutics: C Lycored: C Nano Retina: C,O ONO: C Oxymap: O ScienceBased Health: C Stemnion Inc.: C Husam Ansari MD PhD Andrew Crichton MD Gregg A Heatley MD Ivantis Inc.: S Alcon Laboratories Inc.: L,C Allergan: L,C None Nancy L Flattem MD MS InnFocus: C Isarna Therapeutics: C National Eye Institute: S R Rand Allingham MD Claude F Burgoyne MD Heidelberg Engineering: C,S Vikas Chopra MD Allergan: S E Randy Craven MD None Disclosures current as of 9/23/2016 Check the Mobile Meeting Guide/Online Program for the most up-to-date financial disclosures. Dale K Heuer MD Financial Disclosure 2016 Subspecialty Day | Glaucoma Chris A Johnson PhD Richard A Lewis MD Robert J Noecker MD AGTC: C Ceeable: C Centervue: C Haag-Streit: C JAEB Center: C PanOptica: C Advanced Vision Science: C Aerie: E Alcon Laboratories Inc.: C Allergan: C Glaukos Corp.: C Ivantis: C Malik Y Kahook MD Paul R Lichter MD Abbott Medical Optics: P,S Aerie: C Alcon Laboratories Inc.: C,L,S Allergan Inc.: C,L,S ClarVista Medical: C,P ForSight Vision 5: O,C Mile High Ophthalmics: P,O New World Medical Inc.: P Oasis Medical Inc.: P Shape Ophthalmics LLC: O,P ShapeTech LLC: O,P Shire: C None NeoMedix Corp.: L Aerie: C Allergan: C,L Aquesys: S Beaver-Visitec International Inc.: C,L Diopsys Inc.: C,L Endo Optiks Inc.: C,L Ethis Communications: C Glaukos Corp.: L,S Innfocus: S Inotek: C Iridex: C,L Katena Products Inc.: L Novartis Pharmaceuticals Corp.: C,L Ocular Surgery News: L Ocular T: C,S,O Polyactiva: C Quantel Medical: L Shire: C Sun: C L Jay Katz MD Jeff S Maltzman MD Kouros Nouri-Mahdavi MD None Allergan: C Heidelberg Engineering: S New World Medical Inc.: C Aerie Pharmaceutical: C,S,O Aerpio Therapeutics Inc.: C Alcon Laboratories Inc.: C,L Alimera Sciences Inc.: C Allergan: C,S,L Bausch+Lomb: L Diopsys Inc.: C,S ForSight Vision5: C Glaukos Corp.: C,O InnFocus Inc.: C Inotek Corp.: C Lumenis Inc.: L Mati Therapeutics: C,O Merck & Co. Inc.: L Ocular Therapeutix: C Shan C Lin MD Allergan: C Iridex: C Yao Liu MD None Nils A Loewen MD Kaweh Mansouri MD Sensimed AG: C Cynthia Mattox MD FACS Aerie: C Alcon Laboratories Inc.: C Alimera Sciences Inc.: L Allergan: C,S National Eye Institute: S Ocular Therapeutix: C Transcend: S M Lisa McHam MD None Simon K Law MD Stuart J McKinnon MD PhD None Retroject Inc.: O,P Christopher Kai-shun Leung MD MBChB Felipe A Medeiros MD Alcon Laboratories Inc.: C,L Allergan: C,L Carl Zeiss Meditec: C,L,P,S Glaukos Corp.: L,S Lumenis Inc.: L Santen Inc.: L Tomey Corp.: C,L Topcon Medical Systems Inc.: C,L Alcon Laboratories Inc.: C,S Allergan: S,C Carl Zeiss Meditec: S,C Heidelberg Engineering: S Reichert Inc.: C Topcon Medical Systems Inc.: S Daniel B Moore MD None Marlene R Moster MD Iridex: S Peter Andreas Netland MD PhD PTC Therapeutics: S Disclosures current as of 9/23/2016 Check the Mobile Meeting Guide/Online Program for the most up-to-date financial disclosures. 67 Mildred M G Olivier MD Alcon Laboratories Inc.: C,L National Eye Institute: S Santen Inc.: C Richard K Parrish II MD Aerie Pharmaceuticals Inc.: C,O Alimera Sciences Inc.: C,O American Journal of Ophthalmology: C InnFocus Inc.: C,O National Eye Institute: S Louis R Pasquale MD Allergan: L Bausch+Lomb: C Merck & Co. Inc.: S National Eye Institute: S Novartis Pharmaceuticals Corp.: C Jody R Piltz-Seymour MD Aerie Pharmaceuticals: S Alcon Laboratories Inc.: L Allergan: C Forsight: C Harry A Quigley MD Genentech: C Graybug: C,O Novartis: C Sensimed: C 68 Financial Disclosure 2016 Subspecialty Day | Glaucoma Douglas J Rhee MD Shakeel R Shareef MD Aerie: C,O Alcon Laboratories Inc.: C Allergan Inc.: C,S Glaukos Corp.: S Ivantis: S Merck & Co. Inc.: S Sanofi Fovea: C None Thomas W Samuelson MD Abbott Medical Optics Inc.: C AcuMems: C Aerie Pharmaceuticals: C Akorn Inc.: C Alcon Laboratories Inc.: C Allergan: C AqueSys: C,O Endo Optiks Inc.: C Equinox: C,O Glaukos Corp.: C,O Ivantis: C,O Ocular Surgery News: C Shire: C Slack Incorporated: C Transcend: C Joel S Schuman MD Aerie Pharmaceuticals Inc.: C,S Alcon Laboratories Inc.: C Carl Zeiss Meditec: P DSM Inc.: C Glaukos Corp.: C,S Ocugenix: O,P Opticient: C Pfizer Inc.: C,L Slack Incorporated: C Lucy Q Shen MD LEK Consulting: C Kuldev Singh MD MPH Abbott Medical Optics Inc.: C Aerie: C Alcon Laboratories Inc.: C Allergan: C Carl Zeiss Meditec: C ForSight Vision 5: C InnFocus: C Ivantis: C Mynosys: C National Eye Institute: S National Space Biomedical Research Institute: C Santen Inc.: C Shire: C Thieme Medical Publishers: C Transcend: C U.S. Food and Drug Administration: C Arthur J Sit MD Aerie Pharmaceuticals Inc.: S Allergan: C Glaukos Corp.: S George L Spaeth MD FACS None Tak Yee Tania Tai MD None Adrienne Williams Scott MD Allergan: C Therapeutic Proteins International (TPI): C ThromboGenics Inc.: S Disclosures current as of 9/23/2016 Check the Mobile Meeting Guide/Online Program for the most up-to-date financial disclosures. Clement C Y Tham FRCS MBBS FCOphthHK Abbott Medical Optics Inc.: S Aeon Astron Corp.: S Alcon Laboratories Inc.: C,L,S Allergan Inc.: C Bausch+Lomb: C Icare Finland: S IOPtima Ltd.: C Merck & Co. Inc.: C,L Pfizer Inc.: C,L,S Santen Pharmaceutical Co., Ltd.: C,S Sensimed: S Steven D Vold MD Aerie Pharmaceuticals: C,S Alcon Laboratories Inc.: C,S Allergan: L,S Alphaeon: C,O AqueSys: C,S Bausch+Lomb: S Calhoun Vision Inc.: S Carl Zeiss Meditec: C,S Forsight Labs: C,S Glaukos Corp.: C,S InnFocus: C,S Iridex: C,S Ivantis: C,S Lumenis Inc.: C NeoMedix Corp.: L Ocular Therapeutix: C,S Ocunetics: O Transcend Medical: C,P,S TrueVision Systems: C,O Volk Optical: P Kelly Walton Muir MD None Joanne C Wen MD None 2016 Subspecialty Day | Glaucoma Presenter Index Ahmed*, Iqbal K 54 Allingham*, R Rand 37 Ansari*, Husam 60 Burgoyne*, Claude F 33 Caprioli*, Joseph 31 Chang*, Robert T 57 Chauhan*, Balwantray C 4 Chopra*, Vikas 44 Craven*, E Randy 55 Flattem, Nancy L 17 Giaconi, JoAnn A 61 Girkin, Christopher A 14 Goldberg*, Jeffrey L 40 Greenwood*, Michael 62 Harris*, Alon 35 Johnson*, Chris A 10 Kahook*, Malik Y 56 Leung*, Christopher Kai-shun 9 Lewis*, Richard A 26 Lichter, Paul R 25 Lin*, Shan C 1 Liu, Yao 64 Maltzman, Jeff S 28 Mattox*, Cynthia 39 McHam, M Lisa 18 McKinnon*, Stuart J 15 Medeiros*, Felipe A 6 Moore, Daniel B 58 Moster*, Marlene R 52 Netland*, Peter Andreas 50 Noecker*, Robert J 49 Nouri-Mahdavi*, Kouros 12 Olivier*, Mildred M G 47 Parrish*, Richard 27 Pasquale*, Louis R 41 Quigley*, Harry A 13 Rhee*, Douglas J 46 Samuelson*, Thomas W 22 Shareef, Shakeel R 63 Singh*, Kuldev 8 Sit*, Arthur J 30 Spaeth, George L 21 Tai, Tak Yee Tania 48 Tham*, Clement C Y 42 Vold*, Steven D 19 Wen, Joanne C 59 * Indicates that the presenter has financial interest. No asterisk indicates that the presenter has no financial interest. Presenter Index 69
