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Kansas Kansas EyeCon EyeCon

May 11 & 12, 2018 The Venue 4800 W 135th St., Ste. 108 Leawood, KS 66209

Sponsored by the University of Kansas Department of and the Lemoine Alumni Society

Kansas EyeCon 2018 We wish to acknowledge and sincerely thank these organizations for exhibiting at this conference: Platinum Sponsors: Glaukos Corporation Halozyme Therapeutics IRIDEX Corporation Regeneron Pharmaceuticals, Inc. Saving Sight

Silver Sponsors: Alcon Surgical Allergan Carl Zeiss Meditec, Inc. Leica Microsystems, Inc. Marco Novartis/Alcon Pharmaceuticals Bronze Sponsor: KU Audio‐Reader Network

Kansas EyeCon 2018 May 11 & 12, 2018

Program Overview ‐ This conference is intended to provide ophthalmologists with an educational forum to learn about new developments in the profession and their application to patient care. Covering a cross‐section of all sub‐specialties, physicians can expect to walk away having heard evidence‐based presentations. Target Audience ‐ This program is designed to meet the needs of practicing ophthalmologists. Learning Objectives ‐ Upon completion of the educational activity, participants should be able to:

Cornea and Orbital Session 1. Examine complication rates as well as visual outcomes of resident‐performed surgery at a VA Medical Center; 2. Compare outcomes and complication rates between senior and non‐senior residents; 3. Recognize indications for MSICS/Extracapsular ; 4. Identify the steps for performing MSICS; 5. Recognize conclusions from published results of DREAM Study; 6. Discuss the practical applications; 7. Compare DREAM to other recent publications on role of Omega 3 oils in ocular surface health; 8. Analyze patterns of oculofacial injury due to hoof‐kicks from horses; 9. Determine the severity, outcome, and management of patients who sustained oculofacial injuries as a result of being kicked by a horse; 10. Establish how oculoplastics training in residency affects resident’s perceived comfort level with common oculoplastics procedures; 11. Describe the pathophysiology of thyroid ; 12. Discuss a case series of patients who underwent orbital decompression for thyroid orbitopathy and demonstrated radiographic expansion of post‐operatively; 13. Demonstrate a successful insertion of a scleral fixated intraocular through a small corneal incision; 14. Discuss the clinical findings of cavernous hemangioma; 15. Recognize the surgical approaches for removal; 16. Examine the historical origins and basic principles of laser photodisruption and photocoagulation, contrast sensitivity and variable contrast acuity testing, scanning laser and aspheric ophthalmoscopy and radiant energy protective intraocular lenses. and Anterior Segment Session 17. Describe the anatomic and physiologic role of the lens in angle closure glaucoma; 18. Explain the benefits of lens extraction in treating angle closure glaucoma and compare with alternative treatments; 19. Discuss the fundamental limitations affecting management of glaucoma; 20. Familiarize with new developments in glaucoma; 21. Discuss anatomy and 360 degree treatment vs 180 degree treatment; 22. Analyze resident laser data to determine results and efficacy; 23. Identify different types of MIGS procedures; 24. Recognize when/if it is appropriate to utilize different types of MIGS procedures. Pediatric and Session 25. Recognize the clinical presentation of ocular juvenile xanthogranuloma; 26. Describe management of ocular juvenile xanthogranuloma; 27. Analyze the differences in diagnosis and treatment between adults and children; 28. Describe the current controversies in the field of corneal crosslinking; 29. Discuss therapeutic options for central serous chorioretinopathy; 30. Explain outcomes of patients undergoing treatment for central serous chorioretinopathy; 31. Explain the concept of the ophthalmic endoscope; 32. Recognize current role of ophthalmic endoscopy in vitreoretinal surgeries.

Method of Participation Statements of credit will be awarded based on the participant's attendance and will be available upon completion of an online evaluation/claimed credit form available at akhinc.formstack.com/forms/kseyecon. Alternatively, a statement of credit will be awarded based on the participant’s attendance and submission of the activity evaluation form. A statement of credit will be available upon completion of an evaluation/claimed credit form that should be turned in at the end of the meeting. If you have questions about this CME activity, please contact AKH Inc. at [email protected]. This activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of AKH Inc., Advancing Knowledge in Healthcare and the University of Kansas, Department of Ophthalmology and The Lemoine Alumni Society. AKH Inc., Advancing Knowledge in Healthcare is accredited by the ACCME to provide continuing medical education for physicians. AKH Inc., Advancing Knowledge in Healthcare designates this live activity for a maximum of 7.0 AMA PRA Category 1 Credit(s)™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

CME Credit Provided by AKH Inc., Advancing Knowledge in Healthcare Physicians

FACULTY DISCLOSURES Name Relationship Commercial Interest Radwan Ajlan, MD N/A Nothing to Disclose Neeti Alapati, MD N/A Nothing to Disclose Denise Capps, MD N/A Nothing to Disclose Luke Dolezal, MD N/A Nothing to Disclose Speakers Bureau Aerie Pharmaceuticals Inc.; Allergan Inc.; Novartis Pharmaceuticals Corp. Consultant Aerie Pharmaceuticals Inc.; Allergan Inc.; Novartis Scott Fudemberg, MD Pharmaceuticals Corp. Michael Gilbert, MD N/A Nothing to Disclose Christina Donaghy Gillmor, MD N/A Nothing to Disclose Yong Kam, MD N/A Nothing to Disclose Joshua Jones, MD N/A Nothing to Disclose Katie Keck, MD N/A Nothing to Disclose Martin Mainster, MD N/A Nothing to Disclose Jonathan Manhard, MD N/A Nothing to Disclose Reid Mollman, MD N/A Nothing to Disclose Jason Sokol, MD N/A Nothing to Disclose Erin Stahl, MD N/A Nothing to Disclose John Sutphin, MD N/A Nothing to Disclose W. Abraham White, MD N/A Nothing to Disclose Thomas Whittaker, MD N/A Nothing to Disclose Annie Wishna, MD N/A Nothing to disclose PLANNER DISCLOSURES KUMC/KSEPS Staff and Planners N/A Nothing to Disclose AKH Staff and Planners N/A Nothing to Disclose

Commercial Support There is no commercial support for this activity. Disclosures It is the policy of AKH Inc. to ensure independence, balance, objectivity, scientific rigor, and integrity in all of its continuing education activities. The author must disclose to the participants any significant relationships with commercial interests whose products or devices may be mentioned in the activity or with the commercial supporter of this continuing education activity. Identified conflicts of interest are resolved by AKH prior to accreditation of the activity and may include any of or combination of the following: attestation to non‐commercial content; notification of independent and certified CME/CE expectations; referral to National Author Initiative training; restriction of topic area or content; restriction to discussion of science only; amendment of content to eliminate discussion of device or technique; use of other author for discussion of recommendations; independent review against criteria ensuring evidence support recommendation; moderator review; and peer review. Disclosure of Unlabeled Use and Investigational Product This educational activity may include discussion of uses of agents that are investigational and/or unapproved by the FDA. Please refer to the official prescribing information for each product for discussion of approved indications, contraindications, and warnings.

Disclaimer This course is designed solely to provide the healthcare professional with information to assist in his/her practice and professional development and is not to be considered a diagnostic tool to replace professional advice or treatment. The course serves as a general guide to the healthcare professional, and therefore, cannot be considered as giving legal, nursing, medical, or other professional advice in specific cases. AKH Inc. specifically disclaim responsibility for any adverse consequences resulting directly or indirectly from information in the course, for undetected error, or through participant's misunderstanding of the content.

LEMOINE DISTINGUISHED ALUMNI LECTURERS

LECTURER TITLE DATE

Timothy W. Olsen, MD Rock Chalk Retina Talk: 100 year KU 5/9/2014 KU SOM MD ‘89

Luther L. Fry, MD Standard Cataract Surgery: Tips & Tricks 5/8/2015 KU SOM MD ‘67 Learned after 40,000+ Cases

John D. Hunkeler, MD Continuous Education 4/8/2016 KU SOM MD ‘67 KU Eye Residency ‘73

William A. Godfrey, MD Quality of Life for Ophthalmology: 5/12/2017 KU SOM MD ’65 A Perspective KU Eye Residency ‘71

Martin A. Mainster, PhD, MD, A Physicist’s Adventures in RetinaLand 5/11/2018 FRCOphth, Luther & Ardis Fry Professor Emeritus Alumni Speakers

Scott Fudemberg, MD Residency: 2007

Erin Stahl, MD Residency: 2009; Fellow: 2011

Thomas J. Whittaker, MD MD: 1990

AGENDA

Kansas EyeCon May 11 – 12, 2018 The Venue

Friday, May 11, 2018

12:00 p.m. Registration and lunch with exhibitors

1:00 p.m. Welcome: Neeti Alapati, MD and Orbital Session

1:05 p.m. Michael Gilbert, MD, Comparative Review of Complication Rates and Visual Outcomes in Cataract Surgery between Senior and Non-Senior Residents at a VA Medical Center

1:18 p.m. W. Abraham White, MD, Back to the Future: Manual Small Incision Cataract Surgery (MSICS)

1:43 p.m. John Sutphin, MD, DRy Eye Assessment and Management (DREAM) Update

2:08 p.m. Denise Capps, MD, Patterns of Oculofacial Injury in Equestrians due to Hoof-Kicks

2:22 p.m. Reid Mollman, MD, Correlating Projected Comfort Level of Ophthalmology Residents in Performing Oculofacial Plastics Procedures with Ophthalmology Residency Program Characteristics

2:35 p.m. Christina Donaghy Gillmor, MD, Expansion of Extraocular Muscles Following Orbital Decompression in Thyroid Eye Disease

2:48 p.m. Yong Kam, MD, A Novel Scleral Fixated Intraocular Lens Insertion Technique through a Small Corneal Incision

3:01 p.m. Break

3:29 p.m. Jason Sokol, MD, Cavernous Hemangioma: What are you? Where are you? And how are we going to get you out?

3:54 p.m. Introduction of Dr. Mainster: John Sutphin, MD

4:00 p.m. Martin Mainster, PhD, MD, FRCOphth, Lemoine Distinguished Alumnus Lecturer, A Physicist’s Adventures in RetinaLand

5:00 p.m. Session Adjourns

On site reception immediately following University of Kansas Department of Ophthalmology and The Lemoine Alumni Society

Kansas EyeCon May 11 – 12, 2018

Saturday, May 12, 2018

7:30 a.m. Breakfast with exhibitors

8:00 a.m. Welcome – Neeti Alapati, MD

Glaucoma and Anterior Segment Session

8:05 a.m. Luke Dolezal, MD, Lens Extraction in Angle Closure Glaucoma

8:18 a.m. Scott Fudemberg, MD, Glaucoma 2018: Roadblocks and Detours

9:18 a.m. Josh Jones, MD, Selective Laser Trabeculoplasty: Resident Experiences and Results at the KCVA

9:31 a.m. Anne Wishna, MD, Microinvasive Glaucoma Surgery (MIGS) from a Comprehensive Perspective

9:56 a.m. Break Pediatric and Retina Session

10:21 a.m. Katie Heck, MD, Ocular Findings of Juvenile Xanthogranuloma

10:33 a.m. Erin Stahl, MD. Pediatric Corneal Crosslinking for Keratoconus

10:58 a.m. Jonathan Manhard, MD, Central Serous Chorioretinopathy: Outcomes and Experience

11:11 a.m. Radwan Ajlan, MBBCh, FICO, FRCS(C), DABO, Endoscopic Vitreoretinal Surgery

11:36 a.m. Thomas J. Whittaker, JD, MD, Professor, Vice-Chairman and Residency Program Director, Closing Remarks: Future of KU Eye

12:00 p.m. Session Adjourns

University of Kansas Department of Ophthalmology and The Lemoine Alumni Society

ABSTRACTS

Comparative Review of Complication Rates and Visual Outcomes in Cataract Surgery between Senior and Non- Senior Residents at a VA Medical Center

Michael Gilbert, MD, Resident, Class of 2019 Primary Supervisor: W. Abraham White, MD

Cataract surgery is the most commonly procedure performed by ophthalmologists in the United States, and learning how to perform cataract surgery is a key part of the surgical training of the resident ophthalmologist. A significant portion of the volume of cataract surgeries performed by residents is done at VA medical centers. As a general rule, with each successive year of training, a higher volume of cataract surgery is performed; thus, most cataract surgeries during a resident ophthalmologists’ training is done in their 3rd and final year. However, it is also performed by 2nd and 1st year residents, although at lower volumes. Studies in other specialties have shown that higher surgical volume is associated with lower complication rates. Thus, it is important to have appropriate surgical oversight, as well as to choose cases of appropriate difficulty, based on the training surgeon’s level of skill and experience.

We examined visual outcomes and complication rates from cataract surgeries performed at a VA Medical Center by residents of all levels of training, and then separated and compared the data, based on whether the surgery was performed by a senior or non-senior resident, to evaluate differences in outcomes and complication rates between the two groups.

MSICS: Not Your Father’s Disclaimer and Extracap Acknowledgement

• I have no financial interests to disclose • The views expressed do not necessarily W. Abraham White, MD Assistant Professor, represent those of the Federal Government or Dept. of Ophthalmology the Department of Veterans Affairs University of Kansas Chief of Ophthalmology, KCVA • Special thanks to Scott Hickman and Allen KU EyeCon 2018 Foster for providing graphics and videos

Overview Global Blindness • Epidemiology • In 2015: • What is MSICS? – 36 million blind (20/400 or worse) • What are the indications for MSICS? – 217 million visually impaired (20/70‐20/400) • Patient selection • Rates decreasing, but overall numbers are • Utility of MSICS in the industrialized world increasing due to population growth – Only 31 million blind in 1990 • Tips and tricks • Most blindness is due to cataract worldwide

Global Blindness Global

• 35% Cataract • 49%

• 21% Uncorrected refractive error • 26% Cataract

• 8% Glaucoma • 4% ARMD Cataract Surgery in US Phacoemulsification in the Developing World

• Cataract treatment relatively expensive • Not practical or cost effective in developing nations • Requires specialized equipment • Advanced pathology often not easily • Extensive training necessary amenable

• Lack of trained providers

What is MSICS? Cost/Equipment comparison

MSICS Phacoemulsification • Manual Small Incision Cataract Surgery • Microscope/Light source • Microscope/Light source • First described by Blumenthal et al in 1994 • Single instrument tray • Instrument tray • Minimal equipment requirements • Simcoe I/A • Handpieces • +/‐ Cautery unit • Disposable packs • Can be performed relatively quickly and at • +/‐ Sutures • Phaco Machine low cost • Cost ‐ $10‐20 (India/Nepal) • Cost ‐ ~$50 (India), >$1,000 US

MSICS Peritomy Scleral Tunnel MSICS Scleral Tunnel MSICS Keratotomy

MSICS Cataract Removal 2 Hand Technique

Sandwich Technique Fishhook technique MSICS IOL Insertion MSICS Indications

• Anyone with a visually significant cataract

– Soft lenses more difficult

• Results comparable

• Ruit vs Chang (Nepal)

For Your First Cases Utility of the Technique

• Have a mentor available • Very robust, can be used on almost any • Avoid these patients cataract – Large brow – Traumatic cataract/PXE/Bad zonules • The incision is also useful for other things – Small – Secondary ACIOL – Anxious patients – Large implant placement – Poor communication (deaf/no interpreter) • Take your time! • Good fallback if zonules are weak

Tips for Phaco Surgeons Pitfalls

• Go Big or Go Home! • Try to make AC entry in one cut – Incision – Capsulorrhexis • POD1 IOP of 6 or less = leak

• Wet field cautery to maintain visibility – Don’t be afraid to place a suture (or 3) • Trypan blue is your friend • Keep clear of lens loop • Plan your block • Dropped nucleus possible but rare • 3 Piece IOL recommended Resources

• Ruit S, Tabin G, Chang D, et al. A prospective randomized clinical trial of phacoemulsification vs manual suturelesssmall-incision extracapsular cataract surgery in Nepal. Am J Ophthalmol. 2007;143:35 • Tabin, G., Feilmeier, M. Cataract Surgery in the Developing World. Focal Points Clinical Modules for Ophthalmologists. Volume 29:9. September 2011 • Manual Small Incision Cataract Surgery, Bonnie An Henderson editor, 2016, Springer.

Financial Support

• National Institutes of Health, • Department of Health and Human Services Update on the DREAM Study • Grant Numbers: U10 EY022881 and U10 EY022879 John Sutphin, MD Luther and Ardis Fry Professor and Chair University of Kansas

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Goals Dry Eye Definition

• What is the Dry Eye Assessment and • DEWS Report (The Ocular Surface, 2007) Management Study – “Dry eye is a multifactorial disease of the tears – Basics of Dry Eye Disease and ocular surface that results in symptoms of discomfort, visual disturbance, and tear instability – Design of the study with potential damage to the ocular surface. It is – Intervention accompanied by increased osmolarity of the tear – Results coming in December 2017 film and inflammation of the ocular surface.” • Inflammation  Tear Film Disorder  Ocular Surface Damage • What are we learning about diagnosis? • Affects 14% ‐ 33% of the population – DREAM enrollment data • 5 Million Americans over age 50 have dry eye • Untreated dry eye progresses

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Dry Eye Disease (DED) Recognizing Dry Eye

May be the most common complaint for office visit • • History Economic Burden of DED • – Blurred vision – Medical treatment costs: $700 ‐$1300 per patient per year – Artificial tear reliance – For USA, this is ~$3.8 billion per year – – Productivity losses: $12,000 to $18,000 per patient per year – Sandy/gritty feeling – For USA, this is over $55 billion per year! – Burning/stinging • Significant impact on quality of life, productivity, surgical – Itching outcomes, and patient satisfaction – Dryness – Pain – Medications – Diabetes, thyroid disease Table 2

Key screening questions for dry eye disease. The Dry Eye Assessment and Management Study A patient reporting ‘Yes’ to any of the following warrants a full ocular examination

How often do your eyes feel dryness, discomfort, or irritation? Would you say it is often or constantly? (Y/N) John Sutphin, MD University of Kansas Prairie Village, KS When you have eye dryness,discomfort, or irritation, does this impact your activities

(e.g. do you stop or reduce your time doing them)? (Y/N) Supported by The National Eye Institute National Institutes of Health, Department of Health and Human Services Do you think you have dry eye? (Y/N) Grant Numbers: U10 EY022881 and U10 EY022879

≥ 2 of the following 4 signs in the same eye at BACKGROUND: ELIGIBILITY: screening and baseline visits (Same signs at both • The DRy Eye Assessment and • Ocular Surface Disease Index (OSDI) Management (DREAM) Study is a multicenter, score: visits) randomized clinical trial of omega-3 (ω-3) fatty  25-80 at Screening Visit acid supplementation for the treatment of dry eye  21-80 at Baseline Visit (2 weeks after disease screening) • ≥ 2 of the following 4 signs in the same eye PURPOSE: at screening and baseline visits (Same signs at Conjunctival staining present ≥ 1 (out of • To describe the result of application of both visits) eligibility criteria selected to include patients with  Conjunctival staining present ≥ 1 (out of 6) 6) moderate to severe dry eye disease  Corneal fluorescein staining present ≥ 4 (out mouth of 15)  Tear film break up time (TBUT) ≤ 7 seconds Corneal fluorescein staining present ≥ 4 DREAM TREATMENTS:  Schirmer’s test ≥ 1 to ≤ 7 mm/5min • Randomized assignment to • At least 1 eligible eye (out of 15)  2000mg EPA and 1000mg DHA daily (5 • Symptoms of dry eye disease for ≥ 6 softgels) months OR • Use of or desire to use artificial tears ≥2 Tear film break up time (TBUT) ≤ 7  Placebo (5 softgels) times/day in last 2 weeks • Age ≥ 18 years seconds OTHER KEY DESIGN FEATURES: • Most concomitant dry eye treatments • Recruitment via 25 ophthalmology and allowed as long as the patient commits to optometry clinical centers in the United States continued use during the 1-year follow-up period, Schirmer’s test ≥ 1 to ≤ 7 mm/5min • Main study follow-up period: 1 year including • Primary outcome measure: Mean change in  Topical cyclosporine OSDI score  Up to 1200 mg per day of ω-3 fatty acids by • Sample size: 535 (completed July 2016) mouth 9 10

Testing

• Tear Break Up Time (TBUT) Evaluate evaporative state – Flourescein and no anesthesia

Figure 2. Meniscus volume imaged using a video meniscometer in a: (A) normal eye, (B) dry eye, and (C) dry eye with punctal plugs. Please note the different widths.

Anthony J. Bron, Alan Tomlinson, Gary N. Foulks, Jay S. Pepose, Christophe Baudouin, Gerd Geerling, Kelly K. Nichols, Michael A. Lemp Rethinking Dry Eye Disease: A Perspective on Clinical Implications

The Ocular Surface , Volume 12, Issue 2, Supplement, 2014, S1–S31

http://dx.doi.org/10.1016/j.jtos.2014.02.002 Lissamine Green Testing

• Vital Stains – Rose Bengal – Lissamine Green – Flourescein

Testing Meibomian Expression

• Schirmer Test – Without Anesthetic • Maximal tear production – With Anesthetic • Basal secretion (DREAM) – NO consensus as to best method – 43% of PRK patients were abnormal, 1996

Infrequent tests Age of DREAM Patients (N=535)

• Flourescein Dye Disappearance 50% • Osmolarity (DREAM) 40% 35% • Lactoferrin Mean = 59.0 Yrs • Fluorophotometry 30% 26% • Evaporation 20% 13% • Biopsy 10% 13% 10% 3% 0% <40 40-49 50-59 60-69 70-79 ≥80 Years Gender of DREAM Patients Race of DREAM Patients (N=535) (N=535)

100% 100% 81% 90% 90% 74% 80% 80% 70% 70% 60% 60% 50% 50% 40% 40% 30% 30% 19% 20% 12% 20% 4% 3% 8% 10% 10% 0% 0% Female Male White Black Asian Other Unable to Answer Race

Ethnicity of DREAM Patients Smoking Habit of DREAM Patients (N=535) (N=535)

100% 87% 100% 90% 90% 80% 80% 69% 70% 70% 60% 60% 50% 50% 40% 40% 26% 30% 30% 13% 20% 20% 5% 10% 1% 10% 0% 0% Hispanic Not Hispanic Unable to Answer Never Former Current Ethnicity

Systemic Disease in DREAM Patients Current Meds in DREAM Patients (N=535) (N=535)

100% 100% 90% 90% 80% 80% 70% 70% 60% 60% 50% 50% 40% 40% 22% 30% 19% 30% 20% 10% 12% 9% 20% 6% 10% 10% 0% 0% Sjogren's Thyroid Diabetes Rheumatoid Causing Ocular Dryness Corticosteroids or Arthritis Immunosuppressive Current Ω‐3 Use in DREAM Patients Dry Eye Treatments in DREAM Patients (N=535) (N=535)

100% 100% 90% 79% 90% 75% 80% 80% 70% 70% Median daily dose: 60% 60% 600mg 50% 38% 50% 40% 40% 21% 25% 30% 30% 12% 18% 20% 11% 20% 10% 10% 0% 0% No Yes

Eyes Eligible for DREAM OSDI Score Average of Screening and Baseline (N=535) (N=535)

100% 91% 50% 90% Mean = 44.4 80% 40% 70% 26% 60% 30% 24% 50% 18% 40% 20% 16% 30% 10% 20% 9% 10% 6% 10% 0% 0% 12 23-30 31-40 41-50 51-60 61-70 71-80 Eyes of the Patient Meeting Eligibility Criteria Score

OSDI at Screening and Baseline ≥ 2 of the following 4 signs in the same eye at screening and baseline visits (Same signs at both (N=535) visits)

80 Screening 70 Baseline 59.1 Conjunctival staining present ≥ 1 (out of 60 52.6 48.0 6) 50 46.8 45.1 42.0 40.3 40 35.1 Corneal fluorescein staining present ≥ 4 30 (out of 15) 20 10 Tear film break up time (TBUT) ≤ 7 0 seconds Overall Vision Symptoms Environmental Triggers Schirmer’s test ≥ 1 to ≤ 7 mm/5min ‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐Subscales ‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐‐ 30 Baseline Conjunctival Staining Score Baseline Corneal Staining Score (1024 Eyes) (1024 Eyes)

50% 50% Mean = 3.0 Mean = 3.9 40% 40% 34%

30% 30%

20% 20% 20% 14% 15% 13% 13% 12% 13% 11% 10% 10% 11% 10% 9% 10% 9% 5% 1% 0% 0% 0123456 01234567≥8 Score (maximum of 6) Score (Maximum of 15)

Baseline Tear Break‐Up Time Baseline Schirmer Test Score (1024 Eyes) (1024 Eyes)

50% 50% Mean = 3.1 Mean = 9.4

40% 40%

33% 31% 30% 28% 30%

21% 22% 20% 20% 20% 18%

10% 8% 10% 6% 6% 3% 2% 2% 1% 0% 0% ≤234567≥8 0 1--5 6,7 8--10 11--20 21-30 ≥31 Seconds (rounded to the next full second) mm per 5 minutes

SUMMARY:

• The mean OSDI score at Screening and at Baseline is in the severe category (>33 points1)

• The DREAM Study population is inclusive in representing patients with more than mild dry eye disease Patients with systemic diseases associated with dry eye disease (e.g., Sjogren Syndrome)

Patients (25%) taking Ω-3 fatty acids at a dose well below the dose in the supplements (3000mg)

Patients using a variety of other treatments, including topical cyclosporine

• DREAM Study eyes – signs indicate more than mild disease, usually in both eyes (91%)

The 2 criteria met most frequently (>95%) were conjunctival staining and TBUT

Corneal staining and for Schirmer testing criteria each met for approximately 50% of eyes

Approximately 32% of eyes met all 4 criteria

CONCLUSION:

• Despite use of a variety of common treatments for dry eye disease, DREAM patients have symptoms and signs indicating more than mild dry eye disease

1Miller KL, Walt JG, Mink DR, et al. Minimal clinically important difference for the Ocular Surface Disease Index. Arch Ophthalmol 2010; 128:94-101. 35 36 Which Patients Are Classification of DES Candidates for Therapy? • Aqueous Tear Deficiency • There is no single method for determining if a Volume deficient patient is a candidate for dry eye therapy • Aqueous Tear Dysfunction • Criteria for starting therapy may include – Patient symptoms Evaporative excess – Corneal and conjunctival staining – Meibomian gland issues – Decreased TBUT – Schirmer scores – Exposure • Patient symptoms and clinical signs should be – Blink rate and completeness considered when deciding on therapeutic • Combination intervention

Artificial Tear Replacement Demulcents 1900’s

Normal Artificial Healthy Tears • Cellulose derivatives Tears 1. Carboxymethylcellulose sodium, 0.2% to 2.5% 2. Hydroxyethyl cellulose, 0.2% to 2.5% 3. Hydroxypropyl methylcellulose, 0.2% to 2.5% • Artificial tears contain electrolytes – 4. Methylcellulose, 0.2% to 2.5% But they lack the complex mixture of proteins, mucins and other factors found in normal healthy tears • Provide temporary, palliative relief

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Demulcents Emollients

• Dextran 70 • Lanolin preparations 0.1% when used with another polymeric demulcent agent 1. Anhydrous lanolin, 1% to 10% in combination with one or more oleaginous emollient • Gelatin agents 0.01% 2. Lanolin, 1% to 10% in combination with one or more oleaginous emollient agents • Liquid polyols 1. Glycerin, 0.2% to 1% Oleaginous ingredients 2. Polyethylene glycol 300, 0.2% to 1% 1. Light mineral oil, up to 50% in combination with one or more emollient 3. Polyethylene glycol 400, 0.2% to 1% agents 4. Polysorbate 80, 0.2% to 1% 2. Mineral oil, up to 50% in combination with one or more emollient agents 5. Propylene glycol, 0.2% to 1% 3. Paraffin, up to 5% in combination with one or more emollient agents • Polyvinyl alcohol* 4. Petrolatum, up to 100% 0.1% to 4% 5. White ointment, up to 100% 6. White petrolatum, up to 100% • Povidone 7. White wax, up to 5% in combination with one or more emollient agents 0.1% to 2% 8. Yellow wax, up to 5% in combination with one or more emollient agents • Polyacrylic acid 0.2%*

41 42 Cochrane Database Syst Rev. 2016 Treatments for Dry Eye

• Tear conservation Overall, we found OTC artificial tears – Permanent may be safe and effective at treating occlusion (1936) dry eye; however, no one product – Punctal Plugs (1975) analyzed in this review stands out as a superior dry eye treatment.

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Treatments for Dry Eye Omega‐3 Fatty Acids

• Evaporative prevention • Omega‐3 is a polyunsaturated fatty acid –Tarsorrhaphy – Named for the location of the first double bond – Eicosapentaenoic acid (EPA) –Goggles – Docosahexaenoic acid (DHA) • Secretagogues • Found in: fish, flax seed oil – Salagen • Has been associated with anti‐inflammatory effects in – Evoxac inflammatory diseases • – Rheumatoid arthritis Anti‐inflammatory – Cardiac disease – Steroids (1990s)

Omega‐3 and Dry Eye Disease Comparing DREAM to PRN

• If DED is an inflammatory disease of the ocular surface and Feature DREAM PRN Omega‐3 has anti‐inflammatory properties… Active daily dose 2000mg EPA/ 1000mg DHA 1680mg EPA/ 560mg DHA – Could Omega‐3 be used to treat DED? Placebo content Olive oil 3 gm Safflower oil 3 gm • As of 2014, only 13 randomized controlled trials performed Predominant fatty acid Oleic acid (Ω‐9) Linoleic acid (Ω‐6) using Omega fatty acids in DE patients Primary outcome Change in OSDI score Change in tear omolarity – 13 different treatments (Omega‐3 alone, Omega‐6 alone, Time 1 year 12 weeks Omega‐3 + Omega‐6) Secondary outcomes Change in signs Change in OSDI – Single site, over 1‐3 months Change in signs – No consistency in improvement of signs or symptoms Change in MMP9 positivity – The jury is still out! Randomized patients 535 (2 Active: 1 Placebo) 122 (1 Active: 1 Placebo) – DREAM will provide answers Patients lost 5% at 12 wk, 9 % at 1 yr 14% at 12 wk

Epitropoulos, Cornea, 2016 48 PRN eligibility Baseline

• Exclusions for PRN, not DREAM Characteristic DREAM PRN

Tear osmolarity of < 312 in both eyes (2 visits, 1 week Age ‐ mean (SD) 58 (13) 57 (17) apart) Gender ‐ female 81% 71% Use of cyclosporine (Restasis) Use of steroid eye drops Race ‐ White 74% 75% Use of omega-3 supplements Use of medication known to cause ocular dryness Ethnicity ‐ Hispanic 13% 2% Use of systemic corticosteroids or other OSDI score ‐ mean (SD) 44 (14) 30 (22) immunosuppressive agents Tear osmolarity ‐ mean Meibomian gland loss > 50% in either eye (SD) 303 (17) 326 (16)

TBUT, sec ‐ mean (SD) 2.8 (1.7) 4.7 (2.8) 49 50

Results in PRN trial DREAM

• Enrollment complete Changes from Baseline at 12 Weeks • Follow through July 2017 Difference Characteristic Active (mean (SD)) Placebo (mean (SD)) 95% CI p • Results late 2017, early 2018

Tear osmolarity 11.1 (3.5, decrease 19.4 (2.7) 8.3 (2.8) 18.7) 0.004 12.0 (4.5, OSDI decrease 17.0 (2.6) 5.0 (2.7) 19.4) 0.002

TBUT increase 3.5 (0.5) 1.2 (0.5) 2.3 (0.9, 3.7) 0.002

51 52

Anti‐inflammatory Therapy for KCS SS KCS

• Anti‐inflammatory therapy makes sense Steroids based on etiology effectively treat • Addresses the underlying mechanism of KCS disease (Marsh, – Potential to heal vs lubricate Ophthalmol 1999) • Targeted therapy has longer duration and more convenient dosing

Post Steroids Do Patients Need to Use Steroid Toxicity Artificial Tears with Restasis? • Dry eye is a chronic disease and requires • For additional comfort and relief of dry eye prolonged Rx symptoms, some patients may still need to use • Toxicity of corticosteroids limit their long term artificial tears potential – Nonpreserved artificial tears (Refresh®) were used in – OHT the Restasis® Phase 3 clinical trials – PSC • Need for concomitant use should decrease over – Infection time

When to use punctal plugs?

• Evidence for neurotrophic component • Severe disease with minimal flow, but not in purely evaporative dry eye • Failure to respond to tear substitute or cyclosporine • Army study; 0.25% LASIK AND 0.04% PRK needed plugs post op

58

Current Treatment for Dry Eye Lifitegrast 5%

• OPUS‐1 – Vs placebo, phase 3, n=565, superior in total corneal stain,total LG • A majority of patients (74%) do not obtain stain, mean dryness score and ocular discomfort score at 12 weeks satisfactory relief from dry eye symptoms with • OPUS‐2 – Vs placebo, in artificial tear users, symptoms improved but no artificial tears change in inferior corneal stain • Punctal plugs are not effective for all patients • OPUS‐3 – Vs placebo, n=331, targeted symptoms. Showed trends for corneal • Many dry eye patients (34%) wish there was an flourescein, conj LG stain, Schirmer and conj redness effective therapy available for treating their dry • SONATA eyes – 2014, safety, vs placebo, 1 year, 50% side effects (mild) • FDA approval June 2016

60 Gallup Poll, Data on file, Allergan Lifitegrast vs Cyclosporine Rebamipide

• Both anti‐inflammatory • Secretogogue – Xiidra inhibits T‐cell inflammation by blocking • Not yet approved in US Lymphocyte function‐associated antigen (LFA‐1) and intercellular adhesion molecule (ICAM‐1)

– Restasis inhibits T‐cell proliferation and subsequent T‐ cell mediated responses through calcineurin inhibition

– Different pathways, but no evidence for competition, indifference or facilitation of effects

61 62

Diquafasol Devices in development

• Purinergic agonist of P2Y2 receptor • Oculeve Neurostim Device • Promotes mucin secretion – Nasal stimulation, wireless controller • 2010, approved in Japan • Ocular Ionotphoesis with EG‐437 • Variable clinical results in US and not – Dexamethasone approved – Did not meet endpoints of corneal staining and ocular discomfort

63 64

Pharmaceuticals Platelet Lysate

• Phase 2 trials 2015 • In vivo confocal study • Recombinant Human Serum Albumnin • Effective in Sjogrens patients as eye drop – 6x daily – Increased basal cells, corneal nerves, decreased – Safety over 12 weeks Langerhans cells – No improvement in corneal staining – Autologous, platelets >100,000/ul • KPI‐121/LE‐MMP 0.25% Loteprednol Mucus‐ – 30 patients Penetrating Particle glucocorticoid agonist – Turin – QID, 28 days, improved hyperemia, not in ocular • KUMC planning study in GVHD patients with discomfort allographic platelets

65 66 Conclusions

• Dry eye symptoms have an adverse effect on patients’ lives – DED interferes with daily activities at home and at work – DED worsens over time • Treatment and avoidance can now address the underlying pathophysiology Figure 1. Etiopathogenic classification (modified from 2007 DWES report).1

Hui Lin, Samuel C. Yiu

Dry eye disease: A review of diagnostic approaches and treatments

Saudi Journal of Ophthalmology, Volume 28, Issue 3, 2014, 173–181

http://dx.doi.org/10.1016/j.sjopt.2014.06.002

Dry Eye Recommendations

Pflugfelder Ther ATD ATD Exposure MGD OCP Updates 2004 No reflex

Artificial Tears XX X X X Secretagogue X± Questions? Punctal occlusion XX X Serum XX Restasis XX ±± Steroids XXX Doxycycline Xx Tarsorrhaphy X 70

71 72 73 74

Combinations of Signs in Patients

Other 5%

Conj Stain + TBUT All 4 19%

40%

Conj Stain + Schirmer + 15% TBUT

21% Conj & Corneal Stain + TBUT

75

Specific Aims of the DREAM Study

• Aim 1: Determine the efficacy and safety of oral omega‐3 compared to placebo in patients with dry eye disease over 1 year. • Aim 2:To describe and evaluate a comprehensive set of features of dry eye disease and treatment (signs, symptoms, biomarkers, and economic factors) over one year of observation. • Aim 3: To determine the long term effects of omega‐3 essential fatty acids through 2 years.

77 DREAM Collaborators DREAM CLINICAL CENTER LOCATIONS

Study Chair Office Coordinating Center Icahn School of Medicine at Mount University of Pennsylvania School Sinai of Medicine

Principal Investigator Principal Investigator Penny A Asbell, MD, MBA, FACS Maureen G. Maguire, PhD

Project Manager Project Directors Eric Kuklinski, BA Ellen Peskin, MA, CCRP Biomarker Laboratory Kathleen McWilliams, CCRP Yi Wei , PhD

DREAM CLINICAL TRIAL DESIGN Outcome Measures

Primary Secondary Exploratory Candidate •Change in Ocular Surface • Compliance with the study treatment • Contrast Sensitivity Patients Disease Index (OSDI) score from protocol as measured by changes in • Signs measured by keratography: 24 Month baseline blood levels of essential fatty acids and  TBUT, TMH, redness, 1/2  Follow-up pill counts. meibography 12 Month Active 3 Exam Active 3 Follow-up Exam Randomize • Change in Signs of DED (conjunctival and • Tear osmolarity corneal staining, TBUT, Schirmer’s test) • Meibomian gland secretion • Use of artificial tears or other treatments • Biomarker levels: Randomize 2/3 24 month for DED  MMP‐9, tear cytokine levels, 1/2 Follow-up Eligible Placebo Exam • Quality of life as measured by the SF‐36 HLA‐DR expression. Patients 1/3 • Change in Brief Ocular Discomfort Index  Blood‐ autoimmune biomarkers (BODI) score. Follow-up 12 Month Placebo Exam • Incidence of ocular and systemic adverse events, changes in VA and IOP • Cost‐effectiveness of using Omega‐3

Primary Trial Randomized Extension Study (12 months) (12 months)

Eligibility Criteria –Primary Trial Treatment Assignment

• ≥ 2 of the following 4 signs in the same eye at screening and • Treatments baseline visits (Same signs) – Active supplements  Conjunctival staining present ≥ 1 (out of 6)  Corneal fluorescein staining present ≥ 4 (out of 15) (2000 mg EPA and  Tear film break up time (TBUT) ≤ 7 seconds 1000 mg DHA per day)  Schirmer’s test ≥ 1 to ≤ 7 mm/5min – Placebo supplements • Ocular Surface Disease Index (OSDI) score: • Patients are randomized to a supplement group – 25‐80 at screening • 2:1 ratio active:placebo – 21‐80 at baseline • Symptoms of DED ≥ 6 months • Double masked –patient and evaluators do not know treatment assignment • Use of (or desire) artificial tears ≥2 times/day in last 2 wks Eligibility Criteria –Extension Study Visit Schedule • Assigned to active supplements in Primary Primary Trial Extension Study Trial and willing to continue taking – Screening Visit  Month 15: “Check In” Telephone Call supplements – Month 00: Baseline Visit  Month 18: • We believe this operational definition will – Month 03  Month 21: “Check In” Telephone Call select for patients who perceive benefit from – Month 06  Month 24 their active supplements – Month 09: “Check In” Telephone Call

– Month 12

DREAM Name City State

Stephen Cohen OD Scottsdale AZ • DRy Eye Assessment and Management Study Joanne Shen MD Scottsdale AZ Milton Hom OD Azusa CA – The first major, non‐pharmaceutical funded trial Robert Pendleton MD PHD Oceanside CA on Dry Eye Disease Meng Lin OD PHD Berkeley CA Damien Goldberg MDDREAM InvestigatorsTorrance –Part 1 CA – Unique opportunity to study Dry Eye Disease in a Lee Shettle OD Largo FL

well‐defined cohort of DE patients Harvey Dubiner MD Morrow GA – Will allow us to evaluate the role of Omega‐3 in Sandeep Jain MD IL Dry Eye Disease and in ocular inflammatory Kathleen Kelley OD IN processes John Sutphin MD Prairie Village KS Jack Greiner OD PHD Winchester MA

Reza Dana MD Boston MA

Pedram Hamrah MD Boston MA

Ocular Surface Disease and Refractive Name City State Surgery Roni Shtein MD Ann Arbor MI

David Hardten MD Bloomington MN

Joseph Tauber MD Kansas City MO • Meibomian Gland Dysfunction and Steven Silverstein MD Kansas City MO Rosacea Sean Mulqueeny OD Creve Coeur MO – Treat Aggressively pre operatively or Carol Aune OD DREAM InvestigatorsRaleigh –Part 2 NC Penny Asbell MD New York NY before any Enhancement Holly Hindman MD Rochester NY • Lid Hygiene Loretta Szczotka‐Flynn OD PHD Cleveland OH • Topical Antibiotic Steroid Ointment Marc Jones MD Stow OH • Oral Doxycycline Vatinee Bunya MD PA – 20, 50 or 100 mg; minocycline Michael Christensen OD PHD Memphis TN

Inder Paul Singh MD Racine WI • Flaxseed Oil 1000 mg PO BID • Omega 3 Dietary Supplementation

Patterns of Oculofacial Injury in Equestrians due to Hoof‐Kicks

Denise Capps, MD, Resident, Class of 2020 Primary Supervisor: Jason Sokol, MD

Participation in equestrian sports is on the rise. Interaction with horses is dangerous to both mounted and unmounted equestrians. Current safety recommendations include use of protective headwear while on and off a horse. There are no current recommendations on protective eyewear. Observational data indicate a potential rising incidence of severe oculofacial trauma after interaction with horses, specifically after a horse kick. We aim to survey the pattern and extent of oculofacial injury after horse kicks, specifically in regard to oculofacial fracture.

This presentation will review cases of oculofacial injury sustained by hoof‐kicks in equestrians seen at KUMC and KU Eye Clinic. We will discuss the severity, pattern of injury, outcome, and management of patients who sustained oculofacial injuries as a result of being kicked by a horse.

Correlating Projected Comfort Level of Ophthalmology Residents in Performing Oculofacial Plastics Procedures with Ophthalmology Residency Program Characteristics

Reid Mollman, MD, Resident Class of 2018 Primary Supervisor: Jason Sokol, MD

Introduction: Oculofacial plastic surgery procedures are vital to the training of ophthalmology residents. We sought to assess the projected comfort level of ophthalmology residents in performing 22 common oculoplastic procedures, and correlating this with varied training program characteristics as well as resident level of training.

Methods: A nine‐question web‐based anonymous survey was created, and sent to the program coordinators of all accredited ophthalmology programs, as listed on the ACGME website, who then forwarded the survey link to residents of their individual programs. Responses were solicited between May 18th and May 26th, 2017.

Results: A total of 129 ophthalmology programs were contacted in the survey, which generated a total of 149 completed surveys during the solicitation window. The majority of resident respondents were PGY‐2 (35.6%), followed by PGY‐3 (33.6%) and PGY‐4 (29.5%). The procedures, in which the residents were the most comfortable performing, included excision (94.6%), laceration repair (91.3%) and lacrimal probing and irrigation (90.6%). The procedures the residents were the least comfortable performing included orbitotomy (2.7%), cicatricial repair (3.4%) and orbital fracture repair (4.0%). Program characteristics, which portend a higher comfort level in performing procedures, include programs with an associated oculofacial plastics fellowship, and those who primarily generate cases through a VA resident clinic.

Expansion of Extraocular Muscles Following Orbital Decompression in Thyroid Eye Disease

Christina Donaghy Gillmor, MD, Resident, Class of 2020 Primary Supervisor: Jason Sokol, MD

Thyroid eye disease (TED) is a complex orbital inflammatory condition whereby orbital fibroblasts are activated secondary to auto-antibodies. Severe forms of the disease can lead to compressive or that are visually significant. Orbital decompression is a commonly performed surgery that aims to relieve compression on the , reduce proptosis, and improve eyelid position in TED patients. This case series will review several cases of patients with severe TED who underwent orbital decompression surgery at the University of Kansas and then demonstrated post-operative radiographic expansion of extraocular muscles. Pre-operative and post-operative imaging studies will be reviewed with detailed analysis of extraocular muscle dimensions.

A Novel Scleral Fixated Intraocular Lens Insertion Technique through a Small Corneal Incision

Yong Kam, MD, Resident, Class of 2020 Primary Supervisor: Mary Champion, MD

Objective: To demonstrate a successful insertion of a scleral fixated intraocular lens through a small corneal incision.

Purpose: To describe a technique facilitating insertion of a suture threaded intraocular lens by using an intraocular lens injector through a small corneal incision, avoiding the need to create a large incision with potentially devastating complications.

Method: This is a retrospective two-surgical case report describing a novel surgical technique. This technique utilizes an intraocular lens injector model VIS100 or AI-28 to insert a Gore-Tex suture threaded Akreos AO60 lens through a 1.8 mm to 2.8 mm corneal incision.

Results: This novel technique facilitates successful, safe and efficient insertion and scleral fixation of the intraocular lens with excellent post-operative outcome.

Case 1: A 52-year-old male with history of OS status post pars plana vitrectomy and cryotherapy presented with a count fingers at 3 feet visual acuity from ruptured posterior capsule and with crystalline lens in the vitreous chamber. Patient underwent 25 gauge pars plana vitrectomy, pars plana lensectomy and secondary scleral fixated lens using our novel technique. On postoperative week 1, patient had a visual acuity of 20/500, pinholed to 20/125 and of 19.

Case 2: A 33-year old male presented with a hand motion visual acuity from a traumatic cataract with poor capsular support. Patient underwent 23 gauge pars plana vitrectomy, pars plana lensectomy, and secondary scleral fixated lens using our novel technique. On postoperative week 1, patient had a visual acuity of 20/20 and intraocular pressure of 15.

Conclusion: Creation of a large incision in order to insert a scleral fixated intraocular lens is a high risk maneuver. A suture-threaded intraocular lens for scleral fixation can be successfully inserted through a 1.8 - 2.8 mm corneal incision using an intraocular lens injector, and a larger wound and its associated complications can be avoided.

Cavernous Hemangioma- Objectives Where are you? What are  Overview of the clinical findings of Cavernous you? And how are we Hemangiomas going to get you out?  Review of orbital anatomy  Overview of different surgical approaches for removal

Jason A Sokol, MD Oculofacial Plastic and Orbital Surgery

Cavernous Hemangioma

 Most common benign orbital tumor in adults

 Typically present in middle age (30-50y) with slight female predilection

 Often present with slowly progressive proptosis

 Imaging shows homogeneously enhancing encapsulated mass

 Histology shows encapsulated lesion with large cavernous spaces containing red blood cells with walls containing smooth muscle

 Treatment is surgical excision via orbitotomy. Approach is based on location of lesion. Case 1 Physical Exam

 VA Distance (SC)  Adnexa: 3mm proptosis OD  Chief complaint: dimmed vision OD  OD 20/30+1  : white and quiet OU  HPI: 40yoWM who is otherwise healthy presents with 8  OS 20/10-2 months of persistent stable dimmed vision OD. He also  Cornea: clear OU notes that his vision OD dims more when looking to the  IOP OD 12, OS 10  AC: Deep/Quiet OU side. He denies pain.  Pupils: 3+APD OD  Iris: round OU  Motility: -0.5 ABduction and attempted supraduction OD,  Lens: clear OU otherwise full OU  Vitreous: clear OU What now?

DDx Orbital Mass Combined medial lateral orbitotomy with bone flap  Cavernous Hemangioma  Hemangiopericytoma  Orbital Varix  Lymphoma  Meningioma  Schwannoma  Metastasis Treatment Treatment

Treatment POW5

 VA Distance (SC)  Adnexa: WNL OU

 OD 20/20-2  Conjunctiva: white and quiet OU  OS 20/15-  Cornea: clear OU  IOP OD 10, OS 11  AC: Deep/Quiet OU  Pupils: PERRL, no APD

 Motility: Full OU Case 2

Lateral orbitotomy with bone flap Case 3

Nasal Orbital Anatomy

Trans nasal orbital approach References Questions?

 McNabb A, et al. The anatomical location and laterality of orbital cavernous haemangiomas. . 2014 Oct; 33(5):359-62

 Orbit, , and Lacrimal System. Section 7. Basic and Clinical Science Course, AAO. 2013-2014

 Rootman DB, et al. Cavernous venous malformations of the orbit (so- called haemangioma): a comprehensive evaluation of their clinical, imaging and histiologic nature. Br J Ophthalmol. 2014 July;98(7):880-8.

Mainster, RetinaLand, EyeCon 2018, Page 1

A Physicist’s Adventures in RetinaLand 2018 Lemoine Lecture, May 11, 2018 Martin A. Mainster, Ph.D., M.D., FRCOphth. Department of Ophthalmology, University of Kansas School of Medicine Prairie Village, Kansas, USA, E-mail: [email protected] Educational objectives To examine the historical origins and basic principles of photodisruption, variable contrast acuity testing, slitlamp contact lens ophthalmoscopy and ultraviolet protective intraocular lenses

Reference abbreviations [TI] Technology Incorporated, 1968-72; [S&W] Scott and White Memorial Hospital, 1976-79; [SERI] Schepens Eye Research Institute, 1979-85; [KUEye] University of Kansas, 1985-present Photodisruption Photodisruption occurs in Nd:YAG laser capsulotomy when extremely high infrared laser irradiance ionizes target tissue molecules, disintegrates focal target tissue and causes a perifocal shock wave that fragments adjacent tissue. Latent tissue stress when present causes further tissue disruption. High irradiance (power/area) is achieved by focusing a very brief (nanosecond) laser pulse into a tiny area in the focal plane using a short focal lens. The laser beam diverges rapidly posterior to the focal plane. Retinal irradiance is negligible and “plasma shielding” is unnecessary for retinal safety during capsulotomy. Accurate axial-localization of the focal point of the treatment beam is achieved using a static crossed laser- beam aiming system, similar to the crossed searchlight altitude-localization system used in the 1943 British low-altitude nighttime bomber raid on Ruhr Valley dams in World War II. In the 1983 article I wrote for Ophthalmology, I coined the term “photodisruption” now commonly used in medical laser applications, provided the biophysics of ionizing laser-tissue interactions, proved that picosecond “plasma-shielding” wasn’t needed to protect the retina during capsulotomy (thereby permitting the use of less costly nanosecond lasers) and introduced the static crossed-beam axial target localization system integrated into hundreds of thousands of laser photodisruptors since 1983. Mainster MA, Sliney DH, Belcher CD III, Buzney SM. Laser photodisruptors: Damage mechanisms, instrument design and safety. Ophthalmology 90:973-91, 1983. [SERI] Fourier, contrast sensitivity and variable contrast acuity testing Joseph Fourier (1768-1830) showed that real-world signals or patterns (periodic waveforms) are equal to the sum of their sinusoidal components. Breaking waveforms down into their sinusoidal components is known as Fourier analysis. Real-world signals and patterns can be studied from our familiar time-domain perspective of time and space or from an alternative but equally complete frequency-domain (Fourier- domain) viewpoint of frequency, amplitude and phase. The Fourier transform is the portal between these alternate universes, allowing us to travel back and forth between these two equivalent mathematical representations of reality. Problems that are difficult or impossible to solve in the time-domain can often be solved easily in the frequency domain. For example, spectral-domain and swept-source optical coherence tomography (OCT) capture spectral interference data simultaneously from all chorioretinal depths. The period of spectral oscillations is proportional to the depth of tissue interfaces, so taking the Fourier transform of these spectral data provides A-scans. Capture rate is vastly higher than in time-domain OCT, allowing OCT angiography. Lenses are Fourier transforms in the spatial domain. Visual target information can be decomposed into its spatial sinusoidal components. The eye’s MTF (modulation transfer function) describes how efficiently a target’s spatial information is transmitted through the cornea and lens at different spatial frequencies. I used Fourier optics in 1969 to compute retinal images of bright light sources including lasers and the sun. These data combined with the spectral transmittance of ocular media and the spectral absorption of the RPE and allowed calculation of where and how much chorioretinal thermal energy was produced. I then used Fourier’s heat conduction equation and the finite element modeling techniques we pioneered to compute retinal temperature increases from clinical and military light sources. Our 1970-1 series of articles provided a quantitative basis for clinical retinal photocoagulation, permitting laser exposures to be scaled for Mainster, RetinaLand, EyeCon 2018, Page 2 different spot sizes, wavelengths and pulse durations. This methodology is incorporated in international ocular safety standards for non-ionizing radiation that have been used for over four decades. It takes more contrast to see fine detail than it does to see coarse detail. Overall human contrast sensitivity generally decreases with increasing spatial frequency because the contrast sensitivity of the retina and brain decrease with increasing spatial frequency, as does the contrast transmitted by the cornea and lens. The CSF (contrast sensitivity function) describes the overall sensitivity of the eye and brain to different spatial frequencies. In the frequency domain, the CSF is the product of the optical cornea-lens MTF and neural NTF (retinal-brain neural transfer function) at each spatial frequency. Modern reduced contrast acuity testing developed from variable contrast testing that Dr. George Timberlake and I developed in 1981. The MTF is a widely used measure of the performance of optical devices including intraocular lenses. Any change in MTF due to an individual’s optical aberrations produces an equivalent change in their overall CSF. Patients with macular disease may benefit visually from cataract surgery even when it doesn’t improve their high contrast visual acuity. Contrast sensitivity loss from lens opacities and macular abnormalities are additive, so implant surgery may improve medium spatial frequency performance even though a patient’s high spatial frequency (fine detail) ability has been destroyed permanently by macular scarring or atrophy. Mainster MA, White TJ, Tips JH, Wilson PW. Retinal temperature increases produced by intense light sources. J Opt Soc Am 1970; 60:264-270. [TI] Mainster MA. Contemporary optics and ocular pathology. Surv Ophthalmol 1978; 23:135-142. [S&W] Mainster MA, Timberlake GT, Schepens CL. Automated variable contrast acuity testing. Ophthalmology 1981; 88:1045- 1053. [SERI] Mainster MA, Turner PL. Multifocals and . In: Chang DF, ed. Transitioning to Refractive IOLs – the Art and Science: a Clinical Manual. Slack Inc., 2008; Chapter 110, pp. 389-394. [KUEye] Aspheric lenses and scanning laser ophthalmoscopes The Persian mathematician Ibn Sahl (940–1000) formulated Snell’s law in 984, 600 years before the Dutch astronomer . Sahl used the law to design aspheric “burning” lenses and mirrors. Francis Smethwick produced the first high-quality aspheric lenses in 1667. Hermann von Helmholtz invented the ophthalmoscope in 1851. Allvar Gullstrand showed fifty years later that separating illumination from observation in a patient’s minimizes reflections and improves ophthalmoscopic image quality. Modern flood illumination fundus cameras use Gullstrand’s principle, projecting light into the eye through the pupillary periphery and collecting retro-reflected light through the central pupil. Slitlamp ophthalmoscopic lenses illuminate a narrow pupillary cross-section, collecting light from the rest of the pupil and relying on observers’ skill to dodge anterior segment light reflections. Harold Ridley used a different approach in 1949, illuminating the retina with a scanning spot rather than flooding it with light. He didn’t have the technology then to produce clinically-useful images, but Rob Webb solved the problem in 1980 when he invented the scanning laser ophthalmoscope (SLO). An SLO scans a raster of illuminated points on the retina. Light scattered back from each retinal point is collected and displayed on a monitor to produce a dynamic video image of the retina. The laser beam occupies only a tiny pupillary area at any moment, so the rest of the pupil is available for light collection. SLOs are highly light efficient, allowing dynamic retinal imaging at low, very comfortable light levels. George Timberlake and I helped develop SLO clinical applications beyond clinical ophthalmoscopy. Modulation of the scanning laser beam produces retinal patterns visible simultaneously to patients and observers, thereby permitting retinal perimetry, analysis of low vision reading and other retina-based psychophysical analyses. The Goldmann 3-mirror lens was introduced in 1938. It remained the best available slitlamp ophthalmoscopy lens for several decades despite its narrow 36-degree field of view. That situation changed when Professor Hans-Joachim Schlegel developed his 120-degree contact Panfundoscope lens in 1969 and Dr. David Volk introduced non-contact aspheric slitlamp ophthalmoscopy in the late 1970s. I used aspheric optics in 1986 to solve the image distortion and laser beam problems of the Panfundoscope’s spherical objective lens. Aspheric contact ophthalmoscopic lenses are now used for most retinal photocoagulation procedures. Each lens is a trade-off between magnification and field of view, balancing other variables including resolution, image plane location and the ratio of monocular to binocular field size. Hundreds of thousands of aspheric contact ophthalmoscopic lenses with different designs have been produced since the first “Standard” “Mainster” lens. Mainster MA, Timberlake GT, Webb RH, Hughes GW. Scanning laser ophthalmoscopy: clinical applications. Ophthalmology 1982; 89:852-857. [SERI] Mainster, RetinaLand, EyeCon 2018, Page 3

Timberlake GT, Mainster MA, Peli E, Augliere RA, Essock EA, Arend LE. Reading with a macular : retinal location and fixation area. Invest Ophthalmol Vis Sci 1986; 27:1137-1147. [SERI] Mainster MA, Crossman JL, Erickson PJ, Heacock GL. Retinal laser lenses: magnification, spot size and field of view. Br J Ophthalmol 1990; 74:177-179. [KUEye]

Ultraviolet-blocking filters in intraocular lenses Photic (retinal phototoxicity) is caused by intense light exposures lasting several seconds to minutes that would be well tolerated if experienced only momentarily. Illuminances far exceed ordinary environmental light levels but chorioretinal temperature elevations are too low for photothermal damage. In retinal phototoxicity, optical radiation produces highly reactive oxygen radicals that are damaging to retinal cell membranes, proteins, carbohydrates and nucleic acids. The most common signs of clinical acute retinal phototoxicity are small yellowish-white foveolar lesions in solar or welding arc maculopathy. Larger sometimes extrafoveal lesions occur in operating microscope or endoilluminator injuries. Photic retinopathy can be divided into the photopigment-mediated (Class-1) phototoxicity discovered by Werner Noell and the photosensitizer-medicated (Class-2) phototoxicity discovered by Bill Ham and Dave Sliney. Photopigment-mediated phototoxicity has an action spectrum similar to that of rhodopsin. It has been demonstrated only in rodents. Photosensitizer-mediated retinal phototoxicity is the probable cause of clinical photic retinopathy. Its action spectrum increases rapidly with decreasing wavelength, similar to the absorption spectrum of lipofuscin in the retinal pigment epithelium which is its primary mediator. Class-2 phototoxicity became known as the “blue light” hazard but really should be called the “UV radiation” hazard Professor Ridley invented the IOL based on his observation that PMMA shards from a shattered Spitfire canopy did not cause inflammation in an injured pilot’s eye. He implanted the first IOL in 1949, the same year he pioneered ophthalmic video broadcasting. IOL transmittance was ignored until 1978 when I observed that early polymethylmethacrylate IOLs allowed ultraviolet (UV) radiation to reach the retina. I knew that UV radiation could cause retinal phototoxicity and that it wasn’t useful for human photoreception so blocking it with UV-absorbing IOL chromophores wouldn’t adversely affect human vision. I published these data during the second year of my ophthalmology residency and UV-protective intraocular lenses have been implanted in hundreds of millions of people who have had cataract surgery over the past forty years. Sensitivity spectra show that the ideal IOL for dim light vision and circadian photoreception is a colorless IOL that transmits as much blue light as possible. Mainster MA. Destructive light adaptation. Ann Ophthalmol 1970; 2:44-48. [TI] White TJ, Mainster MA, Wilson PW, Tips JH. Chorioretinal temperature increases from solar observation. Bull Math Biophys 1971; 33:1-17. [TI] Mainster MA. Spectral transmittance of intraocular lenses and retinal damage from intense light sources. Am J Ophthalmol 1978; 85:167-170. [S&W] Mainster MA. Solar , photic maculopathy and the pseudophakic eye. J Cataract Refract Surg 1978; 4:84-86. [S&W] Mainster MA, Ham WT Jr, Delori FC. Potential retinal hazards: instrument and environmental light sources. Ophthalmology 1983; 90:927-931. [SERI] Mainster MA. The spectra, classification, and rationale of ultraviolet-protective intraocular lenses. Am J Ophthalmol 1986; 102:727-732. [KUEye] Mainster MA. Light and : a biophysical and clinical perspective. Eye 1987; 1:304-310. [KUEye] Turner PL, Mainster MA. Circadian photoreception: aging and the eye’s important role in systemic health. Br J Ophthalmol; 2008; 92:1439-44. [KUEye] Mainster MA, Turner PL. Blue-blocking IOLs decrease photoreception without providing significant photoprotection. Surv Ophthalmol 2010; 55:272-83. [KUEye] Mainster MA, Turner PL. Ultraviolet-B phototoxicity and hypothetical photomelanomagenesis: intraocular and crystalline lens photoprotection. Am J Ophthalmol 2010; 149:543-9. [KUEye] Turner PL, Someren EJW, Mainster MA. The role of environmental light in sleep and health: effects of ocular aging and cataract surgery. Sleep Medicine Reviews 2010; 14:269-80. [KUEye] Mainster MA, Turner PL. Blue-blocking IOLs. Ophthalmology 2011; 118:1898-9. [KUEye] Mainster MA, Turner PL. Glare’s causes, consequences and clinical challenges after a century of ophthalmic study. Am J Ophthalmol 2012; 153:587-93. [KUEye] Mainster, RetinaLand, EyeCon 2018, Page 4

Selected publications: a chronology with citations [the number in square brackets is the number of times an article has been cited by other scientific publications as of April 2, 2018] Technology Incorporated, San Antonio, TX, 1968-72 Mainster MA, White TJ, Tips JH, Wilson PW. Retinal temperature increases produced by intense light sources. J Opt Soc Am 1970; 60:264-270. [182] Mainster MA, White TJ, Allen RG. Spectral dependence of retinal damage produced by intense light sources. J Opt Soc Am 1970; 60:848-855. [101] Mainster MA, White TJ, Tips JH, Wilson PW. Transient thermal behavior in biological systems. Bull Math Biophys 1970; 32:303-314. [50] White TJ, Mainster MA, Tips JH, Wilson PW. Chorioretinal thermal behavior. Bull Math Biophysics 1970; 32:315-322. [54] Mainster MA, White TJ, Tips JH. Corneal thermal response to the CO2 laser. Applied Opt 1970; 9:665-667. [15] White TJ, Mainster MA, Wilson PW, Tips JH. Chorioretinal temperature increases from solar observation. Bull Math Biophys 1971; 33:1-17. [62] Mainster MA, Wilson PW, Tips JH. Calculation of photopic and scotopic parameters. Vision Res 1971; 11:1011-4. [2] Mainster MA, White TJ, Stevens CC. Mathematical analysis of photopigment kinetics. Vision Res 1971; 11:435-447. [15] Mainster MA, White TJ. Calculation of absorption spectra for mixtures of human rhodopsin and its photoproducts. Vision Res 1972; 12:151-60 [2] Mainster MA, White TJ. Photoproducts of retinal photopigments & visual adaptation. Vision Res 1972; 12:805-823. [11] Mainster MA. Retinal transport and the regeneration of human cone photopigment. Nature New Biol 1972; 238:223-4. [10]

Scott and White Memorial Hospital (ophthalmology residency), Temple, TX, 1976-1979 Mainster MA. Spectral transmittance of intraocular lenses and retinal damage from intense light sources. Am J Ophthalmol 1978; 85:167-170. [156] Mainster MA. Solar retinitis, photic maculopathy and the pseudophakic eye. J Cataract Refract Surg 1978; 4:84-86. [81] Mainster MA. Contemporary optics and ocular pathology. Surv Ophthalmol 1978; 23:135-142. [15] Mainster MA. Corneal endothelial dynamics and intraocular lens implantation. J Cataract Refract Surg 1978; 4:4-6. [1] Mainster MA. Ophthalmic applications of infrared lasers. Invest Ophthalmol Vis Sci 1979; 18:414-420. [112] Mainster MA, Dieckert JP. A simple haploscopic device for quantitating color brightness comparison. Am J Ophthalmol 1980; 89:58-61. [10] Mainster MA, Sewell JJ. Small computers in the private ophthalmic practice. Surv Ophthalmol 1980; 24:315-321. [5]

Schepens Eye Research Institute/Harvard Medical School, Boston, MA, 1979-1985 Delori FC, Parker JS, Mainster MA. Light levels in fundus photography and fluorescein angiography. Vision Res 1980; 20:1099-1104. [16] Timberlake GT, Mainster MA, Schepens CL. Automated clinical visual acuity testing. Am J Ophthalmol 1980; 90:369-373. [24] Mainster MA, Timberlake GT, Schepens CL. Automated variable contrast acuity testing. Ophthalmology 1981; 88:1045-1053. [17] Timberlake GT, Mainster MA, Webb RH, Hughes GW, Trempe CL. A new method for direct localization of scotomata. Invest Ophthalmol Vis Sci 1982; 22:91-97. [124] Mainster MA, Timberlake GT, Webb RH, Hughes GW. Scanning laser ophthalmoscopy: clinical applications. Ophthalmology 1982; 89:852-857. [174] Mainster MA, Ham WT Jr, Delori FC. Potential retinal hazards: instrument and environmental light sources. Ophthalmology 1983; 90:927-931. [163] Mainster MA, Sliney DH, Belcher CD III, Buzney SM. Laser photodisruptors: damage mechanisms, instrument design and safety. Ophthalmology 1983; 90:973-991. [186] Mainster MA. Finding your way in the photoforest: laser effects for clinicians. Ophthalmology 1984; 91:886-888. [20] Timberlake GT, Mainster MA, Peli E, Augliere RA, Essock EA, Arend LE. Reading with a macular scotoma: retinal location and fixation area. Invest Ophthalmol Vis Sci 1986; 27:1137-1147. [302]

Mainster, RetinaLand, EyeCon 2018, Page 5

University of Kansas, Department of Ophthalmology, Prairie Village, KS, 1985-present Mainster MA. Wavelength selection in macular photocoagulation: tissue optics, thermal effects and laser systems. Ophthalmology 1986; 93:952-958. [187] Mainster MA. The spectra, classification, and rationale of ultraviolet-protective intraocular lenses. Am J Ophthalmol 1986; 102:727-732. [92] Mainster MA. Light and macular degeneration: a biophysical and clinical perspective. Eye 1987; 1:304-310. [122] Mainster MA. Henle fibers may direct light toward the center of the fovea. Lasers Light Ophthalmol 1988; 2:79-86. [8] Mainster MA, Crossman JL, Erickson PJ, Heacock GL. Retinal laser lenses: magnification, spot size and field of view. Br J Ophthalmol 1990; 74:177-179. [45] Mainster MA. The fractal properties of retinal vessels: embryological and clinical implications. Eye 1990; 4:235-241. [185] Mainster MA. Cellular automata: retinal cells, circulation and patterns. Eye 1992; 6:420-427. [4] Mainster MA, Sliney DH, Marshall J, Warren KA, Timberlake GT, Trokel SL. But is it really light damage? Ophthalmology 1997; 104:179-180. [20] Mainster MA, Sliney DH, Timberlake GT, Warren KA. Pointers on laser pointers. Ophthalmology 1997; 104:1213-4. [35] Mainster MA. Solar eclipse safety. Ophthalmology 1998; 105:9-10. [16] Mainster MA. Blinded by the light - NOT! Arch Ophthalmol 1999; 117:1547-1548. [14] Mainster MA, Reichel E. Transpupillary thermotherapy for age-related macular degeneration: long-pulse photocoagulation, apoptosis and heat shock proteins. Ophthalmic Surg Lasers 2000; 31:359-373. [284] Mainster MA, Reichel E, Warren KA, Harrington PG. Ophthalmoscopy and vitreoretinal surgery in patients with an ARRAY refractive multifocal intraocular lens implant. Ophthalmic Surg Lasers 2002; 33:74-6. [17] Mainster MA, Timberlake GT. Why HID headlights bother older drivers. Br J Ophthalmol 2003; 87:113-117. [51] Mainster MA, Stuck BE, Brown J Jr. Assessment of alleged retinal laser injuries. Arch Ophthalmol 2004; 122:1210-17. [77] Luttrull JK, Musch DC, Mainster MA. Subthreshold diode micropulse photocoagulation for the treatment of clinically significant diabetic . Br J Ophthalmol 2005; 89:74-80. [202] Staurenghi G, Viola F, Mainster MA, Graham RD, Harrington PG. Scanning laser ophthalmoscopy and angiography with a wide-field contact lens system. Arch Ophthalmol 2005; 123:244-252. [95] Mainster MA. Violet and blue blocking intraocular lenses: photoprotection vs. photoreception. Br J Ophthalmol 2006; 90:784-92. [214] Zhao H, Mainster MA. Chromatic dispersion and pseudophakic optical performance. Br J Ophthalmol; 2007; 91:1225-9. [75] Turner PL, Mainster MA. Circadian photoreception: aging and the eye’s important role in systemic health. Br J Ophthalmol; 2008; 92:1439-44. [201] Mainster MA, Turner PL. Blue-blocking IOLs decrease photoreception without providing significant photoprotection. Surv Ophthalmol 2010; 55:272-83. [101] Symons RCA, Mainster MA, et al. Solar maculopathy in a young child. Br J Ophthalmol; 2010; 94:1258-9, 1269. [10] Mainster MA, Turner PL. Ultraviolet-B phototoxicity and hypothetical photomelanomagenesis: intraocular and crystalline lens photoprotection. Am J Ophthalmol 2010; 149:543-9. [31] Turner PL, Van Someren EJW, Mainster MA. The role of environmental light in sleep and health: effects of ocular aging and cataract surgery. Sleep Medicine Reviews 2010; 14:269-80. [120] Mainster MA, Turner PL. Blue-blocking IOLs vs. short wavelength visible light: hypothesis-based vs. evidence-based medical practice. Ophthalmology 2011; 118:1-2. [30] Mainster MA, Turner PL. Glare’s causes, consequences and clinical challenges after a century of ophthalmic study. Am J Ophthalmol 2012; 153:587-93. [60] Citation analysis, April 2, 2018, Google Scholar h-index: 38 quantifies impact and significance of research; mean h-index in academic ophthalmology: full professor, 16.7; associate professor, 8.2; assistant professor, 3.5 i10 index: 83 number of publications with at least 10 citations Total number of citations: 5589 Peer-reviewed articles: 127 (first author: 83) Average number of citations/per publication: 44 Note: 90% of articles in scientific journals are never cited; up to 50% of articles are never read except by their authors Meho LI. The rise and rise of citation analysis. Physics World 2007; 20:32-6. Doja A, Eady K, et al. The h-index in medical education: an analysis of medical education journal editorial boards. BMC Med Educ 2014; 14:251. Huang G, Fang CH, et al. Impact of fellowship training on research productivity in academic ophthalmology. J Surg Educ 2015; 72:410-7 Mainster, RetinaLand, EyeCon 2018, Page 6

International lectures: a chronology

First international lecture series, 1984-1993

27 Jan 1984 University Eye Institute of Munich, Clinical Lecture Series MUNICH, GERMANY Lecture: Scanning laser ophthalmoscopy and low vision rehabilitation

18 June - 24 June 1984 American-Israeli Ophthalmological Society and Israeli Ophthalmological JERUSALEM, ISRAEL Society, International Ophthalmic Laser Symposium Lecture: Wavelength considerations for macular photocoagulation Lecture: New developments in ophthalmic laser technology

25 Jun 1984 Technical University of Munich, Clinical Symposium MUNICH, GERMANY Lecture: Clinical uses of the Nd:YAG laser

27 Jun 1984 University Eye Institute of Munich, Clinical lecture MUNICH, GERMANY Lecture: Principles of clinical photocoagulation

28 Jun - 29 Jun 1984 Rothschild Foundation, International Symposium on Surgical Lasers PARIS, FRANCE in Ophthalmology FRANCE Lecture: Photodisruptor Instrumentation

11 Sept - 12 Sept 1986 Ophthalmological Society of the United Kingdom, Cambridge Ophthalmological CAMBRIDGE Symposium, The Aging Eye UNITED KINGDOM Lecture: Light and macular degeneration: a biophysical and clinical perspective

4 June - 6 June 1987 First International Congress on Laser Technology in Ophthalmology CRANS-MONTANA Lecture: Laser therapy for neovascular macular degeneration: SWITZERLAND analysis of mechanisms

25 May 1988 San Raffaele Hospital and the University of Milan, Clinical Conference Series MILAN, ITALY Medical of Recognition, Italian Laser Society Lecture: Macular edema: mechanisms and therapy

27 May - 28 May 1988 University of Genova, International Meeting on the Retinal Pigment Epithelium SANTA MARGHERITA, ITALY Lecture: Retinal axon fiber optics

29 Oct - 3 Nov 1988 Royal Australian College of Ophthalmologists, 1988 Annual Meeting, Invited lecturer SYDNEY Lecture: Trends in laser development and relevant clinical applications Panelist: Problem cases in macular and retinal vascular disease

21 May - 24 May 1989 Eighth Biennial Meeting of the Paul Cibis Club, Washington University School of Medicine LUGANO, SWITZERLAND Lecture: Retinal light hazards of clinicians

24 May - 27 May 1989 Second International Congress on Laser Technology in Ophthalmology LUGANO, SWITZERLAND University of Kansas School of Medicine Lecture: Laser therapy for diabetic macular edema: analysis of mechanisms

2 June - 5 June 1993 Fourth International Congress on Laser Technology in Ophthalmology, LUGANO, SWITZERLAND University of Kansas School of Medicine SWITZERLAND Lecture: Retinal image processing and photocoagulation

28 Oct - 29 Oct 1998 St. Thomas' Hospital, Trends in Ophthalmology Conference LONDON, UNITED KINGDOM Lecture: Retinal imaging: principles and progress

26 Mar - 28 Mar 2000 International Commission on Non-Ionizing Radiation Protection, 8th Annual Meeting PARIS, FRANCE Meeting of Standing Committee IV, Optical Radiation Panelist: Retinal hazards from laser radiation

Mainster, RetinaLand, EyeCon 2018, Page 7

Second international lecture series, 2005-2011

1 – 3 Apr 2005 Canadian Society of Cataract and Refractive Surgery, 12th Annual Meeting, Keynote Lecturer, OTTAWA, CANADA Lecture: Retina protective IOLs: photoprotection vs. photoreception

19 – 22 May 2005 Retinal Physician Symposium, 2005 PARADISE ISLAND Lecture: Blue blocking IOLs: vision vs. protection BAHAMAS Lecture: Decreasing retinal laser damage: TTT and micropulsing

18 – 21 Jan 2006 Zermatt Ophthalmology Academy, Annual Meeting XV ZERMATT, SWITZERLAND Lecture: Visible light blocking IOLs: photoreception vs. photoprotection SWITZERLAND 6 – 7 May 2006 Société Française d'Ophtalmologie (SFO), 2006 annual meeting. PARIS, FRANCE Lecture: Visible light blocking IOLs

14 – 17 Jul 2006 Australian Society of Cataract and Refractive Surgery, 2006 Annual Meeting HAYMAN ISLAND Lecture: IOL performance: what do MTF’s really tell you? AUSTRALIA Lecture: Visible light blocking IOLs: photoprotection vs. photoreception

19 Jul 2006 University of Malaysia Medical Centre, Guest lecturer series KUALA LUMPUR, MALAYSIA Lecture: Retinal light injuries and intraocular lenses MALAYSIA 20 – 21 Jul 2006 National University Hospital; Tan Tock Seng Eye Institute; Singapore Eye Research Institute, SINGAPORE, SINGAPORE Invited speaker Lecture: Retinal imaging, photoreception and photoprotection

9 – 13 Sep 2006 European Society of Cataract and Refractive Surgeons, XXIV Congress LONDON, UNITED KINGDOM Lecture: Optimizing IOL chromophore photoreception and photoprotection

23 – 26 May 2007 5th International Congress of Italian Society of Ophthalmology, Keynote lecturer ROME, ITALY Lecture: Keynote: The important role of blue light in good health and vision Lecture: How chromatic dispersion affects intraocular lens performance

28 – 30 Sep 2007 20th Annual meeting, Asia-Pacific Association of Cataract & Refractive Surgeons, Invited speaker HANOI, VIETNAM Lecture: The important role of blue light in vision and health Lecture: Chromatic dispersion’s effect on pseudophakic optical performance

2 Oct 2007 Hong Kong Eye Hospital, Chinese University of Hong Kong, Visiting Scholar HONG KONG, CHINA Lecture: The important role of IOL materials in photoreception

6 Oct – 7 Oct 2007 Taiwanese Society of Cataract and Refractive Surgeons and Taiwan Academy KAOHSIUNG, TAIPEI of Ophthalmology Annual Meeting, Keynote Speaker and TAICHUNG, TAIWAN Lecture: The impact of blue light on vision and health Lecture: The important role of IOL materials in photoreception

1 Feb – 3 Feb 2008 31st Annual Meeting of Japanese Society of Ophthalmic Surgeons, Invited Speaker YOKOHAMA, JAPAN Lecture: Blue light’s important role in vision and health

28 Jun – 2 July 2008 World Ophthalmic Congress 2008, Invited Speaker HONG KONG, CHINA Lecture: Pseudophakic optical performance: IOL materials and photoreception Lecture: Visible light blocking IOLs Lecture: The impact of IOL materials on visual quality and health

Mainster, RetinaLand, EyeCon 2018, Page 8

Second international lecture series, 2005-2011 (continued)

15 May 2009 Cymru (Wales) Anterior Segment Symposium, Keynote lecturer CARDIFF, UNITED KINGDOM Lecture: Photoreception, health and blue light

18 May 2009 United Kingdom & Ireland Society of Cataract and Refractive Surgery, Guest lecturer BIRMINGHAM, UK Lecture: The effects of blocking blue light with IOL chromophores

20 – 23 May 2009 7th International Congress of Italian Society of Ophthalmology ROME, ITALY Lecture: IOLs: Lighting, aging and circadian physiology Lecture: Optimizing IOL optic material performance

25 – 30 August 2009 14th National Congress of Chinese Ophthalmological Society, Guest Lecturer CHONGQING, CHINA Lecture: The impact of IOLs, lighting and aging on visual quality and health Lecture: The important role of blue light in vision and health

12 – 16 September 2009 XXVII Congress of European Society of Cataract and Refractive Surgeons BARCELONA, SPAIN Lecture: Optimizing optic material performance in intraocular lenses Lecture: IOLs, crystalline lenses and UV-B radiation: retinal phototoxicity and photomelanomagenesis Lecture: Additivity of pseudophakic optical performance losses due to IOL spherical aberration, chromatic dispersion & chromophore design Lecture: Concentric ring dysphotopsias in diffractive bifocal pseudophakia

30 June – 4 July 2010 Fusion, 2010 annual meetings of AUSCRS and APACRS, Invited Lecturer CAIRNS, AUSTRALIA Lecture: Blue light’s important role in good vision and health Lecture: Age-related phototoxicity & photoreception: IOLs vs. crystalline lenses Lecture: UV-B radiation and the pseudophakic eye Lecture: Cataract surgery can improve systemic health

16 – 20 September 2010 25th Asia-Pacific Academy of Ophthalmology Congress and 15th Congress of the BEIJING, CHINA Chinese Ophthalmological Society Course: Why cataract surgery and refractive lens exchange can improve health Lecture: IOL materials and the many myths of blue-blocking IOLs

16 – 18 June 2011 Japanese Society of Cataract and Refractive Surgery, 2011 Annual Meeting FUKUOKA, JAPAN Lecture: The important role of blue light in good vision & health and common misconceptions about its retinal phototoxicity

10 August 2011 Narayana Nethralaya (Eye Hospital), Visiting professor BANGALORE, INDIA Lecture: Photoreception and photoprotection in pseudophakic eyes

11 August 2011 Grant Government Medical College and JJ Hospital, Guest Lecturer, “Meet the Professor” MUMBAI, INDIA Lecture: Circadian photoreception, cataract surgery and health

13 – 14 August 2011 Intraocular Implant and Refractive Society, India, 2011 Annual Meeting NEW DELHI, INDIA Keynote Lecturer and International Gold Medal Recipient Lecture: Cataract surgery can improve health as well as vision Lecture: Glaring misperceptions: disability, dazzle and photostress Lecture: Blue-blocking IOLs decrease photoreception without significant clinical benefit

15-20 September 2011 XXVII Congress of European Society of Cataract and Refractive Surgeons VIENNA, AUSTRIA Lecture: Glare: mechanisms, measurements and misperceptions Course: How cataract surgery can improve health & increase longevity

13 – 16 October 2011 Annual meetings of KSCRS and APACRS, Invited Lecturer SEOUL, KOREA Lecture: Glare’s causes, consequences and clinical challenges Lecture: Optic material optics: light scattering, reflections and images

Lens Extraction in Angle Closure Glaucoma

Luke Dolezal, MD, Resident, Class of 2018 Primary Supervisor: Neeti Alapati, MD

Primary angle-closure glaucoma is a leading global cause of irreversible blindness. Previously, the standard of care for primary angle closure and primary angle-closure glaucoma had been laser peripheral iridotomy and medical management with eye drops to reduce intraocular pressure. If this did not control the disease, the next step would be surgery, often trabeculectomy, which can be associated with serious complications. Because the crystalline lens has a major anatomic and mechanistic role in the development of angle closure, lens extraction has been explored as an alternative initial treatment. In 2016, a large, randomized, controlled, prospective trial entitled, “Effectiveness of early lens extraction for the treatment of primary angle-closure glaucoma (EAGLE),” published data on this question. They found that clear-lens extraction showed greater efficacy and was more cost-effective than laser peripheral iridotomy, and that it, “should be considered as an option for first-line treatment.”

This presentation will review cases of lens extraction for primary angle closure and primary angle-closure glaucoma performed at KU Eye. We will discuss the outcomes of these cases and considerations for patient selection for this intervention.

Glaucoma 2018: Roadblocks and Detours

Scott J. Fudemberg, MD Guest Speaker; Residency Alumnus Class of 2007

Objectives:

Discuss the fundamental problems affecting the field of glaucoma Identify and review innovations in glaucoma diagnosis, medical & surgical management

Roadblocks in Glaucoma

-Purpose of glaucoma treatment and relationship to visual disability -Challenges in determining the burden of disease -Why do people still go blind from glaucoma? -The problem with intraocular pressure -Difficulty in finding modifiable risk factors for glaucoma -Limitations of judging progression: visual field imprecision

Detours in Glaucoma

-Investment in glaucoma research and innovation -Potential diagnostic tools & the biomarker initiative -New glaucoma medications -Nitric oxide in glaucoma -Rho-kinase inhibition -Drug delivery platforms -Surgical advances -New MIGS -New but more invasive surgical procedures

Selective Laser Trabeculoplasty: Resident Experiences and Results at the KCVA

Joshua Jones, MD, Resident, Class of 2018 Primary Supervisor: William Bray, MD

Purpose: To evaluate the efficacy of Selective Laser Trabeculoplasty in patients with primary open-angle glaucoma by senior ophthalmology residents at a VA medical Center.

Design: Case series by retrospective chart review from January 2017 to April 2018 where we reviewed patient charts treated for primary open-angle glaucoma, using Selective Laser Trabeculoplasty performed by senior ophthalmology residents. Patients meeting criteria for inclusion had a history of mild or moderate primary open-angle glaucoma managed with one or more intraocular pressure (IOP) lowering drops with or without previous glaucoma surgery.

Methods: Preoperative and postoperative evaluations were performed within 1 month of surgery, as well as 1 day, 1 week, 1 month and 3 months post-operatively. Evaluations included IOP measurements, topical ocular hypotensive medication use, cup/disc ratio, best corrected visual acuity, complications and adverse events.

Patients: All patients had been previously diagnosed with mild to moderate primary open-angle glaucoma and were receiving treatment with 1-3 IOP lowering medications. Patients were not excluded if they had previous incisional glaucoma surgery.

Conclusions: Selective Laser Trabeculoplasty is a viable option for intraocular pressure lowering in the correct patient population. Further evaluation needs to be performed to assess long term results in this patient population. MIGS: What is MIGS? From a Comprehensive Perspective  Minimally Invasive Glaucoma Surgery  Ab-Interno approach that is minimally traumatic

Anne B. Wishna, MD  Performed through clear corneal incision Clinical Assistant Professor  Do not require conjunctival dissection University of Kansas School of Medicine  Most procedures enhance either trabecular or May 12, 2018 uveoscleral outflow

What is MIGS? Safety of MIGS

 At least modest efficacy that is sustainable  Complications/risks are similar to cataract  Extremely high safety profile surgery   Rapid recovery with minimal impact on  Peripheral anterior synechiae quality of life  IOP spikes  Mostly quick to resolve

Safety of MIGS MIGS

 Traditional transcleral glaucoma filtering:  Implants  Hypotony  3 approaches:  Suprachoroidal hemorrhage  Canal-based  Suprachoroidal  Long-term risk of  Subconjunctival  Destruction of the trabecular meshwork  Blade  Micro-cautery  Canaloplasty MIGS Canal-based Implants

 Implants  Canal-based – trabecular micro-bypass  Implanted at the time of cataract surgery stent (iStent)  FDA approved for mild to moderate glaucoma  Learning curve for insertion  Risk of bleeding, improper device placement, post-op IOP spike, and hypotony  IOP reduction of 16-33%  Require intraoperative gonioscopy  Reduction in medication by 0.5 to 21  May require open angle

Multiple Stents iStent – complications3

 119 patients randomized with unmedicated pre-operative IOP  Stent obstruction or malposition most common 22-38 mm Hg were randomized to 1, 2, or 3 iStents with phaco. (single site, multiple surgeons)2  Posterior capsular opacification  Reduction in IOP at 36 months:  Corneal edema  1 stent: 30%  Elevated IOP  2 stents: 37%  Blurred vision  3 stents: 43%  Iridodialysis or iris trauma  ≥20% reduction in IOP off meds at 42 months:  Iritis  1 stent: 61%  2 stents: 91%  Subconjunctival hemorrhage  3 stents: 91%  Disc hemorrhage

iStent iStent

 First implanted in 2005  Titanium – MRI safe  1.0 mm long, 0.33 mm in height  FDA approved in 2012 In the Pipeline microstent (Ivantis)

 An “intracanalicular scaffold” designed for implantation in conjunction with cataract surgery  iStent inject – 0.23 mm x 0.36 mm  Under FDA investigation  Made of a biocompatible alloy, nitinol, which makes it highly elastic   The microstent measures 8 mm in length and is implanted into Already approved for use internationally Schlemm’s canal by a unique injector through a clear corneal incision under gonioscopic view  Comparing effectiveness to SLT   The implant is designed to place approximately 3 clock hours of TM Also seeking approval for a version to use on stretch, thereby increasing outflow in pseudophakic patients

Hydrus microstent (Ivantis)

 Similar to the iStent, the Hydrus has a lumen which projects into the AC, allowing aqueous to flow directly into Schlemm’s canal and bypass the trabecular meshwork

 The device is currently under FDA investigation

Uveoscleral outflow enhancing Hydrus microstent (Ivantis) procedures

 CyPass microstent  Samuelson et al conducted a prospective randomized single- masked controlled study assessing the safety and efficacy of combined CE with Hydrus microstent placement versus CE  iStent Supra alone.  STARflo  20% reduction in washed out diurnal IOP (DIOP):  CE + Hydrus - 80% ; mean IOP 16.9±3.33 mmHg  CE alone - 46% ; mean IOP 19.2±4.7 mmHg

 Patients not requiring hypotensive medications were higher in the combination group (73% vs 38%)

 VA outcomes and rates of adverse events were similar between the two groups4 Uveoscleral outflow enhancing CyPass microstent procedures  Uveoscleral outflow thought to play a greater role in aqueous drainage (20-50%)  COMPASS trial  20-40% drop in IOP, superior to phaco alone  Devices increasing uveoscleral outflow essentially  Mean 24-month medication use was 67% create a surgical cyclodialysis cleft lower in stent patients; 59% of controls vs.  Advantage is that EVP does not limit extent of IOP 85% of stent subjects were medication free reduction  5.3% underwent subsequent ocular surgeries5

 Limitations: scarring of the cyclodialysis cleft and  Approved in US July 2016 potential loss of the suprachoroidal space where aqueous is shunted

CyPass microstent CyPass microstent

 Contraindications:  Angle-closure glaucoma  Traumatic, malignant, uveitic, or neovascular glaucoma  MRI safe

CyPass microstent Subconjunctival Implant

 15.4% incidence of transient hypotony  Xen 45 Gel Stent  8.8% rate of stent obstruction by iris6  Can be done independently of cataract surgery  Approved November 2016

 InnFocus Microshunt – similar product in this category Xen Gel Stent (Allergan)

 Tube implanted through a clear corneal incision using a pre-loaded injector through the angle into the subconjunctival space  6 mm long stent  2 mm subconjunctival space  3 mm intrascleral  1 mm in anterior chamber

 Results in bleb

 The material of the gel stent is highly pliable, theoretically allowing it to mold to ocular structures and potentially reducing the rate of tube erosion, migration, and corneal endothelial damage

 This feature of the tube material eliminates the need for scleral patch graft reinforcement

 Mitomycin C may be injected at time of shunt placement to further reduce the rate of scarring

Xen Gel Stent Xen Gel Stent

 Approved for refractory glaucoma  At 12 months 76.3% achieved ≥20% IOP  Prior failure of glaucoma procedure reduction from baseline on the same or  Uncontrolled IOP on max meds fewer medications  Mean medications reduced 3.5 to 1.7

Destruction of TM - Xen Gel Stent Microcautery  Complications  Does not require an implant  Needling – most common  Can be done at time of cataract surgery  BCVA loss of ≥2 lines (81% self-resolved)  Can be used to treat severe glaucoma  Transient hypotony  Risks  Increased IOP  Post-op IOP spike (4.9%)  Secondary surgical intervention  Hyphema (23.3%)8  NO intraoperative complications, sustained hypotony, severe complications reported in initial study7 Destruction of TM - blade Kahook Dual Blade

 Blade is passed through a clear corneal incision and used to make two parallel incision in the TM and inner wall of Schlemm’s canal  Mild to moderate glaucoma  Can be used in patients with chronic angle closure, pseudoexfoliation, and pigmentary glaucoma

Kahook Dual Blade Ab Interno Canaloplasty

 Requires intraoperative gonioscopy  Performed through clear corneal incision  Can be done at time of cataract surgery  Illuminated microcatheter is threaded through Schlemm’s canal 360 degrees  Resulted in a decrease of IOP from 18.3±1.7 mmHg to 11.3±1.0 mmHg  Space is visco-dilated and catheter is withdrawn  69% had reduction in medication usage by  Mild to moderate glaucoma at least one medication8  Mean IOP reduction of 28.49% at six months and over half of patients were medication free at six months

Ab Interno Canaloplasty MIGS

 Requires intraoperative gonioscopy  Preparing:  Less risk of bleeding  Assess severity of glaucoma  Considerable learning curve9,10  What are the patients goals?  Perform gonioscopy  Make sure there are no peripheral anterior synechiae, rubeosis, or other angle abnormalities that would limit visualization  Patients with rapidly progressing glaucoma may not be good candidates Pros and Cons Pros and Cons

 Time  Learning curve  Cataract surgery can be as much as 50%  Direct gonioscopy is the main skill to master longer  Can also use a viscoelastic cannula to  Time to counsel patients on options practice maneuvering inside the eye during  Saves time for doctor, patient, and staff when gonioscopy refills, compliance, and side effects of drops are not an issue

Pros and Cons Pros and Cons

 Availability  Less recovery  Many MIGS devices are covered by most insurances  MIGS does not usually inhibit the excellent  Need to have the devices approved at your refractive outcomes that patient’s expect institution Pros and Cons

 Cost  Increases cost of procedure, but reduces cost burden of drops  Ocular surface  Getting patients off drops decreases surface disease  MIGS procedures are conj-sparing – traditional glaucoma surgery is still an option

Ocular Findings of Juvenile Xanthogranuloma

Katie Keck, MD, Children’s Mercy Fellow Primary Supervisor: Erin Stahl, MD

Case 1 5-month-old healthy female presented with spontaneous hyphema of the left eye. She underwent exam under anesthesia, which revealed a small, yellow lesion in the superonasal angle with adjacent conjunctival injection. She was treated with subconjunctival Solu-Medrol as well as topical pred forte for presumed juvenile xanthogranuloma (JXG) with resolution of hyphema. Topical pred forte was tapered over four weeks and stopped. A few weeks later, she had recurrence of hyphema and was restarted on topical pred forte, which was slowly tapered over a two month period with resolution of hyphema. Again, she had recurrence of hyphema approximately one month after discontinuation of pred forte drops. Differential diagnosis at this time included JXG, melanoma, medulloepithelioma, and retinoblastoma. She was sent to Wills Eye Hospital for further evaluation, where JXG was confirmed. She is currently on a four-month taper of topical pred forte.

Case 2 16-year-old healthy female presented with an asymptomatic iris lesion of the right eye she had noticed one month prior, while looking in the mirror. On exam, she was noted to have a whitish lesion of the inferior iris with trace overlying inflammation. Differential diagnosis included JXG, melanoma, and Langerhans histiocytosis. She was also evaluated at Wills Eye Hospital and underwent fine needle aspiration biopsy, which revealed atypical histiocytic tumor consistent with JXG. She was started on topical pred forte.

Clinical Features of JXG - JXG is a benign non-Langerhans cell histiocytosis that most often involves the skin, but may also affect the eye. - Ocular JXG most commonly affects the iris and is often isolated without skin involvement. - The most common presenting features are eye redness, eye mass and hyphema.

Management of JXG - Topical or periocular corticosteroids are the mainstay of treatment for JXG of the iris. - - Rarely, JXG can be recurrent despite treatment with corticosteroids.

References 1. Samara WA, Khoo CTL, Say EAT, et al. Juvenile xanthogranuloma involving the eye and ocular adnexa: tumor control, visual outcomes, and salvage in 30 patients. Ophthalmol 2015;122(10):2130-8.

Pediatric Corneal Crosslinking for Keratoconus

Erin Stahl, MD Volunteer Faculty, KU Eye

Outline: • Historical Overview o US Adult studies o Adult experience OUS o Pediatric experience OUS

• US Crosslinking – Current Status o Avedro approved 2016 o IDE sites still running o Status on insurance reimbursement

• Personal Experience with Pediatric Crosslinking o Making the diagnosis . Using all of your tools o Stopping the itch o Surgical planning . Anesthesia considerations . Planning for postoperative pain . Second eye timing . Severe pediatric cases o Intraop tips and tricks . Managing a thin cornea o Postop management . Pediatric pain control . Healing cycle . Time to stabilization o Visual rehabilitation . Specialized contact lenses . management . Managing fluctuating vision and optics

Central Serous Chorioretinopathy: Outcomes and Experience

Jonathan Manhard, MD, Resident Class of 2019 Primary Supervisor: Mary Champion, MD

Central serous chorioretinopathy (CSC) is an idiopathic disease classically characterized by a well-circumscribed, localized serous retinal detachment involving the macula, which is thought to be secondary to leakage from the choroid due to altered retinal pigment epithelium function. This condition primarily affects young to middle-aged men, causing symptoms, which include blurred vision, metamorphosia, and micropsia. While the etiology of CSC is unknown, risk factors may include steroids, hypercortisolism, pregnancy, and sleep apnea. Multimodal imaging helps to ensure accurate diagnosis. The prognosis is often good, with many patients improving with observation alone. Medical therapy and laser treatment can also be considered for persistent fluid leakage or severe disease.

This presentation will review cases of central serous chorioretinopathy seen at KU Eye Clinic. We will discuss clinical features, multimodal imaging, therapeutic options, and outcomes. Endoscopy Assisted Vitrectomy Endoscopic vitreoretinal Flexible fiberoptic endoscopy probes - Illuminated probe surgery - Illuminated probe with laser

Radwan Ajlan, MBBCh, FRCSC, FICO, DABO Assistant Professor, Retina and Vitreous Department of Ophthalmology University of Kansas School of Medicine

Improving Image and Field Unique Intraocular Optical of View Properties Circumventing anterior segment opacities

Unique Intraocular Optical Unique Intraocular Optical Properties Properties Surgeon’s perspective Visualization of very anterior disease • unique intraoperative view that is up to 90 • unobstructed and undistorted views of off the conventional viewing axis the space between vitreous base and posterior iris. Unique Intraocular Optical Unique Intraocular Optical Properties Properties Improved visualization of Differential light illumination anteroposteriorly oriented disease

• Reflected (coaxial) versus transmitted (dissociated)

Unique Intraocular Optical Endoscopy Assisted Pars Properties Plana Vitrectomy Indications • Anterior segment opacities and temporary keratoprosthesis • Difficult-to-access diseases • Complex retinal detachment • Pediatric vitreoretinal surgery

Endoscopy Assisted Pars Diabetic Retinal Detachment Plana Vitrectomy

11 12 Diabetic Retinal Endophthalmitis Detachment Surgery

13 14

Thank you

15

KU MD and Residency Alumni

Wayne Anliker MD Ann Bidwell MD William Campbell MD MD Class: 1997 MD Class: 1980 MD Class: 1965 Emporia, KS Round Lake, IL Ottawa, KS

Miranda Bishara MD Thomas P. Campbell MD Thomas Ashley MD Residency Class: 2010 Residency Class: 1986 MD Class: 1984 Overland Park, KS Wheat Ridge, CO Topeka, KS

Thomas C. Black MD Patrick K. Canon MD Adam AufderHeide MD Residency Class: 1968 Residency Class: 2001 Residency Class: 2014 Kansas City, MO Colorado Springs, CO Medford, OR

Audrey Blacklock MD Timothy Cavanaugh MD Douglas B. Babel MD MD Class: 2006 MD Class: 1986 MD Class: 1992 Liberty, MO Residency Class: 1990 Residency Class: 1997 Overland Park, KS Erie, PA Jeffrey A. Boomer MD

MD Class: 2001 Mary Champion MD Hasan Bahrani MD Wichita, KS Residency Class: 2015 Residency Class: 2009 Prairie Village, KS Houston, TX Michelle Boyce MD

Residency Class: 2016 Ryan Christensen MD Richard Barr MD Kansas City, MO MD Class: 2004 (Wichita) MD Class: 1957 Residency Class: 2008 Residency Class: 1964 Lance Brown MD Shawnee Mission, KS Overland Park, KS Residency Class: 2001

Joplin, MO Amy Ciccio MD Donald E. Beahm MD MD Class: 2002 MD Class: 1971 Emily Broxterman MD Residency Class: 2006 Great Bend, KS Residency Class: 2015 Kansas City, MO Kansas City, MO

William R. Beck MD Justin T. Cohen MD MD Class: 1983 Michael Brusco MD Residency Class: 1977 Newton, KS Residency Class: 2011 Wheat Ridge, CO Kalamazoo, MI

Deloris W. Bell MD Trey M. Butler MD Sam N. Cohlmia, MD MD Class: 1968 Residency Class: 1993 MD Class: 1993 Residency Class: 1972 Joplin, MO Wichita, KS Overland Park, KS

Anita Campbell MD Brian E. Conner MD Ravi B. Berger MD MD Class: 2010 MD Class: 1972 Residency Class: 2006 Residency Class: 2014 Salina, KS Cleveland, OH Wichita, KS KU MD and Residency Alumni Terry A. Cox MD Alina Dumitrescu MD Kenneth J. Frank MD MD Class: 1975 Residency Class: 2015 MD Class: 1992 Residency Class: 1979 Iowa City, IA Ottawa, KS Columbia, SC David S. Dyer MD Eric L. Fry MD Charles H. Cozean MD MD Class: 1989 MD Class: 2003 MD Class: 1962 Overland Park, KS Residency Class: 2007 Residency Class: 1966 Garden City, KS Richard J. Eggleston MD Cape Girardeau, MO Residency Class: 1974 Luther L. Fry MD Valerie Crandall MD Clarkston, WA MD Class: 1967 Residency Class: 1982 Garden City, KS Ft. Myers, FL Mark D. Emig MD MD Class: 1988 Terrence Curran MD Residency Class: 1993 MD Class: 1972 Scott Fudemberg MD Omaha, NE Residency Class: 1977 Residency Class: 2007

Prairie Village, KS Nicholoas Engelbrecht MD Philadelphia, PA MD Class: 1996 Mohammad Dastjerdi MD St. Louis, MO Valerie Garden MD Residency Class: 2013 Fellow: 2000 Newark, NJ Richard Falter MD Santa Rosa, CA MD Class: 1967 Sujote David MD Hutchinson, KS Amy Gemperli MD MD Class: 1991 MD Class: 1992 Residency Class: 1994 Cynthia A. Ferreira MD Residency Class: 1996 Kansas City, KS Residency Class: 2005 Kansas City, MO Reno, NV Brandon Davis MD Residency Class: 2007 Michael Floyd MD Darrell E. Genstler MD New Orleans, LA Resdency Class: 2010 Residency Class: 1981 Bloomington, MN Albany, OR John Doane MD MD Class: 1990 Michael Foote MD James A. Gessler MD Residency Class: 1995 Residency Class: 2002 MD Class: 1974 Leawood, KS El Paso, TX Springfield, MO

Charles R. Ford MD Luke Dolezal MD Michael Gilbert, MD MD Class: 1963 Residency Class: 2018 Residency Class: 2019 Shawnee, KS Prairie Village, KS Prairie Village, KS

John Frangie MD Erin Gilliland MD Thomas G. Duckett MD MD Class: 1987 MD Class: 1999 MD Class: 1967 Greenfield, MA Broomfield, CA St. Joseph, MO KU MD and Residency Alumni

William A. Godfrey MD K. Dwight Hendricks MD Srinivas Iyengar MD MD Class: 1965 Residency Class: 1983 Residency Class: 2008 Residency Class: 1971 Kansas City, KS Encinitas, CA Prairie Village, KS James A. Hiatt MD Randolph Jackson MD Robert T. Goetzinger MD MD Class: 1999 Residency Class: 2004 MD Class: 1971 Residency Class: 2003 Kansas City, KS Residency Class: 1976 Mesa, AZ Riverdale, GA Derek Horkey MD Russell Jayne MD Residency Class: 2017 Fellow: 1997 Andre J. Golina MD Independence, MO Las Vegas, NV Residency Class: 1979 West Palm Beach, FL Alan Hromas MD Andrew J. Jefferson MD Residency Class: 2014 Residency Class: 1986 Charles E. Graham MD Wichita, KS Leawood, KS Residency Class: 1993 Ana G. Huaman MD Las Vegas, NV Faisal Jehan MD MD Class: 1984 MD Class: 1998 Residency Class: 1996 R. Bruce Grene MD Residency Class: 2003 Albuquerque, NM MD Class: 1978 Fontana, CA

Wichita, KS Quentin C. Huerter MD Cindi Kalin Johnson MD MD Class: 1959 Hasan Hakim MD Residency Class: 1994 Residency Class: 1969 Residency Class: 1997 Leavenworth, KS Leawood, KS Dearborn, MI

Josh Jones MD Denise A. Hug MD James R. Hardin MD Residency Class: 2018 MD Class: 1996 Residency Class: 1997 Prairie Village, KS Kansas City, MO Salisbury, NC

Raymond E. Kandt MD John D. Hunkeler MD David Hardten, MD Residency Class: 1967 MD Class: 1967 MD Class: 1987 Prairie Village, KS Residency Class: 1973 Minneapolis, MN Overland Park, KS Neda Karimi MD

Toby Hartong MD MD Class: 2001 Joel Hunter MD Residency Class: 1982 Residency Class: 2005 Fellow: 2010 Leawood, KS Santa Monica, CA Orlando, FL

James D. Haug MD Richard L. Irwin MD Rickey D. Kellerman MD MD Class: 1981 MD Class: 1975 MD Class: 1978 Residency Class: 1985 Residency Class: 1980 Wichita, KS Atchinson, KS Putnam, CT KU MD and Residency Alumni Daniel M. King MD Ryan Larscheid MD Mark Mazow MD MD Class: 1974 Residency Class: 1974 Residency Class: 1990 Residency Class: 1982 Fountain Valley, CA Dallas, TX Red Bluff, CA Diana Lind DO Thomas L. McDonald MD David A. Kingrey MD Residency Class: 1997 MD Class: 1984 MD Class: 1994 Kearney, NE Residency Class: 1988 Wichita, KS Timothy Lindquist MD Hays, KS Residency Class: 2012 Jess Koons MD Overland Park, KS Lynne G. McElhinney MD MD Class: 1957 MD Class: 1995 Liberal, KS Rebecca Linquist MD Kansas City, MO

Residency Class: 2013 Wilber McElroy MD Ernest Kovarik MD Rapid City, SD MD Class: 1961 Residency Class: 1969 Topeka, KS Shawnee Mission, KS Robert A. Lowenthal MD Residency Class: 1994 Frank E. McKee MD Randall J. Kresie MD Springfield, IL MD Class: 1970 MD Class: 1984 Overland Park, KS Residency Class: 1988 Barry C. Malloy MD Topeka, KS Residency Class: 1989 Peter Mitrev MD Wyomissing, PA Residency Class: 1998 Kartik Kumar MD Chesapeake, VA Residency Class: 2011 Jonathan Manhard, MD Houston, TX Residency Class: 2019 Reid Mollman MD Prairie Village, KS Residency Class: 2018 Leila Kump MD Prairie Village, KS Residency Class: 2010 Babak Marefat MD Gaithersburg, MD Louis Monaco DO MD Class: 1999 DO Class: 1982 Topeka, KS Bradley R. Kwapiszeski MD Clinton, MO MD Class: 1991 John Marsh MD Shawnee Mission, KS MD Class: 1992 Susan K. Mosier MD Residency Class: 1996 MD Class: 1995 Brian A. LaGreca MD Topeka, KS Lawrence, KS Residency Class: 1992 Everett C. Moulton MD Billings, MT Federico Mattioli MD Residency Class: 1979 Residency Class: 2000 Ft. Smith, AR Dale Laird MD Houston, TX MD Class: 1968 Andrew Moyes MD Residency Class: 1974 Donald Maxwell MD MD Class: 1989 Belton, MO Residency Class: 1986 Kansas City, MO Oklahoma City, OK KU MD and Residency Alumni

Brian C. Mulrooney MD Anna (Berry) Parlin MD Anjulie Quick MD Residency Class: 1999 Residency Class: 2016 Residency Class: 2017 Huntsville, AL New Orleans, LA Prairie Village, KS

Forrest P. Murphy MD Theodore Pasquali MD Deborah Reid MD MD Class: 1978 Fellow: 2013 Fellow: 2000 Residency Class: 1985 Lakewood, CA Annapolis, MD Rancho Mirage, CA Michael Pekas MD John S. Reifschneider DO Todd Nickel DO Residency Class: 1976 DO Class: 1981 DO Class: 2000 Sioux Falls, SD Leavenworth, KS Residency Class: 2004 Tyler, TX Cindy Penzler MD Martin Reinke MD MD Class: 1985 Residency Class: 1995 Robert Null MD Residency Class: 1989 Southlake, TX Residency Class: 2017 Topeka, KS Pittsburgh, PA Donald A. Relihan MD Ryan Pine MD MD Class: 1954 Bruce B. Ochsner MD Residency Class: 2012 Residency Class: 1957 MD Class: 1965 Charleston, IL Wichita, KS Wichita, KS Kenneth C. Place MD Garrick Rettele MD Sara O'Connell MD MD Class: 1973 MD Class: 1991 MD Class: 1994 Olathe, KS Coffeyville, KS Overland Park, KS John Pokorny MD Michael G. Reynolds MD Timothy Olsen MD MD Class: 1989 MD Class: 1988 MD Class: 1989 Hays, KS Emporia, KS Rochester, MN Patrick (Frank) Price MD Geoffrey L. Rice MD Lynn W. O'Neal MD MD Class: 1975 Residency Class: 1985 MD Class: 1977 Blue Springs, MO Ukiah, CA Lawrence, KS Bradford S. Prokop MD James R. Rinne MD Richard A. Orchard MD Residency Class: 1961 MD Class; 1984 MD Class: 1965 Ft. Myers, FL Residency Class: 1988 Lawrence, KS Campbellsville, KY Gary V. Puro MD David S. Rothberg MD Residency Class: 1975 Charles F. Palmer MD Residency Class: 1983 Santa Fe, NM Residency Class: 2000 Palm Harbor, FL Cheyenne, WY

KU MD and Residency Alumni

John Rufe MD Wallace B. Smith MD Timothy M. Stout MD MD Class: 1950 MD Class: 1954 MD Class: 1995 Shawnee Mision, KS Residency Class: 1962 Residency Class: 1999 Lees Summit, MO Leawood, KS Roland Sabates MD Ryan Smith MD Manju Subramanian MD MD Class: 1973 Fellow: 2009 Residency Class: 2002 Kansas City, MO Augusta, GA Boston, MA Beatty G. Suiter MD E. Michael Sarno MD David L. Spalding MD MD Class: 1999 Residency Class: 1981 MD Class: 1959 Residency Class: 2004 West Des Moines, IA Residency Class: 1965 Rogersville, MO Fellow: 2009 Shawnee Mission, KS Roger B. Schlemmer MD Jennifer Spiegel MD Kevin Toller MD MD Class: 1968 MD Class: 2009 MD Class: 1994 Residency Class: 1973 Residency Class: 2013 Grove, OK Springfield, MO Thousand Oaks, CA

Albert W.G. Schubert MD Erin D. Stahl MD Patricia L. Turner MD MD Class: 1974 Residency Class: 2009 Residency Class: 1984 Residency Class: 1977 Fellow: 2011 Reno, NV Charleston, IL Kansas City, MO

Perry Schuetz MD Larry Stauffer MD Chris Ullrich DO, FACS MD Class: 1971 MD Class: 1969 DO Class: 1992 Residency Class: 1975 Residency Class: 1975 Washington, MO Great Bend, KS Jefferson City, MO Michael Seligson MD Ann Stechschulte MD Steven Unterman MD MD Class: 1991 Residency Class: 2005 Residency Class: 1987 Santa Fe, NM Shawnee Mission, KS Prairie Village, KS

My Le Shaw MD Richard A. Stein MD Trent Vande Garde MD Residency Class: 2012 Residency Class: 1994 MD Class: 1995 Linden, MI Leavenworth, KS Topeka, KS Michael P. Varenhorst MD C. Eric Shrader MD Michael Stiles MD Residency Class: 1984 MD Class: 1978 MD Class: 1985 Wichita, KS Wichita, KS Residency Class: 1989 Overland Park, KS C. Byron Smith MD Carl Stout MD Natalia Villate MD Residency Class: 1980 Residency Class: 1976 Residency Class: 2008 Billings, MT Independence, MO Boca Raton, FL

KU MD and Residency Alumni

Them Vu MD Stewart M. Wilson MD MD Class: 2000 MD Class: 1968 Plano, TX Residency Class: 1974 Roseburg, OR

Brian Boxer Wacher MD Terria Winn MD Fellow: 1998 MD Class: 1982 , CA Wichita, KS

Matthew Wayner MD Chauncey B. Witcraft MD Residency Class: 1990 Residency Class: 1984 Kerrville, TX Miami, OK

Walter Dan Weaver MD Jerry B. Wurster MD MD Class: 1969 MD Class: 1964 Residency Class: 1973 Residency Class: 1968 Topeka, KS Scottsdale, AZ

Gary Weiner MD Lillian Yang MD MD Class: 1990 Residency Class: 2016 Salina, KS Stockton, CA

Robert Weir MD Michelle Yao MD Residency Class: 1967 Residency Class: 2009 Kansas City, MO Woodbury, NY

Mark L. Wellemeyer MD MD Class: 1988 Wichita, KS

Kent L. Wellish MD Residency Class: 1992 Las Vegas, NV

Thomas J. Whittaker MD, JD MD Class: 1990 Prairie Village, KS

Thomas Williams MD Residency Class: 1994 Hickory, NC

Contact information:

KU Eye Center, Optical Shop & University of Kansas Hospital Specialty Surgery Center: 7400 State Line Rd., Prairie Village, KS 66208

KU Eye Miller Clinic and Optical Shop: 3901 Rainbow Blvd., Miller Building, First Fl., Ste. 1011, Kansas City, KS 66160

Administration: 913-588-6605

State Line Optical Shop: 913-588-6600, Option 4 Miller Clinic Optical Shop: 913-588-6674

Billing: 877-287-6268 LASIK and Refractive Surgery: 913-588-0105

Medical Records: Phone: 913-588-6645 and Fax: 913-588-6655

The University of Kansas Hospital Specialty Surgery: 913-588-2020

Physician Referral and Consultation Urgent and Same-Day Transfers 913-588-1227, 913-588-5862 or 877-588-5862 For emergencies, after hours and weekends, call 913-588-6600 and press "0" to ask for the doctor on-call.