Glaucoma 2016 Syllabus

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 2010 Rohit Varma MD MPH 1996 M Bruce Shields MD
Joel S Schuman MD Leon W Herndon MD E Michael Van Buskirk MD
Program Director 2009 Donald L Budenz MD MPH 1995 Reay H Brown MD
Rohit Varma MD MPH Mary Gerard Lynch MD
Jody R Piltz-Seymour MD
2008 Henry D Jampel MD MHS 1994 Richard A Lewis MD
Program Director
Donald L Budenz MD MPH
Meenakshi Chaku MD 2007 Anne Louise Coleman MD PhD Subspecialty Day Advisory Committee
Andrew CS Crichton MD FRCS Henry D Jampel MD MHS Daniel S Durrie MD
David S Greenfield MD 2006 Christopher A Girkin MD Associate Secretary
Gregg A Heatley MD Anne Louise Coleman MD PhD Julia A Haller MD
Shan C Lin MD 2005 Claude F Burgoyne MD Francis S Mah MD
Nils A Loewen MD PhD Christopher A Girkin MD R Michael Siatkowski MD
Cynthia Mattox MD FACS 2004 David S Greenfield MD Kuldev Singh MD MPH
Kelly W Muir MD Claude F Burgoyne MD Nicolas J Volpe MD
Lucy Q Shen MD 2003 Kuldev Singh MD MPH
Arthur J Sit MS MD David S Greenfield MD Jonathan B Rubenstein MD
2002 Theodore Krupin MD Secretary for Annual Meeting
Former Program Directors Kuldev Singh MD MPH
2015 James D Brandt MD Staff
2001 Robert D Fechtner MD
Joel S Schuman MD Ann L’Estrange, Scientific Meetings
Theodore Krupin MD
2014 David S Friedman MD MPH PhD Specialist
2000 Jeffrey M Liebmann MD
James D Brandt MD Melanie R Rafaty CMP DES, Director,
Robert D Fechtner MD
2013 Thomas W Samuelson MD Scientific Meetings
1999 Robert N Weinreb MD
David S Friedman MD MPH PhD Lisa Romero, Presenter Coordinator
Jeffrey M Liebmann MD
2012 Wallace L M Alward MD Debra Rosencrance CMP CAE, Vice
1998 George A Cioffi MD
Thomas W Samuelson MD President, Meetings & Exhibits
Robert N Weinreb MD
2011 Leon W Herndon MD Patricia Heinicke Jr, Copy Editor
1997 Richard A Lewis MD
Wallace LM Alward MD Mark Ong, Designer
George A Cioffi MD
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

Program Director Program Director
Aerie Pharmaceuticals Inc.: C,S Aerie Pharaceuticals: S
Alcon Laboratories Inc.: C Alcon Laboratories Inc.: L
Carl Zeiss Meditec: P Allergan: C
DSM Inc.: C Forsight: C
Glaukos Corporation: C,S
Ocugenix: O,P
Opticient: C
Pfizer Inc.: C,L
SLACK Incorporated: C
No photo
available
Meenakshi Chaku MD Andrew Crichton MD FRCS David S Greenfield MD

None Alcon Laboratories Inc.: C,L Aerie: C
Allergan: C,L Alcon Laboratories Inc.: C
Allergan: C
Bausch+Lomb: C
Biometric Imaging: C
Glaukos Corporation: C
Quark: C
2016 Subspecialty Day | Glaucoma Planning Group iii
Gregg A Heatley MD Cynthia Mattox MD FACS Arthur J Sit MS MD

None Aerie: C Aerie Pharmaceuticals Inc.: S
Alcon Laboratories Inc.: C Allergan: C
Alimera Sciences Inc.: L Glaukos Corporation: S
Allergan: C,S
National Eye Institute: S
Ocular Therapeutix: C
Transcend: 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
iv Planning Group 2016 Subspecialty Day | Glaucoma
2016 Subspecialty Day R Michael Siatkowski MD AAO Staff

Advisory Committee (Pediatric Ophthalmology)
National Eye Institute: S Ann L’Estrange
Daniel S Durrie MD, Chair None
(Refractive Surgery) Kuldev Singh MD MPH
Abbott Medical Optics: L,S (Glaucoma) Melanie Rafaty
AcuFocus Inc.: C,L,O,S Abbott Medical Optics Inc.: C None
Alcon Laboratories Inc.: S Aerie: C
Allergan: S | Alphaeon: C,L,O Alcon Laboratories Inc.: C Lisa Romero
Avedro: L,O,S Allergan: C None
Hoopes Durrie Rivera Research Carl Zeiss Meditec: C
Center: C ForSight Vision 5: C Debra Rosencrance
Strathspey Crown LLC: C,L,O InnFocus: C | Ivantis: C None
Wavetec: O Mynosys: C
National Eye Institute: S Beth Wilson
Julia A Haller MD (Retina) National Space Biomedical Research None
Celgene: O | Janssen: C Institute: C
KalVista: C | Merck & Co. Inc.: C Santen Inc.: C | Shire: C
ThromboGenics Inc.: S Thieme Medical Publishers: C
Transcend: C
Francis S Mah MD (Cornea) U.S. Food and Drug
Abbott Medical Optics Inc.: S,L,C Administration: C
Aerie: C
Alcon Laboratories Inc.: L,S,C Nicholas J Volpe MD
Allergan: S,L,C (Neuro-Ophthalmology)
Bausch+Lomb: C,L Opticent Inc.: O
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 Contents v
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
vi CME Credit 2016 Subspecialty Day | Glaucoma
CME Credit
Academy’s CME Mission Statement ments is available at http://abop.org/maintain-certification/

part-2-lifelong-learning-self-assessment/sacme/.
The purpose of the American Academy of Ophthalmology’s
NOTE: Credit designated as “self-assessment” is AMA PRA
Continuing Medical Education (CME) program is to present
Category 1 Credit™ and is also preapproved by the ABO for
ophthalmologists with the highest quality lifelong learning
the Maintenance of Certification (MOC) Part II CME require-
opportunities that promote improvement and change in physi-
ments.
cian practices, performance, or competence, thus enabling such
physicians to maintain or improve the competence and profes-
sional performance needed to provide the best possible eye care Teaching at a Live Activity
for their patients.
Teaching instruction courses or delivering a scientific paper or
poster is not an AMA PRA Category 1 Credit™ activity and
2016 Glaucoma Subspecialty Day Meeting Learning should not be included when calculating your total AMA PRA
Objectives Category 1 Credits™. Presenters may claim AMA PRA Cat-
egory 1 Credits™ through the American Medical Association.
Upon completion of this activity, participants should be able to:
To obtain an application form please contact the AMA at
■ Describe innovations in the diagnosis and management of www.ama-assn.org.
glaucoma within their historical context
■ Manage complex cases of glaucoma when other eye dis-
Scientific Integrity and Disclosure of Financial
eases are present
Interest
■ Evaluate the current status of optic disc and retinal nerve
fiber layer imaging and its role in diagnosing and manag- The American Academy of Ophthalmology is committed to
ing glaucoma ensuring that all CME information is based on the application
■ Demonstrate familiarity with current issues in medical of research findings and the implementation of evidence-based
and surgical therapy for glaucoma, both open-angle and medicine. It seeks to promote balance, objectivity, and absence
angle-closure variants of commercial bias in its content. All persons in a position to
■ Identify and manage glaucoma surgical complications 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
2016 Glaucoma Subspecialty Day Meeting Target
being delivered to the learners.
Audience
The Academy requires all presenters to disclose on their first
This activity has been designed to meet the educational needs of slide whether they have any financial interests from the past 12
general ophthalmologists, glaucoma specialists and other oph- months. Presenters are required to verbally disclose any finan-
thalmologic subspecialists, and allied health personnel who are cial interests that specifically pertain to their presentation.
involved in the management of glaucoma patients.
Control of Content
2016 Glaucoma Subspecialty Day CME Credit
The Academy considers presenting authors, not co-authors, to
The American Academy of Ophthalmology is accredited by be in control of the educational content. It is Academy policy
the Accreditation Council for Continuing Medical Education and traditional scientific publishing and professional courtesy
(ACCME) to provide continuing medical education for physi- to acknowledge all people contributing to the research, regard-
cians. less of CME control of the live presentation of that content. This
The American Academy of Ophthalmology designates this acknowledgement is made in a similar way in other Academy
live activity for a maximum of 7 AMA PRA Category 1 Cred- CME activities. Though they are acknowledged, co-authors do
its™. Physicians should claim only the credit commensurate not have control of the CME content and their disclosures are
with the extent of their participation in the activity. not published or resolved.
Self-Assessment Credit Attendance Verification for CME Reporting

This activity meets the Self-Assessment CME requirements Before processing your requests for CME credit, the Academy
defined by the American Board of Ophthalmology (ABO). must verify your attendance at Subspecialty Day and/or AAO
Please be advised that the ABO is not an accrediting body for 2016. In order to be verified for CME or auditing purposes, you
purposes of any CME program. The ABO does not sponsor this must either:
or any outside activity, and the ABO does not endorse any par- ■ Register in advance, receive materials in the mail, and
ticular CME activity. Complete information regarding the ABO
turn in the Subspecialty Day Syllabi exchange voucher(s)
Self-Assessment CME Maintenance of Certification require-
onsite;
2016 Subspecialty Day | Glaucoma CME Credit vii
■ Register in advance and pick up your badge onsite if mate- The Academy transcript cannot list individual course atten-
rials did not arrive before you traveled to the meeting; dance. It will list only the overall credits spent in educational
■ Register onsite; or activities at Subspecialty Day and/or AAO 2016.
■ Scan the barcode on your badge as you enter an AAO Nonmembers: The Academy will provide nonmembers with
2016 course or session room. verification of credits earned and reported for a single Acad-
emy-sponsored CME activity.
CME Credit Reporting
Proof of Attendance
Academy Resource Center, Booth 508 and South Level 2.5
The following types of attendance verification will be available
Attendees whose attendance has been verified (see above) at
during AAO 2016 and Subspecialty Day for those who need it
AAO 2016 can claim their CME credit online during the meet-
for reimbursement or hospital privileges, or for nonmembers
ing. Registrants will receive an email during the meeting with
who need it to report CME credit:
the link and instructions on how to claim credit.
Onsite, you may report credits earned during Subspecialty ■ CME credit reporting/proof-of-attendance letters
Day and/or AAO 2016 at the CME Credit Reporting booth. ■ Onsite registration receipt
Academy Members: The CME credit reporting receipt is not ■ Instruction course and session verification
a CME transcript. CME transcripts that include AAO 2016
Visit www.aao.org/cme for detailed CME reporting informa-
credits entered onsite will be available to Academy members on
tion.
the Academy’s website beginning Nov. 10, 2016.
After AAO 2016, credits can be claimed at www.aao.org/
cme.
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 Dis- a Distinguished Research Award when he was an ophthalmol-
tinguished Scholar in Ophthalmology at Harvard Medical ogy resident at Temple University Hospital. He was recognized
School. In addition to directing the Glaucoma Service at Mas- as an Irving H Leopold honoree, and he received a Physician
sachusetts Eye and Ear Infirmary (MEEI), he directs the Glau- Scientist Award from Research to Prevent Blindness in 2009.
coma Fellowship Program and the MEEI Teleretinal Program He is recognized for his dedication to teaching, having been
and codirects Harvard’s Glaucoma Center of Excellence. nominated twice by Harvard Medical School for excellence in
Dr. Pasquale received his medical degree with distinction in mentoring and once by the Harvard ophthalmology residents
research from the State University of New York, Stony Brook. for Outstanding Teaching. He was acknowledged for service to
He completed an internal medicine internship at Bronx Munici- ARVO and the Academy with a Silver Fellow award and Secre-
pal Hospital affiliated with the Albert Einstein School of Medi- tariat Award, respectively.
cine. After completing an ophthalmology residency at Temple Dr. Pasquale has dedicated himself to serving as a physi-
University School of Medicine, he completed a 2-year glaucoma cian scientist who seeks opportunities to translate basic science
fellowship at the Wilmer Ophthalmological Institute. discoveries into better treatments for glaucoma patients. He is
Dr. Pasquale is a member of the editorial boards for PLoS an NIH Principal Investigator, with continuous support since
One and American Journal of Ophthalmology. He currently 2006. His research, which leverages the rich resources available
serves as chair of the American Glaucoma Society Research in the Nurses’ Health Study, the Health Professional Follow-up
Committee and was chair of the Glaucoma Section, ARVO Study, and the Women’s Genome Health Study, focuses on the
Meeting Program Committee for 2016. He currently serves discovery of primary prevention strategies in the open-angle
on the National Eye Institute Advisory Council. Dr. Pasquale glaucomas.
was awarded the 2006 American Academy of Ophthalmology He has published over 160 peer-reviewed articles in scien-
Achievement Award and the 2009 Physician Scientist Award by tific journals and 68 reviews / book chapters / editorials. He has
Research to Prevent Blindness. delivered numerous named lectures and has given many talks
Dr. Pasquale has received numerous awards for scientific and courses around the world.
achievement, including Sigma Xi from Manhattan College and
2016 Subspecialty Day | Glaucoma Faculty Listing ix
Faculty
Iqbal K Ahmed MD Claude F Burgoyne MD Robert T Chang MD

Mississauga, ON, Canada Portland, OR Palo Alto, CA
Assistant Professor Senior Scientist and Director Assistant Professor
University of Toronto Optic Nerve Head Research Laboratory Byers Eye Institute at Stanford
Clinical Professor, University of Utah Devers Eye Institute University
Clinical Professor of Ophthalmology
Oregon Health Sciences University
No photo
available
R Rand Allingham MD Balwantray C Chauhan PhD

Durham, NC Halifax, NS, Canada
Professor of Ophthalmology Joseph Caprioli MD FACS Professor and Research Director
Duke University Eye Center Los Angeles, CA Department of Ophthalmology and
Professor and Senior Consultant Professor of Ophthalmology Visual Sciences
Duke – National University of Singapore David Geffen School of Medicine
University of California, Los Angeles
Chief, Glaucoma Division
Jules Stein Eye Institute
No photo
available
Vikas Chopra MD
Husam Ansari MD PhD Santa Monica, CA
Needham, MA Associate Clinical Professor
Glaucoma Service David Geffen School of Medicine at
Ophthalmic Consultants of Boston Meenakshi Chaku MD UCLA
Chicago, IL Medical Director – Pasadena
Director, Glaucoma Service Doheny Eye Centers UCLA
Assistant Professor of Ophthalmology
Loyola University, Chicago
x Faculty Listing 2016 Subspecialty Day | Glaucoma
E Randy Craven MD JoAnn A Giaconi MD David S Greenfield MD

Baltimore, MD Los Angeles, CA Palm Beach Gardens, FL
Chief of Glaucoma Health Sciences Associate Professor of Professor of Ophthalmology
King Khaled Eye Specialist Hospital, Ophthalmology Bascom Palmer Eye Institute
Saudi Arabia Jules Stein Eye Institute University of Miami Miller School of
Associate Professor University of California, Los Angeles Medicine
Wilmer Eye Institute Chief of Ophthalmology
Johns Hopkins University Veterans Administration of Greater Los
Angeles
Michael Greenwood MD
Fargo, ND
Andrew Crichton MD Cataract, Refractive, Glaucoma, Cornea
Calgary, AB, Canada Christopher A Girkin MD Surgeon
Clinical Professor Birmingham, AL Vance Thompson Vision
University of Calgary Chairman and Professor
Department of Ophthalmology
University of Alabama at Birmingham
School of Medicine
Chief Medical Officer
Callahan Eye Hospital
No photo
available
Alon Harris PhD

Nancy L Flattem MD MS Indianapolis, IN
Colorado Springs, CO Letzter Endowed Professor of
Ophthalmologist / Glaucoma Specialist Ophthalmology
Colorado Permanente Medical Group Indiana University School of Medicine
Professor of Cellular & Integrative
Jeffrey L Goldberg MD PhD Physiology
Palo Alto, CA Director of Clinical Research
Professor and Chair Indiana University School of Medicine
Byers Eye Institute
Stanford University
2016 Subspecialty Day | Glaucoma Faculty Listing xi
Gregg A Heatley MD Malik Y Kahook MD Christopher Kai-shun Leung MD

Madison, WI Denver, CO MBChB
Associate Professor of Ophthalmology Professor of Ophthalmology Ho Man Tin, Hong Kong
Vice Chair, Clinical University of Colorado School of Professor, The Chinese University of
University of Wisconsin-Madison Medicine Hong Kong
Dale K Heuer MD L Jay Katz MD Richard A Lewis MD

Milwaukee, WI Philadelphia, PA Sacramento, CA
Professor & Chair of Ophthalmology & Professor of Ophthalmology Past President, American Glaucoma
Visual Sciences Thomas Jefferson University Society
Medical College of Wisconsin Director of Glaucoma Service Past President, American Society of
Director, Froedtert & The Medical Wills Eye Hospital Cataract and Refractive Surgery
College of Wisconsin Eye Institute
Simon K Law MD Paul R Lichter MD

Chris A Johnson PhD Los Angeles, CA Ann Arbor, MI
Iowa City, IA Professor, Stein Eye Institute Professor of Ophthalmology and Visual
Professor, Department of Sciences
Ophthalmology and Visual Sciences W K Kellogg Eye Center
University of Iowa University of Michigan
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 Tucson, AZ Durham, NC
Professor of Clinical Ophthalmology Associate Professor of Ophthalmology
University of California, San Francisco and Neurobiology
Director, Glaucoma Service Duke University Medical Center
San Francisco General Hospital Staff Ophthalmologist
VA Medical Center
Kaweh Mansouri MD
Lausanne, Switzerland
Yao Liu MD
Madison, WI Felipe A Medeiros MD
Assistant Professor of Ophthalmology San Diego, CA
University of Wisconsin School of Professor of Ophthalmology
Medicine and Public Health University of California, San Diego
Cynthia Mattox MD FACS No photo

Boston, MA available
Associate Professor of Ophthalmology
Tufts University School of Medicine
Director, Glaucoma and Cataract
Service
New England Eye Center
Nils A Loewen MD Daniel B Moore MD
Pittsburgh, PA Lexington, KY
Associate Professor of Ophthalmology Assistant Professor
University of Pittsburgh Department of Ophthalmology and
Director, Glaucoma and Cataract Visual Sciences
Service No photo University of Kentucky
University of Pittsburgh Medical Center available
M Lisa McHam MD
Quincy, MA
Partner, Eye Health Services
2016 Subspecialty Day | Glaucoma Faculty Listing xiii
Marlene R Moster MD Kouros Nouri-Mahdavi MD Louis R Pasquale MD

Bala Cynwyd, PA Los Angeles, CA Boston, MA
Professor of Ophthalmology Associate Professor of Ophthalmology Professor of Ophthalmology
Thomas Jefferson University School of Stein Eye Institute Harvard Medical School
Medicine University of California, Los Angeles Director, Glaucoma Service
Attending Surgeon Massachusetts Eye and Ear Infirmary
Glaucoma Service
Wills Eye Hospital
Mildred M G Olivier MD
Hoffman Estates, IL Jody R Piltz-Seymour MD
Professor of Surgery Huntingdon Valley, PA
Peter Andreas Netland MD PhD Department of Ophthalmology Clinical Professor of Ophthalmology
Charlottesville, VA Rosalind Franklin University of Perelman School of Medicine
Vernah Scott Moyston Professor and Medicine and Science at Chicago University of Pennsylvania
Chair Medical School Glaucoma Specialist
University of Virginia School of Associate Professor of Ophthalmology Valley Eye Professionals and Wills Eye
Medicine Midwestern University Hospital
Robert J Noecker MD Richard K Parrish II MD Harry A Quigley MD

Fairfield, CT Miami, FL Baltimore, MD
Director of Glaucoma Professor and Director, Glaucoma A Edward Maumenee Professor of
Ophthalmic Consultants of Connecticut Service Ophthalmology
Assistant Clinical Professor of Bascom Palmer Eye Institute Glaucoma Center of Excellence
Ophthalmology University of Miami Miller School of Wilmer Eye Institute
Yale School of Medicine Medicine Johns Hopkins University
Associate Dean for Graduate Medical
Education
University of Miami Miller School of
Medicine, Jackson Health System
xiv Faculty Listing 2016 Subspecialty Day | Glaucoma
Douglas J Rhee MD Adrienne Williams Scott MD Kuldev Singh MD MPH

Cleveland, OH Baltimore, MD Palo Alto, CA
Professor & Chair Assistant Professor of Ophthalmology Professor of Ophthalmology
Case Western Reserve University School Wilmer Eye Institute Stanford University
of Medicine Johns Hopkins University School of Director, Glaucoma Service
Director, University Hospitals Eye Medicine Stanford University
Institute
Shakeel R Shareef MD Arthur J Sit MD

Thomas W Samuelson MD Rochester, NY Rochester, MN
Minneapolis, MN Associate Professor Associate Professor of Ophthalmology
Consultant, Glaucoma and Anterior Flame Eye Institute Mayo Clinic College of Medicine
Segment Surgery University of Rochester Consultant, Mayo Clinic, Rochester
Minnesota Eye Consultants School of Medicine
Adjunct Associate Professor of
Ophthalmology
University of Minnesota
George L Spaeth MD FACS

Lucy Q Shen MD Philadelphia, PA
Boston, MA Esposito Research Professor of
Assistant Professor of Ophthalmology Ophthalmology
Joel S Schuman MD Harvard Medical School Wills Eye Hospital / Jefferson Medical
New York, NY Massachusetts Eye and Ear Infirmary College
Professor and Chairman of
Ophthalmology
NYU Langone Medical Center
NYU School of Medicine
2016 Subspecialty Day | Glaucoma Faculty Listing xv
Tak Yee Tania Tai MD Steven D Vold MD Joanne C Wen MD

New York, NY Fayetteville, AR Seattle, WA
Assistant Professor of Ophthalmology Cataract & Glaucoma Surgery Assistant Professor
Icahn School of Medicine of Mt. Sinai Consultant University of Washington
Adjunct Attending Vold Vision, PLLC
New York Eye and Ear Infirmary
Kelly Walton Muir MD

Clement C Y Tham FRCS MBBS Durham, NC
FCOPHTHHK Associate Professor of Ophthalmology
Kowloon, Hong Kong Duke Eye Center
Professor, The Chinese University of Career Development Awardee
Hong Kong VA Health Services Research and
Honorary Chief of Service Development
Hong Kong Eye Hospital
xvi Mobile Meeting Guide 2016 Subspecialty Day | Glaucoma
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 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 Shan C Lin MD* 1
a Normal Visual Field
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 Felipe A Medeiros MD* 6
OCT Changes Alone? Yes, I Do!
8:22 AM Point – Counterpoint: Do You Make Treatment Decisions on Kuldev Singh MD MPH* 8
OCT Changes Alone? No, I Don’t!
8:26 AM Rebuttal Felipe A Medeiros MD*
8:27 AM Rebuttal Kuldev Singh MD MPH*
8:29 AM Case Presentation #2: Mild Progression of Visual Field Loss in Patient Christopher Kai-shun Leung 9
With Primary Open-Angle Glaucoma MD MBChB*
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 Kouros Nouri-Mahdavi MD* 12
Visual Field Progression? Yes, I Do!
8:44 AM Point – Counterpoint: Do You Advance Treatment Whenever There Is Harry A Quigley MD* 13
Visual Field Progression? No, I Don’t!
8:48 AM Rebuttal Kouros Nouri-Mahdavi MD*
8:49 AM Rebuttal Harry A Quigley MD*
8:51 AM It’s Not Always Glaucoma: Visual Field Loss due to Neurological Causes Christopher A Girkin MD 14
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.
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 Nancy L Flattem MD MS 17
Time? Pro
9:10 AM Controversy #1: Should Surgery Be Performed in Both Eyes at the Same M Lisa McHam MD 18
Time? Con
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— Steven D Vold MD* 19
Are We Preserving Quality of Life? Pro
9:27 AM Controversy #2: Glaucoma Surgery in the Elderly— George L Spaeth MD FACS 21
Are We Preserving Quality of Life? Con
9:32 AM Rebuttal Steven D Vold MD*
9:33 AM Rebuttal George L Spaeth MD FACS
9:35 AM Discussion
9:39 AM Controversy #3: Should We Adopt New Surgical Techniques Early On? Pro Thomas W Samuelson MD* 22
9:44 AM Controversy #3: Should We Adopt New Surgical Techniques Early On? Con Paul R Lichter MD 25
9:49 AM Rebuttal Thomas W Samuelson MD*
9:50 AM Rebuttal Paul R Lichter MD
9:52 AM Discussion
9:56 AM Controversy #4: Combining Glaucoma Surgeries— Richard A Lewis MD* 26
Does It Add Benefit? Pro
10:01 AM Controversy #4: Combining Glaucoma Surgeries— Richard K Parrish II MD* 27
Does It Add Benefit? Con
10:06 AM Rebuttal Richard A Lewis MD*
10:07 AM Rebuttal Richard K Parrish II MD*
10:09 AM Discussion
10:13 AM Advocating for Patients Jeff S Maltzman MD 28
10:18 AM REFRESHMENT BREAK and AAO 2016 EXHIBITS
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 Arthur J Sit MD* 30
Optic Nerve Progression at “Low” IOP—What’s Going On?
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

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* 41
12:15 PM Presentation of the Award David S Greenfield MD*
12:16 PM LUNCH and AAO 2016 EXHIBITS
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 Clement C Y Tham FRCS 42
MBBS FCOphthHK*
1:35 PM Audience Vote
1:36 PM Panel Discussion
1:42 PM Case #2: High IOP in Microphthalmia Vikas Chopra MD* 44
1:54 PM Case #3: Pseudopigmentary Glaucoma From One-Piece IOL Douglas J Rhee MD* 46
2:06 PM Case #4: Pseudoexfoliation With Subluxed Lens and High IOP Mildred M G Olivier MD* 47
2:18 PM Case #5: Cataract and Glaucoma in a Myope 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 50
PhD*
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

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 Malik Y Kahook MD* 56
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* 57
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 58
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 59
4:38 PM Evidence Presentation Joanne C Wen MD
4:43 PM Case Follow-up Joanne C Wen MD
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*

2016 Subspecialty Day | Glaucoma Section I: Is It Progression? Is It Glaucoma? 1
Case Presentation #1: OCT Changes in a Glaucoma

Suspect With a Normal Visual Field
Shan Lin MD
Clinical Data Exam Data

■ 43-year-old white male physician at UC, San Francisco ■ VA with correction: 20/20 O.U.
■ CC: treated by in past for glaucoma and then followed as ■ Manifest refraction: Plano O.U.
suspect ■ IOP: mid-high teens O.U.
■ Family history: no glaucoma ■ Central corneal thickness: 611 μm O.D., 623 μm O.S.
■ Medical history: otherwise healthy, normal BP, no DM, ■ Gonio: Open to SS 360° O.U.
no sleep apnea, no migraines, no Raynaud’s
Figure 1.
Figure 2.
2 Section I: Is It Progression? Is It Glaucoma? 2016 Subspecialty Day | Glaucoma
Figure 3.
Figure 4.
Figure 5.
Figure 6.
What Do These OCT Changes Mean?

Balwantray C Chauhan PhD
Introduction Hence, the change observed in the patients is attributed to glau-

coma alone. However, recent evidence shows that aging is an
Optical coherence tomography (OCT) is transforming diag-
important contributor to the changes observed in glaucoma,6,7
nostics and measurement of treatment efficacy in many areas
with the pattern of topographical changes being similar. The
in ophthalmology. In glaucoma, OCT is becoming the most
ability to separate normal aging (which has significant interin-
common mode of imaging for evaluating the optic nerve head
dividual variability) from glaucomatous change adds another
(ONH), retinal nerve fiber layer (RNFL), and macular thick-
layer of complexity to determining clinically meaningful pro-
ness.
gression.
Proving the Value of OCT

Other Signs From OCT
As with any new technology in glaucoma, the most obvious
Most of the evidence to date on the merit of OCT relates to
question is whether it offers improvement over our currently
changes in the RNFL. However, OCT also images the neuro-
accepted standards. This perennial question has posed a signifi-
retinal rim with anatomically accurate landmarks,8 the anterior
cant challenge in our field with the development of each new
laminar surface,9 choroid,10 and even sclera.11 It is plausible
imaging or perimetric modality, as their merit is compared to
that changes in these structures, especially in the ONH, pre-
the “accepted” standard of sound clinical observation of the
cede RNFL changes.12,13 Future research on the role of laminar
optic disc and RNFL, or analysis of standard automated peri
changes, such as disinsertion or migration from the sclera, and
metry. When a new test has fewer positive results than the cur-
changes in scleral shape or canal opening will provide clinicians
rently accepted standards, the test is deemed to be insensitive;
with other markers of disease progression.
when it yields more positive results, then it is either more sensi-
tive or has more false-positive results. Investigators thus conduct
longitudinal studies to determine whether changes found previ- References
ously with the new techniques are predictive of changes that we
1. Williams ZY, Schuman JS, Gamell L, et al. Optical coherence
accept today as clinical standards, assuming that the biological tomography measurement of nerve fiber layer thickness and
progressive “event” is the same in both cases. the likelihood of a visual field defect. Am J Ophthalmol. 2002;
Unfortunately, proving the clinical value of changes observed 134:538-546.
with OCT requires numerous years of observation. This is
2. Kuang TM, Zhang C, Zangwill LM, et al. Estimating lead time
because the relative infrequency of examinations carried out by
gained by optical coherence tomography in detecting glaucoma
most clinicians (1 or 2 per year) is probably statistically inad- before development of visual field defects. Ophthalmology 2015;
equate given that glaucoma usually develops and progresses 122:2002-2009.
slowly and that measurement noise represents a challenge.
Ultimately, the value of OCT will be proven when clinical deci- 3. Miki A, Medeiros FA, Weinreb RN, et al. Rates of retinal nerve
fiber layer thinning in glaucoma suspect eyes. Ophthalmology
sions made on the basis of OCT observations lead to improved
2014; 121:1350-1358.
outcomes, such as better visual preservation and quality of life.
Several centers globally have made meaningful progress in these 4. Zhang X, Loewen N, Tan O, et al. Predicting development of
issues. glaucomatous visual field conversion using baseline Fourier-
domain optical coherence tomography. Am J Ophthalmol. 2016;
163:29-37.
Current Evidence That OCT Changes Are Clinically
5. Gracitelli CP, Abe RY, Tatham AJ, et al. Association between
Meaningful
progressive retinal nerve fiber layer loss and longitudinal change
Evidence that baseline measurements of RNFL thickness are in quality of life in glaucoma. JAMA Ophthalmol. 2015; 133:384-
predictive of visual field change emerged as early as 2002;1 390.
however, it was recognized that the high false-positive rate 6. Leung CK, Ye C, Weinreb RN, et al. Impact of age-related change
with the older time domain–based instruments required better of retinal nerve fiber layer and macular thicknesses on evaluation
resolution. More recent evidence that spectral domain–based of glaucoma progression. Ophthalmology 2013; 120:2485-2492.
OCT devices are predictive of visual field loss has emerged from
7. Vianna JR, Danthurebandara VM, Sharpe GP, et al. Importance
numerous groups.2-4 Of relevance to clinical outcomes, RNFL of normal aging in estimating the rate of glaucomatous neuroreti-
changes with OCT have been associated with a decreased qual- nal rim and retinal nerve fiber layer loss. Ophthalmology 2015;
ity of life.5 122:2392-2398.
8. Reis AS, O’Leary N, Yang H, et al. Influence of clinically invisi-
Importance of Changes due to Aging ble, but optical coherence tomography detected, optic disc margin
anatomy on neuroretinal rim evaluation. Invest Ophthalmol Vis
Most studies on rates of glaucomatous changes in the ONH, Sci. 2012; 53:1852-1860.
RNFL, and visual field do not contain parallel control subjects.
9. Park SC, De Moraes CG, Teng CC, et al. Enhanced depth imaging
optical coherence tomography of deep optic nerve complex struc-
tures 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: fac-
tors 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 tomog-
raphy 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 experimen-
tal 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 tomog-
raphy in early experimental glaucoma. Invest Ophthalmol Vis Sci.
2014; 55:574-586.
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 progres- during the course of the disease. Imaging measurements seem
sive retinal ganglion cell (RGC) loss associated with charac- to have most utility for detecting change in early stages of the
teristic structural changes in the optic nerve and retinal nerve disease, while perimetry seems to perform better when visual
fiber layer. The neural insult can result in functional losses field losses are already present.5 The disagreement between the
and decrease in vision-related quality of life. Detection of pro- tests can be used to our advantage, by improving the chances
gression and estimation of rates of disease deterioration are of detecting progressive changes over time. However, the diffi-
essential in order to evaluate risk of functional impairment and culty lies in how best to integrate their results without increas-
establish treatment strategies. ing the chance of false-positives. Several methods of combining
Even though standard automated perimetry (SAP) has structural and functional measurements have been proposed,
been used as the gold standard for diagnosis and assessment including using sophisticated statistics10-12 and by a single
of progression in glaucoma, there is substantial evidence indi- combined structure function index.12 These combined mea-
cating that many patients may show substantial structural surements have been shown to outperform isolated measure-
changes despite absence of detectable or statistically significant ments of structure and function for diagnosis and assessment
changes on SAP.1-4 These structural changes may be detected of disease progression and are finding their way into clinical
by tests such as OCT assessment of the retinal nerve fiber layer practice.
(RNFL), macula, and optic disc. Contrary to long-standing
teachings in glaucoma that prescribe that one should always
References
search for a correlation between structural and functional
losses when evaluating progression, evidence has shown that 1. Kass MA, Heuer DK, Higginbotham EJ, et al. The Ocular Hyper-
with currently available testing methods, agreement seems to tension Treatment Study: a randomized trial determines that topi-
be the exception rather than the rule. In most eyes, progressive cal ocular hypotensive medication delays or prevents the onset of
structural changes are seen in the absence of visual field loss primary open-angle glaucoma. Arch Ophthalmol. 2002; 120:701-
713.
and vice versa. Therefore, requiring that functional changes
must be present in order to confirm clinically significant struc- 2. Medeiros FA, Alencar LM, Zangwill LM, et al. Prediction of
tural findings is counterproductive. functional loss in glaucoma from progressive optic disc damage.
Even though the disagreement between structural and Arch Ophthalmol. 2009; 127:1250-1256.
functional changes may seem puzzling, it can be easily under- 3. Liu T, Tatham AJ, Gracitelli CP, Zangwill LM, Weinreb RN,
stood when considering the properties of the tests available to Medeiros FA. Rates of retinal nerve fiber layer loss in contralat-
measure structure and function, such as their different scales, eral eyes of glaucoma patients with unilateral progression by con-
variability, and dynamic range.5 If methods for assessing struc- ventional methods. Ophthalmology 2015; 122:2243-2251.
tural and functional progression were to agree perfectly, there 4. Kuang TM, Zhang C, Zangwill LM, Weinreb RN, Medeiros FA.
would be no need to use both in monitoring progression. One Estimating lead time gained by optical coherence tomography in
test would suffice. detecting glaucoma before development of visual field defects.
Importantly, in order to justify decision making based on Ophthalmology 2015; 122(10):2002-2009.
results of OCT only, these results need to be of demonstrable
5. Medeiros FA, Zangwill LM, Bowd C, et al. The structure and
clinical relevance and predictive of outcomes that are clinically function relationship in glaucoma: implications for detection of
relevant for patients. It is crucial to demonstrate that progres- progression and measurement of rates of change. Invest Ophthal-
sive structural changes are actually predictive of outcomes mol Vis Sci. 2012; 53:6939-6946.
that are clinically relevant for patients. Several studies have
6. Medeiros FA, Lisboa R, Zangwill LM, et al. Evaluation of pro-
shown consistent data in this regard.6-8 OCT abnormalities
gressive neuroretinal rim loss as a surrogate end point for devel-
have been identified up to 8 years before field loss in some opment of visual field loss in glaucoma. Ophthalmology 2014;
patients.4 Using spectral domain OCT, rates of RNFL thinning 121:100-109.
were shown to be significantly faster in eyes that eventually
developed a visual field defect compared to those that did not, 7. Miki A, Medeiros FA, Weinreb RN, et al. Rates of retinal nerve
fiber layer thinning in glaucoma suspect eyes. Ophthalmology
with each 1-μm per year faster RNFL loss associated with a
2014; 121:1350-1358.
greater than 2 times higher risk of developing a future field
defect. Measurement of progressive structural change has also 8. Chauhan BC, Nicolela MT, Artes PH. Incidence and rates of
been shown to be predictive of further visual field progression visual field progression after longitudinally measured optic disc
in eyes with established perimetric defects, at least in early to change in glaucoma. Ophthalmology 2009; 116:2110-2118.
moderate disease. Progressive RNFL thinning has also been 9. Gracitelli CP, Abe RY, Tatham AJ, et al. Association between pro-
shown to be associated with quality of life outcomes in patients gressive retinal nerve fiber layer loss and longitudinal change in
with glaucoma, as measured by the National Eye Institute quality of life in glaucoma. JAMA Ophthalmol. 2015; 133:384-
Visual Function Questionnaire (NEI VFQ-25).9 390.
Studies of the structure-function relationship in glaucoma
have also attempted to identify when to use one vs. another test
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 inte-
grate 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.
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 and normal appearing optic nerves as determined by ophthal-
purpose of a debate. moscopy, who are found to have below average retinal nerve
fiber layer thickness on imaging tests, may be told that they
The goal of glaucoma management is to preserve vision. While have glaucoma and prescribed IOP lowering treatment. The rate
there is often good correlation between structural and func- of false positives with OCT testing may be unacceptably high
tional measures of optic nerve damage in glaucoma popula- for us to solely use this technology to diagnose and treat glau-
tions, there is tremendous interpatient variability with regard to coma and glaucoma progression.
such correlation using currently available tools to assess these Longitudinal assessment of the rate of structural optic nerve
parameters. While OCT is undoubtedly helpful in categorizing change remains critical in distinguishing between one patient
patients as having or not having glaucomatous disease, par- who is classified as having glaucomatous disease from another
ticularly in circumstances when visual field testing cannot be who continues to be labeled a “glaucoma suspect.” The rapid
performed, the incremental benefit of such structural measures advances in imaging technology, with less than optimal back-
beyond visual field testing in determining when to begin or ward compatibility, have made it difficult to longitudinally
advance treatment for glaucoma has remained controversial. assess structural change.
Some have advocated that OCT is most helpful in assessing ocu- Classifying a patient as having “glaucoma” and commit-
lar hypertensives and glaucoma suspects relative to those with ting them to a lifetime of IOP lowering therapy, which may or
moderate to severe glaucoma who already have reproducible may not be necessary or effective, should not be taken lightly in
visual field abnormalities. individuals who demonstrate no measurable visual abnormal-
It is difficult to argue against the benefit of knowing that ity from the disease. Similarly, advancing therapy in glaucoma
one has glaucoma sooner rather than later and OCT can help patients who show changes in retinal nerve fiber layer thickness
towards that end. Nevertheless, there are some potential pitfalls on OCT testing without measurable changes on perimetric mea-
related to glaucoma therapy in patients with normal visual sures of visual function can also be problematic, particularly
function as confirmed by modern automated perimetry. Not all given that it may be difficult to accurately distinguish structural
patients with apparent structural optic nerve damage will go progression related to aging versus disease.
on to develop visual abnormalities and there is little evidence to While the advent of OCT has undoubtedly improved our
suggest that waiting to see early mild visual field defects prior understanding of glaucomatous disease, an incremental benefit
to starting or advancing therapy will generally result in greater in terms of visual preservation beyond previously existing struc-
lifetime glaucoma related visual disability than treating based tural and functional parameters, including stereoscopic exami-
solely on apparent structural progression. nation of the optic nerve and automated perimetry, has not been
Despite the significant advances in assessing structural dam- proven with this technology. Similarly, composite structural
age to the optic nerve over the past two decades, the diagnosis and functional measurements have not been proven to be bet-
of glaucoma is not always clear cut, with many patients sus- ter in terms of increasing the likelihood of visual preservation
pected of having the disease based on OCT testing not showing relative to functional measurements alone. Not surprisingly, the
the natural history one would expect with such a diagnosis, best measure of the glaucoma patient’s present visual function,
even without treatment. The ever increasing resolution of imag- and predictor of future visual function, is testing that measures
ing devices to compare structural optic nerve parameters of visual function.
“glaucoma suspects” with age matched “normal” individuals
has undoubtedly led to increased utilization of such devices, but
Reference
the impact of these advances on the positive and negative pre-
dictive value of making definitive cross-sectional diagnoses of Singh K, Van Buskirk EM and Spaeth G. A Blink at Diagnosing Glau-
glaucomatous disease have been modest. Such increased resolu- coma Suggests that More May Be Less. Ophthalmology 114(7): 1239-
tion of imaging tools has created a clinical phenomenon where 1240. July, 2007.
patients with average intraocular pressures, normal visual fields
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 discus-
sion on management approaches.
How to Best Assess Visual Field Progression

Chris A Johnson PhD
I. Key Points to classify groups (eg, normal vs. glaucoma, pro-

gressors vs. nonprogressors). It is a forecasting
There are difficulties with assessing glaucomatous
model.
visual field progression:
4. Kalman filters
A. More than just one visual impairment (cataract
or corneal problems, retinal disease, other optic A dynamic model that continually updates
neuropathies, chiasm, optic tract, optic radiations, knowledge about an individual’s visual field
cortical pathways) or systemic condition (diabetes, status and clinical findings to forecast future
inflammatory, infiltrative, or compressive lesions) outcomes
can also be involved.
5. Cluster analysis
B. Visual field testing usually involves subjective
This procedure uses clusters of points in the
responses, and reliability can be compromised.
visual field that correspond to the arcuate nerve
C. There can be considerable variability from one test fiber bundle patterns that are characteristic of
to the next. the distribution of optic nerve fiber patterns that
enter the optic disc.
D. Medical or surgical management of the patient may
change over time. 6. Polar trend analysis
II. Methods of Determining Progression Performs linear regression of visual field sensitiv-
ity values that are contained in various sectors of
A. Clinical evaluation
the visual field. It is used as a method of deter-
Determination of improvement, progression, or mining visual field progression for various local
stability by experienced practitioners regions of the visual field, and as a simple means
of comparing functional visual field changes with
B. Classification systems
structural variations produced by glaucoma.
Divide the range of visual field stages from normal
7. ANSWERS (Analysis with Non-Stationary
to blind into discrete segments
Weibull Error Regression and Spatial Enhance-
C. Event analysis ment)
Determines the change in visual field properties for A linear regression model that incorporates the
the current visual field in comparison to baseline nonstationary variability at different levels of
values visual field sensitivity determined as mixtures
of Weibull functions, and that also includes the
D. Trend analysis
spatial correlation measurements obtained at
Determines the best fit of visual field sensitivity neighboring locations
over time (regression). In most instances this is a
8. Permutation analysis
linear fit, but exponential Tobit, polynomial, and
spline fits have also been employed. Permutation of pointwise linear regression
(PoPLR) is a linear regression procedure that
E. New methods
performs a random permutation of the order of
1. Bayesian procedures visual fields to find the best estimate of visual
field progression
Forecasting techniques that use prior probabili-
ties and other useful information that are modi- 9. Least absolute shrinkage and selection operator
fied by the responses of the individual being (LASSO)
tested
Uses robust regression and several other meth-
2. Support vector machine ods to provide the best prediction of future
visual field status
A heuristic method of using a machine classifier
that develops a model based on a small learning 10. Visual field index (VFI)
set to classify different groups using a variety
A scale from 0 to 100 that classifies glaucoma-
of mathematical techniques (eg, quadratic dis-
tous visual fields on the basis of mean deviation
criminant analysis, Gaussian kernels)
(MD) neighboring points, provides more weight
3. Classification and regression trees (CART) to central points, and includes other informa-
tion. It has a ceiling and a floor effect, which
A decision tree procedure that uses recursive
limits its use for early or advanced glaucoma-
partitioning of numerical and categorical data
tous visual field loss.
III. What Methods Have Been Used for Multicenter IV. How Do the Methods Compare?
Clinical Trials?
A. Clinical vs. trend
A. Clinical assessment
Trend analysis performs better than highly trained
Clinical evaluation of Goldmann kinetic visual clinicians’ evaluations.
fields was used in the Collaborative Normal Glau-
B. Event vs. trend
coma Tension Study (CIGTS). To achieve good sen-
sitivity and specificity, progression was determined Event analysis usually detects progression earlier
by 2 out of 3 visual fields within 6 months demon- (sensitivity), but trend analysis has higher specificity.
strating progression followed by 2 out of 3 showing
C. Criteria for identifying progression
progression in the following 6 months.
Depending on what criteria are used for any of the
B. Classification
analysis procedures, there are large differences in
In the Advanced Glaucoma Intervention Study sensitivity to detect change, specificity for distin-
(AGIS) and CIGTS multicenter trials, a 20-point guishing stable from changing visual fields, and the
glaucoma visual field severity scale was used, and a time required to detect change. Agreement among
4-point deterioration was an endpoint. Advantages: the various methods occurs only about 50%-60%
quantitative. Disadvantages: Not sure whether dif- of the time.
ferences from one point to another are the same
D. Continuous vs. discrete functions
across the whole scale.
Continuous functions contain more information
C. Event
that discrete functions (eg, classification systems).
The Early Manifest Glaucoma Trial (EMGT) used
V. Pearls to Remember
event analysis, which consisted of determination of
a change in the current visual field from baseline A. When in doubt, repeat the test, and compare with
(average of 2 visual fields). To improve specificity, other structural and clinical information.
confirmation of a minimum number of abnormal
B. Individual changes are better than comparison to
points were required on 2 subsequent tests. This
population-based information.
formed the basis for the Glaucoma Progression
Analysis (GPA). C. Progression procedures should be simple and easy
to interpret in a clinical setting.
D. Trend
D. Asking the right questions, being a good listener,
Linear regression analysis (the Progressor program)
and interaction with the patient are vital.
was used in the Primary Treatment Trial (Moor-
fields Eye Hospital). Progressor performs linear E. One test or examination is usually not sufficient to
regression analysis of individual test locations and provide a complete answer to progression.
has procedures for minimizing the influence of
“outliers” (measures that are inconsistent with the
remainder of the data).
E. ANSWERS
By analyzing several large visual field datasets,
ANSWERS demonstrated superior performance
when compared to linear regression and permuta-
tion analysis (PoPLR).
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 stan-
dard achromatic perimetry remains the gold standard for esti-
mating 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 pro-
gression 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.
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 glau-
coma treatment. While these arguments should have been obvi-
ous to my opponent prior to his acceptance of this assignment,
I’m sure he will agree once he thinks it over during the debate.
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 F. Congenital disc abnormalities (pits, tilted discs,
etc.)
G. Age
G. Toxic optic neuropathy
H. Headache
H. Neurodegenerative disease
II. Examination
I. Retrochiasmal disease
A. The optic nerve head
IV. Glaucomatous Neuro-Ophthalmic Imitators
1. Rim pallor
A. Old pressure elevation (eg, “burned out” pigmen-
2. Rim volume preservation
tary glaucoma)
3. Less connective tissue remodeling
B. The small optic disc
B. Visual field
C. IOP variation
1. Vertical midline respect
D. Senile sclerotic glaucoma (rim pallor)
2. Central loss
E. Acquired optic nerve pits (paracentral loss com-
3. Inconsistent with optic nerve contour changes mon)
C. Pupillary function
D. Color vision/perception
E. Other neurologic signs
New and Future Technologies:

mERG, mfVEP, Ganglion Cell Markers
Electrophysiology: Not Just for Retina Anymore!
Stuart J McKinnon MD PhD
Description 3. Basic Clinical Science Courses: “Alternative” to

visual field testing
Review of acceptance and clinical application of visual electro-
physiology in glaucoma management 4. American Board of Ophthalmology
5. Preferred Practice Patterns: “Additional test”
Objective
B. International Society for Clinical Electrophysiology
■ To learn about the Academy’s inclusion of visual electro- of Vision (ISCEV)
physiological tests
1. Technical standards
■ To understand the subclinical nature of glaucoma
■ To recognize the need for clinical application of visual 2. Clinical indications
electrophysiology
C. American Optometric Association
■ To incorporate comparative data for medical decision
making and glaucoma care plan Clinical Practice Guidelines: “Supplemental” test-
ing defined
Course Outline III. Clinical Applications
I. Introduction A. Electroretinography (ERG) – dysfunction of retina:
stimuli
A. Diagnostic tests for glaucoma
1. Pattern ERG: ganglion cells
1. Structure
a. Glaucoma
a. Fundus photos
i. Early detection
b. Heidelberg Retina Tomography
ii. Ganglion cell recovery
c. OCT
b. AMD
2. Function
i. Early detection
a. Visual acuity
ii. Macular function recovery
b. Central visual fields
c. Plaquenil
c. Automated perimetry
i. Early detection
d. Color vision
ii. Appropriate testing timeframe
e. Pupils
d. Diabetic retinopathy/diabetic macular edema
B. Limitations of current technologies
2. Full field flash ERG: photoreceptors
1. Patient limitations
a. Inherited retinal dystrophies
2. Neuro-ophthalmic/subclinical nature of glau-
coma b. Opacities (cataracts+retina concerns):
comorbidities
3. Subjective vs. objective: advantages of objective
testing c. Flicker
a. Detection of early disease B. VEP: electrical activity from retina, through optic
nerve, pathway to visual cortex
b. Management of early disease and known
pathology 1. Stimuli
II.
Historical Acceptance of Visual Electrophysiology a. Pattern visual evoked potentials (VEP)
Technology
b. Flash VEP: poor acuity / opacities
A. The Academy and visual electrophysiology
1. Residents Content Outline
2. Core Knowledge
2. VEP applications E. Discuss the results and implications of the exami-

nation with the patient
a. Optic nerve function (eg, glaucoma)
F. Initiate an appropriate management plan, includ-
b. Multiple sclerosis
ing determination of the frequency of future visits,
c. Ischemic optic neuropathy further diagnostic tests, referral, or treatment
d. Traumatic brain injury V. Conclusions
e. Malingering A. Historically proven and accepted ancillary testing
f. Amblyopia B. Sensitive and specific for subclinical concerns on
the rise
IV. Clinical Objectives
C. Objective vs. subjective alternative for equivocal,
A. Detect and diagnose ocular abnormalities and dis-
differential diagnostic circumstances or patient
eases
limitations
B. Identify risk factors for ocular disease
D. Provides quantitative data to aid in initial diagno-
C. Identify risk factors for systemic disease based on sis and subsequent treatment, “to treat, or not to
ocular findings treat”
D. Establish the presence or absence of ocular signs or
symptoms of systemic disease
2016 Subspecialty Day | Glaucoma Section II: Controversies 17
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 num-
bers whenever possible
3. Use of disposables as much as possible to mini-
mize 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
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 cata- Selected Readings
ract surgery (SBCS) is being considered as an efficient strategy 1. Arshinoff S, Bastianelli P. Incidence of postoperative endophthal-
for delivering cataract care. When following stringent antisepsis mitis after immediate sequential bilateral cataract surgery. J Cata-
guidelines, it appears that the risk of bilateral endophthalmitis ract Refract Surg. 2011; 37:2105-2114.
is extremely low. Although some surgeons argue that refractive
2. Chen PP, Lin SC, Junk, et al. The effect of phacoemulsification
outcome in the first eye may guide adjustments for the second
on intraocular pressure in glaucoma patients: a report by the
eye, current biometry technology has reached a level of accuracy
American Academy of Ophthalmology. Ophthalmology 2015;
that this advantage may be of minimal or no clinical signifi- 122:1294-1307.
cance for eyes with typical measurements. In normal, healthy
eyes, the benefits of SBCS in terms of faster visual rehabilita- 3. Slabaugh MA, Bojikian KD, Moore DB, Chen PP. Risk factors for
tion, patient convenience, and decreased postoperative visits are acute postoperative intraocular pressure elevation after phaco-
emulsification in glaucoma patients. J Cataract Refract Surg.
compelling.
2014; 40:538-544.
When it comes to glaucoma patients, however, the risk-
benefit 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 appropri-
ate 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.
Controversy #2: Glaucoma Surgery in the Elderly—

Are We Preserving Quality of Life? Pro
Steven D Vold MD
I. Glaucoma Laser Surgery II. Microinvasive (Minimally Invasive) Glaucoma

Surgery (MIGS)
A. Laser iridotomy (used for narrow angles / angle-
closure glaucoma) A. Trabecular bypass procedures (eg, Trabectome,
gonioscopy assisted transluminal trabeculotomy
1. Risks
(GATT), Visco360, Trab360, iStent, Hydrus)
a. Cataract
1. Risks
b. Other visual symptoms (glare, monocular
a. Hyphema
diplopia)
b. Cleft or stent closure / failure
c. Iridotomy closure
c. Postoperative infection
d. IOP elevation
2. Benefits
e. Chronic inflammation
a. Efficacious in lowering IOP into mid-high
2. Benefits
teens
a. Alleviates relative pupillary block in patients
b. Easily combined with cataract surgery
with angle closure
c. Excellent safety profile
b. Rapid postoperative recovery
d. Rapid postoperative recovery
B. Laser trabeculoplasty (used for open-angle glau-
coma) B. Suprachoroidal microstents (CyPass, iStent Supra,
iStar)
1. Risks
1. Risks
a. Inadequate response
a. Hyphema
b. Early failure
b. Device failure
c. IOP elevation
c. Postoperative infection
2. Benefits
2. Benefits
a. Excellent safety profile
a. Efficacious in lowering IOP into mid-high
b. May reduce patient dependency on glaucoma
teens
medication
b. Easily combined with cataract surgery
C. Cyclophotocoagulation (used for angle-closure and
open-angle glaucomas) c. Excellent safety profile
1. Risks d. Rapid postoperative recovery
a. Chronic inflammation III. Filtration Surgery
b. Hypotony A. Newer subconjunctival devices (Ex-Press, XEN,
InnFocus)
c. Phthisis bulbi
1. Risks
d. Sympathetic ophthalmia
a. Bleb failure
2. Benefits
b. Hypotony
a. May be done from both transscleral and
endoscopic approaches c. Postoperative infection
b. Micropulse technology has dramatically 2. Benefits
improved safety and postoperative recovery
a. Efficacious in lowering IOPs into low-mid
profiles.
teens
b. Excellent safety profile
c. More rapid recovery when compared to stan-
dard filtration surgery
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 thera-
peutic option
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 diag-

nosis or treatment that is based on “risk factors, most especially
age.”
It is routine to hear recommendations based on chrono-
logical 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 bio-
logical 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.
Controversy #3: Should We Adopt New Surgical

Techniques Early On? Pro
Thomas W Samuelson MD
Introduction majority.” Moore reasons that “trying to convince the mass of a

new idea is useless. It is better to convince innovators and early
As with most “point-counterpoint” discussions, the truth is
adopters first” (see Figure 2).
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 Innovation and Glaucoma Surgery
only drivable road is in the middle.”
Progress in any field requires thoughtful assessment of the
Similarly, the somewhere near the middle is where the major-
status quo, critical analysis of established methods, and incre-
ity of surgeons rightly reside on this topic. Of course we should
mental modification. The safer and more efficacious the cur-
not all be early adopters. Nor should none of us be early adopt-
rent standard, the higher the bar for the next innovation (think
ers. Absolutely someone needs to pioneer and adopt innovative
prostaglandins).
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 dis-
cussion to the adoption of glaucoma surgeries. First a few basic
comments concerning the innovative process and diffusion of
innovations.
Diffusion of Innovation
In his book Diffusion of Innovation,1 now in its fifth edition,
EM Rogers describes a model that classifies individuals accord-
ing to their adoption of innovation (see Figure 1).
Geoffrey A Moore’s book Crossing the Chasm2 further char-
acterizes the diffusion process of innovation. The chasm specifi-
cally refers to the difficult step during which innovations are
transferred from “early adopters” to pragmatists, or the “early Figure 2. From Crossing the Chasm by GA Moore.
Figure 1. The Rogers Innovation Curve.

Traditional glaucoma surgery has significant risk, and in my Of the “out of pocket” surgical options I can offer, such as
opinion that risk and a surgeon’s understandable reluctance to LASIK, toric or multifocal IOLs, or excimer enhancement after
perform marginally safe surgery often result in unrealistic medi- cataract surgery, etc., I feel that femto cataract surgery brings
cation regimens, often to the point of surface toxicity. the least value to patients. Therefore I have not yet adopted it for
Few if any could objectively read the literature concerning routine use. Even so, I am pleased that other surgeons have been
the safety of trabeculectomy and tube shunts and not recognize early adopters, so that the technology will continue to improve.
the significant need for innovation in glaucoma surgical strate- It is quite likely that it will evolve so that one day I will find it
gies for mild to moderate glaucoma. That we need innovation is beneficial.
simply without question.
Consider trabeculectomy, which is highly efficacious but
Who Should Be an Early Adopter?
far from safe. There are many uncontrollable variables. For
example, despite perfect surgery the success of the procedure Early adoption of new technology isn’t for all surgeons. While
is predicated on the healing whim of the conjunctiva, which most surgeons may eventually adopt certain technologies (think
is generally out of the surgeon’s control. Even if the periopera- phacoemulsification), the first surgeons to adopt should be
tive period is navigated without incident, late hypotony or bleb those that are most facile with current surgical options. For
leaks may ensue 5-10 years later. Perhaps most concerning is example, when lecturing on the intricacies of canal-based sur-
the fact that late bleb-related endophthalmitis, a devastating gery and the inherent learning curve, I tell surgeons that if they
complication, remains a possibility as long as the bleb remains are above-average phaco surgeons and above-average glaucoma
functional. These complications are completely unrelated to surgeons, they will be able to adopt canal-based surgery. Most
the disease process and are a direct consequence of the surgical surgeons know if they are a “better than average” surgeon or
treatment itself. not. It is not a crime to be average, and such surgeons might not
Such risk is unacceptable with mild to moderate glaucoma at be best served by paving the way and adopting new technolo-
relatively low risk of functional impairment, by far the largest gies. Early adoption requires critical self-assessment of the sur-
population of patients afflicted with glaucoma. Safer surgical gical skills required for each procedure.
options are welcomed, even if they are only modestly effica-
cious. In my opinion, the high-risk situations that we routinely
Patient-First Mentality
put patients in with trabeculectomy and tube shunts mandate
innovation. We have been too accepting of the poor safety pro- As with all of medicine, innovation must have a patient-first
file of some of our glaucoma interventions. 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 motiva-
Early Adopters
tions. With rare exception, physicians who spend time in the
That said, who should be an early adopter? innovative process do so at a financial loss rather than a gain.
In order to justify the risks inherent in the adoption of inno- Without question, a surgeon generally does better financially by
vation, someone must benefit from each specific innovation, spending time in clinic or the operating room serving patients
preferably more than one party. than spending time in wet labs, advisory board meetings, and
In order of priority, these are: clinical trial meetings. Adopting new technology is very labor
intensive and time consuming, although it is rewarding when it
1. Patients
leads to safer procedures that benefit patients.
2. Society at large
Informed consent is mandatory when adopting new pro-
a. Cost savings
cedures. I actually prefer to think of the process as “informed
b. Healthier society
choice,” a phrase that I first heard from my fellowship men-
3. Surgeons
tor, George Spaeth. In my experience, many patients enjoy
a. Efficiency
participating in clinical trials and make an informed choice to
b. Capacity to serve more patients
do so. Other patients prefer time-tested, traditional interven-
c. Safer surgery makes it easier to sleep at night!
tions. Informed patient choice is mandatory, and basic clinical
I consider myself an early adopter, but in order for me to research principles disallow employing unproven technologies
champion a new surgical procedure I must be convinced that it on vulnerable populations.
will benefit patients.
There have been several new technologies that I became
Summary
certified to perform but have never adopted. Two examples are
holmium laser sclerostomy and transscleral / subconjunctival Innovation is necessary for quality medical care. Whether or
placement of the Ex-Press mini-shunt (without the overlying not to become an early adopter is a complex decision best made
scleral flap). In fact, although I became certified early, I never by individual surgeons. Each situation is different and multifac-
performed a single case of either procedure, as they simply torial. Patient-related considerations are paramount. Societal
didn’t pass my “gut check” threshold. I declined the early and surgeon considerations are subordinate to the needs and
adopter option in those instances. care of the patient.
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.
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, Schiff-
man 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, Schiff-
man JC; on behalf of the Tube Versus Trabeculectomy Study
Group. Postoperative complications in the Tube Versus Trabecu-
lectomy (TVT) study during five years of follow-up. Am J Oph-
thalmol. 2012; 153:804-814.
6. Samuelson TW. Microinvasive glaucoma surgery: coming of age.
J Cataract Refract Surg. 2014; 40:1253-1254.
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.
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 expe-
ditious
II. Defining the Term “Combined”
Usually means cataract plus …
III. Cataract surgery is glaucoma’s safest, most predict-
able, 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).
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 IOP-
lowering effect and c or d have some IOP-lowering effect.
When does 1 + 1 = 0? (a + c) When both a or c have compa-
rable moderate IOP-lowering effects.
When does 1 + 1 = −1? (a + d) When both a and d have sub-
stantial 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.
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 whether with time or money. Currently, only a minority of
requires active participation with and commitment to advocacy ophthalmologists have realized the vital importance of contrib-
efforts. Contributions to the following three critical funds by all uting to OPHTHPAC and the other funds. Right now, major
ophthalmologists is part of that commitment: transformations are taking place in health care and we need
participation from the majority of ophthalmologists so that we
1. OPHTHPAC® Fund
have the resources to better our profession and ensure quality
2. Surgical Scope Fund (SSF)
eye care for our patients.
3. State Eye PAC
Among the significant impacts made by OPHTHPAC are the
Your ophthalmologist colleagues serving on Academy com- following:
mittees—the Surgical Scope Fund Committee, the Secretariat ■ Repealed the flawed Sustainable Growth Rate (SGR)
for State Affairs, and the OPHTHPAC Committee—are dedi-
formula
cating significant time to advocating for patients and the profes- ■ Blocked the unbundling of Medicare global surgery pay-
sion. The OPHTHPAC Committee is identifying congressional
ments
advocates in each state to maintain close relationships with fed- ■ Removed a provision in Medicare fraud and abuse legisla-
eral legislators in order to advance ophthalmology and patient
tion that targeted eyelid surgery
causes. The Secretariat for State Affairs is collaborating closely ■ Working to reduce the burdens from Medicare’s existing
with state ophthalmology society leaders to protect Surgery by
quality improvement programs, such as the EHR Mean-
Surgeons at the state level. Both groups require robust funds
ingful Use program
from both the Surgical Scope Fund and the OPHTHPAC Fund ■ Working in collaboration with subspecialty societies to
in order to protect quality patient care.
preserve access to compounded and repackaged drugs
These committed ophthalmologists serving on your behalf
such as Avastin
have a simple message to convey: “It takes the entire commu- ■ Working to get the Centers for Medicare and Medicaid
nity of ophthalmologists” to be effective.
Services to revisit drastic Medicare fee cuts to glaucoma
■ We need each member of the ophthalmology community and retinal detachment surgeries
to contribute to each of these 3 funds. ■ Working to protect your ability to perform in-office ancil-
■ We need each member of the ophthalmology community lary services in your office
to establish relationships with state and federal legislators.
Contributions to OPHTHPAC can be made here at AAO
■ We need each member of the ophthalmology community
2016 or online at www.aao.org/ophthpac.
to make a commitment to protect quality patient eye care
Leaders of the American Glaucoma Society (AGS) are part
and the profession.
of the American Academy of Ophthalmology’s Ophthalmic
Advocacy Leadership Group (OALG), which has met for the
OPHTHPAC® Fund past nine years in January in the Washington, DC, area to pro-
vide critical input and to discuss and collaborate on the Acad-
OPHTHPAC is a crucial part of the Academy’s strategy to
emy’s advocacy agenda. The topics discussed in the 2016 OALG
protect and advance ophthalmology’s interests in key areas,
agenda included the impact of the Medicare Access and the
including physician payments from Medicare as well as pro-
CHIP Reauthorization Act (MACRA); the IRISTM Registry and
tecting ophthalmology from federal scope of practice threats.
quality reporting under Medicare; data transparency and public
Established in 1985, OPHTHPAC is one of the oldest, largest,
reporting, and a roundtable to discuss challenges for surgical
and most successful political action committees in the physician
specialties. At Mid-Year Forum 2016, the Academy and the
community. We are very successful in representing your profes-
AGS ensured a strong presence of glaucoma specialists to sup-
sion to the U.S. Congress. As one election cycle ends, a new one
port ophthalmology’s priorities, and a record number of oph-
starts. OPHTHPAC is always under financial pressure to sup-
thalmologists visited members of Congress and their key health
port our incumbent friends as well as to make new friends with
staff to discuss ophthalmology priorities as part of Congressio-
candidates. These relationships allow us to have a seat at the
nal Advocacy Day. The AGS remains a crucial partner with the
table and legislators willing to work on issues important to us
Academy in its ongoing federal and state advocacy initiatives.
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 Surgical Scope Fund (SSF)
to ophthalmology involve seats in Congress. The entire House
The Surgical Scope Fund (SSF) provides grants to state ophthal-
of Representatives and one-third of the Senate is up for elec-
mology societies to support their legislative, regulatory, and
tion. Several physicians need our help—and we have many new
public education efforts to derail optometric surgery proposals
friends to make.
that pose a threat to patient safety, quality of surgical care, and
In order for ophthalmology to remain seated at the table, we
surgical standards. Since its inception, the Surgery by Surgeons
need to be heavily invested in this year’s election. That takes
campaign—in partnership with state ophthalmology societies
investment by each member of the ophthalmology community,
and with support from the SSF—has helped 32 state / territo-
2016 Subspecialty Day | Glaucoma Advocating for Patients 29
Surgical Scope Fund OPHTHPAC® Fund State EyePAC

To derail optometric surgical scope of practice Ophthalmology’s interests at the federal level / Support for candidates for State House and
initiatives that threaten patient eye safety and support for candidates for U.S. Congress Senate
quality of surgical care
Political grassroots activities, lobbyists, and Campaign contributions, legislative education Campaign contributions, legislative education
media; No funds may be used for candidates
or PACs
Contributions: Unlimited Contributions: Limited to $5,000 Contribution limits vary based on state
regulations.
Individual, practice, and organization
Contributions are 100% confidential. Contributions above $200 are on the public Contributions are on the public record depending
record. upon state statutes.
rial ophthalmology societies reject optometric scope of practice Please respond to your Academy colleagues and be part of
expansion into surgery. the community that contributes to OPHTHPAC, the Surgical
In 2016, thanks to Surgical Scope Fund support by Academy Scope Fund, and your State Eye PAC. Please be part of the com-
members and tireless advocacy by state ophthalmology society munity advocating for your patients now.
leaders, ophthalmology continues to champion surgical safety
at state capitols across the country. State ophthalmological soci-
*OPHTHPAC Committee
eties and the Academy’s Secretariat for State Affairs faced eight
concurrent Surgery by Surgeons battles, in Alaska, California, Donald J Cinotti MD (NJ) – Chair
Delaware, Illinois, Iowa, Massachusetts, Pennsylvania, and Janet A Betchkal MD (FL)
Puerto Rico. William S Clifford MD (KS)
In each of these legislative battles, the benefits from Surgical Sidney K Gicheru MD (TX)
Scope Fund distributions are crystal clear. The fund has allowed
Michael L Gilbert MD (WA)
for successful implementation of patient safety advocacy cam-
paigns, which result in defeating attempts by optometry to Gary S Hirshfield MD (NY)
expand their scope of practice to include surgery. David W Johnson MD (CO)
The Academy relies not only on the financial contributions Jeff Maltzman MD (AZ)
to the Surgical Scope Fund from individual ophthalmologists Lisa Nijm MD JD (IL)
and their practices, but also on the contributions made by oph- John D Roarty MD (MI)
thalmic state, subspecialty, and specialized interest societies.
Diana R Shiba MD (CA)
The AGS contributed to the Surgical Scope Fund in 2015, and
the Academy counts on its contribution in 2016. Woodford S Van Meter MD (KY)
Contributions to the SSF can be made here at AAO 2016 or John (“Jack”) A Wells III MD (SC)
online at www.aao.org/ssf. Charles M Zacks MD (ME)
Ex Officio Members
State Eye PAC
Daniel J Briceland MD (AZ)
It is also important for all ophthalmologists to support their David W Parke II MD (CA)
respective State Eye PACs because PAC contributions to legisla- Michael X Repka MD (MD)
tors at the state level must come from individual ophthalmolo-
William L Rich III MD FACS (VA)
gists and cannot come from the Academy, OPHTHPAC, or the
Surgical Scope Fund. The presence of a strong State Eye PAC, George A Williams MD (MI)
providing financial support for campaign contributions and
legislative education to elect ophthalmology-friendly candidates **Surgical Scope Fund Committee
to the state legislature, is critical as scope of practice battles and
Kenneth P Cheng MD (PA) – Chair
many regulatory issues are all fought on the state level.
Matthew F Appenzeller MD (NC)
Ronald A Braswell MD (MS)
Action Requested: ADVOCATE FOR YOUR PATIENTS
John P Holds MD (MO)
Academy Surgical Scope Fund contributions are used to sup- Cecily A Lesko MD FACS (NJ)
port the infrastructure necessary in state legislative / regulatory C Blake Myers MD (SC)
battles and for public education. PAC contributions are neces-
William (“Chip”) W Richardson II MD (KY)
sary at the state and federal level to help elect officials who will
support the interests of our patients. Contributions to each of David E Vollman MD MBA (MO)
these three funds are necessary and help us protect sight and
Ex Officio Members:
empower lives. Surgical Scope Fund contributions are com-
pletely confidential and may be made with corporate checks or Daniel J Briceland MD (AZ)
credit cards, unlike PAC contributions, which must be made by Kurt F Heitman MD (SC)
individuals and are subject to reporting requirements.
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 underwent a combined cataract extraction and trabeculectomy
glaucoma 11 years ago. At the time of her diagnosis, her IOP with mitomycin C in the right eye, with a good outcome, and
was 21 mmHg in the right eye and 20 mmHg in the left eye. IOP remained between 7 and 9 mmHg over the next 2 years.
She was pseudophakic in the left eye. Her family history was Soon afterward, however, she developed a superior arcu-
significant for a sibling also diagnosed with glaucoma. Her ate defect in the left eye with split fixation. She underwent a
central corneal thickness was 590 µm in the right eye and trabeculectomy with mitomycin C in the left eye and had a
580 µm in the left eye. Past medical history was not significant. postoperative IOP of 6 to 9 mmHg. Despite apparently well-
She was started on medical therapy in both eyes with latano- controlled IOP, her visual fields have continued to decline in
prost and timolol and had a good response. Over the next 9 both eyes.
years, her IOP was apparently well controlled between 11 and Reduction of IOP, even to low therapeutic levels, is not suffi-
14 mmHg. cient to stop glaucoma progression in all patients. This session
Her visual fields and optic nerve remained stable until 2 will explore how IOP of any magnitude may contribute to glau-
years ago, when she started developing an inferior arcuate coma progression, and what factors beyond IOP may contrib-
defect in the right eye, which progressed to encroach upon fixa- ute to the disease. Treatment options for glaucoma other than
tion. An MRI of the head and orbits was unremarkable. She reduction of IOP will be discussed as well.
2016 Subspecialty Day | Glaucoma Section III: Glaucoma—It’s Not Just About IOP 31
Is IOP Fluctuation Important?

Joseph Caprioli MD FACS
I. IOP Fluctuation: Definitions of AGIS data shows association of IOP fluc-

tuation with progression in eyes with low
A. Instantaneous: caused by saccades, blinks, rubbing,
mean IOPs.
etc.
b. Collaborative Initial Glaucoma Treatment
B. Diurnal-nocturnal (nyctohemeral)
Study (CIGTS) data showed that peak IOP,
1. Circadian SD of IOP, and range of IOP are all more
important than mean IOP in visual field
2. Central, humoral
worsening.
C. Short term: days–weeks
c. Other retrospective and prospective studies
D. Long term have implicated IOP fluctuation as an impor-
tant risk factor in glaucoma progression. See
1. Months–years
CIGTS data cited below.
2. Intervisit in-office IOP measurements
d. Some studies have found no influence of IOP
II. Evidence for Effect of IOP Fluctuation on Glaucoma fluctuation and glaucoma progression (eg,
Progression Ocular Hypertension Treatment Study, Early
Manifest Glaucoma Trial, European Glau-
A. Instantaneous
coma Prevention Study EGPS, and OHT
1. No evidence in the Diagnostic Innovations in Glaucoma
Study). These have in common:
2. Interesting to speculate about effects of brief
high peaks in susceptible eyes and high strain i. Higher IOP
from IOP stress
ii. Earlier glaucoma damage
B. Diurnal-nocturnal (nyctoheneral)
iii. Modest treatment or no treatment
1. No evidence
e. These varied findings are not contradictory,
2. Speculation about why these may not be impor- but rather complementary.
tant:
2. Causes for faster rates of progression with
a. Higher nocturnal IOP in humans largely due higher IOP fluctuation are unknown. Specula-
to supine position tion:
b. Increased perfusion pressure in supine posi- a. Lack of steady state
tion may counteract IOP effects on suscep-
b. Long-term uncompensated loading / unload-
tible tissues.
ing of stresses may break down homeostatic
c. Increased CSF pressure may counteract mechanisms.
stresses caused by IOP on nerve head.
c. Irregular and uncompensated excursions
d. Homeostatic mechanisms exist to compen- into IOP levels that are damaging
sate for regular rhythms.
III. Relevance
e. Difficult to measure nocturnal IOP without
Consider IOP “modulation” rather than “reduction”:
disturbing the IOP: Heisenberg-like uncer-
tainty A. Quantity and quality of IOP control
C. Short term: no evidence B. Target for progressing primary open-angle glau-
coma at high risk
D. Long term (intervisit IOP measurements)
1. Low IOP (low mean, area under curve)
1. Evidence exists that larger long-term IOP fluc-
tuations are important in the progression of 2. Constant IOP (reduce fluctuation and peaks),
glaucoma: especially in patients who progress at low mean
IOPs
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
References
1. Mahdavi K, Hoffman D, Coleman AL, Liu G, Li G, Gaaster- 4. Hong S, Seong GJ, Hong YJ. Long-term intraocular pressure fluc-
land D, Caprioli J. Predictive factors for glaucomatous visual field tuation and progressive visual field deterioration in patients with
progression in the Advanced Glaucoma Intervention Study. Oph- glaucoma and low intraocular pressures after a triple procedure.
thalmology 2004; 111:1627-1635. Arch Ophthalmol. 2007; 125:1010-1013.
2. Caprioli J, Coleman AL. Intraocular pressure fluctuation a risk 5. Lee PP, Walt JW, Rosenblatt LC, et al. Association between intra-
factor for visual field progression at low intraocular pressures ocular pressure variation and glaucoma progression: data from a
in the Advanced Glaucoma Intervention Study. Ophthalmology United States chart review. Am J Ophthalmol. 2009; 144(6):901-
2008; 115(7):1123-1129. 907.
3. Bengtsson B, Leske MC, Hyman L, et al. Fluctuation of intra- 6. Musch DC, Gillespie BW, Niziol LM, et al. Intraocular pressure
ocular pressure and glaucoma progression in the Early Manifest control and long-term visual field loss in the Collaborative Initial
Glaucoma Trial. Ophthalmology 2007; 114:205-209. Glaucoma Treatment Study. Ophthalmology 2011; 118:1766-
1773.
Does Ocular Biomechanics Define Tissue Damage?

Claude F Burgoyne MD
I. Alternative Titles/Questions 6. ONH geometry / architecture

A. Does biomechanics underlie or explain optic nerve 7. ONH material properties
head (ONH) tissue damage in glaucoma?
B. Ocular / ONH local tissue immunity
B. Can eye-specific ONH biomechanics predict where
C. Ocular cellular “senescence” (regardless of age or
a given ONH will become damaged from glaucoma
at any age)
and the IOP at which that damage will occur?
D. All non-ocular systemic factors
C. Will eye-specific ONH biomechanics tell us how to
“strengthen” an ONH or make it less susceptible? 1. Immune / inflammatory
D. Answer to all of the above: Yes, these are all goals/ 2. Genetic
working hypotheses of ONH biomechanics.
V. IOP
II. Why the ONH? Does Biomechanics (Ocular or Other-
A. IOP is not the only thing that contributes to ONH
wise) Apply to Other Sites of Damage?
biomechanics – see above.
A. Retinal ganglion cell (RGC) / non-RGC retina?
B. IOP contributes to ONH biomechanics at all levels
B. Retinal RGC axon? of IOP.
C. Orbital RGC axon? C. All IOP-related and non-IOP-related determinants
of ONH physiology are likely influential at all lev-
D. Lateral geniculate?
els of IOP.
E. Visual cortex?
D. The magnitude of non-IOP related determinants of
F. Answer: Maybe, but most data to date suggest ONH physiology should be independent of the level
ONH is the primary site of damage. of IOP (or we would identify them as IOP-related);
this is not the same as saying that they are more
G. Primary insults to all other sites of damage have
important at low levels of IOP or less important
not been shown to cause a glaucomatous optic neu-
when IOP is high.
ropathy.
1. We should look for them and treat them at all
III. Ocular and Orbital Determinants of ONH
levels of IOP.
Biomechanics
2. Systemic BP, CSF pressure, cellular senescence,
A. IOP magnitude / fluctuation
EOM insertion and ocular movement effects …
B. Orbital (atmospheric) pressure
VI. How Do IOP-Related and Non-IOP Related Risk Fac-
C. CSF pressure / fluctuation tors Interact?
D. Blood pressure / fluctuation Working prediction: The presence and magnitude of
non-IOP related risk factors likely influence the level
E. Extraocular muscle (EOM) / dural insertion anat-
of IOP at which the ONH tissue will be “stable” or
omy
change the least.
F. ONH geometry / architecture
VII. Important Next Steps in ONH Biomechanics
G. ONH material properties
A. Build clinical tools to predict where a given ONH
IV. Ocular, Orbital, and Systemic Determinants of ONH will be damaged regardless of the level of IOP at
Physiology which that damage will occur
A. ONH biomechanics B. Predict the level of IOP at which protective remod-
eling will occur and where
1. IOP magnitude / fluctuation
C. Predict the level of IOP at which RGC axon dam-
2. Orbital (atmospheric) pressure
age and loss will occur
3. CSF pressure / fluctuation
D. Construct a strategy for staging the optic neuropa-
4. Blood: pressure / fluctuation / flow / autoregula- thy of glaucoma that is separate from the magni-
tion tude of axon loss
5. EOM / dural insertion anatomy
E. Construct experimental models of the optic neu- 2. Burgoyne CF, Downs JC. Premise and prediction: how optic nerve
ropathy of glaucoma that do not require IOP eleva- head biomechanics underlies the susceptibility and clinical behav-
tion ior of the aged optic nerve head. J Glaucoma. 2008; 17:318-328.
F. Understand how and why the ONH becomes more 3. Burgoyne CF. A biomechanical paradigm for axonal insult within
the optic nerve head in aging and glaucoma. Exp Eye Res. 2011;
susceptible to axonal injury with age
93:120-132.
G. Determine if those same processes contribute to 4. Sigal IA, Flanagan JG, Ethier CR. Factors influencing optic nerve
glaucoma susceptibility at all ages head biomechanics. Invest Ophthalmol Vis Sci. 2005; 46:4189-
H. Generate ONH-targeted, non-IOP lowering neuro- 4199.
protective interventions 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.
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.
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 Novel interdisciplinary approaches are needed to build an
action of IOP, are involved in the pathophysiology of glau- integrated view of the diverse data coming from experimen-
coma dates back more than a century. The last decades have tal and clinical studies, in order to provide attending physi-
witnessed significant advancements of imaging technologies cians with effective tools to assess the relative weight of the
utilized to visualize and quantify hemodynamic and vascular various glaucoma risk factors in a given patient and to better
parameters within the eye. These technologies have generated tailor treatment and management strategies. Recent results
large amounts of varied data but have also led to many new obtained by analyzing experimental and clinical studies using
questions on the appropriate interpretation of this data from the a novel synergistic combination of statistical and biophysical
clinical viewpoint, such as whether vascular changes are pri- approaches show great promise for advancing individualized
mary or secondary to the disease process and what is the rela- glaucoma care. The main rationale of the combined approach
tionship between vascular, structural, and functional changes. is that statistical methods can unveil correlations among risk
Many population-based studies have identified decreased factors, and that biophysical methods, based on, for example,
ocular perfusion pressure, calculated as differences between the laws of mass transport, fluid and tissue mechanics, and
blood and intraocular pressures, to be associated with increased biochemistry, can elucidate cause-effect relationships among
prevalence and incidence and the progression of glaucoma. The factors.
development of imaging modalities has allowed for many direct For example, many studies have identified high IOP, low
vascular tissue defects in glaucoma to be identified, including blood pressure, low ocular perfusion pressure, and low intra-
disturbances in vascular autoregulation and comparatively cranial pressure as glaucoma risk factors. While the sole
lower blood flow measures in retinal, choroidal, and retro- statistical analysis of data has not been able to explain how
bulbar tissues. Several studies have also found these vascular these factors combine to determine disease status and progres-
biomarkers to be associated with visual field and structural sion in a given patient, a combined statistical and biophysical
glaucomatous damage. Retinal oximetry has demonstrated approach can help us solve the riddle. By combining statistical
metabolic disturbances, including lower extraction of oxygen, and biophysical methods, we have shown that (1) patients with
in glaucoma patients, while very recent advances in angiogra- low blood pressure may be more susceptible to glaucomatous
phy OCT have produced pilot data on optic nerve capillary loss damage even at relatively low IOPs due to the reduced effective-
and perfusion deficits. ness of vascular regulatory compensatory mechanisms and
The ocular circulation is complex and influenced by many the increased venous collapsibility, (2) an elevation in IOP or a
factors that combine to give rise to what is actually measured in decrease in intracranial pressure may have similar implications
each specific patient. These factors may be local to the eye (eg, in terms of optic nerve head biomechanics, but very different
IOP, axial length, optic disc structure) or non-local (eg, blood consequences on retrobulbar and retinal blood flow, and (3) the
pressure, cerebrospinal fluid pressure, vascular regulation, body clinically observed increase in retinal venous oxygen saturation
mass index), and it is extremely difficult to disentangle and may be due to a decrease in oxygen demand in patients with
quantify their individual effect when analyzing the combined elevated IOP and to an impairment of vascular regulation in
data. Indeed, all these factors coexist in each patient, but not normal-tension glaucoma patients.
always with the same relevance. For example, many glaucoma As the advancement of ocular imaging modalities produces
patients continue to experience disease progression despite sig- an ever-increasing number of biomarkers, including vascular
nificant reduction of IOP via medical and/or surgical interven- parameters, the investigation, integration, and comprehensive
tion. Additionally, vascular factors seem to be more pronounced understanding of their importance becomes paramount. Inter-
in some patient subgroups, including those of African descent disciplinary approaches combining clinical research studies and
and those suffering from diabetes. biophysical modeling of outcomes, in combination with other
In order to advance the current understanding of vascular clinical, diagnostic, and demographic factors, will likely be
risk factors in glaucoma, long-term studies that comprehen- required to reveal their importance in glaucoma management
sively assess all risk factors across patient subgroups are indeed and to devise effective tools to better tailor management and
necessary. However, the implementation of such research has therapeutic strategies to each individual patient.
historically been arrested by several limitations. For example,
clinical studies provide data on humans, but they are limited
Selected Readings
in the type of measurements and procedures that can be per-
formed. Animal studies allow more invasive measurements and 1. Weinreb RN, Harris A. World Glaucoma Association Consensus
procedures, but they are limited in the translation of the results Series, no. 6: Ocular blood flow in glaucoma. Amsterdam: Kugler
to humans. Biological studies provide data on cell functions and Publications; 2012.
activities, but they are limited in the integration of the results 2. Chen CL, Bojikian KD, Gupta D, et al. Optic nerve head perfu-
with all other ocular and systemic risk factors. Further, even sion in normal eyes and eyes with glaucoma using optical coher-
advancements in imaging of ocular vascular tissue often assess ence tomography-based microangiography. Quant Imaging Med
only few selected aspects of total perfusion. So how can all this Surg. 2016; 6(2):125-133.
data be rationalized, interpreted, and utilized to better serve
each individual patient coming to the clinic?
3. Gross JC, Harris A, Siesky BA, Sacco R, Shah A, Guidoboni G. 7. Guidoboni G, Harris A, Cassani S, et al. Intraocular pressure,
Mathematical modeling for novel treatment approaches to open- blood pressure and retinal blood flow autoregulation: a math-
angle glaucoma. Expert Rev Ophthalmol. In press. ematical model to clarify their relationship and clinical relevance.
Invest Ophthalmol Vis Sci. 2014; 55(7):4105-4118.
4. Guglielmi A, Guidoboni G, Harris A. Role of ocular perfusion
pressure in glaucoma: the issue of multicollinearity in statistical 8. Guidoboni G, Harris A, Arciero JC, et al. Mathematical modeling
regression models. J Modeling Ophthalmol. In press. approaches in the study of glaucoma disparities among people of
African and European descents. J Coupled Syst Multiscale Dyn.
5. Prada D, Harris A, Guidoboni G, Siesky B, Huang AM, Arciero J.
2013; 1(1):1-21.
Autoregulation in the optic nerve head. Surv Ophthalmol. 2016;
61(2):164-186. 9. Arciero J, Harris A, Siesky B, et al. Theoretical analysis of vas-
cular regulatory mechanisms contributing to retinal blood flow
6. Carichino L, Harris A, Guidoboni G, et al. A theoretical inves-
autoregulation. Invest Ophthalmol Vis Sci. 2013; 54(8):5584-
tigation of the increase in venous oxygen saturation levels in
5593.
advanced glaucoma patients. J Modeling Ophthalmol. 2016;
1(1):64-87.
CSF Pressure: Is It an Important Part of Glaucoma?

R Rand Allingham MD
Introduction and that the CSFp is even lower in patients with normal-tension
glaucoma (NTG). In addition, both groups have shown that
Biological processes essential to life invariably utilize, mitigate,
ocular hypertensive patients without glaucoma have a higher
or confront forces, one of which is pressure. Glaucoma is a dis-
CSFp than controls, which suggests that higher CSFp may be
ease intimately related to the stress and strain produced by vari-
protective for glaucoma.
ous pressures on the optic nerve.
What Biological Factors Alter CSFp, and Are These

Does CSF Pressure Play a Role in Glaucoma?
Associated With POAG?
The damaging effects of elevated IOP and damage on the optic
Ren and co-workers reported that blood pressure and IOP are
nerve observed in patients with glaucoma have been known
positively associated with CSFp in normal individuals but not
since the mid-19th century. In the early 20th century, the first
in people with POAG. Body mass index (BMI) is positively
questions arose about the role of cerebrospinal fluid pressure,
associated with CSFp, so in general, patients with lower BMI
or CSFp, as a counterbalance to IOP. More specifically, does
have a lower CSFp. Consistent with these findings, Pasquale
the pressure difference between IOP and CSFp at the lamina
et al reported that higher BMI was associated with reduced
cribrosa (the translaminar pressure [TLP]) contribute to optic
risk of POAG in women. Asrani et al found that NTG patients
nerve damage in glaucoma? (See Figure 1.)
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 reduc-
tion is remarkably similar to that observed for increasing preva-
lence of POAG.
Figure 1. The lamina cribrosa is the location where IOP comes in con-
tact with the CSF pressure that surrounds the optic nerve.
Does Altering CSFp (and TLP Difference) Affect the

Optic Nerve? Figure 2. CSFp progressively decreases in people after age 50, very
similar to the age when POAG prevalence rises.
Altering CSFp in an animal model was first shown to cause an
optic neuropathy similar to glaucoma by Yablonski and co-
workers in a cat model. Morgan et al showed that the mechani- CSFp and Its Implications for Clinical Practice
cal movement of the lamina cribrosa caused by altering CSFp
was equivalent to that caused by changing IOP in a dog model. There is growing evidence that lower CSFp (and higher TLP dif-
More recently, Wang and co-workers found that chronically ference) increases risk of POAG and NTG and that higher CSFp
reduced CSFp produces retinal nerve fiber thinning that resem- reduces glaucoma risk. Other biological factors that are asso-
bles glaucoma in a monkey model. ciated 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.
What Is the Evidence that CSFp Affects Risk for The ability to measure CSFp noninvasively and then calculate
Glaucoma in Our Patients? TLP difference could provide a potentially powerful approach
In retrospective studies by Berdahl et al and prospective studies to treating our patients with POAG and NTG.
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,
References
1. Marek B, Harris A, Kanakamedala P, et al. Cerebrospinal fluid
pressure and glaucoma: regulation of trans-lamina cribrosa pres-
sure [review]. Br J Ophthalmol. 2014; 98(6):721-725.
2. Yang D, Fu J, Hou R, et al. Optic neuropathy induced by experi-
mentally 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. Ophthal-
mology 2008; 115(5):763-768.
4. Berdahl JP, Fautsch MP, Stinnett SS, Allingham RR. Intracranial
pressure in primary open angle glaucoma, normal tension glau-
coma, and ocular hypertension: a case-control study. Invest Oph-
thalmol 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):259-
266.
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).
Novel Treatment Options for IOP:

Independent Factors
Cynthia Mattox MD FACS
I. Targets for IOP: Independent Factors on Optic Nerve, 3. Kang JH, Pasquale LR, Willett WC, et al. Dietary fat consump-
Retinal Ganglion Cells tion and primary open-angle glaucoma. Am J Clin Nutr. 2004;
79(5):755-764.
A. Ischemia, blood flow autoregulation
4. Passo MS, Goldberg L, Elliot DL, et al. Exercise training reduces
B. Deprivation of growth factors, trophic factors, intraocular pressure among subjects suspected of having glau-
nourishment coma. Arch Ophthalmol. 1991; 109:1096-1098.
C. Excitotoxicity 5. Baskaran M, Raman K, Ramani KK, Roy J, Vijaya L, Badrinath

SS. Intraocular pressure changes and ocular biometry during sir-
D. Oxidative stress sasana (headstand posture) in yoga practitioners. Ophthalmology
2006; 113:1327-1332.
E. Current drugs, or drugs in development
6. Schuman JS, Massicotte EC, Connolly S, Hertzmark E, Mukherji
II. Lifestyle
B, Kunen MZ. Increased intraocular pressure and visual field
A. Diet1-3 defects in high resistance wind instrument players. Ophthalmol-
ogy 2000; 107:127-133.
B. Body mass
7. Dewundara SS, Wiggs JL, Sullivan DA, Pasquale LR. Is estrogen
C. Exercise: Likely IOP effects, but blood flow, perfu- a therapeutic target for glaucoma? Sem Ophthalmol. 2016; 31(1-
sion pressure also affected 2):140-146.
1. Aerobic exercise 8. Kang JH, Pasquale LR, Rosner BA, et al. Prospective study of
cigarette smoking and the risk of primary open-angle glaucoma.
2. Isometric exercise, weight lifting Arch Ophthalmol. 2003; 121:1762-1768.
3. Yoga, inversion vs. flow5 9. Wise LA, Rosenberg L, Radin RG, et al. A prospective study of
diabetes, lifestyle factors, and glaucoma among African-American
D. Wind or other resistance instruments6
women. Ann Epidemiol. 2011; 21(6):430-439.
E. Eye rubbing, Valsalva maneuvers 10. Kim KN, Jeoung JW, Park KH, Kim DM, Ritch R. Relationship
III. Concurrent Systemic Factors between preferred sleeping position and asymmetric visual field
loss in open-angle glaucoma patients. Am J Ophthalmol. 2014;
A. Estrogen7 157:739-745.
B. Smoking8,9 11. Malihi M, Sit AJ. Effect of head and body position on intraocular
pressure. Ophthalmology 2012; 119:987-991.
C. Systemic hypertension control, nocturnal hypoten-
sion 12. Gunasekera V, Ernst E, Ezra DG. Systematic internet-based
review of complementary and alternative medicine for glaucoma.
IV. Body Position Ophthalmology 2008; 115(3):435-439.e2.
A. Sleep10 13. Law SK, Lowe S, Law SM, Giaconi JA, Coleman AL, Caprioli J.
Prospective evaluation of acupuncture as treatment for glaucoma.
B. Neck flexion, hyperextension11 Am J Ophthalmol. 2015; 160(2):256-265.
V. Complementary and Alternative Treatments12 14. Her JS, Liu PL, Cheng NC, et al. Intraocular pressure-lowering
A. Acupuncture, acupressure13,14 effect of auricular acupressure in patients with glaucoma: a pro-
spective, single-blinded, randomized controlled trial. J Altern
B. Herbals and supplements15-17 Complement Med. 2010; 16(11):1177-1184.
C. Meditation 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.
References
16. Lee J, Sohn SW, Kee C. Effect of ginkgo biloba extract on visual
1. Kang JH, Willett WC, Rosner BA, Buys E, Wiggs JL, Pasquale field progression in normal tension glaucoma. J Glaucoma. 2013;
LR. Association of dietary nitrate intake with primary open-angle 22:780-784.
glaucoma: a prospective analysis from the Nurses’ Health Study
and Health Professionals Follow-up Study. JAMA Ophthalmol. 17. Wang SY, Singh K, Lin SC. Glaucoma prevalence and the intake
2016; 134(3):294-303. of iron and calcium in a population-based study. Curr Eye Res.
2013; 38(10):1049-1056.
2. Giaconi J, Yu F, Stone KL, et al; Study of Osteoporotic Fractures
Research Group. The association of consumption of fruits/veg-
etables with decreased risk of glaucoma among older African-
American women in the study of osteoporotic fractures. Am J
Ophthalmol. 2012; 154: 635-644.
Innovations in Neuroprotection
Jeffrey L Goldberg MD PhD
■ Glaucoma is a neurodegenerative disease. ■ Advances in clinical trial design, patient selection, and
■ In glaucoma, retinal ganglion cells (RGCs) and their outcome measures support the premise that clinical trials
axons in the optic nerve degenerate. for neuroprotection can be designed and implemented.
■ Progressive optic nerve degeneration leads to progressive ■ Ciliary neurotrophic factor (CNTF) is a protein normally
vision loss and blindness. expressed at low levels in the visual system.
■ Typically, treatment includes reducing IOP. ■ CNTF has been shown in preclinical research to improve
■ However, not all patients with glaucoma have elevated survival and regeneration of RGCs in a variety of optic
IOP, and lowering IOP is not sufficient to completely neuropathies.
block progression in many patients. ■ CNTF has been tested in human patients with retinitis
■ Current glaucoma research aims to find complimentary pigmentosa, macular degeneration, and, in two Phase 1
therapies to decreasing IOP to promote neuroprotection, open label trials, nonarteritic ischemic optic neuropathy
regeneration, and neuroenhancement of RGCs and their and glaucoma.
axons in the optic nerve. ■ Data from human patients suggest that CNTF can
●● “Neuroprotection” refers to keeping retinal ganglion increase retinal thickness and may stabilize or reverse
cells alive. visual dysfunction.
●● “Regeneration” refers to promoting the regrowth of ■ Based on Phase 1 data, CNTF is hypothesized to prevent
axons from damaged RGCs down the optic nerve. loss of vision (neuroprotection) and/or improve visual
●● “Neuroenhancement” refers to augmenting or function (neuroenhancement) in patients with diagnosed
enhancing the function of residual RGCs. glaucoma.
■ Some therapeutics may promote more than one of these. ■ A clinical trial has been designed to test this hypothesis in
a sham controlled, randomized, masked Phase 2 trial.
2016 Subspecialty Day | Glaucoma The AGS Subspecialty Day Lecture 41
Primary Open-Angle Glaucoma Redefined

Louis R Pasquale MD
I. Ground Rules F. Impaired glucose metabolism8

A. Primary open-angle glaucoma (POAG) ≠ “high- G. Pro-apoptotic genetic environment (p53)
tension glaucoma” (HTG)
VI. Selected POAG Cases Redefined
B. POAG = “HTG” + “NTG” (normal-tension glau-
VII. Conclusion
coma).
Current treatments for POAG are inadequate in that
C. “Low pressure glaucoma” (LPG) is a confusing
side effects are more prominent than the disease early
term that should be discarded.
on and halting neuronal progression when the disease
D. POAG ≠ glaucoma is advanced does not seem possible. In the future we
will have a better understanding of the natural history
II. POAG
of POAG, and we will avert iatrogenic injury induced
POAG is a heterogeneous group of IOP-related pro- by our treatments. POAG is really several diseases,
gressive optic nerve diseases in which multiple mecha- some of which are best defined by declining sex hor-
nisms of neuronal degeneration are implicated. It is mones; others described by impaired nitric oxide
not an idiopathic condition. Rejection of the notion signaling; and still others, by insulin resistance. There
that the cause of the disease is unknown will lead to are other disease mechanisms in POAG that remain
more rational treatments that prevent and/or slow dis- undefined. Ultimately the terms “NTG,” “HTG,” and
ease progression. “POAG” will be replaced by biochemical pathway and
molecular profiles that will lead to precision medicine
III. Strategy for Redefining POAG
solutions. Armed with such information we may be
Identify the upstream causes of POAG so that more able to predict who will develop POAG and draw up
rational drug targets are identified. Upstream factors pre-emptive strategies to avert visual field loss.
that simultaneously contribute to variable outflow
impairment and increased optic nerve vulnerability to
References
degeneration are particularly attractive candidates.
1. Bailey JN, Loomis SJ, Kang JH, et al. Genome-wide association
IV. Tools Used to Redefine POAG analysis identifies TXNRD2, ATXN2 and FOXC1 as suscepti-
A. Genetics/genomics bility loci for primary open-angle glaucoma. Nat Genet. 2016;
48:189-194.
National Eye Institute Human Glaucoma Human
2. Hysi PG, Cheng CY, Springelkamp H, et al. Genome-wide analy-
Genetics Collaboration Heritable Overall Opera-
sis of multi-ancestry cohorts identifies new loci influencing intra-
tional Database / International Glaucoma Genetics ocular pressure and susceptibility to glaucoma. Nat Genet. 2014;
Collaboration1,2 46:1126-1130.
B. Population-based studies with incident POAG 3. Kang JH, Willett WC, Rosner BA, Buys E, Wiggs JL, Pasquale
LR. Association of dietary nitrate intake with primary open-angle
1. 20-year Ocular Hypertension Treatment Study
glaucoma: a prospective analysis from the Nurses’ Health Study
cohort and Health Professionals Follow-up Study. JAMA Ophthalmol.
2. Nurses Health Study 2016; 134:294-303.
3. Health Professionals Follow-up Study3 4. Kim DW, Jeoung JW, Kim YW, et al. Prelamina and lamina
cribrosa in glaucoma patients with unilateral visual field loss.
C. Carefully performed clinical studies4 Invest Ophthalmol Vis Sci. 2016; 57:1662-1670.
D. Animal models with relevance to the human disease 5. Lei Y, Zhang X, Song M, Wu J, Sun X. Aqueous humor outflow
physiology in NOS3 knockout mice. Invest Ophthalmol Vis Sci.
1. Nitric oxide synthase 3 knockout mouse5 2015; 56:4891-4898.
2. Soluble guanylate cyclase knockout mouse6 6. Buys ES, Ko YC, Alt C, et al. Soluble guanylate cyclase alpha1-
deficient mice: a novel murine model for primary open angle glau-
V. Putative Upstream Causes of POAG
coma. PLOS ONE 2013; 8, e60156.
A. Alteration in sex hormones7 7. Vajaranant TS, Pasquale LR. Estrogen deficiency accelerates aging
B. Endothelial (outflow + vascular) dysfunction of the optic nerve. Menopause 2012; 19:942-947.
C. Mitochondrial dysfunction 8. Shen L, Walter S, Melles RB, Glymour MM, Jorgenson E. Diabe-
tes pathology and risk of primary open-angle glaucoma: evaluat-
D. Oxidative stress ing causal mechanisms by using genetic information. Am J Epide-
miol. 2016; 183:147-155.
E. Neuroinflammation (excess TNF alpha)
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 B. Topical pilocarpine

A. 51-year-old Asian woman with normal visual acu- 1. Advantage
ity and IOP in clinic now, without medications
Constricts pupil and widens angle pharmaco-
B. 180-degree appositional angle closure on dark- logically, without risk of laser or surgical inter-
room gonioscopy despite patent laser peripheral ventions
iridotomy (LPI). No peripheral anterior synechiae
2. Disadvantages
(PAS).
a. Long-term drug application is required to
C. LPI performed previously elsewhere, for ocular
keep angle open, with both short- and long-
hypertension (OHT) (O.D.: 32 mmHg; O.S.: 28
term adverse drug effects.
mmHg), “angle closure,” and iris bombé.
b. Drug compliance may be an issue, especially
D. No functional or structural evidence of glaucoma-
with adverse effects such as compromised
tous optic neuropathy
night vision, accommodative change, head-
E. History suggestive of 1 to 2 episodes of possible ache and brow-ache, and ocular irritation.
acute OHT since LPI
c. May make subsequent lens / cataract surgery
Episodic “acute blurring” in the evenings, with more difficult
halo (?). Not sure whether affecting one eye or
3. Comment: Patients of this active age group
both. Occasional headache. No obvious redness,
are unlikely to be able to tolerate regular drug
nausea, or vomiting.
administration and adverse effects in the long
F. Imaging suggestive of plateau iris configuration (or term.
even syndrome if episodes of raised IOP confirmed)
C. Laser peripheral iridoplasty
II. Treatment Options
1. Advantages
A. Observation
a. Noninvasive office procedure
1. Advantages
b. Effectively opens up appositionally closed
a. As episodes of acute OHT are not yet con- angle in one setting, with no patient compli-
firmed, this may merely be a case of primary ance issue. Effect can be maintained in long
angle closure suspect (PACS) with plateau term.1,2
iris configuration.
c. Lower risk of surgical complications com-
b. Least risk of adverse effects or complica- pared to lens extraction
tions arising from the treatment, among the
2. Disadvantage
options listed here
Risk of laser complications (eg, iris atrophy,
2. Disadvantages
damage to corneal endothelium, etc.), especially
a. Risk of acute primary angle closure (APAC) if not properly applied2
attack, which may result in irreversible
3. Comment: May be a suitable approach, espe-
structural damage or even visual loss if not
cially if recent episodic OHT likely. Even better
promptly diagnosed and treated
justified if OHT is confirmed, or glaucomatous
b. Risk of progression to PAC, or even PACG, optic neuropathy is documented.
in the long term, especially if patient lost
D. Lens extraction
from follow-up subsequently
1. Advantages
3. Comment: Observation may be one possible
approach, especially if patient is able and willing a. Most effective means to deepen anterior
to seek prompt ophthalmic attention if APAC chamber and widen drainage angle3
occurs and will likely comply with regular
b. Decreases IOP and need for glaucoma drugs4
follow-up arrangements.
c. Eliminates future need for cataract surgery
2016 Subspecialty Day | Glaucoma Section IV: The “New Patient” in Your Clinic—Treatment Options 43
2. Disadvantages B. With either approach, regular follow-up is neces-

sary, in particular to monitor angle status, IOP, and
a. Major surgery and risk of complications4
signs of glaucoma.
compared to more conservative options above
C. Patient should be educated about symptoms of
b. May introduce presbyopia if not already
acute OHT and advised to seek prompt ophthalmic
present, though this can be partially allevi-
attention should any of these arise.
ated with monovision or multifocal IOL
3. Comment: Clear lens extraction probably not
References
justified in the absence of documented OHT or
glaucomatous optic neuropathy. Lower thresh- 1. Ritch R, Tham CC, Lam DS. Long-term success of argon laser
old for cataract extraction may be considered. peripheral iridoplasty in the management of plateau iris syn-
drome. Ophthalmology 2004; 111(1):104-108.
E. Alternative potential treatment option: Photoco-
agulation and shrinkage of prominent ciliary pro- 2. Ritch R, Tham CC, Lam DS. Argon laser peripheral iridoplasty
(ALPI): an update. Surv Ophthalmol. 2007; 52(3):279-288.
cesses using endoscopic approach
3. Tham CC, Leung DY, Kwong YY, Li FC, Lai JS, Lam DS. Effects
1. Partially reversing plateau iris configuration of phacoemulsification versus combined phaco-trabeculectomy on
2. Experimental and not evidence-based yet drainage angle status in primary angle closure glaucoma (PACG).
J Glaucoma. 2010; 19(2):119-123.
3. Best to combine with lens extraction
4. Tham CC, Kwong YY, Baig N, Leung DY, Li FC, Lam DS. Phaco-
4. Comment: Not recommended for routine clini- emulsification versus trabeculectomy in medically uncontrolled
cal practice, due to lack of evidence chronic angle-closure glaucoma without cataract. Ophthalmol-
ogy 2013; 120(1):62-67.
III. Conclusions
A. Depending on how likely it is that those were epi-
sodes of OHT, presenter is inclined toward offering
observation or laser peripheral iridoplasty, with the
aim of minimizing adverse effects, risk of complica-
tions, and need for patient compliance in the long
term.
Case #2: High IOP in Microphthalmia

Vikas Chopra MD, Brian A Francis MD
The patient is a 54-year-old monocular female with microph- C. Very high IOP: Risk of decompression
thalmia, aniridia, and aphakia. The IOP is 52 mmHg on
D. Aphakia
maximum glaucoma medications including oral acetazolamide.
There is advanced visual field loss with split fixation in the 1. Unicameral eye
superior quadrant and severe glaucomatous optic nerve damage
2. Vitreous
(0.9–0.95).
3. Refractive issues
I. Key Features of the Clinical Case
III. Surgical Options
A. Patient has glaucoma with multiple mechanisms:
A. Microinvasive glaucoma surgery, angle based, and
1. Aniridia – secondary angle closure
suprachoroidal shunt procedures
2. Aphakia
B. Trabeculectomy
3. Microphthalmia – primary and secondary angle
C. Tube shunt: Ahmed
closure
D. Tube shunt: Baerveldt
B. Patient is monocular. What was the cause of vision
loss in the fellow eye? This will help guide surgical E. Transscleral cyclophotocoagulation (CPC) or
approach. micropulse diode CPC
1. Choroidal hemorrhage? F. Endoscopic cyclophotocoagulation (ECP)
2. Uncontrolled IOP and glaucoma damage? G. Secondary IOL implantation
3. Endophthalmitis? H. Glaucoma surgery combined with pars plana
vitrectomy
4. Hypotony and phthisis?
IV. Conclusions
C. Extent of optic nerve damage and target IOP
A. Clinical case management
D. Prior surgeries in the operative eye and fellow eye?
B. Follow-up for clinical case
1. Glaucoma surgeries
C. Management is individualized, depending on his-
2. Retinal procedure (vitrectomy)
tory of prior treatment and response, stage of dis-
E. Aphakia: Can patient see with contact lens, or is a ease, visual potential, and other factors.
secondary IOL needed?
1. This greatly increases the complexity of the Selected Readings
case.
1. Nelson LB, Spaeth GL, Nowinski TS, et al. Aniridia: a review.
2. Scleral IOL fixation Surv Ophthalmol. 1984; 28:621-642.
II. Management Issues 2. Grant WM, Walton DS. Progressive changes in the angle in con-
genital aniridia, with development of glaucoma. Am J Ophthal-
A. Microphthalmia mol. 1974; 78:842-847.
1. Axial length: 21 mm or less 3. Wiggins RE, Tomey KF. The results of glaucoma surgery in
aniridia. Arch Ophthalmol. 1992; 110:503-505.
2. Autosomal dominant, autosomal recessive and
sporadic 4. Walton DS. Aniridic glaucoma: the results of goniosurgery to
prevent and treat this problem. Trans Am Ophthalmol Soc. 1986;
3. Isolated vs. syndromic 84:59-70.
4. Microphthalmia–anophthalmia–coloboma 5. Chen TC, Walton DS. Goniosurgery for prevention of aniridic
spectrum (genetic testing) glaucoma. Arch Ophthalmol. 1999; 117(9):1144-1148.
5. High risk for choroidal hemorrhage or effusion 6. Adachi M, Dickens CJ, Hetherington J, et al. Clinical experience
(intraoperatively and postoperatively) of trabeculotomy for the surgical treatment of aniridic glaucoma.
Ophthalmology 1997; 104:2121-2125.
B. Aniridia
7. Molteno ACB, Ancker E, Van Biljon G. Surgical technique for
1. Angle anatomy advanced juvenile glaucoma. Arch Ophthalmol. 1984; 102:51-57.
2. Compromised outflow pathways (both trabecu-

lar and suprachoroidal)
8. Billson F, Thomas R, Aylward W. The use of two-stage Molteno

implants in developmental glaucoma. J Pediatr Ophthalmol Stra-
bismus. 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. Ophthalmol-
ogy 1998; 105:1921-1927.
11. Kirwan JF, Shah P, Khaw PT. Diode laser cyclophotocoagulation:
role in the management of refractory pediatric glaucomas. Oph-
thalmology 2002; 109:316-323.
Case #3: Pseudopigmentary Glaucoma From

One-Piece IOL
Douglas J Rhee MD
I. Key Features of Clinical Case B. Laser: Argon laser cautery if neovascularization of

the angle or iris is seen
A. Clinical history of intermittent spiking IOPs
C. Surgery
B. Patient has presence of inflammation.
1. If caught early, simple removal of IOL can be
C. Clinically had appearance of IOL very close to
curative.
pupillary margin
2. If condition has been present for > 6-12 months,
D. External sutures are close to the limbus.
will likely need IOP-lowering procedure along
E. Plateau iris appearance in only one eye with IOL removal.
F. Ultrasound biomicroscopy is diagnostic. III. Surgical Options
G. Others possible findings but not seen in this case: A. IOL rotation if there is iris entrapment with an
pigment dispersion, iris transillumination defects, anterior chamber IOL (AC-IOL)
microhyphema
B. IOL exchange
II. Management Issues
1. Remove the offending IOL
A. Medical
2. Options for replacement include: AC-IOL,
1. Pilocarpine to decrease IOL chaffing sutured (scleral or iris) or glued posterior cham-
ber IOL
2. Palliative care
IV. Conclusions
a. Usual antiglaucoma medications to lower
IOP and blunt the IOP spikes A. Most important aspect is recognition, as this condi-
tion is potentially reversible.
b. Stop aspirin, NSAIDs, warfarin (ie, antico-
agulation) if microhyphema is a significant B. Surgical intervention is most often needed.
component.
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 2. Transscleral: Video presentation, compliments
of Brock Blakewell MD
E. Mechanism of action
VI. Surgical Options
II. Key Features of Clinical Case
A. Laser trabeculoplasty
A. Poor vision O.S.
B. Trabeculectomy or Ex-Press shunt
B. Uncontrolled IOP O.S. of 31 mmHg
C. Trabectome
C. On maximum tolerated medical therapy (MTMT)
D. Glaucoma drainage device
D. Subluxated IOL O.S.
E. Micropulse G probe
E. Gonioscopic evaluation O.S. open-angle glaucoma /
narrow angle O.D. F. Cyclophotocoagulation
F. Progressing visual fields G. Endoscopic cyclophotocoagulation
III. Other Clinical Features H. Minimally invasive glaucoma surgery
A. Unilateral vs. bilateral VII. Conclusions
B. Frequency of evaluations A. Patient expectations regarding visual rehabilitation
IV. Genetic / Environmental Influences B. Uncontrolled left eye pressure on MTMT
A. Affected populations: Scandinavian / Bantu C. Pseudoexfoliation of the lens O.D. with narrowing
chamber
B. Alleles
D. Instability/subluxation of the IOL in the left eye
1. LOXL 1
E. Language/culture
2. CACNA1A
3. Clusterin
References
C. Environmental factors
1. Kim KE, Kim MJ, Park KH, et al; Epidemiologic Survey Commit-
1. Light exposure tee of the Korean Ophthalmological Society. Prevalence, aware-
ness, and risk factors of primary open-angle glaucoma: Korea
2. Latitudes (northern) National Health and Nutrition Examination Survey 2008-2011.
Ophthalmology 2016; 123(3):532-541.
3. Caffeine
2. Lam D, Lee J, Jonas J, et al. Glaucoma: today and tomorrow. Asia
V. Cataract Challenges Pac J Ophthalmol (Phila). 2016; 5(1):2-4.
A. Capsular tension rings 3. Wiggs JL. Association between LOXL1 and pseudoexfoliation.
B. Zonular dehiscence / laxity Arch Ophthalmol. 2008; 126(3):420-421.
Case #5: Cataract and Glaucoma in a Myope

Tak Yee Tania Tai MD
I. Case Features C. Combined cataract with glaucoma filtration surgery

A. Patient referred for glaucoma evaluation; cataract 1. Pro: Can achieve low pressures
surgery planned, but referring ophthalmologist
2. Pro: Patient may not need another surgery.
questions possible need for a combined procedure.
3. Con: Possible lower success rate for filtration
B. Exam shows cataract.
surgery
C. High myopia
4. Con: Bigger surgery and longer surgical time for
D. Gonioscopy shows angle open to ciliary body band. a complex eye may lead to even higher chance of
complications.
E. IOP elevated despite multiple medications.
D. Combined cataract with microinvasive glaucoma
F. Advanced disc cupping
surgery (MIGS) procedure
II. Management Considerations
1. Pro: Options for future filtration surgery
A. Cataract is visually significant.
2. Pro: Little additional surgical time compared to
B. IOP is higher than optimal. phacoemulsification alone
C. High myopia is associated with increased risks and 3. Pro: Low risk of hypotony / choroidal hemor-
challenges for cataract extraction. rhage
1. Posterior capsule tear 4. Con: May not achieve the necessary IOP lower-
ing
2. Zonular dehiscence
3. Anterior capsule tear
References
4. Reverse pupillary block
1. Zuberbuhler B, Seyedian M, Tuft S. Phacoemulsification in
5. Retinal detachment eyes with extreme axial myopia. J Cataract Refract Surg. 2009;
35(2):335-340.
6. Refractive error
2. Dodick JM, Kahn JB. Special considerations for cataract surgery
D. High myopia is associated with increased risks and in the face of pathologic myopia. In: Spaide RF, Ohno-Matsui K,
challenges for glaucoma filtration surgery. Yannuzzi LA, eds. Pathologic Myopia. New York: Springer Sci-
ence and Business Media; 2014:313-314.
1. Thinner, more flexible sclera
3. Sergienko NM, Shargorogska I. The scleral rigidity of eyes with
2. Intraoperative suprachoroidal hemorrhage different refractions. Graefes Arch Clin Exp Ophthalmol. 2012;
250:1009-1012.
3. Hypotony maculopathy
4. Matsumoto Y, Fujihara M, Kanomori A, Yamada Y, Nakamura
4. Delayed suprachoroidal hemorrhage
M. Effect of axial length reduction after trabeculectomy on the
III. Surgical Options development of hypotony maculopathy. Jpn J Ophthalmol. 2014;
58:267-275.
A. Cataract surgery alone
5. Jeganathan VSE, Ghosh S, Ruddle JB, Gupta V, Coote MA,
1. Pro: IOP-lowering effect of cataract surgery Crowston JG. Risk factors for delayed suprachoroidal hemorrhage
following glaucoma surgery. Br J Ophthalmol. 2008; 92:1393-
2. Con: Risk for IOP spike following cataract sur- 1396.
gery
6. Vijaya L, Manish P, Ronnie G, Shantha B. Indian J Ophthalmol.
3. Con: IOP-lowering effect of cataract surgery 2011; 59(suppl 1):S131-S140.
may not be significant and may not last long.
7. Lochhead J, Casson RJ, Salmon JF. Long term effect on intraocu-
B. Glaucoma surgery first lar pressure of phacotrabeculectomy compared to trabeculectomy.
Br J Ophthalmol. 2003; 87:850-852.
1. Pro: Possibly better success for trabeculectomy
later 8. Chen PP, Lin SC, Junk AK, Radhakrishnan S, Singh K, Chen TC.
The effect of phacoemulsification on the intraocular pressure in
2. Pro: Can revise filtration surgery during cata- glaucoma patients: a report by the American Academy of Oph-
ract extraction thalmology. Ophthalmology 2015; 122(7):1294-1307.
3. Con: Likely inevitable second surgery 9. Rebolleda G, Muñoz-Negrete, FJ. Phacoemulsification in eyes
with functioning filtering blebs: a prospective study. Ophthalmol-
4. Con: Patient and referring physician less happy ogy 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 pro- The most common cause of failure in filtering surgery is
cedure for the surgical treatment of glaucoma. Historically, subconjunctival fibrosis. Recognition that certain popula-
the common denominator of filtration surgery has been the tion groups (patients of African American descent, younger
creation of a hole through the sclera into the anterior chamber patients, or those who have been using glaucoma medications
so that aqueous flow can occur into the subconjunctival space, for prolonged periods) are prone to inflammation and scarring
thus lowering IOP. In the short term, the sclera and its ostium postoperatively has been an important facet of filtration surgery
control outflow, while in the longer term, aqueous flow is con- management. Therefore anti-inflammatory therapy has played
trolled by the resistance of the conjunctiva. an important role in the management of filtration surgery.
The earlier forms of filtration surgery involved scleral drain- Corticosteroids, both systemic and topical, have always been
age sites that were full thickness through the sclera. While these the mainstay of anti-inflammatory therapy. Antimetabolites
procedures were effective in lowering IOP in the longer term, were initially introduced in the form of 5-fluorouracil and were
the short-term postoperative period typically involved signifi- typically administered postoperatively twice a day via subcon-
cant hypotony, which caused significant morbidity and required junctival injections after surgery. While this regimen was effec-
intense management in an in-patient setting. The unregulated tive, it was uncomfortable for the patient and for the glaucoma
early flow was managed by full-time patching of the eye and fellow assigned to give the injections.
the use of devices, such as the Simmons shell, that would apply Intraoperative administration of mitomycin C, a more potent
pressure to the ostium and slow flow temporarily. antimetabolite, was introduced in the mid 1980s. This major
The recognition of the difficulties in the early postop period step forward improved the success rate of filtration surgery
associated with full-thickness filtration surgery led to the through controlling subconjunctival fibrosis. The mitomycin is
introduction of guarded filtration techniques. These techniques typically administered on top of the sclera and underneath the
involved the creation of half-thickness scleral flaps that are conjunctiva on sponges soaked in a predetermined concentra-
sutured to mitigate the flow of aqueous from the eye. Sutures tion of solution for a predetermined amount of time and then
are lysed selectively to lower IOP further when the initial post- washed away. The exposure is dictated by surgeon experience
operative period, with its high risk of hypotony and associated and patient risk profile. A newer commercial product has been
complications, has passed. This technique is the still the basis of introduced to standardize the solution and application materi-
modern trabeculectomy and is used today. als.
In an effort to minimize early hypotony even more, tech- While mitomycin C use has become standard in filtration
niques such as deep sclerectomy have been introduced that leave surgery, it has introduced new problems in the longer term. Late
a thin layer or window of the Descemet membrane in place. bleb leaks and prolonged hypotony occur in patients in which
This layer of tissue provides more resistance to outflow and the subconjunctival healing has been retarded too much.
therefore has a lower rate of flow. The downside of this tech- Filtration surgery remains the standard for glaucoma
nique is that completing the procedure in an optimal manner surgery, owing to its ability to deliver efficacy in terms of pro-
requires optimal ocular tissue and exacting tissue dissection. longed IOP lowering at significant levels. The technique has
Also, in some cases, the flow is not vigorous enough to lower evolved over time and may be enjoying a renaissance as newer
IOP adequately in the longer term. devices are introduced that may enhance the safety profile of
Recently, devices have been introduced that attempt to stan- the procedure.
dardize 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 intraopera-
tively, and restrict flow so that there is less early inflammation
and hypotony.
50 Section V: Past, Present, and Future of Surgical Techniques 2016 Subspecialty Day | Glaucoma
Evolution of Tubes
Peter A Netland MD PhD
I. Introduction B. An implant with a pressure-sensitive slit opening

was described in 1976 by Krupin.
A. Use of setons to “wick” aqueous from the anterior
chamber dates back to 1906, with the use of horse- 1. The slit “valve” was prone to variability of effi-
hair to drain aqueous through a paracentesis. Vari- cacy and obstruction by debris.
ous materials, including suture, glass, metals, plas-
2. The Krupin (Eagle Vision) implant is no longer
tic, and biologic material, were used and ultimately
commercially available.
failed due to problems with inflammation, fibrosis,
and infection. C. Various other flow-restrictive implants, including
the Joseph, White, and Optimed implants, were
B. In the 1970s, Molteno pioneered development
developed but did not remain commercially avail-
of a posterior tube shunt implant, with a plate
able.
implanted posterior to the limbus connected to the
anterior chamber by a long silicone tube, thereby D. Ahmed Glaucoma Valve was introduced in 1993.
initiating the modern glaucoma drainage implant
1. The valve is comprised of 2 thin silicone elasto-
era.
mer membranes positioned in a Venturi-shaped
II. Development of Nonrestrictive Implants chamber.
A. Molteno implant variations 2. Different models include polypropylene plates
(single-, double-plate, and pediatric), silicone
1. Polypropylene plates, including single-plate (133
plates (single-, double-plate, and pediatric), and
mm2), double-plate, pressure ridge, and pediat-
a porous polyethylene plate.
ric
a. The silicone single-plate model (FP-7) has
2. Molteno3 implant is a flexible, larger, single-
been popular among clinicians.
plate design (175 mm2 or 230 mm2 plates)
b. The Ahmed Glaucoma Valve is the only avail-
B. Baerveldt implant introduced in 1990
able resistance glaucoma drainage device.
1. Larger (250 mm 2 and 350 mm2) silicone plates
IV. Clinical Experience
2. Intraluminal occlusion sutures and external
A. Various factors associated with success and fail-
ligation of the tube avoided postop hypotony.
ure have been identified, which have clarified the
C. While the Schocket implant is not commercially role of glaucoma drainage implants in the clinical
available, clinicians have attached tubes to previ- management of glaucoma patients and prompted
ously implanted encircling bands to treat patients modifications of the procedure to improve clinical
with elevated IOP after scleral buckle. outcomes (see Table 1).
III. Development of Flow-Restrictive Implants B. Reduction of complications
A. Flow-restrictive implants were developed in order 1. Avoidance of hypotony during the early
to avoid problems associated with early postopera- postoperative period
tive hypotony after drainage implants.
2. Prevention and treatment of other complications
Table 1. Variables Influencing Success or Failure of Glaucoma Drainage Implant Surgery6

Influence on Success or Failure Little or No Effect on Success or Failure
Patient-related Race Age
Previous surgery
Diagnosis Diagnosis
Silicone oil endotamponade Controlled uveitis
Neovascular glaucoma Severe ocular surface disease
Implant-related Implant plate size Adjunctive antifibrosis drugs

Implant plate material Location of implant: Superior versus inferior
C. Improved outcomes for refractory glaucomas VII. Conclusions

1. Ocular surface disease A. Several effective glaucoma drainage implants have
been developed.
2. Silicone oil endotamponade
B. Use of drainage implants has improved the
3. Uveitic glaucoma
prognosis for success for refractory glaucomas.
4. Neovascular glaucoma
C. Complications may be prevented or corrected.
5. Pediatric glaucoma
D. Glaucoma drainage implants have a well-
V. Present Situation established role in the surgical treatment of
glaucoma.
A. Available glaucoma drainage implants
1. Molteno implant (non–flow restrictive)
References
2. Baerveldt implant (non–flow restrictive)
1. Rollett M, Moreau M. Traitement de le hypopyon par le drainage
3. Ahmed Glaucoma Valve (flow restrictive) capillaire de la chamber anterieure. Rev Gen Ophthalmol. 1906;
25:481.
B. Indications
2. Molteno ACB, Luntz MH. The use of plastics in glaucoma
1. Failure of primary glaucoma surgery surgery. Proceedings of the First South African International
Ophthalmological Symposium. London: Butterworths; 1969.
2. Extensive limbal-conjunctival fibrosis / scarring
3. Molteno AC, Straughan JL, Ancker E. Long tube implants in the
3. Failure of other primary glaucoma surgery management of glaucoma. S Afr Med J. 1976; 50:1062-1066.
likely
4. Lloyd MA, Baerveldt G, Heuer DK, Minckler DS, Martone
4. Primary surgery JF. Initial clinical experience with the Baerveldt implant in
complicated glaucomas. Ophthalmology 1994; 101:640-650.
VI. The Future
5. Ahmed AM. Ahmed valve surgery. In: Chen TC, ed. Surgical
A. Improved materials / nanomaterials Techniques in Ophthalmology: Glaucoma Surgery (vol. 4). New
B. Improved modulation of biological response York: Elsevier; 2008:55-73.
C. Improved technology (valves, pumps, sensors) 6. Netland PA. The Ahmed Glaucoma Valve in neovascular
glaucoma. Trans Am Ophthalmol Soc. 2009; 107:325-342.
D. Alternative techniques
Evolution of CPC
Cyclodestructive Procedures: From Past to Present
Marlene R Moster MD
I. It All Began: Cyclocryotherapy E. TSCPC is designed to target the melanin in the pig-
mented ciliary body epithelium, thereby decreasing
A. 1950 Bietti: Freezing the ciliary body resulted in
the rate of aqueous production.
lower IOP.
F. Traditionally, this has been performed using a con-
B. Quigley demonstrated histologically that cryo
tinuous delivery of laser energy.
destroyed the epithelial cells and capillaries of the
ciliary body, resulting in a decrease in aqueous G. The diode continuous mode has been shown to
production and a breakdown of the blood–aqueous cause significant collateral tissue damage to adja-
barrier. cent nonpigmented structures, including the ciliary
stroma and ciliary muscle.
C. Complications: pain, uveitis, extensive posterior
synechiae, pupillary block, cataract, chronic flare, H. The nonselective targeting feature of cyclodestruc-
choroidal detachment, 52% decreased vision, tion is thought to contribute to higher rates of
phthisis 12% overall, with neovascular glaucoma, postoperative complications, including prolonged
22% inflammation and hypotony.
II. Fast Forward: Cyclophotocoagulation (CPC) I. Traditional TSCPC may be associated with serious
complications including uveitis, vision loss, chronic
A. 1961 Weekers, first to use light energy as a means
hypotony, and rarely phthisis bulbi and sympa-
of cyclo destruction. Trans scleral xenon arc photo-
thetic ophthalmia.
coagulation over ciliary body lowered IOP.
J. Newer studies recommend using TSCP for eyes
B. 1985 Beckman used ruby laser than Nd:Yag which
that have better visual potential.
ushered in the present era of cyclophotocoagulation
(CPC) K. Rotchford et al published the results of a study that
evaluated the effects of diode CPC in patients with
C. Nd:Yag CPC is 1064 nm in the infrared spectrum
good (≥ 20/60) visual acuity. The results showed
(2-6 joules)
that 73.5% of patients had a final IOP of 16 mmHg
D. Placed 2 to 3 mm from the limbus with 30 to 40 or less and that only 30.6% lost 2 or more Snellen
applications lines. To compare, in the Tube Versus Trabeculec-
tomy (TVT) study, 63.9% of patients in the tube
E. Pulsed mode: produces mechanical photodisrup-
shunt group and 63.5% of patients in the trabecu-
tion of the ciliary processes with homogeneous
lectomy group had an IOP of 14 mmHg or less.
lesions
Forty-six percent of the tube shunt patients and
F. Continuous mode: energy 1000 times greater than 43% of the trabeculectomy patients lost 2 or more
for YAG iridectomy; full thickness burn to ciliary lines of Snellen visual acuity.
body and a mild thermal effect in the sclera. IOP
IV. Endocyclophotocoagulation (ECP)
decreases 44%-68%. A contact lens delivers the
energy for 360°. A. 1991: ECP first available by Endo Optiks
III. Transscleral Cyclophotocoagulation (TSCPC) 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 1. E2: endoscope + diode laser (pulsed continuous-
glaucoma or palliation of painful eyes with a very wave energy 810-nm laser, video camera,
poor prognosis. helium-neon laser aiming beam, and xenon
light)
B. There has been debate over whether there is a direct
correlation between the amount of laser energy 2. E4: Endoscope only (video and xenon light) for
used and the rate of complications. vitrectomy
C. Concerns regarding postoperative complications 3. Uses a 1.5- to 2.0-mm incision. Expand pos-
must be balanced with concerns for overall efficacy, terior chamber with ophthalmic viscosurgical
as studies have shown that mean IOP reduction is device
strongly correlated with the number of delivered
C. Laser settings: Treat 180 to 360 degrees (make a
laser burns.
second incision 1.5-2 mm, 120 degrees away)
D. Diode laser cyclophotocoagulation emits light near
1. Continuous settings, about 3 seconds for slow
the infrared spectrum at 810 nm, which is strongly
whitening
absorbed by melanin.
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):262-
D. Uses of ECP: phaco/ECP for mild to moderate glau- 267.
coma; target mid-teens
2. Tham YC, Li X, Wong TY, Quigley HA, Aung T, Cheng CY.
E. Advanced refractory glaucoma with prior trabs/ Global prevalence of glaucoma and projections of glaucoma bur-
tube shunts den through 2040: a systematic review and meta-analysis. Oph-
thalmology 2014; 121(11):2081-2090.
F. Eyes that cannot undergo a filtering procedure
(chronic ocular surface disease or high risk of com- 3. Bloom PA, Tsai JC, Sharma K, et al. “Cyclodiode.” Trans-scleral
plications [history of pars plana vitrectomy, apha- diode laser cyclophotocoagulation in the treatment of advanced
refractory glaucoma. Ophthalmology 1997; 104(9):1508-1519,
kia, suprachoroidal])
discussion 1519-1520.
G. Can use at same time or after other angle surgeries 4. Kosoko O, Gaasterland DE, Pollack IP, Enger CL; the Diode Laser
(Trabectome, iStent) as it lowers IOP via a decrease Ciliary Ablation Study Group. Long-term outcome of initial cili-
in inflow ary ablation with contact diode laser transscleral cyclophotocoag-
ulation for severe glaucoma. Ophthalmology 1996; 103(8):1294-
H. Good for anterior segment disease where view is
1302.
poor or in plateau iris as the ECP causes the ciliary
processes to shrink and deepen the angle 5. Mistlberger A, Liebmann JM, Tschiderer H, Ritch R, Ruckhofer
J, Grabner G. Diode laser transscleral cyclophotocoagulation for
V. Micropulse Transscleral Cyclophotocoagulation refractory glaucoma. J Glaucoma. 2001; 10(4):288-293.
(Micropulse TSCPC, MP-TSCPC, IRIDEX IQ810 6. Oguri A, Takahashi E, Tomita G, Yamamoto T, Jikihara S,
Laser Systems; Mountain View, CA) Kitazawa Y. Transscleral cyclophotocoagulation with the diode
laser for neovascular glaucoma. Ophthalmic Surg Lasers. 1998;
A. Micropulse transscleral diode laser CPC uses 29(9):722-727.
micropulse technology to denature the target tissue
while further minimizing collateral tissue damage. 7. Schlote T, Derse M, Rassmann K, Nicaeus T, Dietz K, Thiel
HJ. Efficacy and safety of contact transscleral diode laser cyclo-
B. The device applies a series of short (microsecond), photocoagulation for advanced glaucoma. J Glaucoma. 2001;
repetitive bursts of energy that effectively confines 10(4):294-301.
the thermal effect to the absorbing tissue.
8. Pantcheva MB, Kahook MY, Schuman JS, Rubin MW, Noecker
C. The micropulse delivery mode includes on and off RJ. Comparison of acute structural and histopathological changes
cycles, allowing energy to build up in the targeted of the porcine ciliary processes after endoscopic cyclophotocoagu-
pigmented tissues, eventually reaching the coagula- lation and transscleral cyclophotocoagulation. Clin Exp Ophthal-
mol. 2007; 35(3):270-274.
tive threshold.
9. Tan AM, Chockalingam M, Aquino MC, Lim ZI, See JL, Chew
D. The adjacent nonpigmented structures have time PT. Micropulse transscleral diode laser cyclophotocoagulation
to cool off during the off cycle, thus never reaching in the treatment of refractory glaucoma. Clin Exp Ophthalmol.
the coagulative threshold, which minimizes collat- 2010; 38(3):266-272.
eral tissue damage.
10. Aquino MC, Barton K, Tan AM, Sng C, Li X, Loon SC, Chew PT.
E. Only a few studies have described the outcomes of Micropulse versus continuous wave transscleral diode cyclopho-
this novel treatment for glaucoma. They showed tocoagulation in refractory glaucoma: a randomized exploratory
micropulse transscleral cyclophotocoagulation study. Clin Exp Ophthalmol. 2015; 43(1):40-46.
(MP-TSCPC) to have comparable efficacy with 11. Rotchford AP, Jayasawal R, Madhusudhan S, Ho S, King AJ,
fewer side effects when compared with traditional Vernon SA. Transscleral diode laser cycloablation in patients with
continuous wave mode diode laser delivery. good vision. Br J Ophthalmol. 2010; 94(9):1180-1183.
F. This more favorable side effect profile has the 12. Egbert PR, Fiadoyor S, Budenz DL, et al. Diode laser transscleral
potential to make MP-TSCPC an earlier thera- cyclophotocoagulation as a primary surgical treatment for pri-
peutic option instead of reserving it for end-stage mary open-angle glaucoma. Arch Ophthalmol. 2001; 119:345-
refractory eyes. 350. 
Evolution of MIGS
Iqbal K Ahmed MD
N OTE S
Graveyard of Innovation
E Randy Craven MD FACS
I. Filtration Techniques C. Valve implants

A. Full-thickness procedures: sclerostomies with bleb 1. Schocket and modifications of
1. Laser 2. Krupin valve
a. Holmium 3. White shunt
b. Erbium 4. Susanna implant
c. Nd:YAG II. Cyclodialysis
i. Contact A. With implant, tissue, or space-occupying substance
ii. Noncontact 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 Methods

of anti-VEGF agents. Sustained IOP elevation is less commonly Enzyme-linked immunosorbent assay, size exclusion chroma-
seen but can require medical and/or surgical intervention. The tography, and polyacrylamide gel electrophoresis were used to
mechanism for sustained IOP elevation is not well understood analyze repackaged bevacizumab syringes obtained from three
but has been attributed to trabecular meshwork injury from outside compounding pharmacies and samples obtained directly
repeated injections, a potential toxic or inflammatory reaction from the original vial. Microflow imaging was used to examine
after exposure to the biologic agents and/or vehicle, or mechani- particulate material within samples.
cal blockade of the trabecular meshwork by protein aggregates
or contaminant particles associated with packaging and injec- Results
tion techniques, among other potential causes. Intravitreal All syringes contained statistically similar amounts of protein,
anti-VEGF injections are commonly used to treat neovascular consisting of immunoglobulin (IgG) heavy and light chains
diseases of the eye. Although they have a favorable side-effect (polyacrylamide gel electrophoresis). However, two of the
profile, their use can be associated with both transient and sus- three compounding pharmacies’ batches had significantly less
tained elevation in IOP. Further research is necessary to deter- functional IgG in the solution (enzyme-linked immunosorbent
mine the cause of these findings. assay). Additionally, the compounding pharmacies with the
lowest IgG ( approximately 50%) also contained 10-fold the
Evidence number of micron-sized particulate matter as measured by
microflow imaging.
High-molecular-weight aggregates in repackaged bevacizumab
(Kahook et al.). Conclusion
There are significant differences in IgG concentration measured
Purpose from repackaged bevacizumab syringes. A trend exists for an
The anti-VEGF agents ranibizumab and bevacizumab are used increase in micron-sized protein aggregates with the decrease in
to treat ocular neovascular diseases. There have been recent IgG concentration. Large particulate matter within some sam-
reports of sustained elevation of IOP after use of either agent, ples may lead to obstruction of aqueous outflow and subsequent
which we hypothesize could be because of high-molecular- elevation in IOP. Additional studies are warranted to explore
weight aggregates. these findings.
2016 Subspecialty Day | Glaucoma Section VI: The Intersection of Glaucoma and Retina 57
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 glau-
coma 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.
58 Section VI: The Intersection of Glaucoma and Retina 2016 Subspecialty Day | Glaucoma
Case #3: Managing Neovascular Glaucoma

Daniel B Moore MD
Case Presentation 12:00, 2+ diffuse injection of the conjunctiva, mildly edematous

cornea, deep central anterior chamber, active neovasculariza-
A 42-year-old woman with poorly controlled diabetes mellitus
tion of the iris, and a centered posterior chamber IOL. Gonio
presents for evaluation and management of neovascular glau-
scopy demonstrated active neovascularization of the angle with
coma (NVG) of the left eye. Her referring provider performed a
near circumferential peripheral anterior synechiae rising above
combined cataract extraction and trabeculectomy in the left eye
the pigmented trabecular meshwork. Dilated fundus examina-
two months ago, but the trabeculectomy has failed and her IOP
tion revealed moderate cupping of a slightly pale optic nerve,
is elevated on maximum therapy. She has also undergone pan-
macular edema, and dense peripheral panretinal coagulation.
retinal photocoagulation for her proliferative diabetic retinopa-
thy, but no intravitreal injections. She is relatively monocular,
with light perception vision in the right eye as a result of NVG. Questions to Consider
The right eye had a similar presentation roughly one year ago, ■ How would you surgically manage this patient? Does the
with severely elevated IOP after cataract extraction and trab-
current state of the fellow eye influence your decision?
eculectomy, and she underwent an Ahmed Valve FP7 placement
Would your approach change if she had not previously
in the supratemporal quadrant at that time. She lives 2 hours
undergone trabeculectomy or cataract surgery?
away, is just above the federal poverty level, and is the primary ■ Would you provide an intravitreal anti-VEGF injection?
caregiver for her 2 school-aged children.
Does the timing of this injection make a difference for
On examination, her vision is 20/400 in the left eye. Her IOP
surgical planning?
is 31 and 45 mmHg in the right and left eye, respectively, on 4 ■ Does the patient’s social and financial status play a role in
glaucoma medications, including oral acetazolamide. Slitlamp
surgical decision making?
examination of the left eye reveals a focal, vascularized bleb at
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 Although the IOP initially improves, the patient is ulti-
mately referred back at postoperative week 4 from silicone oil
A 46-year-old African American male with poorly controlled
removal, when the vision is found to be 20/200 O.S. and the
diabetes underwent a pars plana vitrectomy with silicone oil
IOP 32 mmHg. The patient complains of headaches and is on
for extensive tractional retinal detachment secondary to severe
all 4 glaucoma medications. He is no longer able to tolerate
proliferative diabetic retinopathy in the left eye. The patient is
acetazolamide. Slitlamp exam reveals trace corneal edema, deep
referred for a glaucoma evaluation when he presents on post-
anterior chamber with trace pigmented cells, and no obvious
operative week 2 with an elevated IOP. On exam, visual acuity
oil droplets in the anterior chamber. Gonioscopy reveals 360
of the left eye is count fingers at 1 ft with an IOP of 39 mmHg.
degrees of mostly open angles with few scattered PAS inferiorly
Slitlamp exam is significant for corneal edema, formed anterior
and scant “fish egg” oil droplets superiorly.
chamber, iris with an overlying glistening sheen, and a poste-
The decision is made to proceed with placement of a glau-
rior chamber IOL. A peripheral iridotomy (PI) was not seen.
coma drainage device (GDD) into the left eye. While the patient
Gonioscopy is hazy but reveals 360 degrees of mostly open
is supine on the operating table at the beginning of the case, we
angles that have patchy peripheral anterior synechiae (PAS)
note a significant amount of emulsified oil droplets accumulat-
inferiorly. Funduscopic exam reveals a pale, moderately cupped
ing in the anterior chamber. We began the case by performing
nerve with overlying fibrosis and dense panretinal photoco-
a thorough anterior chamber washout. Given the amount of
agulation scars with scattered fibrosis. The retina appears flat
occult emulsified oil droplets, the GDD is placed in the infero-
under oil.
nasal quadrant to minimize risk of occlusion by silicone oil. The
The elevated IOP is felt to be secondary to silicone oil in
patient does well, and at postoperative year 1 his visually acuity
the anterior chamber, and an inferior PI is placed. The patient
is 20/100 and IOP is 15 mmHg on dorzolamide-timolol twice
is advised to assume face-down positioning. Over the next 2
daily.
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 Conclusion
at subsequent follow-ups and by postoperative month 3, the
In patients with high IOP following retina surgery, identifying
IOP is 31 mmHg on 4 glaucoma drops and oral acetazolamide.
the underlying mechanism causing the IOP elevation is essential
The retina surgeon decides to remove the oil to see if this will
for guiding management.
improve the IOP.
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 pre-

sented 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 61
The Hyphema That Keeps on Giving

JoAnn Giaconi MD
A 74-year-old man presented with elevated pressures and recur-

rent 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 high-
lights the difficulty in removing an 8-ball hyphema.
“I See Red”
Michael Greenwood MD
Suprachoroidal hemorrhage is a rare but devastating complica-

tion 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 endocyclo-
photocoagulation 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 Section VII: Video Surgical Nightmares 63
Training for Angle Surgery:

No Good Deed Goes Unpunished
Shakeel R Shareef MD
Brief Synopsis of Video Presentation Recommendations will be made to prevent intraoperative

complications, including (1) use of modified goniolenses for
The rate-limiting step in angle surgery is visualization of angle
better globe control, (2) use of lidocaine jelly not only as a
structures. The video demonstrates an intraocular complication
coupling medium but also as a topical analgesic, providing a
following uncomplicated cataract surgery—iridodialysis—that
decreased sensation of tissue manipulation during angle sur-
resulted during angle surgery training from a Sinskey hook and
gery, and (3) performance of angle surgery prior to PE when
highlights the differences between phacoemulsification (PE)
patient is maximally anesthetized with IV sedation and preop-
and angle surgery: (1) PE is a bimanual intraocular surgery
erative lidocaine jelly.
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 stimula-
tion of the ocular surface with creation of a keratome and side-
port 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.
A Divining Rod for Angle Blood

Yao Liu MD and Michele C Lim MD
Minimally invasive glaucoma surgeries (MIGSs) are generally This video presentation illustrates that as with all surgical
considered to have low-risk safety profiles relative to their tradi- procedures, caution should be taken in performing MIGS in
tional glaucoma surgical counterparts (ie, trabeculectomy and high-risk glaucoma patients. Although MIGSs have a more
tube shunts). Thus they are often selected for surgical manage- favorable risk profile compared to traditional glaucoma surger-
ment in higher-risk glaucoma surgical patients, such as those ies, the resulting complications can have a significant impact on
who are elderly or monocular, use anticoagulants, or have a patient outcomes. An awareness of vision-threatening hyphema
pre-existing bleeding diathesis. as a potential serious complication following MIGS procedures
In this surgical video, we present a case in which a combined can aid in preoperative patient selection and counseling to
cataract and Glaukos iStent trabecular microbypass surgery reduce the risk of adverse outcomes.
(Glaukos Corp.; Laguna Hills, CA, USA) was performed in an
elderly, monocular patient with a prior history of resolved idio-
References
pathic vitreous hemorrhage. Preoperatively, he had a visually
significant cataract and his IOPs were well controlled medically. 1. Wellik SR, Dale EA. A review of the iStent® trabecular micro-
He elected to have iStent combined with cataract surgery to bypass stent: safety and efficacy. Clin Ophthalmol. 2015; 9:677-
reduce his dependence on glaucoma medications. After unre- 684.
markable cataract surgery, two attempts were made to place the 2. Craven ER, Katz LJ, Wells JM, et al. Cataract surgery with tra-
iStent in the trabecular meshwork. becular micro-bypass stent implantation in patients with mild-to-
An intraoperative hyphema developed that was not cleared moderate open-angle glaucoma and cataract: two-year follow-up.
at the time of surgery. Postoperatively, the hyphema was vision J Cataract Refract Surg. 2012; 38(8):1339-1345.
limiting in this monocular patient, and it caused an intractable 3. Patel I, de Klerk TA, Au L. Manchester iStent study: early results
elevation in IOP despite maximal medical therapy. Due to his from a prospective UK case series. Clin Experiment Ophthalmol.
poor vision and need for assistance in instilling IOP-lowering 2013; 41(7);648-652.
medications, the patient was admitted to the hospital for treat-
4. Buchacra O, Duch S, Milla E, et al. One-year analysis of the iStent
ment. Six days later, he underwent a second procedure to clear
trabecular microbypass in secondary glaucoma. Clin Ophthal-
the hyphema, which resulted in improved vision and IOP con- mol. 2011; 5:321-326.
trol. He was then discharged home upon regaining his indepen-
dence. 5. Donnenfeld ED, Solomon KD, Voskanyan L, et al. A prospective
This was an unusual case given that the safety profile of 3-year follow-up trial of implantation of two trabecular microby-
pass stents in open-angle glaucoma. Clin Ophthalmol. 2015;
combined iStent with cataract surgery has been shown to be
9:2057-2065.
comparable to that of cataract surgery alone in multiple pub-
lished 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 pha-
kic patient following implantation of 2 iStents, which required
surgical irrigation of the anterior chamber.5
2016 Subspecialty Day | Glaucoma Financial Disclosure 65
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66 Financial Disclosure 2016 Subspecialty Day | Glaucoma
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Iqbal K Ahmed MD Joseph Caprioli MD FACS JoAnn A Giaconi MD

Abbott Medical Optics: C,L,S Alcon Laboratories Inc.: S None
Aerie Pharmaceuticals: C Allergan: S
Alcon Laboratories Inc.: C,L,S National Eye Institute: S Christopher A Girkin MD
Allergan Inc.: C,L,S New World Medical Inc.: S None
Bausch+Lomb: C RPB: S
Carl Zeiss Meditec: C,L,S Jeffrey L Goldberg MD PhD
Centervue: C Meenakshi Chaku MD Alcon Laboratories Inc.: C
Clarity: C,S None Allergan: C
Envisia: C NIH, DOD, GRF: S
Equinox: C Robert T Chang MD
Eyelight: C Alcon Laboratories Inc.: C David S Greenfield MD
ForSight Labs: C Allergan: C Aerie: C
Glaukos Corp.: C,O,S Carl Zeiss Inc.: S Alcon Laboratories Inc.: C
Iantech: C Healgoo: C Allergan: C
InjectSense: C Kali Care: C Bausch+Lomb: C
InnFocus: C Paxos Scope: P Biometric Imaging: C
Iridex: C Santen Inc.: C Glaukos Corp.: C
Ivantis: C,L,S Transcend Medical: C Quark: C
LayerBio: C Unity Biotechnology: C
Leica: C Michael Greenwood MD
New World Medical Inc.: C,S Balwantray C Chauhan PhD Alcon Laboratories Inc.: L
Oculus Inc.: C Allergan: C,L Imprimis Pharmaceuticals: C
Omega Ophthalmics: C Heidelberg Engineering: S,C
Ono Pharma: C Topcon Medical Systems Inc.: S Alon Harris PhD
PolyActiva: C AdOM: C,O
Sanoculis: C Vikas Chopra MD BioLight: C
ScienceBased Health: C Allergan: S Cipla: C
Stroma: C Isarna Therapeutics: C
Transcend Medical: C E Randy Craven MD Lycored: C
TrueVision: C Allergan Inc.: C,L Nano Retina: C,O
Ivantis: C,S ONO: C
R Rand Allingham MD King Khaled Eye Specialist Hospital: E Oxymap: O
Camras Vision: C Pfizer Inc.: C ScienceBased Health: C
NIH: S Transcend Medical: C Stemnion Inc.: C
Husam Ansari MD PhD Andrew Crichton MD Gregg A Heatley MD

Ivantis Inc.: S Alcon Laboratories Inc.: L,C None
Allergan: L,C
Claude F Burgoyne MD Dale K Heuer MD
Heidelberg Engineering: C,S Nancy L Flattem MD MS InnFocus: C
None Isarna Therapeutics: C
National Eye Institute: S
Disclosures current as of 9/23/2016

Check the Mobile Meeting Guide/Online Program for the most up-to-date financial disclosures.
2016 Subspecialty Day | Glaucoma Financial Disclosure 67
Chris A Johnson PhD Richard A Lewis MD Robert J Noecker MD

AGTC: C Advanced Vision Science: C Aerie: C
Ceeable: C Aerie: E Allergan: C,L
Centervue: C Alcon Laboratories Inc.: C Aquesys: S
Haag-Streit: C Allergan: C Beaver-Visitec International Inc.: C,L
JAEB Center: C Glaukos Corp.: C Diopsys Inc.: C,L
PanOptica: C Ivantis: C Endo Optiks Inc.: C,L
Ethis Communications: C
Malik Y Kahook MD Paul R Lichter MD Glaukos Corp.: L,S
Abbott Medical Optics: P,S None Innfocus: S
Aerie: C Inotek: C
Alcon Laboratories Inc.: C,L,S Shan C Lin MD Iridex: C,L
Allergan Inc.: C,L,S Allergan: C Katena Products Inc.: L
ClarVista Medical: C,P Iridex: C Novartis Pharmaceuticals Corp.: C,L
ForSight Vision 5: O,C Ocular Surgery News: L
Mile High Ophthalmics: P,O Yao Liu MD Ocular T: C,S,O
New World Medical Inc.: P None Polyactiva: C
Oasis Medical Inc.: P Quantel Medical: L
Shape Ophthalmics LLC: O,P Nils A Loewen MD Shire: C
ShapeTech LLC: O,P NeoMedix Corp.: L Sun: C
Shire: C
Jeff S Maltzman MD Kouros Nouri-Mahdavi MD
L Jay Katz MD None Allergan: C
Aerie Pharmaceutical: C,S,O Heidelberg Engineering: S
Aerpio Therapeutics Inc.: C Kaweh Mansouri MD New World Medical Inc.: C
Alcon Laboratories Inc.: C,L Sensimed AG: C
Alimera Sciences Inc.: C Mildred M G Olivier MD
Allergan: C,S,L Cynthia Mattox MD FACS Alcon Laboratories Inc.: C,L
Bausch+Lomb: L Aerie: C National Eye Institute: S
Diopsys Inc.: C,S Alcon Laboratories Inc.: C Santen Inc.: C
ForSight Vision5: C Alimera Sciences Inc.: L
Glaukos Corp.: C,O Allergan: C,S Richard K Parrish II MD
InnFocus Inc.: C National Eye Institute: S Aerie Pharmaceuticals Inc.: C,O
Inotek Corp.: C Ocular Therapeutix: C Alimera Sciences Inc.: C,O
Lumenis Inc.: L Transcend: S American Journal of Ophthalmology: C
Mati Therapeutics: C,O InnFocus Inc.: C,O
Merck & Co. Inc.: L M Lisa McHam MD National Eye Institute: S
Ocular Therapeutix: C None
Louis R Pasquale MD
Simon K Law MD Stuart J McKinnon MD PhD Allergan: L
None Retroject Inc.: O,P Bausch+Lomb: C
Merck & Co. Inc.: S
Christopher Kai-shun Leung MD Felipe A Medeiros MD National Eye Institute: S
MBChB Alcon Laboratories Inc.: C,S Novartis Pharmaceuticals Corp.: C
Alcon Laboratories Inc.: C,L Allergan: S,C
Allergan: C,L Carl Zeiss Meditec: S,C Jody R Piltz-Seymour MD
Carl Zeiss Meditec: C,L,P,S Heidelberg Engineering: S Aerie Pharmaceuticals: S
Glaukos Corp.: L,S Reichert Inc.: C Alcon Laboratories Inc.: L
Lumenis Inc.: L Topcon Medical Systems Inc.: S Allergan: C
Santen Inc.: L Forsight: C
Tomey Corp.: C,L Daniel B Moore MD
Topcon Medical Systems Inc.: C,L None Harry A Quigley MD
Genentech: C
Marlene R Moster MD Graybug: C,O
Iridex: S Novartis: C
Sensimed: C
Peter Andreas Netland MD PhD
PTC Therapeutics: S

68 Financial Disclosure 2016 Subspecialty Day | Glaucoma
Douglas J Rhee MD Shakeel R Shareef MD Clement C Y Tham FRCS MBBS

Aerie: C,O None FCOphthHK
Alcon Laboratories Inc.: C Abbott Medical Optics Inc.: S
Allergan Inc.: C,S Lucy Q Shen MD Aeon Astron Corp.: S
Glaukos Corp.: S LEK Consulting: C Alcon Laboratories Inc.: C,L,S
Ivantis: S Allergan Inc.: C
Merck & Co. Inc.: S Kuldev Singh MD MPH Bausch+Lomb: C
Sanofi Fovea: C Abbott Medical Optics Inc.: C Icare Finland: S
Aerie: C IOPtima Ltd.: C
Thomas W Samuelson MD Alcon Laboratories Inc.: C Merck & Co. Inc.: C,L
Abbott Medical Optics Inc.: C Allergan: C Pfizer Inc.: C,L,S
AcuMems: C Carl Zeiss Meditec: C Santen Pharmaceutical Co., Ltd.: C,S
Aerie Pharmaceuticals: C ForSight Vision 5: C Sensimed: S
Akorn Inc.: C InnFocus: C
Alcon Laboratories Inc.: C Ivantis: C Steven D Vold MD
Allergan: C Mynosys: C Aerie Pharmaceuticals: C,S
AqueSys: C,O National Eye Institute: S Alcon Laboratories Inc.: C,S
Endo Optiks Inc.: C National Space Biomedical Research Allergan: L,S
Equinox: C,O Institute: C Alphaeon: C,O
Glaukos Corp.: C,O Santen Inc.: C AqueSys: C,S
Ivantis: C,O Shire: C Bausch+Lomb: S
Ocular Surgery News: C Thieme Medical Publishers: C Calhoun Vision Inc.: S
Shire: C Transcend: C Carl Zeiss Meditec: C,S
Slack Incorporated: C U.S. Food and Drug Administration: C Forsight Labs: C,S
Transcend: C Glaukos Corp.: C,S
Arthur J Sit MD InnFocus: C,S
Joel S Schuman MD Aerie Pharmaceuticals Inc.: S Iridex: C,S
Aerie Pharmaceuticals Inc.: C,S Allergan: C Ivantis: C,S
Alcon Laboratories Inc.: C Glaukos Corp.: S Lumenis Inc.: C
Carl Zeiss Meditec: P NeoMedix Corp.: L
DSM Inc.: C George L Spaeth MD FACS Ocular Therapeutix: C,S
Glaukos Corp.: C,S None Ocunetics: O
Ocugenix: O,P Transcend Medical: C,P,S
Opticient: C Tak Yee Tania Tai MD TrueVision Systems: C,O
Pfizer Inc.: C,L None Volk Optical: P
Slack Incorporated: C
Kelly Walton Muir MD
Adrienne Williams Scott MD None
Allergan: C
Therapeutic Proteins International Joanne C Wen MD
(TPI): C None
ThromboGenics Inc.: S

2016 Subspecialty Day | Glaucoma Presenter Index 69
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


Glaucoma 2016 Syllabus

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Glaucoma 2016 Syllabus

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Glaucoma 2016

In conjunction with the American Glaucoma Society

Saturday, Oct. 15, 2016

Supported in part by an unrestricted educational grant

2016 Glaucoma Subspecialty Day Planning Group

Joel S Schuman MD Jody R Piltz-Seymour MD

Meenakshi Chaku MD Andrew Crichton MD FRCS David S Greenfield MD

Gregg A Heatley MD Cynthia Mattox MD FACS Arthur J Sit MS MD

Nils A Loewen MD PhD

2016 Subspecialty Day R Michael Siatkowski MD AAO Staff

Glaucoma 2016 Contents

The American Glaucoma Society Subspecialty Day Lecturer viii

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:

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

Academy’s CME Mission Statement ments is available at http://abop.org/maintain-certification/

Self-Assessment Credit Attendance Verification for CME Reporting

The American Glaucoma Society (AGS)

Louis R Pasquale MD FARVO

Iqbal K Ahmed MD Claude F Burgoyne MD Robert T Chang MD

R Rand Allingham MD Balwantray C Chauhan PhD

E Randy Craven MD JoAnn A Giaconi MD David S Greenfield MD

Alon Harris PhD

Gregg A Heatley MD Malik Y Kahook MD Christopher Kai-shun Leung MD

Dale K Heuer MD L Jay Katz MD Richard A Lewis MD

Simon K Law MD Paul R Lichter MD

Shan C Lin MD Jeff S Maltzman MD Stuart J McKinnon MD PhD

Cynthia Mattox MD FACS No photo

Marlene R Moster MD Kouros Nouri-Mahdavi MD Louis R Pasquale MD

Robert J Noecker MD Richard K Parrish II MD Harry A Quigley MD

Douglas J Rhee MD Adrienne Williams Scott MD Kuldev Singh MD MPH

Shakeel R Shareef MD Arthur J Sit MD

George L Spaeth MD FACS

Tak Yee Tania Tai MD Steven D Vold MD Joanne C Wen MD

Kelly Walton Muir MD

Ask a Question Live During the Meeting

To ask a question during the meeting,

■ 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

Glaucoma Subspecialty Day 2016: Innovations in

Section I: Is It Progression? Is It Glaucoma?

* Indicates that the presenter has financial interest.

Section II: Controversies

Section III: Glaucoma—It’s Not Just About IOP

* Indicates that the presenter has financial interest.

The American Glaucoma Society Subspecialty Day Lecture

Section IV: The “New Patient” in Your Clinic—Treatment Options

Section V: Past, Present, and Future of Surgical Techniques

* Indicates that the presenter has financial interest.

Section VI: The Intersection of Glaucoma and Retina

Section VII: Video Surgical Nightmares