ARDS Notes Cover 11

M A R C H 5 – 9, 2 0 11 • S N O W M A S S, C O L O R A D O

Aspen RetinalDetachment Society

Meeting Notes

ARDS

39thAnnual

MEDICAL CONFERENCE PLANNERS, INC.

1251Post Road, Scarsdale, NY10583

914-722-0664

[email protected]

www.medconfs.com

The Aspen Retinal Detachment Society

gratefully acknowledges Genentech, Inc.

for their generous contribution toward

the production of this booklet.

Aspen R

etinal Detachm

ent Society Meeting N

otes 2011

2011

ARDS 11 Notes-Cover final_ARDS Notes Cover 11 5/16/11 12:45 PM Page 1

Dear Aspen Retinal Detachment Society Meeting Participant,

Once again, we are delighted to offer you this booklet of notes, supplemented by the

majority of slide presentations (edited), from our recent meeting. The notes were taken

and assembled by two young, talented, rising retinal stars – Drs. Minhee Cho and

Kevin Suk – who attended every talk and captured the essence of the vigorous

post-talk discussion, for which the ARDS is deservedly famous. We would also like to

acknowledge the editorial assistance of Dr. R.V. Paul Chan.

This work was made possible by a generous contribution provided by Genentech, Inc.

We are grateful to Drs. Cho, Suk and Chan and to all of you for contributing to the

intellectual vibrancy of ARDS. We hope you will find this booklet interesting, and also

of value to you in the care of your patients.

Please join us March 3-7, 2012 for the 40th Annual ARDS Meeting.

Sincerely,

Organizing Committee

Timothy G. Murray, MD, MBA Donald J. D’Amico, MD William O. Edward, MD Ottiwell W. Jones, MD Jerry E. Leclaire, MD

39thAnnual


MeetingMARCH 5–9, 2011 • SNOWMASS, COLORADO

40thAnnual


Meeting

March 3-7,2012The Viceroy Snowmass

MEDICAL CONFERENCE PLANNERS, INC.1251 Post Road, Scarsdale, NY10583

914-722-0664

[email protected]

www.medconfs.com

For information

SAVETHE

DATE

JOINTLY SPONSORED BY THE FLORIDA MEDICAL ASSOCIATION AND THE ASPEN RETINAL DETACHMENT SOCIETY

This activity has been planned and implemented in accordance with the Essential Areas and policiesof the Accreditation Council for Continuing Medical Education through the joint sponsorship ofthe Florida Medical Association and the Aspen Retinal Detachment Society. The Florida MedicalAssociation is accredited by the ACCME to provide continuing medical education for physicians.

The Florida Medical Association designates this educational activity for a maximum of twelve (12.0) AMA PRA Category 1 Credits.™ Physicians should only claim credit commensurate with the extent of their participation in the activity.


39th Annual Meeting Program . . . . . . . . . . . . . . . . . . . . . . . 2

SUNDAY, MARCH 6

I. The New Paradigm for Treatment of DME in the Anti-VEGF Era: An Assessment of the Risks, Benefits, and Costs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5PowerPoint Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . A.2

Harry W. Flynn, Jr., MD

II. Familial Exudative Vitreoretinopathy – Case Report and Genetics . . . . . . . . . . . . . . . . . . . . . . . . . 8PowerPoint Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . A.11

Mina Chung, MD

III. Retinal Detachment Repair: To Buckle or Not. Success Rates from a Single Private Practice. . . . . . . . . . . . . . . . . . . . . . . . . . . 9PowerPoint Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . A.20

Robert L. Avery, MD

IV. Surgery for Complex Retinal Detachment and Proliferative Vitreoretinopathy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11PowerPoint Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . A.26

Allen C. Ho, MD

V. Pediatric Surgery: Surgical Video Review/Presentation . . . . . . . . . . . . . 13Carl Claes, MD

MONDAY, MARCH 7

I. Acquired Vitelliform Lesions: Correlation of Clinical Findings and Multiple Imaging Analyses . . . . . . . . . . . . . . . . . . . . . . . 15PowerPoint Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . A.33

K. Bailey Freund, MD

II. VEGF Trap Update . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17Gregg T. Kokame, MD, MMM

III. Surgical Management of Idiopathic Macular Holes in the SD-OCT Era. . . . . . . . . . . . . . 19PowerPoint Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . A.39

Andre V. Gomes, MD, PhD

IV. Vitrectomy and Pars Plana Baerveldt Glaucoma Implants for Complex Glaucoma . . . . . 21PowerPoint Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . A.43

Robert L. Avery, MD

V. PANEL DISCUSSIONComplex Surgical Case Management: An Interactive Evaluation of Surgical Therapy. . . 23PowerPoint Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . A.48

Contents

TUESDAY, MARCH 8

I. Do We Need a New Classification for Choroidal Neovascularization in Age-related Macular Degeneration?. . . . . . . . . . . . . . 24PowerPoint Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . A.53

K. Bailey Freund, MD

II. Retinal Complications of the Dohlman Keratoprosthesis . . . . . . . . . . . . . . . . . . . . . . . 27PowerPoint Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . A.59

Mina Chung, MD

III. Endophthalmitis after Intravitreal Anti-VEGF Injections: 6 Years Rates and Outcomes of Treatment at BPEI . . . . . . . . . . . . 29PowerPoint Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . A.64

PDF Handout: Allergy to Povidone Iodine and Cephalosporins . . . . . . . . . A.71

Harry W. Flynn, Jr. MD

IV. TAYLOR SMITH LECTUREThe Practice Environment of Retina in 2015: What’s the Prognosis? . . . . . . . . . . . . . . . . . . 33PowerPoint Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . A.74

David W. Parke, II, MD

WEDNESDAY, MARCH 9

I. Microincision Vitrectomy 2011: New Instrumentation and Techniques. . . . . . . . . . . 37PowerPoint Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . A.81

Allen C. Ho, MD

II. Vitreoretinal Management of Anterior Segment Complications . . . . . . . . . . . . . . . . 39PowerPoint Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . A.88

Gregg T. Kokame, MD, MMM

III. PVR and Retinotomies: How Far Should We Go? . . . . . . . . . . . . . . . . . . . . . . . . 42PowerPoint Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . A.94

Andre V. Gomes, MD, PhD

IV. Ocular Trauma Surgery: Surgical Video Review/Presentation . . . . . . . . . . . . . 45Carl Claes, MD

V. Retinoblastoma: Unique Diagnosis and Treatment Paradigms in 2011 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46PowerPoint Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . A.98

Timothy G. Murray, MD, MBA

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . .

2 ASPEN RETINAL DETACHMENT SOCIETY MEETING

ARDS 2011 Program

SundayM A R C H 6

4:00-4:25 PM

The New Paradigm for Treatment of DME in the Anti-VEGF Era: An Assessment of the Risks, Benefits, and CostsHarry W. Flynn, Jr., MD

4:35-5:00 PM

Familial Exudative Vitreoretinopathy – Case Report and Genetics Mina Chung, MD

5:10-5:35 PM

Retinal Detachment Repair: To Buckle or Not. Success Rates from a Single Private PracticeRobert L. Avery, MD

6:15-6:40 PM

Surgery for Complex Retinal Detachment and ProliferativeVitreoretinopathyAllen C. Ho, MD

6:50-7:15 PM

Pediatric Surgery: Surgical Video Review/PresentationCarl Claes, MD

MondayM A R C H 7

4:00-4:25 PM

Acquired Vitelliform Lesions: Correlation of Clinical Findings and Multiple Imaging Analyses K. Bailey Freund, MD

4:35-5:00 PM

VEGF Trap UpdateGregg T. Kokame, MD, MMM

5:10-5:35 PM

Surgical Management of Idiopathic Macular Holes in the SD-OCT EraAndre V. Gomes, MD, PhD

6:15-6:40 PM

Vitrectomy and Pars Plana Baerveldt Glaucoma Implants for Complex GlaucomaRobert L. Avery, MD

6:50-7:30 PM

PANEL DISCUSSIONComplex Surgical Case Management: An Interactive Evaluation of Surgical Therapy

TuesdayM A R C H 8

4:00-4:25 PM

Do We Need a New Classification forChoroidal Neovascularization in Age-related Macular Degeneration?K. Bailey Freund, MD

4:35-5:00 PM

Retinal Complications of the Dohlman KeratoprosthesisMina Chung, MD

MARCH 5–9, 2011 • SNOWMASS, COLORADO 3

39th Annual Meeting Guest Faculty

Robert L. Avery, MDCalifornia Retina Consultants

Santa Barbara, CA

Mina Chung, MDFlaum Eye Institute

University of Rochester, NY

Carl C. Claes, MDSt. Augustinus Hospital

Wilrijk, Antwerp, Belgium

Harry W. Flynn, Jr., MDBascom Palmer Eye Institute

Miami, FL

K. Bailey Freund, MDVitreous Retina Macula Consultants

of New York, NY

Andre V. Gomes MD, PhDUniversity of Sao Paulo

Sao Paulo, Brazil

Allen C. Ho, MDWills Eye Institute

Philadelphia, PA

Gregg T. Kokame, MD, MMMRetina Consultants of Hawaii/

University of Hawaii School of Medicine

Honolulu, HI

Timothy G. Murray, MD, MBABascom Palmer Eye Institute

Miami, FL

David W. Parke II, MD Executive Vice President and CEO

American Academy of Ophthalmology

San Francisco, CA

5:10-5:35 PM

Endophthalmitis after Intravitreal Anti-VEGF Injections: 6 Years Rates andOutcomes of Treatment at BPEIHarry W. Flynn, Jr. MD

6:15-6:45 PM

TAYLOR SMITH LECTUREThe Practice Environment of Retina in 2015: What’s the Prognosis?David W. Parke, II, MD

WednesdayM A R C H 9

4:00-4:25 PM

Microincision Vitrectomy 2011: New Instrumentation and TechniquesAllen C. Ho, MD

4:30-4:55 PM

Vitreoretinal Management of Anterior Segment ComplicationsGregg T. Kokame, MD, MMM

5:00-5:25 PM

PVR and Retinotomies: How Far Should We Go?Andre V. Gomes, MD, PhD

6:00-6:25 PM

Ocular Trauma Surgery: Surgical Video Review/PresentationCarl Claes, MD

6:30-6:55 PM

Retinoblastoma: Unique Diagnosis and Treatment Paradigms in 2011Timothy G. Murray, MD, MBA

4 ASPEN RETINAL DETACHMENT SOCIETY MEETING NOTES

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .

The Aspen Retinal Detachment Societygratefully acknowledges generous contributionsfrom the following companies:

BLACK DIAMOND

Genentech, Inc.

DIAMOND

Insight Instruments, Inc.

PLATINUM

Alcon Laboratories, Inc.

Bausch + Lomb

GOLD

Alimera Sciences

Allergan

Carl Zeiss Meditec

Dutch Ophthalmic, USA

Eyetech, Inc.

Franck’s Compounding Lab, Inc.

Iridex Corporation

MedOne Surgical Inc.

Peregrine Surgical

QLT Ophthalmics, Inc.

Synergetics, Inc.

ThromboGenics Inc.

SPECIAL RECOGNITION

Genentech, Inc.

Insight Instruments, Inc.

1983 Thomas M. Aaberg, Sr., MD

1984 Robert E. Morris, MD

1985 Michael Shea, MD

1986 Alexander Ray Irvine, Jr., MD

1987 William H. Spencer, MD

1988 Victor T. Curtin, MD

1989 Alan Bird, MD

1990 J. Donald M. Gass, MD

1991 Robert J. Brockhurst, MD

1992 Stephen J. Ryan, MD

1993 Wayne E. Fung, MD

1994 Charles P. Wilkinson, MD

1995 George W. Blankenship, MD

1996 Mary Lou Lewis, MD

1997 Donald J. D’Amico, MD

1998 Stanley Chang, MD

1999 Harry W. Flynn, Jr., MD

2000 Ian J. Constable, MD

2001 Thomas R. Friberg, MD

2002 William S. Tasman, MD

2003 Evangelos S. Gragoudas, MD

2004 Steve Charles, MD

2005 Thaddeus P. Dryja, MD

2006 Jerry A. Shields, MD

2007 Mark S. Blumenkranz, MD

2008 Allan E. Kreiger, MD

2009 Alexander R. Gaudio, MD

2010 Carmen A. Puliafito, MD, MBA

2011 David W. Parke, II, MD

Taylor Smith Lecturers Corporate Partners

SundayM A R C H 6

I. The New Paradigm for Treatment of DME in the Anti-VEGF Era: An Assessment of the Risks, Benefits, and CostsHarry W. Flynn, Jr., MD

PRESENTATION

A new paradigm for the treatment ofDME includes anti-VEGF agents. TheDRCR Network published data from Protocol I, demonstrating that use of

ranibizumab, with or without laser treatment, resulted inbetter vision than using laser treatment alone in patientswith DME and VA ≤ 20/32 (ETDRS). The patientstreated with ranibizumab plus either prompt or deferredlaser gained approximately 9 letters at both the one andtwo-year time points with a decreased OCT thickness of131/137 and 144/170, respectively. Other studies reportingpositive results include the READ 2, RESTORE, andVEGF TrapEYE studies. The Intravitreal Bevacizumab or Laser Therapy (BOLT) Study also recently released12-month data. Mean change in ETDRS visual acuity at12 months in the laser group was a loss of 0.5 letters,while the bevacizumab group gained a mean of 8 lettersduring the same time period.

The cost-effectiveness of ranibizumab is obviously lessthan bevacizumab. The DRCR patients in theranibizumab groups received a mean of 8 injectionsduring the first year of the study and 3 injections duringthe second year. Using costs derived from the 2009National Medicare Fee Schedule reflecting Medicareallowable charges for treatment (approximately $2000per injection) in a physician’s office by an ophthalmologistwho participated with the Medicare program for calendaryear 2009, this leads to nearly $22,000 charges for thedrug alone over 2 years in each of the ranibizumab groups.This further translates to a cost of over $3500 perETDRS letter improvement per eye of the patient in the DRCR study.

Although comparability between clinical trials isdifficult, bevacizumab use could save at least $1500 perinjection, which could yield greater than $10,000 insavings during the first year of treatment alone. Anarticle published in the Wall Street Journal (attributed to2008 data from an unpublished paper of Ross J. Brechnerand others of the federal Centers for Medicare andMedicaid Services and Philip J. Rosenfeld of BascomPalmer Eye Institute) reports approximately 60% of

physicians elect to use bevacizumab over ranibizumab forwet age-related macular degeneration. The percentage of physicians using ranibizumab (currently off-label) forDME may be increasing after recent publications, butinsurance coverage of ranibizumab for DME has been variable.

Further concern with anti-VEGF therapy is the risk of endophthalmitis in the injection groups. While therisk of endophthalmitis for each intravitreal injectionwas only 0.08% in the DRCR, each patient in theranibizumab group received an average of 11 injectionsover the course of 2 years. This yields a risk of endoph-thalmitis approaching 1% in the patient over the 2-yeartime course. With a typical retinal physician treatinghundreds of patients for DME, this could lead to adramatic increase in cases of endophthalmitis in manypractices. Endophthalmitis represents a visually devas-tating disease process requiring further expensiveevaluation and treatment, including more invasiveprocedures and costs.

Further complicating the new treatment pharmaco -therapeutic paradigm, in Protocol I of the DRCR, thesubgroup of pseudophakic eyes at baseline assigned tocorticosteroid plus prompt laser performed better thanlaser alone and equivalent to the ranibizumab groups.Similar positive studies include dexamethasone andfluocinolone implants. The question remains whetherthis is a reasonable alternative in pseudophakic patientsto more frequent visits and injections with ranibizumabor bevacizumab despite the risks of elevated intraocularpressure and endophthalmitis.

In DME patients with 20/30 or better visual acuity, there are very few randomized clinical trials except theETDRS. The risk/benefit favors photocoagulation in this subset of patients with clinically significant DMEbecause of the low risk and durability of laser treatment.

HIGHLIGHTS

• Focal/grid macular laser remains an effective option for DME with good VA

• Metabolic control of diabetes still remains important

• Several trials have demonstrated the effectiveness ofintravitreal ranibizumab injections for the treatment ofDME compared to macular laser

• Rate of endophthalmitis per patient is a concern foranti-VEGF treatments

NOTES

The old versus new paradigm – CasesThe initial management choices for the treatment ofmacular edema include the following: 1) observation withmedical control, 2) focal/grid laser photocoagulation, 3) intravitreal VEGF or steroid, 4) combination therapy,


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or 5) PPV with membrane peel. These choices demon-strate both the old and new paradigm for the treatmentof DME. Not only has a paradigm shift occurred in thetherapeutic options for DME but also in the tools used toevaluate this pathology, i.e. OCT is surpassing FA in thediagnosis and monitoring of DME. The following casesillustrate the enduring effectiveness of the old paradigm.A 39 year old type 1 diabetic patient presents with a20/20-2 vision in the right eye with diffuse exudates andminimal subfoveal fluid on OCT and 20/70 vision in theleft eye with diffuse macular edema. ETDRS standardizedfocal/grid laser therapy as the first line therapy for clini-cally significant macular edema. Following the oldparadigm, this patient was treated with laser after anevaluation with fluorescein angiography. A 51yo manwith 20/40 vision with subfoveal macular edema onOCT was similarly treated with laser. One year later, hemaintained 20/25 vision. The use of laser for macularedema in patients with good VA still remains aneffective option.

Old paradigm persistsSome elements from the traditional paradigm remainvery important in the treatment of DME. Optimizationof metabolic control including glycemic, hypertensionand lipid control in collaboration with the internists isimportant. Complete ocular evaluation to rule out othertreatable causes of macular edema is vital. Treatmentwith ETDRS-style laser should be considered prior tonewer options such as VEGF inhibition and steroids. The importance of metabolic control is demonstrated inthe following case. An obese patient with hypercholes-terolemia presented with 20/400 vision and massiveexudates in both eyes.

After collaborating with the internist and undergoing aweight loss program, the exudates resolved, and theretinopathy and vision improved to 20/200. Severalstudies have demonstrated that glycemic control reducesthe complication rates of diabetes. Diabetes Control andComplications Trial (DCCT) and UK ProspectiveDiabetes Study (UKPDS) showed relative risk reductionranging from 23% to 46% per 10% decrease in HbA1Cin type 1 and 2 diabetes. Elevated serum lipids have alsobeen shown to be a risk factor for visual loss; severity ofhard exudates directly correlated with the level ofcholesterol and the risk of 15 letter loss at 5 years.

New paradigm in clinical trials: The treatment paradigm for DME has shifted since theintroduction of various intravitreal treatments. DRCR,READ 2, RISE, RIDE, RESOLVE and RESTORE have demonstrated the effectiveness of intravitrealranibizumab; BOLT, DRCR and PACORES investigatedintravitreal bevacizumab; Macugen DRS looked at theuse of pegaptanib; DaVINCI is studying the effectivenessof VEGF-trap in the treatment of DME. Intravitreal

steroids that have been used to treat DME include triamcinolone, Retisert (Fluocinolone), Ozurdex(Dexamethasone), Illuvien (Fluocinolone). The safetyprofiles of these treatments should be kept in mind. Risksof intravitreal anti-VEGF injections include endoph-thalmitis, retinal detachment, inflammation, cataract,increased IOP, glaucoma surgery, and adverse cardiovas-cular events. Other treatment options include vitreolyticagent like microplasmin which creates a posteriorvitreous detachment. Systemic agents such as fenofibrate,rosiglitazone and ruboxistaurin have not been shown tobe effective and have serious side effects.

PPV for DME was popularized in the early 2000s, butnow is performed in select cases with vitreoretinaltraction. This is based on the DRCR protocol D findings.This protocol studied PPV for DME with vitreomaculartraction versus DME alone and found that despite a 2-fold reduction in central retinal thickness, visual acuityremained about the same at 6 month follow up in patientwho underwent PPV.

Anti-VEGF treatment for DME has been analyzed viaseveral randomized controlled trials. DRCR net protocolI evaluated intravitreal ranibizumab plus prompt/deferredlaser or triamcinolone plus prompt laser versus macularlaser alone for DME with vision 20/30 or worse. Atprimary endpoint (2 years), ranibizumab with prompt/deferred laser had the best outcome compared to theother 2 groups; this group had an average gain of 9 letters(compared to laser with 3 letter gain) and greaterreduction of macular thickness on OCT. When subgroupanalysis was performed, pseudophakic patients receivingtriamcinolone and prompt laser had equivalent outcometo ranibizumab with prompt/deferred laser, possiblysuggesting this as an option to reduce the treatmentburden of ranibizumab injections on pseudophakicpatients. Of note, patients with vision better than 20/32were not included. Also, there was 1% rate of endoph-thalmitis in patients receiving ranibizumab.

READ2 study showed that intravitreal ranibizumab wassuperior to laser or combined laser/ranibizumab treat-ments. RESOLVE was a European trial that showed at 12month, intravitreal ranibizumab was superior to shaminjection with an average gain of 8 letters. The rate ofendophthalmitis was high in this study (2%). DAVINCI(DME And VEGF Trap-Eye: INvestigation of ClinicalImpact) compared focal laser to different doses of VEGFTrap at different treatment intervals. At 1 year primaryendpoint, there was 9.7-13.1 letter gain in the VEGFTrap groups compared to loss of 1.3 letter in the lasergroup. The reduction of retinal thickness was greater inthe VEGF Trap groups. The rate of endophthalmitis washigh at 2.3%. BOLT was a single-center study thatincluded patients that failed initial laser treatment with20/40 or worse vision. Repeat laser was compared to


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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .

intravitreal bevacizumab. After a mean of 9 injections,the bevacizumab group had an average gain of 8 letterscompared to 0.5 loss of letters in the laser group

Future trials include DRCR protocol J which will inves-tigate whether prior anti-VEGF (ranibizumab) or steroid(triamcinolone) injections can reduce the risk of VA lossin eyes with DME receiving focal/PRP treatment.Protocol R will study the effect of nevanac onnoncentral DME with vision 20/32 or better. Safetyoutcomes measured will include corneal adverse effectssuch as keratitis, ulcer, melting and infection.

Cost and risks of the new paradigmDespite the effectiveness of the new paradigm for thetreatment of DME (anti-VEGF), two major points needto be considered: Cost and Endophthalmitis risks. Thecost of intravitreal ranibizumab injections is a societalburden. Assuming 8 injection in year 1 and 3 in year 2,the total cost of administering the treatment includingthe drug cost and staffing has been estimated to be$28,000. Although the rate of endophthalmitis is 0.08%per injection over the course of 2 years according to theDRCRnet, each patient received an average of 11 injec-tions, which increases the risk of endophthalmitis perpatient to 0.8%. The Wall Street Journal reported thetotal cost to Medicare with ranibizumab injection was$537 million ($1600/injection) in 2008 in contrast tobevacizumab injections which was 20 million dollars($42/injection).

INTERACTIVE QUESTIONS

Q: What is your initial approach for treatment-naïve eye with diffuse DME (20/40)? (n=94)

Observe/medical control . . . . . . . . 0%Focal/grid laser . . . . . . . . . . . . . . . . 9%Bevacizumab . . . . . . . . . . . . . . . . 19%Monthly ranibizumab . . . . . . . . . . 2%Triamcinolone . . . . . . . . . . . . . . . . 0%Anti-VEGF + steroid. . . . . . . . . . . 2%Anti-VEGF + focal/grid laser . . 67%Anti-VEGF + steroid + laser. . . . . 1%

Q: In a Medicare Plus supplemental patient with DME, does the cost of treatment matter? (n=84)

Yes . . . . . . . . . . 84.5%No . . . . . . . . . . . 15.5%

DISCUSSION

Q: Do you recommend bariatric surgery for these patients?

A: Sometimes for morbidly obese patients and those with high risk for systemic problems. More doctors arerecommending it now that the complication profile hasimproved.

Q: Is the definition of CSME as used in ETDRS relevantin this era of OCT?

A: No. I believe this is largely a historical term. Thecutoff of 500 microns from the center of fovea is lessrelevant with the use of OCT.

Q: In BOLT study, how was failed laser treatment defined?

A: Patient only needed to fail one prior laser. Patientcontinue to have central macular thickness of >200, VAloss or vision 20/30 or worse with persistent centralinvolvement.

Q: In anti-VEGF non-responders without any vitreo-macular traction who are young, phakic and steroidresponsive, what do you recommend?

A: I would consider intravitreal steroid. If the patient hassevere glaucoma, I would individualize treatment basedon the level of VA. I am more aggressive for VA 20/50 orworse.

Q: In RISE, there was a selection bias in the studybecause the investigators were less prone to recruit forlaser if the patient was a good candidate for intravitrealbevacizumab. How about for DRCRnet studies?

A: Patients with persistent macular thickness greaterthan 250 um with vision 20/32 or worse were recruited.Many patients had already had PRP with regressed PDR,which may mean an entirely different disease.

Q: What did protocol I show in terms of diffusepersistent ME?

A: With diffuse ME, it took longer to achieve thinningof macula. Anti-VEGF may result in a more rapidresponse. At least 3 injections seemed to be required fora fair trial before deciding on a poor response.

Q: What do you do with patients who claim allergy topovidone iodine?

A: Ask the patients what type of allergic reactions theyhave had previously. Careful history-taking is important.Most of the times, it’s contact dermatitis. Iodine has noallergic component where as povidone can. If they havehad hives, test povidone on the arm. I have NEVERNOT used povidone before injections.

Q: The reported 1-2% of endophthalmitis seems veryhigh compared to everyday practice.

A: DRCRnet followed all the protocols for avoidinginfection (lid speculum, povidone). Other studies maynot have been as diligent. Using 4th generation fluoro-quinolone instead of povidone may not be enough. 1%needs to be considered in context: the Bascom Palmerstudy showed 1/10000 incidence when considering thenumber of total injections and 1/1000 individual riskover time.

See Flynn PowerPoint presentation, A.2


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II. Familial ExudativeVitreoretinopathy –Case Report and Genetics Mina Chung, MD

PRESENTATION

A case of FEVR, including differentialdiagnosis and surgical management, willbe presented. The inheritance pattern and features of the pedigree will be

discussed. Recent advances in the understanding ofmolecular genetics will be reviewed.

HIGHLIGHTS

• Choroidal nonperfusion on FA, RRD, and abnormalvitreoretinal adhesion may be nonclassical features ofFEVR

• Always examine family members of FEVR suspect forperipheral retinal changes

• Always examine the fellow eye of the patient

NOTES

A 10 year old otherwise healthy, full-term girl presentedwith exotropia and blurred vision in the left eye for 6months. She had no skin lesions. The fundus photographof the right eye (VA 20/25) showed vessel straighteningand exudates in the temporal macula with fibrosis andischemia. The fundus photograph of the left eye (20/200)showed macula-involving TRD with NV. FA of the lefteye showed active NV, telangiectatic vessels and non -perfusion in both retinal and choroidal layers in theperiphery. FA of the right eye showed mottled choroidalvasculature temporally with leakage and nonperfusion in the periphery. The right eye received laser treatmentto the ischemic area; left eye underwent PPV withmembrane peel, endolaser and anti-VEGF injections.

The family pedigree showed half brothers and sisterswithout any problems, indicating an autosomal recessiveinheritance pattern. The differential diagnoses includeROP, Coats, and incontinentia pigmenti (although noneof the daughters had skin findings). On paternal side ofthe family, a half-sister was reported to have myopia andlattice-like changes. However, the fundus photograph ofthe right eye (VA 20/40) revealed fibrosis with retinalischemia, not lattice degeneration. FA showed telang-iectatic vessels with leakage. A half-brother on thepaternal side also demonstrated fibrosis with largerchoroidal vasculature in both eyes. Additionally, heshowed same telangiectatic vessels in the periphery withchoroidal abnormality and nonperfusion. When thefather, a possible carrier, was examined, the FA showeddelayed transit with mottled choroidal vasculature. Hewas also myopic. One year later, he presented with RRDwith superior HST and underwent PPV with endolaser.

A year later, he presented with a posterior tear and wastreated with pneumatic retinopexy. This indicated anautosomal dominant inheritance pattern, leading to thediagnosis of possible FEVR with nonclassical features.

FZD4 gene abnormality was found in all affectedmembers, which has been associated with FEVR in someJapanese families. This genetic abnormality affects WNTreceptor, which is important in cell fate signaling, andhas a Norrin ligand. In retina, Norrin signaling pathwayis very important in the retinal vascular developmentand involves Frizzed-4 and Tspan12. TSPAN12 promotesNorrin signaling. A few unexplained FEVR cases fromIowa were also found to share FZD4 mutation. Thisfamily was traced back to a consanguinous Amish familyin Nebraska. Two abnormal copies of FZD4 gene leads toa very severe phenotype due to the double dominanteffect.

Retinal ischemia, telangiectasia, neovascularization, andtractional retinal detachment are classic manifestationsof FEVR; choroidal nonperfusion, RRD, and abnormalvitreoretinal adhesion may be nonclassical manifesta-tions of FEVR.


Q: What is the mode of inheritance of FEVR in thiscase? (n=70)

Autosomal dominant . . . . . . . 95.7%Autosomal recessive . . . . . . . . . . 4.3%X-linked recessive . . . . . . . . . . . . 0.0%X-linked dominant . . . . . . . . . . . 0.0%

Q: Which of the following genes have been associated with FEVR? (n=66)

Frizzled 4 . . . . . . . . . . . . . . . . . . 16.7%LRP5 . . . . . . . . . . . . . . . . . . . . . . 1.5%Norrin . . . . . . . . . . . . . . . . . . . . . 4.6%TSPAN 12 . . . . . . . . . . . . . . . . . 6.1%All of the above . . . . . . . . . . . 71.2%

DISCUSSION

Comment: An 18yo with unexplained neovascularizationwith vitreous hemorrhage in my practice was found tohave a telomerase mutation.

Comment: Dr. Kim Drenser is investigating WNT signal -ing pathways. TSPAN12 pathway in her studies did notshow much abnormality.

Comment: It is important to always examine the felloweye. FA may be very important in detecting some of thesubtle changes. Coats disease can also be a bilateraldisease. FEVR may show asymmetry.

See Chung PowerPoint presentation, A.11


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III. Retinal Detachment Repair –To Buckle or Not? Success Rates from a Single Private PracticeRobert L. Avery, MD

PRESENTATION

Techniques of repair of retinaldetachment have advanced over the pastfew decades, and controversy remains in regard to the role of different techniques.

Scleral buckling was once the only technique available,but with the advent of vitrectomy, the role of bucklinghas decreased. In addition, pneumoretinopexy has beenshown to be a useful technique in select cases, but inmany practices, it is rarely used due to its lower successrate. Some retinal surgeons profess never to use a buckle,even as an adjunct to vitrectomy. With this backgroundof controversy, we retrospectively reviewed the charts ofpatients undergoing repair of a primary retinal detach -ment in an attempt to evaluate the success rates of thesedifferent techniques.

This study is an IRB approved, retrospective chart reviewof consecutive patients undergoing repair of primary retinaldetachment in a single private practice. Patients were ex -cluded if they had concurrent ruptured globe or penetratinginjury, giant retinal tear (> 3 clock hours), or proliferativediabetic retinopathy. To be included, a minimum of 3months follow up was required. Over 900 patients wereevaluated in this study. Pneumoretinopexy had the lowestanatomic success rate (sustained retinal reattachmentwithout need for a second retinal procedure) at about 70%,whereas, scleral buckle alone, buckle with vitrectomy,and vitrectomy alone had anatomic success rates rangingfrom 87% to 94%. The success rate for vitrectomy withscleral buckle was higher than that for vitrectomy alone.

This was not a randomized study, and it is likely therewas a selection bias with the surgeon selecting the moreextensive surgery for the more difficult cases. Nevertheless,the success rate for pneumoretinopexy was the lowestdespite the presumption that these should have been theeasiest cases. Furthermore, one could argue that surgeonsmight elect to use vitrectomy with scleral buckle in casesthat are more difficult than those that they choose totreat with vitrectomy alone. Despite this selection bias,the re-detachment rate was higher in those cases receivingvitrectomy alone instead of vitrectomy and scleral buckle.This observation reinforces the clinical suspicion thatadding a scleral buckle to the vitrectomy may increasethe success rate of primary retinal reattachment. Thereare, however, many disadvantages to scleral bucklingincluding refractive changes, increased surgical time,poor reimbursement, and potential erosion or infection.The advantages and disadvantages will be discussed.

HIGHLIGHTS

• Different options for primary RD repair have shownvariable success rates

• PPV is increasingly being used as the primarytechnique for repairing primary RD

• The appropriate primary technique for pseudophakiceyes may differ from phakic eyes; i.e. SB is a goodoption for phakic eyes and PPV or PPV/SB may lead toa better anatomic outcome in pseudophakic eyes

• Combined PPV/SB as the initial procedure is areasonable choice for complex primary RD repair

NOTES

The best technique for primary retinal detachment (RD) repair remains controversial. This is mainly due tovariable success rates reported in the literature usingdifferent techniques. Randomized prospective studies toevaluate the different techniques are difficult to performbecause every RD is unique. First, the three mostfrequently used techniques for primary RD repair will be reviewed.

Current techniques for RD repairPneumoretinopexy (PR) is the least frequently usedtechnique due to its low success rate. Clement Chanperformed a meta-analysis of 4138 cases from 81 reportsand showed a single operation success rate of 74.4% andfinal success rate of 96%. Phakic eyes had a higher rateof success. PVR occurred in 5.2% of cases. Steamrollingand avoidance of fish eggs are important for flatteningthe macula and preventing the spread of fluid. ShelleyDay performed a Medicare claim analysis to reviewsuccess rates of different techniques and also showed alow rate of success for PR. In her study, 9216 primaryRDs were reviewed. Redetachment rate within 1 yearwas 40.6% for PR, 19.2% for SB and 21.2% for parsplana vitrectomy (PPV).

The role of scleral buckling in the age of PPV isdiminish ing. The advantages of SB include the highsuccess rate (ranging 80-94%), no need for positioning,lack of cataract progression and no air travel restriction.The disadvantages of SB include induced myopia, risk ofextrusion, infection, postoperative pain, and diplopiaespecially with segmental buckles. SB is also technicallymore difficult. A large single surgeon series performed byAlberto Salicone showed the primary success rate of 81%in phakic eyes and 73% in pseudophakic eyes, with finalsuccess rate of 96%. Visual acuity was better than 20/40in 78% of macula-on RD and 28% of macula-off RD.

PPV has become increasingly popular for primary RDrepair. The advantages include less postoperative pain,better visualization, decreased operative time, directrelief of traction, ability to treat complex cases involvingPVR and giant retinal tear, less refractive changes and


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diplopia. The disadvantages include need for positioning,risk of new breaks, air travel restrictions, progression ofcataract, condensation on IOL, risk of wound leak andhypotony. Increased oxygenation after PPV is thought tocause cataract progression.

Clinical trials comparing different techniquesSeveral studies have compared the efficacy of SB versusPPV for primary RD repair. Campo et al performed aretrospective study on 294 pseudophakic eyes andreported 91% success rate for macula-on and 86% successrate for macula-off cases. Oshima reported a study of 102cases and noted 91% single operation success rate forboth SB and PPV. There was better VA outcome withPPV in more severe cases. A bicenter study comparingthe use of SB versus PPV showed that SB was used morefrequently in Vienna and PPV in New York, and bothplaces reported about 85% success rate with similarvisual outcome. Other studies have shown success rateranging from 68% to 83% for SB and 62 to 94% for PPV.

SPR (Scleral buckling versus Primary vitrectomy inRhegmatogenous retinal detachment study group) was amulticenter European study that included 681 patientswith primary RRD from1998-2003 (416 phakic eye, 265 pseudophakic eyes). At 1 year, VA was better in SB group (7 vs 5 lines of VA improvement), primaryanatomic success rate was the same in both groups (only63% but need for secondary ERM peeling was includedas failure), and the redetachment rate was 26% in both.In pseudophakic eyes, VA outcome was similar in bothgroups; however, the primary success rate was better inPPV group (72% versus 53% in SB). The redetachmentrate in the same group was 21% in PPV and 40% in SB.In PPV group, it was left up to the surgeons’ discretion tocombine SB with PPV. 50% of the phakic eyes receivedSB and 67% of the pseudophakic eyes received SB.Redetachment rate in the pseudophakic group was 11%in the combined SB/PPV group and 41% in PPV alone.The study recommended PPV for pseudophakic eyes andconcluded that SB is a reasonable option for phakic eyessince it prevents cataract formation.

SB versus PPV at Dr. Avery’s practiceDr. Avery performed a retrospective chart review ofconsecutive patients undergoing repair of primary retinaldetachment over the past 10 years in his private practice.All patients had a minimum of 3 month follow up.Those with ruptured globe, giant retinal tear, PDR, andPVR greater than grade C were excluded.

Overall, surgeons in this practice, despite variousfellowship trainings, chose similar techniques with themost common being combined PPV/SB. A total of 793patients were included: 72 received PR, 91 SB, 533PPV/SB and 97 PPV. There was a selection bias towardsperforming combined PPV/SB for those with more

complex RDs, e.g. early PVR, vitreous hemorrhage ormacula-off RD. The anatomic outcome was the best inthis group. The redetachment rate was the highest in thePR group (32%), followed by SB (10%), PPV (3%) andPPV/SB (2.4%). In SB group, 6% of phakic eyes and19% of pseudophakic eyes redetached. The redetachmentrate was high in both phakic and pseudophakic eyes inthe PR group even though the RDs repaired tended to be the least severe. The mean final VA was around 20/40despite the failures, however. The phakic group hadhigher redetachment with PPV and had better anatomicoutcome with PR and SB. This may be due to poorvisualization secondary to cataract or inadequate anteriorvitreous base shaving due to the lens. The pseudophakiceyes had better anatomic outcome with SB/PPV and PPV.

The high success rate seen in this study may be due tothe following factors: 1) retrospective study, 2) a lowthreshold to employ combined SB/PPV if the caseconsidered complex, 3) buckle of choice (4050) supportsmore broadly than a 41 or 240 (width double), and 4)exclusion of grade C and worse PVR. When subgroupanalysis including patients with worse PVR was per -formed, the success rate was significantly lower. None ofthe patients in the category received PR or SB only. IfRD repair is successful the first time, there is less risk ofPVR formation. Thus doing everything possible the firsttime, even combined PPV/SB, may be beneficial.


Q: How would you treat a phakic patient with macula-on nasal retinal detachment from a superonasal dialysis?(n=91)

Pneumoretinopexy . . . . . . . . . . . . . . 13%Scleral buckle . . . . . . . . . . . . . . . . . 64% Vitrectomy . . . . . . . . . . . . . . . . . . . . 12% Vitrectomy and scleral buckle . . . . . 11% Other . . . . . . . . . . . . . . . . . . . . . . . . . 0%

Q: How would you treat a phakic patient with macula-off retinal detachment from multiple pathology (a breakat 12 o’clock, 9 o’clock and 6 o’clock)? (n=91)

Pneumoretinopexy . . . . . . . . . . . . . . . 0% Scleral buckle . . . . . . . . . . . . . . . . . . 26% Vitrectomy . . . . . . . . . . . . . . . . . . . . 19% Vitrectomy and scleral buckle . . . . 55% Other . . . . . . . . . . . . . . . . . . . . . . . . . 0%

Q: How would you treat a pseudophakic patient withmacula-off retinal detachment from multiple pathology(a break at 12 o’clock, 9 o’clock and 6 o’clock)? (n=90)

Pneumoretinopexy . . . . . . . . . . . . . . . 0% Scleral buckle . . . . . . . . . . . . . . . . . . . 4% Vitrectomy . . . . . . . . . . . . . . . . . . . . 32% Vitrectomy and scleral buckle . . . . 62% Other. . . . . . . . . . . . . . . . . . . . . . . . . . 1%


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DISCUSSION

Q: I did a similar single surgeon chart review of 150patients over 9 years during which time I transitionedfrom 20g PPV/SB to 20g PPV then 23g. 97% success rate was observed in each of these groups. Endolaser was performed 360 degrees in all cases with posteriordrainage without PFO. 47% were phakic and 67%developed cataract. I noticed patients also preferred PPVbecause it removes floaters. Can you tell us more aboutyour techniques?

A: We do 360 degree laser, posterior drainage withoutPFO in PPV. When we do buckle, we just laser thepathology. Without the additional support from SB, wefind that lasering 360 degrees is helpful. We still likedoing SB in pseudophakic eyes, but some surgeons in mygroup are transitioning into doing primarily PPV only.Patient comfort in the postoperative period is animportant issue. The success rate also depends on thelearning curve.

Q: Cutting the flaps from these tears is important. Adirectional laser to get out to the ora is also important.

A: Advances in technology are making PPV only a verygood option. Combined SB/PPV is still a good optionwith good outcome. However PPV/SB is not necessarilybetter than PPV only (probably due to learning curveinvolving buckle procedures).

Q: How often do you use silicone oil?

A: Less than 10% of the time in primary cases.

Comment: We do more SB primarily than combinedSB/PPV due to inferior VA outcome in SB/PPV. We arewilling to accept higher failure rates that come with SBgroup because of this VA issue. A failed PPV is difficultcase to fix, but failed SB is not as challenging.

Q: Why was the final VA best in the PR group?

A: It may have to do with squeezing out the fluid earlywhich is possible with PR. VA outcome presented in ourstudy, however, was not best-corrected VA, so the finalVA outcome is not really comparable.

Q: Does anyone have better success with PR for PVR cases?

A: A small case series from California reported success inPVR with PR, however, this study had a very selectgroup of patients. This is probably not generalizable.

Q: What gas do you use for how long and how strict areyou with positioning?

A: It depends on whether the patient is phakic or not. In a pseudophakic with inferior pathology, I use C3F8.Other surgeons may use SF6 in such cases. In phakiceyes, I definitely use SF6. I’m also more aggressive aboutpositioning in phakic eyes than in pseudophakic eyesunless there is pathology that needs aggressive positioning.

Q: How do you manage a 65yo who underwent PPV withgas for superior RD, now has a severe white cataractpostoperatively that prevents a satisfactory examinationof the posterior pole? B scan is not conclusive for flatretina.

A: If you position the patient a certain way, the B scanshould be doable. If that doesn’t work and still not sureof the retina status, I would try religious face downpositioning. Once the bubble is sufficiently gone,perform cataract surgery.

Q: I also believe there is a role for SB. Variable successrates shown in different studies are interesting. How doyou do your PPV?

A: I prefer 23g PPV. I like the fluid dynamics of 23gcutter more than 20g and 25g. 23g system is rigid enoughand I can be aggressive with the anterior vitreous basewith scleral depression. We don’t perform lensectomy toshave and to peel PVR. We do posterior retinotomy withPFO for internal drainage. The surgeries are done in ahospital setting. The future policy changes will requirethat everyone perform a sequential introspective reviewof his/her own data every 1, 2 or 3 years to understandthe practice. It is very educational to look through yourfailed cases.

See Avery PowerPoint presentation, A.20

IV. Surgery for Complex RetinalDetachment and ProliferativeVitreoretinopathyAllen C. Ho, MD

PRESENTATION

Although surgical success rates forcomplex retinal detachment complicatedby PVR have improved over the last several decades these cases persist and

continue to pose some of our greatest surgical challenges.While the pathophysiology and cellular components ofPVR are better understood there is a lack of effectivepharmacosurgical adjuncts to help reduce the incidenceof PVR.

The vitreous base is a critical area in the development of PVR and surgical techniques to identify, visualize,illuminate, tissue stain, access and shave this tissue areimportant in primary vitrectomy for retinal detachmentas well as for surgery for complicated recurrent retinaldetachment. Support of the vitreous base can be wellachieved by scleral buckling and should always beconsidered in the setting of primary or recurrent retinaldetachment surgery, particularly in younger and phakicpatients. In some patients, retinectomy will be required


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particularly if the retina is foreshortened by anterior loopPVR; in general, retinectomies should be adequate assmaller retinectomies tend to fail. If there is significantintrinsic retinal fibrosis, then even retinectomy may notachieve retinal reattachment.

Intraocular gases and silicone oil continue to be theprimary vitreous substitute in these cases; in certain casesof inferior PVR short term heavy perfluorocarbon liquidsmay be considered. Future surgical improvements willlikely include pharmacologic adjuncts; the best way,however, to avoid these complicated cases is to performcareful and meticulous initial retinal reattachmentsurgery.

HIGHLIGHTS

• Study individual failed cases; this is the best way tobecome a better surgeon

• In complex RD with PVR cases, thoroughly trim thevitreous base, identify all tears, use oil for severe cases,but otherwise C3F8

• Functional success >5/200 achieved in 50-75% cases

• There is need for development of better instrumen-tation and techniques and possible pharmacologicaltherapy for PVR

NOTES

PVR backgroundWith today’s technology, the reattachment rate for PVR only reaches 60-80%. This points to a need for anon surgical, perhaps, a pharmacological therapy for thetreatment of PVR. PVR is a reason for RD repair in 5-8%of cases. 75% of failed RD repair is from the formation of PVR. An effective prevention and treatment are still lacking.

PVR is a collection of RPE, glial, fibroblast, inflam-matory cells and collagen growing on the retinal surfacethat eventually lead to traction. When PVR formsanteriorly, it can detach the retina towards the iris planeand lead to hypotony and phthisis. Risk factors for PVRinclude previous RD surgery, chronic RD, VH, GRT,multiple tears with exposed RPE cells (reflects differentvitreous characteristics), uveitis, pre- and postoperateivechoroidal detachment, and excessive cryotherapy. Ifmembranes are not visible, tortuosity of retinal vesselsmay still be an indication of PVR. If the patient has amacula-off RD with PVR, the timing of the repair maybe delayed, but earlier repair is recommended for thosewith macula-on RD.

PVR surgical techniquesTreatment options include laser, pneumatic retinopexy(almost never), rarely primary SB or encirclement, andPPV, which is most often employed. A 360 degree laser is

rarely needed unless there is a severe PVR; usually, aselective laser around the pathology is adequate.Anterior trimming of PVR is facilitated by wide angleviewing system (BIOM), vitreous staining with triamci-nolone, scleral depression by an assistant, chandelierlight (although this makes it difficult to see vitreousfibrils), and transillumination techniques. The placementof an encircling buckle is usually performed prior to PPV.If encirclement is used, one must avoid tendency foregoan extensive shaving of the anterior vitreous base. It isvital to always thoroughly shave the vitreous base inevery PVR case.

A dilute solution (1:10) of triamcinolone is adequate forvisualization of the vitreous and can be injected via thecutter into the areas of interest. Heavy liquids can beused in complex cases, especially to stabilize a large RD.Trimming of the anterior flap can be done with the helpof an assistant depressing the area. If a good assistant isnot available, an illuminated curved laser can be usedwith the surgeon depressing while using a chandelier forextra illumination. Trans-scleral transilluminationcontrolled by the surgeon can also be employed for veryanterior vitreous cutting. Fiber optic illuminated scleraldepressor allows surgeon control and bimanual shaving.

Retinotomy or retinectomy may be necessary. Themistake is to make these too small. C3F8 is superior toSF6 or silicone oil. Other surgeons find silicone oil betterfor postoperative vision and hypotonous eyes with lowerrate of reoperation. For severe cases, one can considerleaving PFO in for 2-4 weeks along with the SO untilchorioretinal adhesions form. Complications from PVRrepair lead to more inflammation than primary RD andcan cause severe anterior segment complications as well.Future directions should explore pharmacologic therapyto either prevent or treat PVR. Past attempts withsteroid, 5-FU, accutane or heparin have not shownsignificant effect.


Q: Major failure risk for PVR retinal detachment after retinectomy? (n=66)

Hemorrhage . . . . . . . . . . . . . . . . . . 6%Subretinal air/gas/oil . . . . . . . . . . . 3%Retinectomy too large . . . . . . . . 1.5%Retinectomy too small . . . . . . 89.4%

Q: Complex PVR retinal detachment surgery’s mostsignificant advance? (n=36)

Silicone oil tamponade . . . . . . . . . 6%C3F8 gas tamponade . . . . . . . . . . . 0%Retinectomy. . . . . . . . . . . . . . . . . . 3%Perfluoron liquid . . . . . . . . . . . . . 17%Widefield viewing. . . . . . . . . . . . 75%


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DISCUSSION

Q: How do you start peeling wide-spread membranes andwhich forceps do you use?

A: I use the Alcon 23-g ILM forceps and start by goingin deep into the center of the starfold. One cansometimes visualize the base of the starfold. More peoplestart in the center of the star fold rather than theperiphery because the membrane is thicker in the centerand leads to less shredding.

Q: Do you stain with membrane blue or ICG?

A: In my hands, membrane blue works well. Europeansuse more staining for these membranes.

Q: Do you remove the ILM?

A: Yes. It may prevent PVR formation.

Q: How long do you wait for PVR to mature?

A: The surgeon needs to think about the inflammatorystatus of the eye. I use the visualization of the membraneand quiet eye as guides.

Q: What kind of anesthesia do you use for these complex cases?

A: Local

Comment: Studies have shown that silicone oil and gasare comparable, but we prefer oil for complex casesbecause the incidence of hypotony is lower. We leave theoil in longer in patients who have had multiple RDsurgeries to give the eye a rest. I believe removal of lensin a phakic eye is important for better shaving. Anotherquestion is how much and how long to peel the membranefor? A residual membrane may be peeled once SO isremoved. The use of heavy oil remains controversial. It isless PVR-genic than PFO. The key is to leave the retinadry to prevent emulsification.

A: No benefit was shown with Densiron in clinical trials.The failure and complication rates were higher in thosepatients receiving Densiron. However, the case selectionin the study may have biased towards failure since thosewith most severe PVR RD were enrolled.

Q: Chandlier is crucial for these complex cases. Do you think there is place for cryotherapy with today’stechniques, especially since it may induce PVR?

A: In my practice, cryotherapy is used only in PR andSB, and sometimes intraocular cryotherapy is performedwhen visualization poor. Extensive cryotherapy is nolonger performed, so the effect of cryotherapy on PVRinduction is likely minimal.

See Ho PowerPoint presentation, A.26

V. Pediatric Surgery: Surgical Video Review/PresentationCarl Claes, MD

PRESENTATION

Description of indications andtechniques in Diabetic Vitrectomy, illustrated by surgical videos.

HIGHLIGHTS

• Bimanual dissection is key in complex cases

• Valved cannulas have improved IOP control

• Good wound construction is important for maintainingIOP control

• Heavy silicone oil is inflammatory and PVR-genic and its use is not recommended

NOTES

Repair for ocular traumaA patient presented with an ocular trauma from anexplosion. Preop vision is LP. The repair can be donewith either a 23 or 25g vitrectomy system. The conjunc-tivalized cornea was cleared. Infusion was inserted atapproximately where the pars plana would be. MVR bladewas used to dissect the anterior fibrosis. A temporaryKPro was placed and a total closed-funnel RD wasvisualized. The membranes were removed with the forceps.In these complex cases, the ability to do bimanualdissection is important. I start peeling from the edge ofPVR. Radial incisions in the funnel RD allow someflattening of the retina. Silicone oil was injected and theeye received a PK. Anatomic success is possible in thesecases, but there is a high likelihood of developing PVR.There is less PVR risk in eyes with old trauma.

Vitrectomy for diabeticsAdvanced surgical tools including high speed cutters,improved IOP control with Constellation, valvedcannulas, proportional reflux function, and better woundconstruction have made vitrectomy for complicateddiabetic detachment more effective. The availability ofchandelier light source facilitates bimanual dissection ofdiabetic membranes. I use forceps to circumcisemembranes 360 degrees before delaminating.

In diabetic patients, I do a thorough peripheral shavingwith scleral depression to prevent anterior membraneproliferation. Excellent IOP maintenance makes this partof the procedure not as difficult. One should avoidcreating retinal tears in diabetic TRD cases as this makesmembrane peeling more challenging. An illuminatedspatula can be used to lift the membrane and protect the


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retinal surface while cutting off the membrane. TheUltravit probe has the port very close to the end of thecutter which makes it easier to maneuver the tissue forcutting without damaging the retina.

Importance of IOP control in PPVIOP control in Constellation is excellent combined withthe valved cannula system. Enhanced blade designcreates a linear wound which also contributes to a betterIOP control. IOP can be raised up to 120mmHg in a wetlab with valved cannulas. The removal of a probe fromthe cannula rarely causes a drop in the infusion pressure.Without valved cannulas, removal of the instrument canlead to a 30-100mmgHg pressure drop, which should beavoided during vitrectomy. The use of long tunnel whenmaking a scleral wound is also vital for maintaining agood IOP control. Reliable IOP control allows vitrectomyprocedure to be performed with a low infusion pressurearound 12-15mmHg, which is important especially indiabetic patients to prevent induced retinal ischemia.

Heavy tamponadeRegular silicone oil (SO) has been in use for more than 40 years and is often utilized in complicated cases.Complications that arise from the use of SO is mostlyfrom the wrong use of SO and are preventable. With the introduction of perfluorocarbon liquids, heavy SO analogue was sought and we now have densiron.Densiron shows better inferior tamponade, and this isuseful since most recurrent RDs with PVR occur in theinferior quadrants. However, studies have shown that thenumber of reoperations is not reduced with the use ofdensiron. Densiron leads to a significant intraocularinflammation and has not been shown to preventinferior PVR. The complications that occur with heavySO are much worse than regular SO. Subretinal densironcan stimulate PVR formation. Posterior pole heavy oil isdifficult to remove because it sticks to the retina. Astrong aspiration is needed and this could potentiallylead to a funneling of redetached retina.

In Europe, even primary RDs are being tamponaded byheavy oil. In primary RD repair, I personally never use anencircling band, always use a gas tamponade and utilizehigh speed cutting in the periphery. When I encounter aheavy oil removal case, I push it out of the macular areaand then remove it. The emulsified oil particles areharder to remove since they don’t float. As the heavy oilmoves with the different patient positions, themembranes can form in all levels.

DISCUSSION

Q: When do you decide to leave the oil permanently? Is recurrent RD worth the risk?

A: The removal of oil in PVR cases is more complicatedthan injecting the oil. One always needs to check formore membranes, perform additional laser if needed andeven put back a tamponade (oil or gas). In a very severehypotony case, I do not remove SO.

Q: How often do cases of SO removal lead to reinjection of SO?

A: I see lots of complex referrals that have both heavyand regular SO. I get better results in cases that havebeen operated as our own primary case.

Q: A patient with a small chronic inferior RD under SO with good VA, do I remove or leave the oil?

A: The longer you wait with SO in the eye, the moremembranes will form that need to be removed later andcases become more complex. I recommend an earlierreoperation.

Q: Have you considered two port vitrectomy for RDrepair under oil without infusion?

A: Valved trocars would allow this and have revolu-tionized vitrectomy procedures.


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MondayM A R C H 7

I. Acquired Vitelliform Lesions: Correlation of Clinical Findings andMultiple Imaging Analyses K. Bailey Freund, MD

PRESENTATION

Accumulations of yellowish andpresumably subretinal material can occurin a variety of macular disorders. This finding may be referred to generically as a

vitelliform lesion (VL) to avoid confusion with the termsvitelliform macular dystrophy and vitelliform maculardegeneration. Vitelliform lesions most commonly developsingly beneath the fovea but are occasionally multipleand can occur in other locations within the macularregion. When detected in younger patients, VLs oftenoccur in the setting of Best macular dystrophy (Bestdisease), an autosomal dominant disorder with variablepenetrance and expressivity first described more than acentury ago by Frederic Best. Best disease has beenassociated with a mutation in bestrophin 1 (BEST1), agene on 11q13 that codes for a transmembrane anionchannel found on the basolateral plasma membrane ofretinal pigment epithelial (RPE) cells.

Multiple causative etiologies may produce an acquiredvitelliform lesion (AVL), but only some have knowngenetic associations. Inconsistent terminology prevails inthe literature. The terms pattern dystrophy, adult-onsetvitelliform macular detachment, foveomacular vitelliformdystrophy—adult type, pseudovitelliform macular degen-eration, and adult-onset foveomacular pigment epithelialdystrophy are often used interchangeably in describingthese eyes. Some specific genetic causes of AVLs havebeen identified including mutations in either the Best 1 or the photoreceptor peripherin gene (PRPH2/RDS) onChromosome 6 (6p21.1-cen).

When VLs present in adults without typical findings ofage-related macular degeneration (AMD), the term‘‘pattern dystrophy’’ is commonly used even in theabsence of a known family history of AVLs or a provenmutation in one of the known associated genes. Otherentities associated with AVLs include cuticular drusen,tractional maculopathies, and AMD. The purpose of thispresentation is to correlate clinical observations withmultimodal imaging analysis in a large series of patientswith AVLs due to multiple causes in order to elucidatethe nature, pathogenesis, and natural course of this entity.

HIGHLIGHTS

• Acquired vitelliform lesions (AVLS) are not specificand can occur in many different diseases

• 2 different types exist: extracellular (shed photore-ceptor outer segments) vs intracellular (pigment-ladenmacrophage, RPE)

• 2 mechanisms exist for the formation: Degeneration vsLoss of apposition between photoreceptors and RPEleading to accumulation of materials

• There is no known treatment for AVLS

• VA best correlates with the integrity of the inner andouter segment junction of photoreceptors on OCT


What would you call the funduscopic findings in this70yo male with no family history of macular disease?(n=54)

Pattern dystrophy . . . . . . . . . . . . . . . . . . . . . . . . 5.6%Adult onset vitelliform macular detachment. . 22.2%Foveomacular vitelliform dystrophy-adult type . 25.9%Pseudovitelliform macular degeneration . . . . . 31.5%Adult-onset foveomacular pigment epithelial dystrophy . . . . . . . . . . . . . . . . . . . . . 14.8%

NOTES

The question posed above highlights the various inconsistent terminologies that exist for describing vitelliform lesions. Vitelliform lesions in a familial settingcan be seen in Best disease, pseudoxanthoma elasticumor pattern dystrophy. Acquired form of vitelliform lesions can be seen in central serous chorioretinopathy(CSC) variants, cystoid macular edema or maculartelangiestasia.

Basic features of acquired vitelliform lesionsWe performed a retrospective chart review of 90 eyeswith acquired vitelliform lesions defined as presence of awell-circumscribed area of yellowish subretinal materialdetected in patients older than 40 years. (AVLS)(published in January 2011 issue of Retina). Patients with Best disease and neovascular AMD at baseline wereexcluded. Mostly commonly, patients with VL hadminimal fundus findings (44.4%). They were typicallygiven the clinical diagnosis of a pattern dystrophy oradult-onset foveomacular dystrophy. FA can mimicoccult AMD lesion. OCT shows material in thesubretinal space above the RPE without subretinal fluid(SRF). The material appeared to be predominantly intra-cellular. In patients with larger lesions, two distinct typesof subretinal materials were observed: near infrared lightreflectance with high melanin content vs. extracellularmaterial of presumed outer segment origin. Both thesetypes demonstrated hyperautofluorescence.


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Associated findings with acquired vitelliform lesions:22.2% of the patients had VL associated with cuticulardrusen and other finding of dry AMD. Cuticular drusehave a “starry sky” pattern on FA and are hypoauto -fluorescent because the RPE is thin over the cuticulardruse and there are less lipofusin in the troughs betweenthe cuticular drusen. OCT is distinct for its sawtoothpattern. These patients may present with other types ofdruse like soft druse. 21% of the patients with VL hadassociated dry AMD findings with overlying PED. 3.3%had subretinal reticular drusenoid deposits (above RPEunlike soft druse). 3.3% had PXE and angioid streaks,another 3.3% had vitreomacular traction (like a yellowdot described by Don Gass), and 2.2% had CSC. Theouter segments can continue to shed in the setting ofsubretinal fluid, leading to accumulation of VL. Forexample, we had a chance to follow a patient diagnosedwith CSC (confirmed by thick choroid on EDI OCT)and drusen over a 9 month period with spectral-domainOCT and observed a progressive accumulation of thesubretinal material.

Majority of the patients (79%) had no SRF. No SRF wasseen in the fellow eye without VL. Of the 19 eyes withSRF, 8 eyes (42.1%) had no other fundus abnormalities,5 eyes (26.3%) had cuticular drusen, 3 eyes (15.8%) hadnonneovascular AMD, 2 eyes (10.5%) had PXE, and 1eye (5.3%) had CSC. The SRF may precede the materialor vice versa. 13% of the eyes had a complete resolutionof VL, but VA rarely improved even with the resolutionof VL. This may be because by the time RPE catches up to absorb the VL material, there is advanced loss ofphotoreceptors. Most patients had same or worse VA(20/60 to 20/80 once VL resolved) due to foveal atrophy.A case was followed over 7 months, and the VA deterio-rated from 20/50 to 20/70 with very thin fovea but VLresolution on OCT.

Treatment for acquired vitelliform lesionsThere is no role for anti-VEGF therapy for these eyes.14% of our patients received treatment but no benefitwas seen and the treatment was discontinued. No changewas seen on OCT with anti-VEGF therapy. There maybe a benefit if the patient develops CNV. ICG may behelpful to discern CNV under the VL material. Therewas a patient with VL who presented with hemorrhageand SRF on the initial visit. Both the fluid and VLresolved with lucentis injections. However, the outer

nuclear layer thinned over time on OCT. The baselineheight of ONL inversely correlated with the VA atbaseline and at the last follow up. The IS/OS junctioncorrelates best with the final VA outcome.


Q: What SD-OCT finding best correlates with the visual acuity in eyes with AVLS? (n=58)

Presence/absence of subretinal fluid . 13.8%Height of the AVL . . . . . . . . . . . . . . . . 6.9%Size (GLD) of the AVL . . . . . . . . . . . . 1.7%Integrity of the IS/OS junction. . . . 74.1%ONL thickness . . . . . . . . . . . . . . . . . . . 3.5%

DISCUSSION

Q: I had a 60yo with adult vitelliform dystrophy. The lesion disappeared spontaneously, but then a fewmonths later, VL came back in the same location. Have you seen this?

A: This may be seen in CSC. But I’ve never observedthis in age-related vitelliform dystrophy.

Q: In those cases where RPE appears healthy and there is VMT, would it help to peel the posterior hyaloidwith vitrectomy?

A: The relief of traction may help with the resolution ofVL. Microplasmin may come into use.

Q: What about lasering around the lesion?

A: I have never tried. Others who have lasered foundthat VL resolves after the procedure. Laser is not recom-mended since the laser scars expand and can affect thecentral vision. Clinical examination looking for hemor-rhages is important to detect concurrent CNV. However,these patients rarely develop CNV. IS/OS junction hasbecome the most important factor that correlates withVA in almost all retinal diseases.

Comment: Classically when intraretinal pigmentmigration is seen, this is an indication that there is toomuch production of lipofusin by RPE, leading to atrophy.Some patients present with basal laminar drusen, whichis seen in AMD. It may be difficult to differentiatebetween AMD and VL as a result.

See Freund PowerPoint presentation, A.33


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II. VEGF Trap UpdateGregg T. Kokame, MD, MMM

PRESENTATION

The recent results of VEGF Trap-Eye(Regeneron/Bayer) are very promising asan effective therapy for exudative AMD, central retinal vein occlusion and diabetic

macular edema. Data has recently been released from the phase 3 VIEW trials in wet AMD, the phase 3COPERNICUS trial for macular edema associated withCRVO, and the phase 2 DA VINCI trial for DME.

For wet AMD the VIEW 1 trial from North Americashowed that 2 mg of VEGF Trap-Eye given monthly orevery 2 months resulted in equivalent and non-inferiorstabilization and improvement in vision compared toranibizumab 0.5 mg dosed monthly. There were nosystemic or ocular safety signals in the View 1 trial.

For macular edema associated with CRVO the COPER-NICUS trial at 6 months showed a 56.1% chance of atleast 15 letters of vision improvement with monthly 2 mgVEGF Trap-Eye, compared to only 12.3% in the shaminjection group. The Galileo Trial (Bayer) will bereleasing results for CRVO later in 2011.

The one year results of the DA VINCI trial utilizingVEGF Trap-Eye for DME show stabilization of the visiongain that was initially noted at 24 weeks out to 52 weekswith continued therapy with mean letter improvementranging from 9.7 - 13.1 letters, compared to minus 1.3letters in the laser-treated group. Phase 3 studies for DME are in the planning stages.

HIGHLIGHTS

• VEGF Trap Eye have shown promising results in wet AMD, DME and CRVO

• It’s effective, safe and durable

• In Wet AMD, all doses of VEGF Trap Eye were noninferior to monthly ranibizumab injections, including 2 mg q 2 months

• DME – promising response leading to phase III trialcurrently being organized

• CRVO – 56.1% gained at least 15 letters (6 months)with no rubeosis

NOTES

Current anti-VEGF therapy for neovascular AMD:Advances in AMD treatments have been astonishing.The therapies we had available before the anti-VEGF erawere only able to slow down the progression of thedisease. Now the disease is reversible. After the results

from the MARINA and ANCHOR trials in mid-2000were published, Lucentis was approved for intraocular usein 2006. Intravitreal avastin has been in use since 2005.

Unfortunately, many studies have shown that monthlyinjection of Lucentis is the best way to preserve theimproved vision (PIER, HORIZON, SAILOR), leadingto a heavy treatment burden for the patients. Trials thathave investigated a less frequent use of Lucentis likePRONTO still required that patients come into clinic forexamination and OCT every month. Currently, the treatand extend regimen developed by Dr. Freund is the mostpopular one among the clinicians.

Basic features of VEGF TrapVEGF Trap binds all isomers of VEGF. It is a fusionprotein for both receptors. It also blocks placentralgrowth factor (PIGF). The binding of PIGF may lead toa higher affinity for VEGF. The molecular weight isbetween lucentis and avastin. The Fc portion of IgGantibody is incorporated into the protein prolonging thehalf life up to 8 days. The binding affinity is 40-50x thatof lucentis. Duration of biological activity is estimated tobe 83 days with 2mg of VEGF Trap.

Clinical trials with VEGF Trap for treatment of neo vascular AMDCLEAR-IT2 investigated the optimal dose of Trap. Fixeddosing of 0.5mg q1month, 2mg q1month, 0.5mg q3month,2mg q3month and 4mg q3month was compared for 3months. After the primary endpoint at 3 month, prndosing was used up to a year and then everyone wasswitched to 2mg dosing prn. There was 7.3 letter gain at3 months, 8.4 at 1 year, 6.1 at 2 years. At 1 year, 20% ofthe patients needed no additional injection after month3. The first reinjection was 3.5months (median) later.The 2 year conclusion showed that VA improvement wasmaintained with prn dosing using 2mg. On average,there was 1 injection per every 4.6 month. VEGF Trapwas well-tolerated.

VIEW1 and VIEW2 are phase 3 studies investigating theefficacy of VEGF Trap Eye in wet AMD in US/Canadaand Europe/Asia/Latin America, respectively. They had a total enrollment of 2500. It is a non-inferiority trialcomparing 0.5mg q1month, 2mg q1month, 2mg q2monthof VEGT Trap Eye to 0.5mg q1month of lucentis. In thesecond year, capped prn dosing was started. The studiesincluded those with active primary or recurrent subfovealCNV lesions secondary to AMD. There are a few differ-ences between the two studies. VIEW2 group has slightlyyounger patients. There are 21% Asians in View 2, but very few in View1. Each center also used differentreading centers.


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The primary endpoint was proportion of patients whomaintained vision (loss of fewer than 15 ETDRS letters)at week 52. The 2mg q2month VEGF Trap group hadthe least number of injections (7 vs 12 for the other 3groups). All VEGF Trap dosages were equivalent tolucentis in meeting the primary endpoint, proving non-inferiority. Proportion of the patients who gained visionand had a reduction in retinal thickness was also equiv-alent. 2mg q4month Trap performed significantly betterthan lucentis. In VIEW1, the rate of endophthalmitiswas 0.3% versus VIEW2 which was 0. All groups sharedsimilar systemic safety profiles.

Clinical trials with VEGF Trap for treatment of diabetic macular edemaDAVINCI is a phase 2 trial investigating the role ofVEGF Trap Eye in the treatment of DME. READ-2 trialwith lucentis has shown superiority of lucentis onlytreatment (6.5 letter gain at 1 year) compared to laser (2letter gain) and lucentis/laser combination (4.5 lettergain). Focal laser was compared to different dosages ofTrap in the treatment of center-involving DME of morethan >250microns on OCT. A total of 176 patientscompleted the trial. Retreatment was given following 3months when the criteria are met. At the 1 year primaryendpoint, the most significant improvement in VA andcentral retinal thickness was seen in the 2mg q1monthTrap group. At 2 years, VA improvement in Trap eyesreceiving different dosages was maintained compared tothe focal group which had a loss of 1.3 letters. Theaverage number of Trap injection was 7 in 1 year for the2mg groups. Phase 3 trial is on the way.

Clinical trials with VEGF Trap for treatment of vein occlusionsCOPERNICUS is a phase 3 trial looking at the use ofVEGF Trap Eye in 187 patients with CRVO. The naturalhistory of CRVO leads to 3 letter loss in 1 year. TheCRUISE study showed 15 letter gain in 46% of patientsreceiving lucentis. 2mg q1month dose of Trap wascompared to sham. 56% of patients gained 3 lines ormore vs 12.3% in sham, higher than with lucentis inCRUISE study. The mean change in vision was 17 lettersversus -4 in sham, again better than lucentis. The centralretinal thickness was also significantly improvedcompared to sham (458 micron decrease vs 145).Anterior neovascularization developed less frequently,and the quality of life improved. The rate of endoph-thalmitis rate was 1%. The safety analysis was similar inboth groups.


Q: How will the information on VEGF Trap Eye for agerelated macular degeneration affect your current practicechoice for injectable medicine? (n=76)

No change, will continue to use ranibizumab or bevacizumab as are currently doing . . . . . . . . 16%Will use VEGF Trap Eye as my preferred drug . . 11%Will use VEGF Trap Eye, ranibizumab or bevacizumab depending individual case . . . . . . 74%

Q: What would most influence you on utilizing VEGF Trap Eye in your practice? (n=71)

Duration of biological activity – longer intervals between injections. . . . . . . . . . . 27%Price – still unknown . . . . . . . . . . . . . . . . . . . . 41%Insurance coverage . . . . . . . . . . . . . . . . . . . . . . . . 6%Efficacy and improvement in vision . . . . . . . . . . 27%

Q: What is your first line of therapy for non-centerinvolved clinically significant macular edema? (n=88)

Macular laser treatment. . . . . . . . . . . . . . . . . . . 81%Anti-VEGF therapy . . . . . . . . . . . . . . . . . . . . . . . 17%Injection of steroid drug or implant . . . . . . . . . . . 2%

Q: What is your first line of therapy for center involvedclinically significant macular edema? (n=89)

Macular laser treatment. . . . . . . . . . . . . . . . . . . . 26%Anti-VEGF therapy . . . . . . . . . . . . . . . . . . . . . . 73%Injection of steroid drug or implant . . . . . . . . . . . 1%

Q: What will Trap cost (will you pay)? (n=77)

$1,000 . . . . . . . 70.1%$1,500 . . . . . . . . . 7.8%$2,000 . . . . . . . . . 9.1%$2,500 . . . . . . . . . 6.5%$3,000 . . . . . . . . . 3.9%$3,500. . . . . . . . . . . 0%$4,000 . . . . . . . . . 2.6%

Q: What do you think Trap will cost? (n=68)

$1,000 . . . . . . . . . 5.9%$1,500 . . . . . . . . 11.8%$2,000 . . . . . . . . . 7.4%$2,500 . . . . . . . . 20.6%$3,000 . . . . . . . 32.4%$3,500 . . . . . . . . . 5.9%$4,000 . . . . . . . . 16.2%

DISCUSSION

Q: What about VEGF Trap Eye for BRVO?

A: Currently there is no discussion of starting a trial forBRVO. The cost of VEGF Trap will be based on what’savailable now (lucentis) and what its cost is. It willprobably be more than $2,000 given that its duration islonger than that of lucentis.


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Q: Why not use avastin as the point of reference for pricing?

A: Most audience members believe the pricing should bebased on more than just the cost of lucentis.

Q: What is more important, duration or efficacy for these drugs?

A: Both are important factors.

Q: How will a general retinal specialist deal with thechange that may ensue from monthly injection topossibly bimonthly injection?

A: Currently, we have an optimized practice environ -ment to meet the demands of monthly injections. Theprofit margin will decrease if the practice environmentdoes not adapt to the changes in the practice patterns.

Q: If all drugs are equally effective and the patientprefers a more durable drug, how will this change thephysician preference?

A: It will depend on the individual cases and severalother factors such as insurance, copay, travel time, etc.Always do what’s best for the patients.

Q: How about coumadin for the management of CRVO,keeping the INR at a therapeutic range of 3.5. I had acase of a patient with CRVO, after starting him oncoumain, I saw a dramatic improvement. Hayreh paperfrom 2005 dismissed this option but INR was not strictlycontrolled in that study. If Cardiologists are comfortabledoing this for their patients, why aren’t we doing this forour patients? It benefits acute CRVO, but may be goodfor CRVO of 4-6 months. It is not effective in BRVO.

A: I agree that we are not treating the pathophysiologyof the disease. I haven’t seen any treatment that effec-tively targets the pathophysiology.

For more information visit:http://investor.regeneron.com/search.cfm?method=and&keyword=angiogenesis&CategoryFromPath=

III. Surgical Management of IdiopathicMacular Holes in the SD-OCT EraAndre V. Gomes, MD, PhD

PRESENTATION

Since the magnificent work done byDonald Gass in 1988, many things haveevolved regarding clinical evaluation of the macular holes. Gass classification in

stages 1a, 1b, 1b occult, 2, 3, and 4, was done by meansof biomicroscopy through a slit lamp and no ancillarytests were utilized.

The introduction of Optical Coherence Tomography(OCT) has brought new light into classification, surgicalindications and follow-up of those patients. Up until fewyears ago, surgical indication was based on stages, durationof the disease, size of the hole and pre-op visual acuity.The best case scenario would be a stage 2-3 macular holewith no more than six months of history, a size less than500 microns and a visual acuity not so bad.

Things have changed with the use of OCT technology.Few recent reports involving OCT have demonstratedthat the outer retina plays an important role on visualacuity recovery in successfully operated eyes. OCT hasalso showed that the inner retina and foveal morphologymight not be so important.

Spectral domain technology has dramatically improvedour histological knowledge involving macular holeformation, aging and recovery after surgery. We nowknow that the lesions age in a different fashion. Somebecome larger faster. Others show signs of photoreceptoratrophy sooner. But one can also find older lesions thatare still suitable for surgery and vision gain.

OCT also identify younger lesions that may no benefitfrom surgery as much. OCT also allows us some measure-ments involving height and width of the lesions, whichmay lead to prognostic index for operated eyes.

In conclusion, SD-OCT has changed the way surgeonsmake the diagnosis of macular hole, as well as modifiedthe surgical criteria for such cases. OCT has alsoenhanced our understanding of the closure and visualrecovery of these patients. A case series of operated eyeswill be presented at the talk, as well as a novel techniquefor chronic macular holes and data on this will be revealed.

HIGHLIGHTS

• Preoperative VA and size of the macular hole are themost important criteria for postoperative outcome

• Older holes can carry favorable outcome

• Old chronic holes with cuff of fluid have better closurerate (higher height/inner size ratio)

• Check photoreceptor atrophy at the edges preopera-tively that could indicate poor visual outcome

• Restoration of outer retinal layer goal

• Good case selection is as important as the technique

NOTES

Features of idiopathic macular holeSince the description by Kelly and Wendel in 1991, thepathophysiology of idiopathic macular hole has beenbetter elucidated. The introduction of OCT was criticalto this understanding. Don Gass used clinical observa-tions to describe different stages of MH, stressing the


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importance of vitreomacular traction. OCT of MH atvarious stages has confirmed the stages described by Gass.OCT has made the visualization of the vitreoretinalinterface possible, thus leading to refined surgicaltechniques and development of new instruments. OCTalso allows the differentiation of a pseudohole and alamellar hole from a full-thickness MH. The spectral-domain OCT has even higher resolution, allowingdetection of the location of CME, progression of diseaseand the analysis of the photoreceptor layer so surgeonscan recommend surgery accordingly.

Personal evolution in the surgical technique for macular hole repairIMH surgery is becoming more popular and is enjoyinghigher success rates. My personal techniques performedfor IMH in 1995 differ from that performed in 2005. Inthe former, posterior hyaloid was removed with suctionand the edges of the hole were scratched with occasionalinjection of adjunct like serum. In the latter, theposterior hyaloid is removed followed by the internallimiting membrane removal without staining to avoidICG toxicity and fluid air exchange. Recently, a 27g PPVwith valved trocars has been introduced for macular holerepair. A 29g trocar for chandlier lighting has alsobecome useful for bimanual surgery.

Predictive factors for surgical successVisual and anatomic outcomes of MH surgery are oftenhard to predict. Success of MH surgery involves propercase selection and techniques. Various literatures havereported better anatomic and visual outcome whensurgical repair is performed for macular holes less than 6months of duration. The conventional criteria for recom-mending surgery include the stage, lesion size (smallerthe better according to presentation by Wendel AAO2002), preoperative VA and duration of disease.

With the help of SD-OCT, we can better select surgicalcandidates. For instance, a pilot study evaluated theheight to inner diameter ratio termed macular holeprognostic index (MHPI) and determined that when thisratio is larger than 0.53, the odds of hole closure is signif-icantly higher. When the cuff is preserved, a goodheight/inner diameter ratio is maintained and the holehas a better chance of closing than a flatter hole. Someof the older chronic macular holes may still maintainthis cuff. However, as MH ages, the photoreceptor layerbecomes atrophic.

Flat holes may still be operable. The edge-liftingtechnique is a novel technique for less favorable MHPI(flat holes). A case series of such macular hole repair wasperformed. After a more extensive ILM peel, the marginsof the hole were detached to soften the tissue, thuscreating a higher chance for closure. In 12 patients who

underwent this technique for flat holes, 67% closed and75% gained 2 ETDRS lines.

The goal in IMH repair is not only an anatomic closurebut VA recovery. A retrospective chart review of 63 eyesusing stratus-OCT found a significant correlationbetween the integrity of subfoveal photoreceptor layerand final VA after a successful MH surgery. Many reportsalso demonstrate similar findings. The integrity of theexternal limiting membrane may also be important. In alamellar hole, the outer retina is intact. It is usuallyassociated with ERM, thus may be a pseudohole. Giventhese facts, the surgery is not justified in lamellar holes.


Q: What criteria do you most currently use to adviseIMH surgery? (n=69)

Duration of disease . . . 11.6%Size . . . . . . . . . . . . . . . . 2.9%Stages . . . . . . . . . . . . . . 2.9%Pre-op visual acuity . . 10.1%OCT plus all others. . 72.5%

Q: Do you operate on IMH older than 1 year? (n=73)

Yes. . . . . . . . . . . . . . . . . 89%No . . . . . . . . . . . . . . . . . 11%

Q: Do you operate on lamellar holes? (n=84)

Yes . . . . . . . . . . . . . . . . 36.9%No . . . . . . . . . . . . . . . 63.1%

DISCUSSION

Q: There is about 2% failure even with a meticulous ILM peeling. Sometimes the MH is even bigger post -operatively. Why does this occur?

A: There is a span of 24-72 hours for the hole to close.Positioning and long acting gas are not as important. I often check for “softness” and “rawness” of the holeintraoperatively. If not present, I extend the peeling.

Q: How about inverted flap technique?

A: Having tissue in the fovea may not improve visualoutcome. If the intraoperative anatomy appears unlikelyto close, I may try.

Q: Do you perform FA for prognosis for chronic MH?

A: If there is window defect, there may be RPE damage. I believe OCT is more important for prognosis.

Q: A lamellar macular hole is usually associated withERM. A lamellar hole surgery may still help patients.

A: If there is ERM, you don’t know whether it was theERM removal or the lamellar hole closure that helpedthe patient. Stretching of the cells may account for poorvisual recovery.


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Q: Chronic bilateral MH was repaired with good visual outcome.

A: I also have chronic MH cases with successful repair.FA had window defect. Every patient is different.

Q: We pay little attention to the NFL atrophy. One ofthe postoperative OCT scan presented shows NFLatrophy. Does it have any visual significance?

A: We see this often. But ERG shows no difference.Microperimetry is also normal. Absence of NFL atrophymay actually indicate subtotal removal of ILM.

Q: Size of the IS/OS defect and the area of defect corre-lated with visual acuity after MH repair but not perfectly.There are other factors that can affect the outcome likeprogression of cataract. With longer postoperative period,IS/OS may still be restored.

A: I agree that you should give at least 6 months to see ifthere is any improvement. This should be discussed withthe patients. Improvement may continue for years.

See Gomes PowerPoint presentation, A.39

IV. Vitrectomy and Pars Plana Baerveldt Glaucoma Implants forComplex GlaucomaRobert L. Avery, MD

PRESENTATION

Severe glaucoma is often associated withvitreoretinal disease, especially in casesof neovascular glaucoma (NVG). We have elected to perform combined

vitrectomy and placement of pars plana Baerveldt glau -coma implants in order to treat these complicated cases.There are several potential advantages to this combinedapproach including a single operating room setting, theability to avoid entering the anterior chamber and poten -tially inducing hyphema, better access to the posteriorpole for treatment of the cause of NVG, and betteroxygenation of the posterior pole following vitrectomywhich may reduce hypoxia – part of the pathophysiologyof NVG. Also, in cases following corneal transplantation,posterior placement of the tube may potentially reducethe risk of subsequent graft failure. Disadvantages includemore extensive surgery and the increased risk of compli-cations such as cataract formation and retinal detachment.There is a risk of erosion of the tube, but this may be lesswhen it is inserted more posteriorly at the pars planarather than at the limbus.

We have recently retrospectively reviewed a consecutiveseries of patients from a single private practice who

underwent combined vitrectomy and placement of a pars plana Baerveldt implant utilizing a novel ripcordtechnique. One hundred twenty-four eyes of 120 patientswere identified. Most of these patients had NVG, andmany had prior corneal transplantation. Mean follow-upwas 25 months (3–98 months). Complete success wasdefined as a pressure of 21 or less on no glaucomamedications. Qualified success was defined as thispressure on medications, and a qualified failure wasdefined as a pressure greater than 21 or less than 6.Complete failure was defined as the development ofphthisis, the loss of light perception, or the need foradditional glaucoma surgery for pressure control.

At last follow-up, 60 eyes of 124 eyes (48.4%) werecomplete successes, 48 eyes (38.7%) were considered aqualified success, 6 eyes (4.8%) were qualified failures,and 10 eyes (8.1%) were complete failures. Postoperativecomplications included serous choroidal detachments,hypotony, cataract, tube erosion or obstruction, andretinal detachment. The ripcord technique allows severaladvantages over partially ligated or open tubes that havebeen described in the past. Complete closure of the setontube can be achieved in the early postoperative course to allow use of gas bubble tamponade to treat retinaldetach ment or macular holes. The rip-cord can be easilyremoved in the office at the slit lamp when the fibrosishas formed around the glaucoma plate. This techniqueallows for safe and effective treatment of complexglaucoma combined with retinal disease.

HIGHLIGHTS

• Pars plana placement of tube shunts with simultaneousvitrectomy not only lowers the anterior chambercomplications like corneal decompensation andhyphema but also allows retinal surgeons to treat theposterior disease that led to glaucoma

• Right-angled Baerveldt tube avoids the lens and lowersthe incidence of tube obstruction

• Ripcord technique allows more control of theimmediate postoperative IOP

• Baerveldt implant has a better IOP control but highercomplication rates compared to Ahmed valve at 1 year

NOTES

Posterior segments diseases and glaucomaRetina specialists manage many posterior segmentdiseases that are significantly linked to glaucoma. Forexample, diabetic retinopathy or CRVO can lead toneovascular glaucoma. Posterior uveitis, retained lensfragments and their treatments can lead to uveitic orsteroid-response glaucoma. PPV plays a critical role incontrolling NVG: it clears the media for laser andincreases oxygenation of the retina. Intraoperative laser


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is better and more thorough than an office procedure,thus PPV is able to treat the root cause of NVG.Preoperative avastin can quiet the eye prior to PPV, butthe eye can be hard to tap if the IOP spikes. I use only0.01ml of avastin if IOP is already high; there is no needto use the regular dosage of avastin for NVG.

Surgical options for glaucomaThere are several surgical options for glaucoma:trabeculectomy, tube implants and cyclodestruction.Cyclodestruction using cryotherapy is unpredictable andmay lead to hypotony. This is rarely done in my practice.A prospective study of 276 patients compared the rate ofsuccess and complications of Ahmed valve to Baerveldtat 1 year postoperative follow up. There is no initialrestriction of flow with Baerveldt until a fibrous capsuleforms around the reservoir. Ahmed has a valve whichcontrols the pressure starting postoperative day 1. Thestudy showed that Baerveldt had a better IOP control(13.2 mmHg vs 15.4mmHg in Ahmed), but highercomplication rates (58 vs 43%) secondary to the initialhigh output of fluid.

Pars plana glaucoma shuntsA few retinal surgeons have reported their experiencewith concurrent PPV and glaucoma procedures. Today,Ahmed and Baerveldt valves are primarily used. Manyreports have shown successful lowering of IOP with parsplana valves and simultaneous PPV. In our practice, weuse right-angled Baerveldt for pars plana insertion. Thistype of valve avoids the lens and lowers the incidence oftube obstruction. Pars plana placement of the shunt alsoleads to a better corneal graft survival. This may not justbe due to the increased distance of the tube tip from thecornea but also because the flow of inflammatory cellsand aqueous is directed away from the endothelium. Weperformed a retrospective chart review of 50 patientsthat received right-angled pars plana Baerveldt withsimultaneous vitrectomy. 31 patients had NVG. Post -operative IOP decreased to less than 22 in 47 patients.

There are several advantages to simultaneous vitrectomyand pars plana placement of tube shunts. The shunts areless likely to erode. Media is cleared to evaluate and treatthe posterior pathology. It requires a single operation andavoids anterior chamber complications like hyphema.Posterior segment complication from pars plana shuntincludes retinal detachment, hemorrhage, choroidaldetachment and cataract. There are various ways tolower the rate of early postoperative hypotony fromBaerveldt implant: a two stage procedure, tube fenes-tration, pneumatic stent, absorbable tie (plain-gut suturesare better than vicryl since vicryl takes longer todissolve) and concurrent valved tube. I prefer the ripcordtechnique. A 4-0 prolene suture is threaded into thelumen of the tube to close off the flow; one end of thesuture is buried under the conjunctiva and can be pulled

out in the office at a later time when adequate fibrouscapsule forms around the implant reservoir and the IOPremains controlled.

We performed a retrospective chart review of 119 eyesthat underwent pars plana Baerveldt with ripcordtechnique. 69 eyes had NVG from PDR or RVO. Insome patients who can’t tolerate high postoperative IOP,the tube proximal to the suture was fenestrated. 4patients had elevated IOP despite the valve; one of thepatients had an obstructed tip from a vitreous plugsecondary to choroidal detachment that brought theanterior vitreous closer to the tip. Vitreous plug alwaysneeds to be removed. 86% achieved success (IOPbetween 6 and 21without complications), 4 patients hadIOP <6 or >21, and 12 patients had a complete failurewith NLP and phthisis. NLP vision after surgery was dueto the underlying disease, not due to lack of IOP control.

Retinal surgeons should get involved with pars planatube implantation because patients with NVG andanterior chamber tube have poor prognosis. We can treatthe underlying disease with endolaser during the tubeshunt procedure. PPV can also increase retinaloxygenation. Lastly, the valve surgery is simple.

The steps I perform for pars plana tube shunt are asfollows. First, superotemporal conjunctival peritomy iscarried out. Then I hook the superior and lateral rectusmuscles, and the preloaded valve with an anchoringneedle and ripcord is inserted. The anchoring sutures are passed. A 25g PPV is performed, the superotemporalsclerotomy is enlarged with a straight MVR blade (the19g Baerveldt tube fits snugly), the angled tube end isanchored, and a patch graft is placed over the tube. Imake sure the ripcord is intact in the lumen then I passit through the inferior conjunctiva twice with a smallpart of the suture exposed for pulling at a later time.


Q: Do you currently do combined vitrectomy andglaucoma implant surgery? (n=58)

Yes, doing both components myself . . . . . . 9% (≥ 20%)Yes, with glaucoma specialist doing the implant . . . . . . . . . . . . . . . . . . . 28% (≥ 24%)No, not particularly interested . . . . . . . . . 34% (≥ 20%)No, but may be in the future . . . . . . 29% (≥ 36%)

Q: The Ahmed Baerveldt comparison study found that: (n=72)

Baerveldt implants had lower IOP at one year and fewer complications than Ahmed implants . . . 14%Ahmed implants had lower IOP at one year and fewer complications than Baerveldt implants . . 1%Baerveldt implants had lower IOP at one year and more complications than Ahmed implants . . . 82%Ahmed implants had lower IOP at one year and more complications than Baerveldt implants . . . 3%


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DISCUSSION

Q: When do you pull the ripcord?

A: In about 2-3 weeks

Q: How quiet does the eye need to be before you perform the tube shunt?

A: It is possible to do it even when the eye is veryinflamed. I started doing this procedure before avastinbecame available.

Q: How about performing peripheral retinal laser and/orciliary body cryotherapy for these cases without havingto perform PPV/shunt procedure?

A: That is definitely less invasive, but it is difficult totitrate the IOP after such procedures. One may considerthese procedures in patients with very poor view.

Q: With ripcord, how do you manage postop IOP spike?

A: Usually the postop IOP is low with the ripcord. IfIOP spike is feared, one can also make fenestrations inthe tube. In reality, there may be some leakage from thesclerotomies. Tight PRP may also cause serous choroidaleffusion leading to lower IOP. Glaucoma drops anddiamox can also be restarted.

Q: Do you ever place a regular Baerveldt in pars plana? I have not experienced problems with erosion with theregular Baerveldt.

A: I used to in the past. It gets more easily obstructed. In a phakic eye, good peripheral vitrectomy aroundwhere the tube sits is very difficult and eventually avitreous plug will obstruct the tube. I recommend theright-angled Baerveldt to avoid this problem.

Q: A study was done comparing trabeculectomy to tubeshunts. They were similar but more favorable results wereobserved with the tubes. Thus more glaucoma surgeonsare turning to tube shunts as their primary procedure.Corneal decompensation is often seen, however. Whatdo you think about eliminating all AC shunts andprimarily using pars plana shunts as the initial procedurefor even less complicated glaucoma?

A: This is already being done in a small set of patientpopulation, but mostly when there’s additional posteriorproblems like macular pucker or retained lens. Moreglaucoma specialists are considering the status of corneaand recommend pars plana shunts. In regards to whoactually performs the surgery, some believe the glaucomaspecialists should perform the procedure since they willbe following the patients postoperatively.

Q: In an ASC, stocking shunts may not make financialsense for retinal surgeons who do not perform this proce-dures routinely. If it is done as a staged procedure, whatdo you do with the tube that has not been insertedintraocularly?

A: You can tuck the tube under the conjunctiva. This is more difficult to do with the right-angled tube.

See Avery PowerPoint presentation, A.43

V. Panel Discussion Complex Surgical ManagementHIGHLIGHTS

• Giant retinal tears do better with combined scleralbuckle and vitrectomy

• When confronted with a complex surgical case, doeverything one can with a single operation, but onlywithin one’s comfort level.

• Same day vitrectomy surgery for retained lens is notrecommended except in special circumstances

NOTES

Surgical trends have shown the transition in pars planavitrectomy from 20 gauge instruments to smaller (23 or25 g), sutureless, transconjunctival vitrecomies withtrocar systems. High resolution imaging has contributedsignificantly to our surgical planning and postoperativefollow ups. Adjunct pharmacological agents will furtheradvance our surgical field.

CASE 1: 71yo woman presented with blurred vision aftercataract surgery. Her vision was 20/200. On examination,ACIOL was found to have been inserted upside down(posterior bowing of the iris), dislocated PCIOL wasfound in the posterior chamber with a giant retinal tear.

INTERACTIVE QUESTION

Q: How would you manage this patient’s retinaldetachment? (n=50)

Scleral buckle . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0%Primary pars plana vitrectomy . . . . . . . . . . . . . . . . . 26%Combined scleral buckle and pars plana vitrectomy . 60%

DISCUSSION

The panel would choose combined SB/PPV as well.


Q: How would you manage this patient’s intraocular lens? (n=49)

Remove ACIOL and suture PCIOL . . . . . . . . . . . . 12%Remove ACIOL, PCIOL and replace ACIOL . . . . 16%Remove PCIOL and reposition ACIOL . . . . . . . . . 27%Leave aphakic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45%

DISCUSSION

The panel agrees that they would leave the patientaphakic. There is a trend for anterior segment surgeonsto want the retinal surgeons to suture-fixate dislocatedPCIOL.


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An audience member discussed a similar case. ThePCIOL was placed between the ACIOL and the iris, and 2 months later, the anterior segment surgeonbrought the patient back to the operating room for IOL replacement.

In this particular patient, an encircling band was placed(#41) before vitrectomy, the ACIOL was removed, andPFO was used to remove the PCIOL. After the RD wasrepaired, endolaser was performed 360 degrees, C3F8 gas was used for tamponade, and a new ACIOL wasimplanted. It is important to do everything one can witha single operation, but also important to only do up toone’s comfort level.

The induced myopia with the encirclement needs to betaken into account when calculating the IOL power. Thesurgeon should always review the IOL calculation. Thisparticular case was done with a 20g system, but we arenow shifting to 23g when it is combined with SB or forother complicated cases. In these complicated cases, wehave a higher threshold for suturing the 23g wounds.


Q: 67 year old undergoing planned cataract/IOL surgerywith dropped nucleus. How do you manage? (n=53)

Recommend anterior surgeon complete procedure, clear anterior vitreous, place IOL and refer. . . . . . . 40%Convert case to pars plana vitrectomy, remove nuclear fragments, place IOL . . . . . . . . . . . 60%

DISCUSSION:

The panel would perform a staged procedure because the retinal surgeon has not spoken to the patient prior to surgery and there are medicolegal ramifications.However, exceptions have been made depending on therelationship the vitreoretinal surgeons have with theiranterior segment colleagues.

When removing the retained lens material, the surgeonneeds to be very aggressive about removing the posteriorhyaloid. Occasionally, triamcinolone is used to bettervisualize the vitreous. If fragmatome is needed, one canenlarge one of the sclerotomies with a 20g MVR blade.Soon, a 23g fragmatome will be available in the marketwhich will make the need for sclerotomy enlargementobsolete. A thorough examination for retinal tears is very important at the end of each case.

If preoperative VA is good, same day surgery for retainedlens has shown a very good prognosis. But that alone isnot a rationale for same day surgery after a complicatedcataract removal.

See Panel Discussion PowerPoint presentation, A.48

TuesdayM A R C H 8

I. Do We Need a New Classification for Neovascularization in Age-RelatedMacular Degeneration?K. Bailey Freund, MD

PRESENTATION

Anatomic Classification:1. Type 1 (sub-RPE) neovascularization

a. Case examplesb. Treatment considerations

2. Polypoidal neovascularization (a variant of type 1neovascularization)a. Case examples (simultaneous eye-tracked

SD-OCT/ICG)b. Treatment considerations

3. Type 2 (sub-retinal) neovascularizationa. Case examplesb. Treatment considerations

4. Type 3 (intra-retinal) neovascularization (RAP)a. Case examples

Questions• Is polypoidal a “neovasculopathy” or a “choroidalvasculopathy?”

• What has SD-OCT taught us about Type 3 neovascu-larization (RAP)?

• Can Type 1 neovascularization protect the retina?• Why do some eyes with choroidal neovascularizationdevelop Type 2 neovascularization rather than Type 1?

• Can Type 2 neovascularization become Type 1?

HIGHLIGHTS

• With OCT used increasingly more in managingchoroidal neovascularization, a classification schemebased on anatomic findings rather than fluoresceinpatterns may be more useful.

• Polypoidal vasculopathy is likely a neovasculopathyrather than a choroidopathy.

• Type 3 neovascularization (RAP) may be most easilydetected with SD-OCT.

• In some cases, neovascularization may be protective to the retina.


Q: Where are the polyps in polypoidal vasculopathylocated?

1. Deep Choroid 2. Inner choroid 3. Beneath the RPE 4. Just beneath Bruch’s membrane 5. Sub-retinal space.


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The responses were varied and Dr. Freund commentedthat hopefully the talk will convince us that #2 is notthe correct answer.

Q: Where is the “branching vascular network” of PCV located?

Deep choroid . . . . . . . . . . . . . . . . . 36.0%Inner choroid . . . . . . . . . . . . . . . . . 32.0%Beneath the RPE . . . . . . . . . . . . . 22.0%Just beneath Bruch’s membrane . . . 4.0%Sub-retinal space . . . . . . . . . . . . . . . 6.0%

Q: Early type 3 neovascularization (RAP) is most easilydetected with:

Clinical examination. . . . . . . . . . . 14.3%High-speed ICG. . . . . . . . . . . . . . . 35.7%Fluorescein angiography . . . . . . . . 21.4%SD-OCT . . . . . . . . . . . . . . . . . . . . 23.2%Red-free photography . . . . . . . . . . . 1.8%Fundus autofluorescence imaging . . 3.6%

NOTES

Most of our classification of neovascularization is basedon fluorescein terminology. Now that we’re using OCTmore to image and manage our patients with neovascu-larization, we need a better language to communicate thefindings rather than terms like ‘polyps’ or ‘well defined’.An editorial published in the October 2010 issue ofRetina discusses the rationale for shifting to a differentclassification scheme that is based on anatomic findingsrather than angiographic findings.

Historically, we have used the Gass classification of Type 1 and Type 2 choroidal neovascularization. Type 1neovascularization is where the vessels are confined tothe subRPE space whereas type 2 neovascularizationcorresponds to the classic or well-defined lesion wherethe vessels have eroded through the RPE and are prolif-erating in the sub neurosensory space. There is a thirdtype, that is actually a common type of neovascular-ization, where the vessels are proliferating intraretinallyand forming retinal-choroidal anastamoses. Dr. Freundlikes to call this type 3 neovascularization since it fits inwith the Gass classification.

Then we have polypoidal vasculopathy. Some don’tthink this is even a form of neovascularization, but itmay in fact be a variant of a type 1 growth pattern. So,PCV may not be a choroidal abnormality but a neovas-cular abnormality.

It’s nice to go back to the literature to look at histo -pathological correlation of patients who had neovascularlesions imaged before they died.

Unfortunately, there are not a lot of these in the liter-ature. One example is a recent study by Klein andWilson in the January 2011 issue of Ophthalmology. In

this study, several eyes were examined demonstratingdifferent types of neovascular lesions.

Image: Type 1 vessels in the subRPE space and aboveBruchs membrane.

Image: Type 2 pattern was also shown. This was correlated to fluorescein angiography that showed themore classic, well-defined, type 2 lesion adjacent to anoccult lesion.

Questions to explore:

• Is polypoidal a neovasculopathy or a choroidal vasculopathy, as is commonly believed?

• What has SD-OCT taught us about type 3 neovascularization?

• Can CNV actually protect the retina and beneficial for eyes that develop it?

• Is polypoidal a neovasculopathy or a choroidal -vasculopathy?

As initially described, polypoidal was termed an abnor-mality of the inner choroidal vasculature. However, inlooking at the literature of histopathologic correlations,many of the published reports have found that the polypsare actually above Bruch’s membrane in the sub-RPEspace, suggesting that it may be, in some eyes, a variantof type 1 neovascularization. In OCT correlation, thepolyps are right underneath the RPE and appear to bepart of a larger and extensive type 1 neovascularmembrane. This is a pattern that was seen over and overagain whenever a direct ICG-OCT correlation was done;the polyps were right under the RPE and were usually apart of a much larger complex consistent with a type 1neovascular membrane.

Going back to Klein and Wilson’s recent histopathologiccorrelation, what they describe is that the vessels in thetype 1 neovascular tissue are very small and are mostlyextracellular matrix and fibrous tissue. Type 2 tissue,however, is composed of a more loose matrix and larger vessels.

Case Presentation: Large vessels in type 1 neovasculartissue beneath the RPE, which may be the early origin ofpolypoidal vasculopathy.

Case Presentation: Polyps at the margin of the neovascular lesion.

What about the branching network?

The whole branching vascular network is in the spaceabove Bruchs membrane and above the RPE. Polyps canbe seen at the margin of the larger type 1 vascularnetwork and the vessels may elevate the RPE. Sometimeswhen the RPE is elevated, as in chronic cases, it can liftthe polyps with it. The polyps are actually lifted up onthe back surface of the RPE. Using simultaneous ICG


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and OCT on the Heidelberg system there is point-to-point correspondence which ensures that what lights upon the ICG is what we are seeing on the OCT. Vesselscan also adhere to the back-surface of the RPE. Bruchsmembrane may appear to be pulled up and be adherentto the polyp. He concluded that polypoidal vasculopathyis a neovasculopathy.

What has SD-OCT taught us about type 3 neovascular-ization. (RAP)?

Type 3 neovascularization lesions are often difficult tosee clinically. An orange intraretinal lesion typical oftype 3 neovascularization may be identified. At this stagefluorescein is much more sensitive than ICG. Thebackground fluorescence of ICG overwhelms the smallamount of hyperfluorescence of the lesion and doesn’tlook anything different than a staining drusen. And veryoften, the only way type 3 neovascularization is pickedup is by OCT. On OCT, you can see intraretinal fluidand a vascularized PED. This is a typical configuration of early type 3 lesions. Therefore, overall SD-OCT hastaught us that type 3 neovascularization is detectedearliest with SD-OCT and that there is a characteristicpattern on OCT.

Evolution of Type 3 NeovascularizationThere is gradual thinning of the ONL over a druse(possibly vascularized). Then a hyperrefelctive materialbegins to show in the outer retina. At this point it ishard to tell if the vessels are coming from the deepintraretinal circulation or from the vascularized druse.Over time, intraretinal fluid accumulates. This is aprocess that occurs over a number of months. Althoughwe don’t know if the vessels come from the deepintraretinal circulation, the choroidal circulation or fromthe neovascularization within the druse, we know thatover time, these eyes develop retinal-choroidal anasta-moses. OCT may demonstrate new vessels coming out ofthe neovascular tissue and into the retina. What isconfusing, however, is that in histopathologic cases (byDubovy and Klein), no defects in Bruchs membranecould be found, which strongly suggest that the neovas-cularization originates from the retina.

Can CNV be protective to the retina?

Case Presentation: Patient with a type 1 occult membranewho was asymptomatic and not treated. After 7 years offollow-up, the patient is still 20/30 and the photorecep -tors look healthy over the type 1 neovascular tissue.

Another case was presented. The right eye was 20/40with type 1 neovascularization and geographic atrophy.The other eye had geographic atrophy and no evidenceof neovascularization. The right eye was treated withmonthly ranibizumab for 53 months and maintainedvision. The other eye never developed neovascularization

and the geographic atrophy grew much larger. Over 25months of follow-up there was no change in the right eyewith healthy foveal photoreceptors whereas in the lefteye the geographic atrophy became much larger.Therefore, we can hypothesize that the neovascular-ization is actually perfusing the outer retina helping toprevent the loss of photoreceptors.

Case Presentation: Patient with dry AMD in the right eyeand a large vascularized PED with hemorrhage in the lefteye. The left eye did very well with anti-VEGF therapyfor 22 months and visual acuity improved. In the othereye, the photoreceptors began to atrophy and the visiondecreased.

Looking at the histopathologic correlation of Klein andWilson, the neovascular tissue between the RPE andBruchs membrane corresponds to the occult pattern offluorescein staining. Looking closely in that area, thephotoreceptors are surviving over the neovascular tissue.

Case Presentation: Patient with a history of multiple PDTsand multiple anti-VEGF treatment was able to maintain20/30 vision despite persistent subretinal fluid, whichsometimes involved the fovea. This suggests that theCNV is helping to perfuse the photoreceptors.

So, it appears that CNV can be protective to the retinafor some cases. To be more specific, however, we aretalking about type 1 subRPE vessels and not type 2 ortype 3 neovascularization, which are toxic to thephotoreceptors.

DISCUSSION

Q: Why can’t it be that the treatment of neovasculari -zation is protective, not the CNV itself?

A: You would have to come up with some plausiblerationale of why anti-VEGF would be protective. Wedon’t think it is neuroprotective although it’s possiblethat the anti-VEGF treatment is causing survival of thephotoreceptors.

Q: Could he identify this kind of outcome when lookingback at his practice prior to the anti-VEGF agents?

A: In doing ICG for many years, plaques were often seenin asymptomatic eyes, which indicates that there mayalready be occult vessels in asymptomtic eyes. A similarfinding is seen with OCT, where there seems to be avascularized PED but there is no fluid or hemorrhage.Many of these eyes may have neovascularization for along period of time before they start bleeding, and if yougo back, you can probably see that.

Q: Are we were seeing 2 independent disorders, neovas-cular AMD and GA, with GA progressing despitetreatment of the neovascularization. Or are we treatingneovascularization too aggressively in that a little bit of


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neovascularization is protective and we’re preventingthat from happening?

A: Eyes that have a certain amount of ischemia can godown either 2 paths. They can go to atrophy or developa compensatory response. It is a very complex disease andthere are a lot of different things that can happen. Butthe main point is that some of these eyes with persistentfluid do well. They may gradually lose vision over time,but the concept that we really need to get rid of theneovascular tissue is somewhat flawed. It may backfire atthe end when we look long-term.

Q: All the data we have show that there isn’t an issuewith over treatment. There can be independent compli-cations related to the injection itself, but repetitivemonthly injection of anti-VEGF therapy does not seemto be associated with any significant long term decline invisual acuity.

A: It’s about balancing risks and balances.

Q: Where do you think the vessels in type 3 neovascular-ization come from?

A: Although originally I was adamant that it was fromthe choroid I am not sure now since the histopathologiccorrelations that we have don’t support this. I don’tthink it will be answered necessarily by a next generationOCT but will likely be answered by histopathologiccorrelations that catch the process.

See Freund PowerPoint presentation, A.53

II. Retinal Complications of the Dohlman KeratoprosthesisMina Chung, MD

PRESENTATION

The Dohlman keratoprosthesis offers analternative to penetrating keratoplastywith the potential for faster recovery of clear optical media and reduced post-

operative astigmatism. A case series of vitreoretinalcomplications of the keratoprosthesis will be presented.Types of vitreoretinal complications, special considera-tions for surgical management, and long term outcomeswill be reported.

HIGHLIGHTS

• As the Dolman type I keratoprosthesis has becomemore popular, it has been associated with a rise invitreoretinal complications.

• Important vireoretinal complications include retro-prosthetic membranes and endophthalmitis.

• Treatment with vancomycin is important to preventendophthalmitis.

• There are unique surgical considerations in these eyes.

NOTES

The Dolman type I keratoprosthesis is made of PMMA.The middle part is the donor cornea and is used as abiologic scaffolding. The internal depth of the barrel sitsdeep inside the eye. The lens and iris are usuallyremoved and an anterior vitrectomy is performed.

The KPro is usually used in eyes with extensivepathology and, when it works, can provide a very clearoptical zone very soon after surgery. It has thus become apopular alternative to standard corneal transplantation.

There has been an advent of pediatric cases as well, therationale being that there is a clear visual axis right awaywith no astigmatism or sutures to worry about.

In the last 8 years, 254 cases were performed at Dr.Chung’s institution. Accordingly, there has been a rise in vitreoretinal complications.

In 2007, the retina service looked at all KPro casesassociated with vitreoretinal complications. 22 eyes of 18 patients were identified. There were 14 pediatric and4 adult cases. Most of the complications were retro -prosthetic membranes and endophthalmitis.

Endophthalmitis in KPro PatientsTo look more into endophthalmitis, a retrospective caseseries of all KPro cases over a 4-year period was done.This included 141 eyes of 130 adult patients. All werefollowed for an additional 2 years. The postoperativeregimen included topical steroids, vigamox andvancomycin. A bandage contact lens was placed toprevent drying of the interface between the optic andthe corneal donut. The vancomycin is compounded by apharmacy and only lasts 2 weeks.

Endophthalmitis was defined as vitritis with decreasedvision ± pain and ± injection. Of note, patients do notget a hypopyon since there is no anterior chamber.

Ten cases of endophthalmitis were identified. The meanonset was 1.8 months after surgery, ranging from 2-25months. There were 7 additional eyes with presumedsterile vitritis which were treated with steroids. None ofthe 10 cases of endophthalmitis were on vancomycin atthe time of diagnosis. Some had other procedures prior tothe diagnosis of endophthalmitis. Six eyes had presumedsterile endophthalmitis and were treated with steroids,while 1 eye had a glaucoma valve placement.

After diagnosis, most eyes had a vitrectomy. One patientrefused vitrectomy and had a tap/inject. One eye under-going vitrectomy had a retinal detachment that wasrepaired at the same time.


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All received intravitreal antibiotics and 3 receivedAmphotericin. All eyes undergoing vitrectomy wereculture positive. Most of these specimens were positivewith Staphylococcus and sensitive to vancomycin andresistant to fluoroquinolones. Two cultures were positivewith gram negative rods and none of the fungal cultureswere positive.

All cases resolved after initial treatment but 7 of the 10cases had recurrent endophthalmitis. The mean onset ofrecurrence was 4 months after resolution of the firstepisode. Again, all patients with recurrences had stoppedtaking vancomycin. Five had a tap/inject and 2 receivedvitrectomy with injection. The second time around, thecultures were not as sensitive as five eyes had a negativeculture.

One eye had a third episode of endophthalmitis, whichoccurred 1 month after the previous treatment. Thepatient had stopped using vancomycin in this case aswell.

In this patient, it was decided to exchange the KPRo,but the eye developed a suprachoroidal hemorrhageduring surgery.

Overall, visual acuity results were unfavorable, with mostpatients ending up LP or NLP.

Another study was performed to evaluate pediatric KProcases. Thirty-six eyes of 27 patients were identified over3 years. Median age was 2 years at the time of KProsurgery. Many of the patients had prior retinal pathologyand 3 of 4 cases where there was a prior retinal detach -ment, the retinal detachment was discovered at the timeof KPro placement.

Of new onset complications, 18 of 36 had a retropros-thetic membrane, 10 had a retinal detachment and 2developed endophthalmitis. There was prosthesisextrusion in 5 cases.

If the patient had pre-existing retinal pathology, 75% ofcases had additional complications after the KPro. Ifthere was no prior retinal pathology, patients still had avery high rate of retroprosthetic membrane formationand retinal detachment.

Two patients developed a retinal detachment after theretroprosthetic membrane was treated by an anteriorapproach. Retroprosthetic membranes are initiallymanaged with YAG, which occasionally works. If YAGdoesn’t work, an anterior vitrectomy is performed. But inthese eyes, an anterior vitrectomy is difficult to define.

Videos of surgical case examplesCase 1: A 53 year old with keratoconus and multiple PKshad a KPro placed 11 months prior to presentation. Hehad developed glaucoma for which an Ahmed valve wasplaced. 1 day post Ahmed valve placement, the IOP was

actually increased. This increased IOP was presumed tobe due to vitreous incarceration. To manage this patient,a 25g vitrectomy system was used in an attempt to avoidthe Ahmed valve during surgery. Intraoperatively, it wasseen that there was consolidated vitreous streaming up tothe tube. This vitreous was removed. After thisexperience Dr. Chung suggests doing a vitrectomy at thetime of Ahmed valve placement.

Case 2: A 4 year old boy with multiple graft failures hada KPro placed 10 months prior to presentation. Onfollow up, B-scan ultrasound was concerning for retinaldetachment. The purpose of this video was to show howhard it is to define anatomical features after multiplesurgeries; it is hard to know where the limbus is. In asmaller eye, it can be harder to use a 25/23 g system. So,in this case, a 20g system was used, which allows foreasier removal of scar tissue and also gives more controlof the eye. The contact lens system works relatively wellwith the KPro. There is a decent view of the peripherybut you can’t do scleral depression. In this case, the childdid not have a retinal detachment, but instead hadextensive membranes. Endolaser was applied and a fluidair exchange was performed. Of note, as the infusion wasbeing removed, air could be seen leaking out betweenthe optic and the donut. This indicates that there is anopening between the optic and the corneal donut, eventhough it looks intact and is seidel negative.

Case 3: A 6 year old girl with sclerocornea presentedwith no red reflex. On examination it was found thatblood and retina was consolidated just behind the KPro.Although the view is decent through the contact lens,the ora cannot be visualized. The patient was noted tohave a total funnel retinal detachment. During surgery,membranes were removed and healon was used to helpopen the funnel. A 360 degree retinectomy was alsoperformed and laser was applied. At end of video, theBIOM view was shown, demonstrating that any amountof tilting causes the image to deteriorate.

CONCLUSION

Surgical considerations• It is hard to identify landmarks for sclerotomies.

• Wide angle viewing is very helpful but you still can’tdepress.

• The KPro is very difficult to remove. In a few of thecases where the KPro was attempted to be exchanged,the patient had bad complications.

• Consider primary PPV at time of KPro placement.

For the endophthalmitis series• Consider vancomycin for all patients.

• It is typically a late onset endophtalmitis, similar tohaving a glaucoma tube.


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• Look carefully for thinning between the optic and the donut.

• Have a high degree of suspicion in those cases withvitiris.

• A vitrectomy is more likely to give positive cultureresults than Tap.

Pediatric cases: • Case selection is key.

• It is important to do a careful B scan prior to the KPro.

• If a retroprosthetic membrane develops, have a highsuspicion for retinal pathology.

DISCUSSION

Comment: There has been a large shift toward using theKPro at our institute. However, by 36 months, 33% havea retinal detachment and by 5 years, 50% have a retinaldetachment. At our institute, a vitrectomy is done inevery patient at the time of placement of the KPro. Thisseems to have decreased the incidence of retrokerato-prosthetic membrane. Also, these membranes are nolonger managed by YAG laser but by vitrectomy. Oncethese implants are in place, their complications are ourcomplications, and we will likely be seeing a lot more of these.

Preoperative evaluation with ultrasound is critical andthe contact lens viewing system is superior to the BIOMin these cases.

Comment: Dohlman discovered a few years ago that,without the vancomycin, it’s an end game. At ourinstitute, we take everything out of the eye including thecrystalline lens or IOL and do a complete vitrectomy ± glaucoma tube. There is no proof, but this mightdecrease the rate of some of these complications. On thecornea side, they are moving toward going to the KProearlier. This is because after multiple surgeries, they weregetting good anatomic success, but poor visual outcomes.

Comment: I do not necessarily agree that you need to go to KPro early. It is more important to manage theassociated complications such as glaucoma early. I thinkgoing to KPro early is a mistake if the long term KaplanMeier risk of retinal detachment is 50%.

Comment: In eyes with multiple surgeries, there is a lot ofscar tissue that can cause the glaucoma surgery to fail.

Q: How you can differentiate between a corneal meltand endophthalmitis?

A: It is difficult to tell, but the threshold for diagnosis ofendophthalmitis should be low.

Comment: Experience of the non-Boston KPro in Europe is the same in terms of retinal detachment andretroprosthetic membrane as well as endophthalmitis.

Q: What is your opinion in using an endoscopic approach?

A: Although I don’t have access to it, it may be helpful.


Q: Retinal complications of the keratoprosthesis include:

Retroprosthetic membrane . . . . . 0.0%Retinal detachment . . . . . . . . . . 0.0%Endophthalmitis . . . . . . . . . . . . . 1.4%All of the above . . . . . . . . . . . 98.6%

Q: Long term, topical use of which of the following isrecommended to prevent endophthalmitis?

Tobramycin . . . . . . . . . . . . . . . . . 0.0%Vancomycin . . . . . . . . . . . . . . . 97.0%Moxifloxacin. . . . . . . . . . . . . . . . 1.5%Povidone iodine . . . . . . . . . . . . . 1.5%

See Chung PowerPoint presentation, A.59

III. Endophthalmitis after Intravitreal Anti-VEGF Injections: 6 Years Ratesand Outcomes of Treatment at BPEIHarry W. Flynn, Jr. MD

PRESENTATION

The purpose of this presentation is toassess the rates of as well as to describethe clinical and microbiological features of eyes that develop clinically suspected

endophthalmitis following an intravitreal injection ofvascular endothelial growth factor (VEGF) antagonists.The current study is a retrospective consecutive caseseries from a University-based referral center and threeuniversity-owned satellite clinics, of patients undergoingintravitreal injections of anti-VEGF agents from01/01/2005 through 12/31/2010. The rates of endoph-thalmitis, clinical outcomes, and microbiological featureswill be presented.

Twelve cases (eleven patients) of clinically suspectedendophthalmitis were identified out of a total of 60,322(P=0.02, 95% confidence interval 0.0117 to 0.0359).Eleven of the twelve cases presented within 3 days of theinjection. Of the 7 culture-positive cases, 5 were due toStreptococcus species, 1 was due to Staphylococcusepidermidis, and 1 was due to Bacillus non-anthracis. Ofthe culture-positive cases, 3 achieved visual acuity of20/100 or better, but 4 had hand motions or worse visionat last follow-up. In 4 of the 5 Streptococcus cases, finalvisual acuity was hand motions or worse. Four of the fiveculture negative cases, by contrast, achieved visual acuitybetter than 20/100. The rate of clinically suspectedendophthalmitis was 0.023% after bevacizumab and0.036% after ranibizumab.


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In conclusion, there was a very low rate of endoph-thalmitis after intravitreal injection of anti-VEGF agentsin the current 6-year study. Patients typically presentedwithin three days of injection. Streptococcus species wasthe most common bacteria isolated and it was generallyassociated with poor visual outcomes.

HIGHLIGHTS

• Endophthalmitis after intravitreal injection is anuncommon but dreaded complication.

• A tap and inject is typically performed in these cases,with vitrectomy done in severe cases.

• True allergy to povidone iodine is uncommon.

• 4th generation fluoroquinolones are not effective inpreventing endophthalmitis.

• The use of povidone iodine is the most effective wayto prevent endophthalmitis.

• Post intravitreal injections have become optional formany.

• Although the rates of endophthalmitis after intra -vitreal injection is low, it is more frequently caused byStreptococcus compared to intraocular surgery.

• Antisepsis is more important than antibiotics.

NOTES

Dr. Flynn commented that a KPro is the only indicationthat he knows of where vancomycin should be kept up asa prophylactic drug.

Case Presentation: A photograph of an eye was shown.The patient had presented 1-2 days after intravitrealinjection. All the classic features are seen of endoph-thalmitis: fibrin in the pupil, hypopyon, redness andmajor loss of vision. If it is a bad organism such as strep-tococcus, it can occur very quickly.

Case Presentation: A patient presented with hand motionvision 4 days after ranibizumab injection. There is fibrinand a hypopyon. There isn’t much redness but a densevitritis is present. This patient was treated with tap/inject.

Tap/Inject TechniqueThe intravitreal antibiotics are prepared by the com -pounding pharmacy. Place the patient in the supineposition. Peribulbar anesthesia is used and the procedureis done either with the microscope or with loupes. Afterthe patient is anesthetized, a standard prep using povi -done iodine is used as well as an eyelid speculum. Aflexible 23-g butterfly needle is used to enter the eye.Watch the fluid come up the tubing and stop when thefluid begins to just enter the syringe. The antibiotics canthen be injected sequentially.

In severe cases, however, patients are taken to the ORand vitrectomy should be considered. Dr. Flynn’spreference is to use a 23g system for the vitrectomy and

give the standard intravitreal antibiotics. Fungalinfection after intravitreal injection is uncommon.However, one case of Myocabacterium after intravitrealtriamcinolone has been reported.

Eyes that develop endophthalmitis post intravitrealinjection should be treated like an acute onset postsurgical endophthalmitis after cataract surgery.

Case Presentation: A photograph was shown of a patientone day post treatment for endophthalmitis. Fibrin isseen retracting in the midpupillary space, which is anextremely good sign that the antibiotics are working. Onthe second day post treatment, the fibrin is clearing andthe hypopyon is a pink color, a mixture of blood andpurulent material. This case was coagulase negativestaphylococcus, which is why it presented at 4 daysinstead of one day, which often occurs withStreptococcus. The patient returned to 20/50.

Case Presentation: Photograph was shown to highlight thatthe eyelashes are curling down. It is possible the needletouched a lash and carried the organism into the eye.

Intravitreal Injection TechniqueAt Bascom Palmer, a lid speculum is used after preppingthe lid margins with 10% povidone iodine. No prein-jection antibiotics are used. After the conjunctiva isprepped with 5% povidone iodine, a pledget of lidocaineis used to touch the area of treatment and to massage thearea to lower the IOP. Non-sterile gloves are used duringthe injection. Post injection antibiotics have becomeoptional for many.

Dr. Rosenfeld at Bascom Palmer has performed over6,000 injections with no post injection antibiotics andhas had no cases of post injection endophthalmitis.

Povidone Iodine AllergySo what do we do when a patient states they are allergicto povidone iodine? There is confusion as to what constitutes a true allergy. The most common allergiesimpacting Ophthalmology are povidone iodine andpenicillin. An allergy is a disorder of the immune system.It is classified as types 1-4. Allergy typically refers to atype I reaction in clinical practice. It involves an IgEresponse to repeated exposure to a stimulant with mastcells, eosinophils and immune mediators that can cause a variety of reactions.

A study at the New York Eye and Ear Infirmary looked at8,000 eyes undergoing cataract surgery. Patients wereeither assigned to povidone iodine on the conjunctiva ora silver protein solution. The difference in the rate ofendophthalmitis between the two groups was significant.

Looking more closely at the issue of povidone iodine“allergy”, the most common effect is as an irritant. Thisoccurs in as many as 4% of cases. The povidone iodine


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can cause a chemical burn from prolonged contact. Thisis completely different from an allergy. There may be anallergic contact dermatitis, which occurs in <0.5% ofcases. This can be determined by patch and ROATtesting and is usually a limited effect that patientsrecover from quickly. Anaphylaxis is extremelyuncommon and is limited in the literature to generalsurgery, where large amounts are used and left behindafter surgery. In Ophthalmology, it is a different scenario.There is limited contact and it is washed out.

What about seafood allergy? This is caused by a specificIgE reaction. While seafood contains relatively highlevels of iodine, seafood allergy has nothing to do withiodine content. Therefore, it is important to ask aboutthe specific reaction. Additionally, the structure ofpovidone iodine is not similar to that of contrast media.If there is concern, one should consult an allergist.

The alternatives to povidone iodine are limited.Chlorhexidine (Hibiclins) is most popular in generalsurgery. Phisohex is too toxic to the conjunctiva, andTechnicare was pulled off the market.

Case Presentation: A photograph of a case of chlorhex-idine keratopathy was then shown which occurred after a9 hour face lift with chlorhexidine used to prep the face.

A recent Japanese study examined the effect of constantirrigation with dilute povidone iodine during cataractsurgery. 400 patients were divided into 2 groups. GroupA received no povidone iodine, whereas group Breceived 0.25% povidone iodine as a constant irrigation.There is normally a high rate of positive cultures inroutine surgery. So, a 5% positive culture rate for routinesurgery is typical.

At the start of the case, after standard prep, the culturepositive rate was 5% in both groups. But after constantirrigation during surgery, the anterior chamber cultureshowed 0 culture growth in the povidone iodineirrigation group versus 5% in the other group. There wasno difference in endothelial cell counts, but there was ahigher iodine concentration in group B. Interestingly,this is similar to what we do with intra vitreal injections.We bathe the eye with povidone iodine prior toinjection. So, it is the povidone iodine that is keepingthe rates of endophthalmitis low.

The time kill of povidone iodine is extremely short,being as short as15 seconds in some studies. The insetsays 2 minutes. Thus, the action of povidone iodine isalmost instantaneous.

At Bascom Palmer, in patients who are very concerned,we do a skin test by putting a little swab of povidoneiodine on the inner arm to show the patient thatnothing happens. So, don’t ignore the patient. Workwith them.

FluoroquinolonesThe other question is, do 4th generation fluoro-quinolones prevent endophthalmitis? The answer is no.We know that the fluoroquinolones penetrate into theanterior chamber, but penetration into the vitreous isnegligible. Even if it got there, how does it work againstcoagulase negative staphylococcus?

Looking back over the last 20 years, fluoroquinoloneswere shown to have less than 50% sensitivity tocoagulase negative staphylococcus. So even if it getsthere, it may not be effective. This is particularly truewith MRSA; only 15% were sensitive to fluoro-quinolones. Another study, the Ocular TRUST studyshowed similar findings..

Price is another issue. The average wholesale price offluoroquinolones is more than $90, whereas gentamicinand polytrim are much less expensive.

From Dr. Kokame’s presentation, looking at the 2009data, greater than 1 million injections were performed,one-third being ranibizumab and two-thirds, bevacizumab.Not even looking at the other intravitreal injectionssuch as steroids, this is becoming one of the mostcommon ophthalmic procedures.

A recent study at Bascom Palmer sought to identify therates of endophthalmitis after intravitreal injection inthe cases that were seen from January 1, 2005 toDecember 31, 2010. During this time 60,322 injectionswere performed. There were 12 clinically diagnosed andtreated cases of endophthalmitis. 7 were after bevacizumab,5 after ranibizumab and 0 after pegaptanib injection. 7 were culture positive and 5 were culture negative. The mean age was 80 years. 9 injections were performedby faculty, 3 by fellows and none by residents. Therefore,the rate of endophthalmitis was 12/60322=0.02% andthe culture positive rate was 0.01%. There was no statistical difference between the rates of endophthal -mitis with ranibizumab and bevacizumab, even thoughbevacizumab is prepared by the pharmacy and notprepackaged.

Of the culture positive cases, 5 were streptococcus.Others were caused by Staphylococcus. 5 were culturenegative. The culture negative cases had relatively goodoutcomes. The key is streptococcus. Those with thisinfection generally had bad outcomes.

Meta-Analysis of Endophthalmitis CasesIn this study, over 105,000 cases of injections wereincluded. There were 54 cases of endophthalmitis. Theisolates were divided into non-Streptococcus andStreptococcus. Out of 26 culture positive cases, 8 werestreptococcus and 18 were non-streptococcus, with onebeing bacillus cereus and all others being coagulasenegative staphylococcus. This is similar to what is seen


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after intraocular surgery. However, the rate of infectionsby streptococcus after intraocular surgery is 7-9%,compared to 30% by streptococcus after intravitrealinjections. Thus, there is a much higher rate of endoph-thalmitis caused by streptococcus with intravitrealinjections than with other intraocular procedures.

There may be a danger of breathing or talking orsomehow contaminating the needle prior to entry of theneedle into the vitreous cavity.

IN CONCLUSION

• The rate of endophthalmitis after intravitreal injectionwas very low in the series of 60,000+ injections atBascom Palmer.

• The most common organisms implicated were grampositive bacteria.

• Infections by streptococcus occurs 3-4 times higher withintravitreal injections than with intraocular surgery.

• Prognosis for vision is very poor with streptococcus.

• Antisepsis and proper technique is more importantthan antibiotics.

DISCUSSION

Q: Can you explain again the speed kill of povidoneiodine?

A: The more dilute strength appeared to have a fasterkill rate in the small studies presented. It is counter -intuitive and may be a case where too much of a goodthing is not good.

Q: Is there any role of post injection topical antibiotics?

A: It’s hard to understand the rationale for post injectionantibiotics. The entry point is self-sealing unless there isa large vitreous wick. The only reason is that it is a“community standard”, although there have yet been nocases that went to court for failure to give post injectionantibiotics. It is a disservice to the medical community toimply that you are under the standard if you choose notto use topical antibiotics.

Q: Is there is anything in the literature documenting theefficacy of not using post injection antibiotics?

A: The Bascom Palmer series was the closest, in whichall cases of endophthalmitis received fluoroquinolones.

Comment: The concern in the community is under-standable. Having Dr. Rosenfeld’s series where there wereno infections after using no post-injection antibiotics inthe literature would be very helpful.

Q: Who, in the audience, does not use topical antibioticsafter intravitreal injection?

A: Several raised their hands.

Q: Given the comments on streptococcus, does he use amask for injections?

A: Although some faculty at Bascom Palmer wear amask, I do not. I don’t talk over the patient and I tell thepatient not to talk.

Q: Is there a worry that by doing a tap/inject, we may beunder-treating streptococcus and possibly staph aureus?Should we take the position of being more aggressive inthese rare cases and perform vitrectomy?

A: In a streptococcus case, the horse is already out of thebarn. During vitrectomy in these cases, my experiencehas been that the vessels are sheathed and the retina isfeatureless so that the retina is already necrotic. Thereare no studies looking at this, but there may be some inpress. So, we do not have the answer yet. But, it isimportant to get treatment into the eye as fast as possiblein these cases. Waiting to get to OR may prolong treat -ment. Getting antibiotics on board fast is the concern.

Q: Do the culture results change the management?

A: If I get back streptococcus, I am more ready to re-injectwith vancomycin within 24-48 hours. If it is coagulasenegative staphylococcus, I am not as aggressive.

Q: How do you culture and what plates do you use?

A: If you can get 0.3 cc on blood and chocolate, it isadequate for the lab.

Q: Is using 10% povidone iodine on the eyelids animportant step. Also, if we can compound a 1% povidoneiodine solution, would it make sense to use this based onthe fact that it may have a faster time kill?

A: The studies on killing time have been limited, so wedon’t really know the answer. I am concerned about thelashes and lids especially during the process of insertingspeculum with the patient squeezing. So, cleaning the lidmargins is important, but there is no data to support it.

Comment: There is a dilutional effect on the eye surface,so the 5% used on the eye surface may be effectively less.So, prior to using a more dilute solution, we would wantto compare the efficacy in a study. The best study wasfrom the Japanese, but it was a continuous irrigation andwas with cataract surgery.

Q: Some people wash out the eye after the injection tominimize complaints. Do you do that?

A: In certain cases, but not routinely.

Q: Do you have experience with keeping antibioticsfrozen in the clinic since there’s usually a delay betweendiagnosis and getting the antibiotics prepared, especiallylate at night, and are they still effective?

A: It is done at Bascom Palmer and the shelf life is 30 days.

Q: If you are in a satellite clinic far from a lab, is usingblood culture bottles okay?

A: Pediatric culture bottle gives similar results, but agood microbiology lab is recommended.


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Q: Some people skip the povidone iodine and just usetopical antibiotics. Does anyone in the audience do this?

A: Antibiotics require hours to kill organisms. TheDRCR network will publish some cases of eyes that gotendophthalmitis after receiving only topical fluoro-quinolones when they stated that they had a povidoneiodine allergy.

The audience was then polled with no one using topicalantibiotics instead of povidone iodine.

Comment: With over one million injections that aregiven a year, each patient needs to get a new bottle offluoroqinone each time. So, each time, the fluoro-quinones kill off the good bacteria. What you have leftwith is a hypothetical 80 year old patient coming everymonth to get an injection and every month getting afluoroquinolone, which builds up resistance.

Comment: Culture and sensitivity of the conjunctivalshowed that there was 5% resistance to fluoroquinolonesat 3 months.

A: It is an issue that will probably change people’s minds about antibiotics. Especially in patients that need11-12 injections a year, the fluoroquinolones may reallybe just separating out the bad bugs and letting themthrive while killing off the weaker coagulase negativestaphylococcus.

Comment: There are a handful of cases moving throughthe courts concerning endophthalmitis after intravitrealinjection. The issues in these cases have not been postinjection topical antibiotic use but have been the failureto use povidone iodine. In his opinion it is indefensible.The other issue is the failure to document an informedconsent process in the chart. So, from a risk/litigationperspective, use povidone iodine and have an informedconsent process in the chart.


Q: For my intravitreal injections, I use the followingantibiotic prophylaxis.

Fluoroquinolones . . . . . . . . . . . 26.2%Polymyxin B/trimethoprim. . . . . 9.2%Gentamicin . . . . . . . . . . . . . . . . 13.9%None . . . . . . . . . . . . . . . . . . . . . 50.8%

Q: In the prevention of endophthalmitis, antiseptics are more important than antibiotics.

True . . . . . . . . 100.0%False. . . . . . . . . . . 0.0%

See Flynn PowerPoint presentation, A.64

See PDF handout: Allergy to Povidone Iodine and Cephalosporins, A.71

IV. TAYLOR SMITH LECTUREThe Practice Environment of Retina in 2015: What’s the Prognosis?David W. Parke, II, MD

PRESENTATION

2015 is effectively right around thecorner. The odds are that only about 250of the current population of American vitreoretinal specialists will retire before

that time. Therefore, it matters to just about everyone. It is also to be the ‘tipping point year’ for the Americanphysician community—including vitreoretinal specialists.How the practice of vitreoretinal surgery appears in 2015will give an unusually strong glimpse of the look for thefollowing decade.

What is the prognosis for 2015? It will be driven by some unpredictable factors (meteor strikes, etc) but alsoby some predictable ones. These include:

• The perceived cost trend in healthcare delivery

• Ophthalmology’s (and vitreoretinal surgery’s) disease-specific costing trends

• The funding of healthcare under Medicare/Medicaid

• The delivery structure of healthcare/eyecare underMedicare/Medicaid

• Ophthalmology’s position under Accountable CareOrganizations (or their successor structure) and othermodels of healthcare delivery

• The consolidation of every aspect of the eyecare business

• Demographic issues facing the vitreoretinal community(both supply and demand sides)

• Perception of access issues to vitreoretinal care

• The position of vitreoretinal specialists in thecontinuum of care delivery

• National and local quality of care initiatives in vitreoretinal surgery

• Funding of research and scientific innovation

• Impact of comparative effectiveness research

• New technology

Why focus on 2015? 2015 is projected to be the transitionyear both in the Accountable Care Act and in some ofthe key demographic and economic drivers. If the vitreo-retinal community denies some of the realities facing it,the prognosis will be grim. If individual practitioners andorganizations prepare for it, there are opportunities tonot simply persevere, but to flourish.


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Q: The primary sources of medicare funding are:

Part A (hospitals) from beneficiary premiums and Part B (physicians) from general revenue . . 16%Part A (hospitals) from general revenue and Part B (physicians) from general revenue . . 44%Part A (hospitals) from general revenue and Part B (physicians) from payroll taxes . . . . . 27%Part A (hospitals) from payroll taxes and Part B (physicians) from general revenue . . . . 14%

Q: Most sources estimate that the average medicarerecipient will need to fund how much over their lifespanoutside of medicare’s payments?

$50,000 . . . . . . . 12.1%$100,000 . . . . . . 45.5%$200,000 . . . . . . 31.8%$400,000 . . . . . 10.6%$800,000 . . . . . . . 0.0%

Q: Who said the following: “Because of…the fact thatmost of the coverage provisions [of the Affordable CareAct] would be in effect for only 6 of the 10 years of thebudget period, the cost estimates…do not represent a full 10 year cost for the new legislation”?

President Obama. . . . . . . . . . . . . 4.8%Tom Coburn . . . . . . . . . . . . . . . 14.5%WSJ . . . . . . . . . . . . . . . . . . . . . . 25.8%CMS Chief Actuary . . . . . . . . 32.3%Paul Ginsberg . . . . . . . . . . . . . . 22.6%

NOTES

The Academy’s role is to represent our profession and tofight for the needs of our profession, and recognizing thatour profession’s needs and society’s needs are truly inter-twined. We are a very heterogeneous group. The bottomline is that most of us are confused by the claims andcounterclaims.

The question is, is it a brave new world orArmageddon?Take home messages are:

• Listen to your patients (fellow citizens).

• Put the interest of your patients first.

• We have an opportunity to search for congruencebetween our interests and our patient’s interests.

So, what are the big drivers for the year 2015?• Money

• Demographics

• The ACA bill.

What are these supposed to do?All are supposed to end up decreasing cost. We have todrive total system cost down.

The next is to increase quality. There are great examplesin recent years such as decreasing the rate of infectionswith central lines. It can be done. Secondarily it will cut costs.

Provide “appropriate” access that deals with the issue ofhealth care needs versus health care wishes.

When we talk about the ACA, remember that everypage of legislation typically leads to 10-20 pages ofregulation. The ACA is 2700 pages long. What thismeans is that even though the bill is passed, what willhappen in the next 5-10 years is over 20,000 pages ofregulations will be created. This gives us, as physicians,an opportunity to modify these regulations.

Why focus on 2015?A lot of the major impacts of the ACA come together in2015. Not a lot in 2011 or 2012 have a major impact onus as practicing physicians.

Some background on how we got to where we are. This is an overview of the economics:

Using 2006 as a baseline, there are $2.2 trillion in healthcare costs. It was projected at that time to rise to 20% ofGDP by 2019. That seemed like a long way off in 2006.It’s not a long way off any longer. Interestingly, 22% ofthis goes to physician services, and half is paid by federaldollars. Looking at the 2009 budget, which is a $3.1trillion budget, federal health care expenditures are $700 billion.

Breaking down the federal component, medicare is more than 50% of it. Medicaid is also a large part of it.“Budget dust” remains for the NIH, CDC, FDA. So,really it is medicare and medicaid that run things.

It is important to know how medicare is funded. Part Agets 85% of its funding from payroll taxes. The money isguaranteed and is not really at risk, so the hospitals arenot at risk. Looking at Part B, approximately 75% ofwhat we get paid from medicare is at risk every singleyear. We, as physicians, are the most vulnerable recipientsof medicare compared to hospitals, pharmaceuticals, etc.Going back to the second audience response question, itis estimated by financial institutions that if you retiretoday, you will have to pay $400,000–500,000 aftermedicare. The median value of retirement accounts ofpeople age 65 is $60,000. In other words, they are facinghealth care costs of $400,000 and they only have$60,000. This is the main reason private contracting isdead on arrival. There is no place to shift the costs to.


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Medicare beneficiaries have had a 40% increase inpremiums in recent years. Now they pay between $110-$350 a month depending on income with a 0.9%surcharge on top.

There may still be ways to fix this. Putting the economicstogether, there is no appetite in congress to create a truefix to the SGR for about $600 billion. Switching todemographics, the second driver, the baby boom does nothit until 2010. Between 2010 to 2015, the number ofseniors that we see will increase by 15%. We don’t havethe capacity. Also, the seniors today are using healthcaremuch more intensively than they used to. So, there aremore seniors, and they will be using health care intensively.

The third driver is the ACA. Focusing on physicianpayment, the first thing to know is the IPAB (IndependentPayment Advisory Board). It is a group of individuals(15) that are appointed by the president that isappointed to reduce health care costs. The only tool, bylaw, they will have to bring health care costs undercontrol is to decrease physician payments, not hospitals,overhead, durable goods or pharmaceuticals. Theabsolute top priority of the Academy is to get IPAB outof this. We would rather have congress deal with thisthan have 15 people whose only tool is to cut how muchphysicians get paid.

The next part of this is the value based modifier. As partof the ACA, CMS is mandated to pay more for qualityand efficiency and less for the reverse. Again, 2015 iswhen this will be applied to some physician paymentsand will apply to all by 2017. It will have to be “budgetneutral”, which means there will be winners and losers.Glaucoma and cataract are in the top 25, but rightbehind is diabetic retinopathy. The delta between thebonus and the penalties is unknown, but it’s likely to bearound 10%. We will be measured on our resource useper episode of care or on a per capita population basis,but the details are not yet written.

Those physicians outside 2 standard deviations from themean will be either penalized or rewarded. We knowsome of the problems that will arise such as regression tothe mean and how to make sure patients are not gettingless care than they need. There are a lot of questions andproblems.

Shifting to the SGR, the total physician revenue frommedicare has gone up despite freezes because we are moreproductive than we used to be. Over one decade, eventhough our payment per procedure went down, theamount that Ophthalmologists got paid went from $3.9Billion to $5.1 Billion. This is with about the samenumber of Ophthalmologist and statistically working the

same number of hours per week. The reason for thisincrease in pay is that we are more efficient. However,there is a limit to that. The point is that, so far, we haveabsorbed a lot of this on the basis of increased efficiency.

Shifting topics, the administration wants to get awayfrom the SGR. There is a $62 billion cost just to fix it for 2 years. At this point a 10 year fix, not a total fix, is$315 billion. Why does the government want to fix theSGR? They are worried about access to care.

So, some may propose that we stop seeing medicarepatients. However, there is no data that there is asubstantial amount of physicians dropping out ofmedicare. A few communities and specialties are beingwatched very carefully by CMS, but not Ophthalmology.

Next to geriatrics, Ophthalmology has the highestpercentage of geriatric patients. As medicare goes, so do we. Even if all the SGR cuts went into place, thephysician cost will continue to rise. What a lot of healthcare economists are thinking right now is to discard theSGR and to perhaps index physician payments to themedicare index.

Now, regarding new patients, there will be 33 millionnew patients that will have coverage that didn’t have itbefore. It will not have an impact on medicare or AMD,but to pediatric retina and diabetic retinopathy. Thereare provisions to encourage remote screening for ROPand diabetic retinopathy.

Medicaid will expand. There will be 20 million newmedicaid patients. For those that have been seeingMedicaid patients in the past, it will depend on theregion whether seeing more patients will make up for the cuts.

Shifting to PQRI, Ophthalmology has the highestpercentage of physicians getting PQRI bonuses. PQRIhas now turned into PQRS and the bottom line is thatthe bonuses start to go away and the penalties build up.Now there are a whole series of bonuses and penalties.For example, with e-prescribe, the bonuses turn intopenalties in 2014. The quality issues are focused on agroup of diseases that has been prioritized by the instituteof medicine, and diabetic retinopathy is in the top 100conditions.

The other area of penalties is the EHR. In 2015, theincentives go away and the penalties start to pick up.

The last major topic is ACOs (Accountable care organi-zations). 50% of medicare beneficiaries have 5 or morechronic diseases and are responsible for ¾ of Part A andPart B expenditures. That group of patients has 14different physicians on average. The rationale is that


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getting all these physicians together will improve qualityand lower costs. Within the ACA, there is an ACO.ACOs are similar to other integrated systems such asKaiser, but there are important differences. The first isthat they have to have at least 5000 patients. They alsohave to promote evidence based medicine and have toreport on quality. Data becomes critical. They also haveto coordinate care and be patient centered. There are alot of different types of ACOs – from Kaiser–like systemsto multispeciality groups to virtual physician organiza-tions. CMS wants to encourage virtual physicianorganizations.

ACOs will not be successful unless they substantiallylower costs and maintain or improve quality. Within thebill, it specifically says that the secretary of health andhuman services can, without any further congressionalaction, move to any payment model he/she wants.

What does this mean for us in retina?

All of us will be approached by hospital systems to be apart of their ACO. Everyone in an academic system isalready in an ACO. ACOs are buying doctors andcontracting with those they can’t buy. For the physiciandriven ACO model, it will be an exchange of somefinancial incentive, such as an EHR, for agreeing tofollow the standards and regulations of the system. Thekey is that data is shared with their IT system. Some willbe good systems. Some will have exclusivity agreements.

This kind of integration is intended in the ACA.Vertical integration and physician employment byhospitals is the goal of the bill. For example, 50% ofcardiologists are now employed by hospitals, the numberof orthopedists employed by hospitals have doubled,neurosurgeons and primary care. Ophthalmologists areoff the radar which allows us to retain a potential forindependence.

Interestingly, ophthalmology incomes have beenincreasing greater than the rate of medical inflation dueto efficiency and the E&M payments.

We are moving from a pure fee for service to beingreimbursed per episode basis through an ACO withpossibly a bonus or penalty on outcome and service.

As part of the ACA, there is a physician directory toolcalled physician compare. The goal is that by 2015, a lotof quality metrics and outcome data will populate thiswebsite. However, is the data going to be clean, will it berisk adjusted, etc?

IN CONCLUSION:

• A lot is going to be changing. In the 1960s, medicarewas just a change in payment. What will be changingnow will be: the structure of your practice, how we getpaid, how much we get paid, how your performance isjudged, how you will be valued as a physician.

• There is a lot of pressure to reduce total system cost.

• If we can propagate standards of care based on realdata that we can agree on, it will improve quality.

• We do have opportunities to effect positive regula-tions, such as getting rid of the IPAB.

• We are in a highly desirable position. The hospitalsdon’t want to own us, but they need us. So, we havean opportunity to control our destiny in a way that alot of specialties don’t.

• Every one of us plays a role in advocating.

DISCUSSION

Q: In the initial discussion for this bill, the AMA wasleading the charge. Do they have a better understandingnow?

A: The AMA’s major problem was that the board oftrustees acted without getting enough input at the grass-roots level and without communicating a lot of theissues. The percentage of physicians that are AMAmembers is at an all time low. Which is why specialtyorganizations now have more opportunity to be effective.93% of Ophthalmologists are part of the Academy.

Q: The challenges of the health care system are somassive that the only way this problem will be solved iswith a heavy hand of regulation with a threat ofpenalties and price cuts. As a physician, we can do eitherof 2 extremes: limit what we do, or develop new ways ofdelivering care. I don’t know what those are, but wouldlike your input.

A: There are realities we can’t get away with. Just say nois no longer a strategy. We have to find another pathforward. Our efficiency gains in the past have not beenmaxed out. What we need to look at are new models ofcare. Options include utilizing NPs, PAs, optometrists orcoming to together in larger groups. We are a heteroge-neous group, so there is no single model that will workfor everybody. It is important to go back and look back atwhat we do. If we can increase throughput, keep qualityhigh and not significantly affect service, then we will bein a sweet spot.


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Q: How do ACSs fit in the ACO model?

A: The goal of the ACO is to deliver care at the lowestcost and highest quality. If there is an independent ASCthat demonstrates that, it will be asked to be a part ofthe system. But, it is all about the data – outcomes,processes, etc.

Q: If we cure diabetes, we will cut costs significantly.What do we do to try to educate people?

A: I don’t know the answer, but at the end of the day alot of this is politics and not policy.

Q: Another speaker stated that physicians account for6% of health care expenditures rather than 22%. Also,his vision of ACOs have the hospitals taking the big cutssince they are inefficient?

A: 22% is the correct number for medicare. Althoughthe part physicians get paid is 22%, the part of thehealthcare the physician controls is close to 100%. Thatis why physician behavior is the lynchpin for a lot ofhealthcare reform. The early cuts will come from thehospitals but the long term cuts are from physicians.

Q: 2/3 of us are using Avastin over Lucentis because it’ssaving the government money. Will that be rewarded inthe future or is the pharmaceutical lobby too powerful?

A: The way you get rewarded will be based on cost andquality. What they are looking for is not individual costbut cost per episode care and total system cost, not aquestion of drug A versus drug B.

Q: Can you comment on the optometry bill inKentucky?

A: To summarize, a bill was signed in Kentucky thatgives optometrists the right to do anything they wantbecause one part of the bill allows them to define whatthey want to do. It specifically allows them to giveintravitreal injections. They were given the opportunityto get that out of the bill, but did not. He then gave asynopsis of the events that led to its passage as law. Thebottom line was money. Optometrists contributed$400,000 to state legislatures in the months precedingthe vote. Ophthalmology had given $10,000. There arelessons to be learned from this, but what this means isthat more states will be facing this so that it is an issuefor all of us.

See Parke PowerPoint presentation, A.74

WednesdayM A R C H 9

I. Microincision Vitrectomy 2011: New Instrumentation and TechniquesAllen C. Ho, MD

PRESENTATION

New vitrectomy system platforms haveevolved into integrated surgical systemsthat afford the surgeon greater control in the individual surgical steps of

vitrectomy and also in tissue control and manipulationin the eye. High speed cutting vitrectomy probes withport optimization allow better flow even in smaller gaugevitrectomy. Duty cycle control affords another level oftissue control in the eye, for example, when shavingvitreous near mobile retina.

25g vitrectomy probes, endoilluminators, and handheldinstruments are now more rigid and have improvedperformance -approaching the performance of the 23gplatform. 27g platforms are being developed as well. The vitrectomy probe has become a more sophisticatedinstrument by design and by surgical technique, oftenobviating the need for other instruments such as scissors in cases of diabetic traction retinal detachment.Improved wound architecture created by MVR liketrochar cannula systems have engendered more confi-dence in sutureless microincision vitrectomy and havebeen a significant advance. Illuminated instrumentationsuch as endolaser probes and tissue picks also improveour surgical capabilities.

In many ways, these advances in technology haveimproved the access of high quality vitreoretinal surgicalcare to more patients who require them; that is, theseadvancements are no longer confined to few select insti-tutions but rather are available to most retinal surgeons.

HIGHLIGHTS

• Advances in vitreoretinal surgery have been beneficialfor both surgeons and patients.

• Control of the duty cycle allows for safer and moreefficient vitrectomy.

• Small gauge cutters can minimize the need for otherinstruments.

• Valved cannulas are available and create a more closedsystem during vitrectomy.

• The ozil may be more efficient than the fragmatome inremoving hard nuclear fragments.


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• We are very fortunate to have integrated vitrectomymachines as opposed to the “stack” of years ago. Ourpatients are privileged as well since advanced vitreo-retinal surgical care is now available to everyone andnot limited to a few centers.

• Over the past few years, many people have adoptedsmall incision surgery. There are several systems, all of which are excellent.


Q: When removing an epiretinal membrane (20/50 with mild macular edema), I prefer:

25g peeling ERM . . . . . . . . . . . 11.4%23g peeling ERM . . . . . . . . . . . 18.2%20g peeling ERM . . . . . . . . . . . . 2.3%25g peeling ERM and ILM . . . . 31.8%23g peeling ERM and ILM . . . . 31.8%20g peeling ERM and ILM . . . . . 4.6%

For most of his cases, Dr. Ho will peel both ERM andILM, although he is not sure we have to do both.

Q: When removing hard nuclear retained lens fragmentsafter complicated cataract surgery, I would prefer to use:

25g vitrectomy cutter . . . . . . . . . . . . . . . . . . . . . 0.0%23g vitrectomy cutter . . . . . . . . . . . . . . . . . . . . 13.3%20g vitrectomy cutter . . . . . . . . . . . . . . . . . . . . . 4.4%20g fragmatome. . . . . . . . . . . . . . . . . . . . . . . . . 80.0%20g Ozil phacoemulsification hand piece . . . . . 2.2%

NOTES

Until a few months ago, the fragmatome would be hisgo-to tool, but now with hard pieces, he uses the Ozilafter taking off the infusion portion and enlarging thesclerotomy to a 19g. The technology of the sweepingultrasound seems to give more followability.

Duty cycle is the excursion of the cutter from closed toopen. Core duty cycle is where the cutter is open 70% ofthe time and 30% closed. Shave is where it is flippedwith the cutter open 30% and 70% closed. Shave ishelpful with mobile retina.

VIDEO PRESENTATIONS

Video of 25g+ system used to remove vitreous hemor-rhage. The 25g+ system is a big improvement. It movesvitreous more efficiently and the instrumentation is notas flexible as the previous system.

Video of shave mode at 5000 cuts/minute, which is 160cycles per second. In shave mode, where it is only open30% of the time and closed 70% of the time, it allowsyou to get close to mobile retina.

Video of patient with a giant retinal tear, using shavemode over mobile retina.

The new cutters have reduced the need for other instru-ments since the mouth is larger and moved toward theend, more like a real end cutter. Most complicateddiabetic tractional retinal detachments can now be donewith the vitreous cutter themselves. There has beenalmost a doubling of flow rate between the 25g and 25g+system.

Video of surgery for proliferative diabetic retinopathy/tractional retinal detachment. A chandelier is used toilluminate. Forceps are used in the left hand and thetissue is approached from the top of the tissue, peelingback gently with the forceps to delaminate.

Video of Dr. Berrocal using viscodissection. A 23g cutterwas used to delaminate tissue.

Finding the spaces in between the pegs of attachment isimportant in these cases, as the pegs of attachmentreflect where the neovascularization is. The cutter can beplaced in the potential space to delaminate. Anothertechnique is sitting on top of the tissue and pressingdown. David Boyer coined the term ‘depression delami-nation’ which allows the tissue to fall back into thecutter to allow safe delamination.

When things get difficult, there is a new illuminatedmembrane pick. The end of the pick is malleable so thatthe angle of approach can be modified.

Trocar Insertion: Most surgeons are doing an obliqueincision with conjunctival displacement. There are newvalved cannulas as well as a 6mm infusion cannula. Thenew blade design is a significant improvement. Thewounds look better and are linear internally. The nosecone of the new trocars are longer which allow you toget around the speculum and the back end givesmarkings for trocar placement. Wound closure is veryimportant.

Infusion Cannula: The infusion cannula tubing is alsomodified so that the distal end is more flexible and thebore of the tubing is larger to allow greater flow.

Video: The cannula system is pulled over a solidinstrument to prevent any suction of vitreous into thecannula creating a vitreous wick. Instead of using acotton tip, a solid instrument such as a muscle hook isused to massage the wound. If there is any question, asingle 8-0 vicryl pass is placed across the middle of thewound through conjunctiva and sclera. Subconjunctivalvancomycin and steroids are used in most of the cases.

In pulling out the cannula, support the wall of the eyeand then grab onto the cannula system. Eversion of thewound may cause leaks in the other wound and cause the pressure to drop, subsequently causing choroidalhemorrhage.


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Video: (Valved Cannula) The valves in these cannulasare low friction valves, but sometimes instruments docatch. A new retention feature will prevent pulling outthe valved cannula system. An advantage of the valvedcannulas is that the pressure can be raised to 60mmHgand they do not leak. Valved cannulas help provide IOPcontrol giving a very good closed system which allows usto operate at lower pressures. Instead of 35mmHg, Dr. Hooperates at 20mmHg or lower. Sometimes, however, itcan be difficult to get a soft tip through the cannula andit needs to be fed through.

The valve system also allows ICG staining withouthaving to plug a cannula and can enable shaving withscleral depression with no leakage from the valvedcannulas.

Illumination: Illuminated curved laser probes allowdepression anteriorly. Dr. Ho brings the tissue to wherethe illumination is. The chandeliers are also useful andimproved with much better now with wide illumination.The chandelier is easily placed through a 25 or 23gcannula.

Transillumination techniques for depression are useful for shaving the anterior vitreous base. Even in phakicpatients, this technique can be used to shave the anteriorvitreous without disturbing the lens. Sometimes, theinfusion cannula can be rotated to allow better access.You can’t, however, see the posterior fundus very well,but the area of interest is well illuminated with transillu-mination and tissue staining. Overall, the illumination inthe current systems is much better.

Crystalline Lens Removal: A 25g system can be used inmany cases of retained cortical lens material. In caseswhere there is retained nuclear material, the fragmatomewith poor followability of nuclear fragaments can be veryfrustrating. As an alternative, the anterior segment ozilhandpiece with the infusion sleeve removed can be usedto remove the nuclear fragment. Ozil is a sweeping typeof ultrasound which allows more followability and ismore efficient. There will, however, be a 23g fragmatomecoming out later this year.

Submacular Hemorrhage Video: Extensive submacularhemorrhage in patients with age related macular degen-eration usually indicates the presence of a RPE tear. Ininterested patients, subretinal TPA can be used with a41g needle. The potential space should be opened withadequate fluid and the TPA (25 micrograms/0.1cc)should be injected in the inferior aspect of the hemor-rhage to allow the blood to be displaced inferiorly.

In summary, we are very lucky to be able to provide highquality care to all of our patients.

DISCUSSION

Comment: This talk highlights a quandary of thesemeetings. Some may think that Dr. Ho speaking aboutone platform is a commercial bias, but I believe thatpeople should talk about what they know and do andbring into the discussion other platforms.

Comment: Negative results being presented by presenterswho have had a part in development of the instrumentor platform have been miniscule.

Comment: The number of negative reports, in general,that are presented are negligible regardless of whetherthe presenter has a financial relationship or not.Negative results can be even more important thanpositive ones, but are difficult to publish as demonstratedby the trends in the major Ophthalmology journals. It isnot the financial relationships that sway against negativeresults, but rather personal nature to want to presentpositive results in front of colleagues.

Q: Is there any update on the 27g system?

A: It is in the works.

Q: Have you noticed any decrease in the incidence oflate recurrent vitreous hemorrhage after 25g surgery?

A: It is still a problem and my clinical sense is that it hasnot decreased significantly.

Comment: With valved cannulas, putting in a soft tip canbe difficult and using a 30g needle to displace one of theleaflets during entry can be helpful. Also, one of theconcerns of using the Ozil system is thermal effects.Enlarging the wound allows flow around the instrument,but it is important to watch the sclera.

A: It is important to pay attention. Also, enlarging thesclerotomy to 19g allows flow of fluid and heat transfer.

See Ho PowerPoint presentation, A.81

II. Vitreoretinal Management of Anterior Segment ComplicationsGregg T. Kokame, MD, MMM

PRESENTATION

As anterior segment surgery for cataracthas advanced, the management ofcomplications associated with anterior segment surgery by the vitreoretinal

specialist has also required modification and advances.Manage ment of dislocated implant and dislocatedcapsular tension rings will be discussed, as well as adjust-ments recently made to manage complications related tonew implant design and clinical presentation. In-the-bag


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IOL dislocations have become the most common presen-tation, and management options will be reviewed.Special case situations will be presented withmanagement options.

HIGHLIGHTS

• Many trends in cataract surgery have changed andhave affected how we manage vitreoretinal complica-tions.

• It is important to place a suture in the clear cornealincision prior to vitrectomy.

• Single-piece IOLs are becoming more common. If theyare repositioned, they should not be placed in thesulcus.

• There has been an increase in the number of in-the-bag IOL dislocations.

• For dislocated IOLs, the trend has shifted toward morebeing exchanged rather than being repositioned.

• IOL haptic externalization techniques are safer thaninternal looping when repositioning an IOL.

• A number of things have changed in cataract surgery.One is the change to clear cornea incisions. PMMAoptics to foldable optics is also a very clear trend.Multifocal IOLs and capsular tension rings are alsonow more common.


Q: Do you put a suture in the clear corneal incision priorto beginning vitrectomy, if one is not present?

Yes . . . . . . . . . . . . 59%No . . . . . . . . . . . . 41%

Q: Do you recommend to your anterior segmentcolleagues to put a suture in the clear corneal incision, if they are going to refer for vitreous surgery?

Yes . . . . . . . . . . . . 60%No . . . . . . . . . . . . 40%

It is very difficult thing to ask of the anterior segment,but Dr. Kokame asks his anterior segment colleagues todo that.

NOTES

Clear Corneal IncisionsClear corneal incisions have become very popular andmost surgeons use this now. They are excellent inminimizing astigmatism but there is a significant risk ofleakage since they are temporal. When we put in ourtrocars, we are putting them in temporally, right behindthe clear corneal incision. A lot of times, the wound willopen and the eye will become hypotonous. Therefore, itis very important to put a suture in if there is not onepresent. A series of cases was published where patientslost a significant amount of vision after developing achoroidal hemorrhage from that short period of

hypotony. A simple thing to do is to put a suture in toprevent vision loss.

IOLsAnother thing that has changed is that we have gonefrom rigid PMMA optics to one-piece IOLs. Now wehave the premium multifocal or accommodating IOLs.Foldable IOLs are much more challenging to reposition,but we still can reposition them. The single piece IOLsare much thicker and should not be placed in the sulcus.Placing them in the sulcus can cause significant irischaffing and recurrent vitreous hemorrhages. The under-surface of the iris of an eye with a sulcus placed singlepiece IOL was observed with an endoscope and showedthat it was completely white in the midperipheral iris. Ifyou are going to fixate these lenses, he recommendsgoing further back, to 2-3mm behind the limbus and tonot iris fixate these lenses.

Another trend is the use of capsular tension rings incases of zonular weakness or loss. A capsular tension ring,however, does not prevent an in-the-bag IOL dislo-cation. Many case reports have demonstrated completedislocation of the IOL-bag complex 2-7 years aftersurgery.

Removal of Capsular Tension RingsA case was then shown of a dislocated capsular tensionring. The capsular tension ring has a large diameter andis difficult to remove since the trailing edge can damagethe retina during removal. The other way to remove it isto use the original inserter for the capsular tension ring.During vitrectomy the ring can be placed back into theinserter. This is a very safe way of removing it.

Dislocated IOLs and IOL RepositioningThere has also been a shift in the type of dislocatedIOLs. Dr. Kokame now sees more in-the-bag dislocationsand one-piece IOLs. There are four management optionswhen dealing with a dislocated IOL. The same IOL canbe repositioned. If there is good residual capsule, theimplant can be placed back over the capsule. If goodcapsule support is not present, the IOL can be replacedwith scleral fixation or with iris fixation. The IOL canalso be exchanged with either an anterior chamberimplant or a scleral fixated implant. In some cases it isbetter to just remove the IOL. And, in some cases withpoor prognosis or systemic health, it can be observed.

In 2000, Dr. Kokame presented at the AAO a series of41 cases. At that time, he was repositioning 83%,exchanging 12% and removing 5%. In another seriesfrom Bascom Palmer of 110 cases in the same year, 84%were repositioned, 15% exchanged and 1% removed.The trend has changed with more now being exchangedfor an anterior chamber IOL.


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It is important to note that anterior segment surgeonsconsider 1.25D of astigmatism a complication. Thedemands are much higher now and we should try tominimize astigmatism.

When there is a complete 360 degrees of residual capsule,it is easy enough to position the lens above the capsule;these patients usually do well. If there is less than 5 clockhours of capsule remaining, Dr. Kokame recommendsthat the capsule not be used since they tend to dislocatelater on. With late dislocations, even if the capsule looksintact, there is probably something wrong with the capsuleand zonules, so the capsule should not be used. Anotherpoint was to remove the entire capsule if it is not goingto be used. The capsule will only get in the way.

There is a controversy of IOL repositioning versus exchange.In the US, many people are using ACIOLs. In Hawaii,the referring doctors demand scleral fixated PCIOLs. InAsia, most prefer scleral fixated PCIOLs as well.


Q: What is your first preferred management option fordislocated implants with poor capsular support?

Reposition with scleral fixation sutures . . . . . . . . . . 12%Exchange with anterior chamber IOL . . . . . . . . . . . 73%Exchange with scleral fixated posterior chamber IOL. . 6%Remove IOL . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6%Refer patient . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2%

Comment: There has been a trend toward iris fixationand away from scleral fixation in the past 5 years.

To this, Dr. Kokame stated that it is a fine technique for3-piece lenses, but we will not be seeing a lot of theselenses soon. If it is a 1-piece lens, it should be eitherexchanged or scleral fixated. He emphasized that youshouldn’t iris fixate 1-piece IOLs since they will causevitreous hemorrhage, hyphema and glaucoma.

The advantage of repositioning is that you are using thesame IOL with the same refractive power, there is nolarge limbal incision, which minimizes astigmatism, andthere is less surgical trauma. The disadvantage is redislo-cation risk if the suture slips or degrades, technicaldifficulty and it also takes time and patience.

The other reasonable choice is to exchange the IOL with an ACIOL or a posterior chamber scleral fixatedimplant. It is much quicker, but the disadvantage is thatit induces much more astigmatism and is potentiallymore traumatic.

In terms of repositioning, many techniques have beendescribed. The problem is that it is a difficult procedure.Dr. Kokame believes that any technique using internallooping is not a safe procedure. He has not done any

internal looping for years. Instead, he uses a haptic exter-nalization technique. Clement Chan was the first todescribe it. Whereas he used a par plicata fixationsclerotomy and externalized the haptic through thefixation sclerotomy, Dr. Kokame usually externalizes thehaptics through a clear corneal incision and then passesthe suture back. In hapic externalization, the haptics canbe externalized either through the fixation sclerotomy ora clear corneal incision. Thicker haptics fit through thefixation sclerotomy better. How you suture the haptic tothe sclera is very important. A separate 10-0 prolenesuture is passed to close the fixation sclerotomy site. Thesutures that are around the haptic are then tied in oneknot to the sutures that are closing the fixationsclerotomy site.

In the original publication, there were 15 eyes with alldifferent displacement types: 3 subluxations, 11 disloca-tions into the vitreous cavity, 1 in-the-bag dislocation.Now, the majority of cases are in-the-bag dislocations.The benefit of this technique is that you immediatelystabilize the dislocated implant. There were no signif-icant complications from the clear corneal incision orfrom manipulation of the IOL in the anterior chamber.

Some tips for externalization include using a bimanualapproach, visualizing the tip of the haptic and grabbingthe tip and following the curve during externalization. 1mm may be anatomically correct, but Dr. Kokame prefers2mm for polypropelene haptics and 2-3mm for the thickone-piece IOLs.

VIDEOS

Video of a case in which a sulcus PCIOL was implantedover a capsulorrhexis but there is a dislocated siliconeplate IOL in the vitreous. Dr. Kokame managed the caseby first doing a vitrectomy and removing the siliconehaptic IOL through a 4 mm pars plana incision withpreplaced 8-0 nylon sutures. The patient recovered 20/40 vision and did well.

Video of a complete nucleus on the retina with a dislo-cated IOL on top of the nucleus. With the implant soaccessible, the IOL was first repositioned after avitrectomy. The nucleus was then removed with thefragmatome.

The alternative was to remove the entire nucleus andIOL through a large limbal incision and to place anACIOL.


Q: Have you seen an increased incidence of in-the-bag IOL dislocation?

Yes . . . . . . . . . . . . 60%No . . . . . . . . . . . . 40%


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Dr. Kokame has seen an increased incidence. Pseudo -exfoliation only explains a part of it. He has seen it inuveitis patients and post vitrectomy.

VIDEOS

Video of an in-the-bag IOL dislocation. One option is toremove the entire complex through the limbus andexchange it for an ACIOL or to scleral fixate theimplant, which would induce a significant amount ofastigmatism. Dr. Kokame prefers to remove the capsulefrom the IOL and to refixate the PCIOL.

Video of scleral fixation sclerotomy made 2mm posteriorto the limbus. The capsule was removed from the IOLand the IOL was scleral fixated with no additionalcorneal or limbal incision.

Video of a dislocated synchrony dual optic IOL, which isnot yet FDA approved. It is a large foldable lens thatgoes into the capsular bag. 2 years after implantation, thepatient developed an in-the-bag dislocation. Since it wasa large lens, it was removed through a limbal incision.

The major points are:

1. Place a stitch over the clear corneal incision. It is asimple thing you can do to prevent blindness.

2. PCIOL repositioning is still possible even with the newer IOL designs. He strongly suggests haptic externalization.

DISCUSSION

Q: If there is still viable capsule on one side, why isinternal looping not useful in these cases?

A: In these cases haptic externalization brings theopposite haptic closer to the middle, making it easier toplace it over the residual capsule.

Comment: There are other techniques of fixating thehaptics in a scleral tunnel without sutures.

A: One of my colleagues uses fibrin glue in a similartechnique. It is a potentially good technique but there isnot enough data yet.

Q: Are you not worried that the refraction will bedifferent by going 3 mm back?

A: Although initially concerned about that, I haven’tseen any significant change in the refractive error. A fewstudies that are to be published have demonstrated this.

Comment: There are a lot of risks in working inside theeye to refixate an IOL. Just exchanging the IOL may besafer.

A: This is the exact reason why I am advocating externalhaptic fixation, to minimize intraocular manipulation.

Q: How would you manage toric and multifocal IOLs?

A: With toric IOLs, one must be very careful to get theposition exactly right. So, I exchange these lenses for asingle focus, spherical IOL and have the cornea servicefix the astigmatism.

Q: Have you had any experience with the implantabletelescope?

A: Although I have not seen these yet, since these arelarge bulky lenses, I think there will be a much higherincidence of in-the-bag dislocation of these lenses.

Comment: With multifocal, toric and telescopic lenses, itis better to explant these since they need perfectcentration. Especially, with toric IOLs, it can be difficultto know where the axis should be, let alone where it was.

Q: Do you do any iris fixation at all?

A: I am not opposed to iris fixation as long as it is a 3-piece IOL, but I don’t do them anymore.

Comment: Being able to capture the optic in the anteriorchamber makes iris fixation much easier.

Comment: I have been iris fixating one-piece IOLs formany years without any complications.

A: One-piece IOLs cause iris chaffing resulting inrecurrent vitreous hemorrhage and hyphema. If you lookat the back of the iris, it is white from the IOL chaffing.

See Kokame PowerPoint presentation, A.88

III. PVR and Retinotomies: How Far Should We Go?Andre V. Gomes, MD, PhD

PRESENTATION

Surgery for retinal detachment hasevolved consistently in recent decades.The use of new instrumentation, per fluorocarbon liquids, high speed cutting,

wide angle viewing has brought successful rates to over90%. But even though we operate and see better, we stillface complications. Even less difficult cases may end uprequiring new operations and patients may lose vision.

One of the main sources of complication is proliferativevitreous retinopathy (PVR). Meticulous vitreous baseshaving and even the use of some drugs have decreasedbut not eliminated PVR. When there is no more shavingand peeling to do, with the retina showing some degreeof shortening, we have to count on retinotomy/retinectomy to accomplish reattachment.

It can be a small retinotomy to remove a subretinalmembrane or a very extensive one used as a last resort tosucceed. But is it worth it? Will the patient see with this“new” retina lacking large pieces?


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Studies involving 360 retinotomies for the removal ofsubretinal membranes in AMD, have shown good visualrecovery after the procedures. The patients may not seewell after retinotomies due to many reoperations, or evenbecause the macula was off to begin with. Some damageto the optic nerve may also be present! Post-op poorvisual acuity may not be related to the fact one had toperform a large retinotomy! There are situations in onlyeye patients when everything should be tried to giveback some vision to that eye.

Videos of difficult cases and a case series of greater than180 retinotomies will be presented. I will also reveal somedata on a trial designed to verify if PVR can be minimizedwith the use of some steroid during the surgery.

HIGHLIGHTS

• Proliferative Vitreoretinopathy (PVR) is the mainsource of failure after primary retinal detachmentrepair.

• Intraviteal triamcinolone acetonide may lower the rate of PVR.

• Retinotomies are useful in these cases.

• Earlier use of retinotomies seems to favor betteroutcomes.

NOTES

Studies on proliferative vitreoretinopathy (PVR) aresmall and are hard to compare. PVR is a cell mediatedevent where the RPE cells reach the vitreous cavity andproliferate along with glial cells to form epiretinalmembranes. These membranes contract and forshortenthe surface of the retina.

PVR is the main source of failure after surgery forrhegmatagenous retinal detachment. A reliable tool oragent for decreasing its formation is yet to be found.

Although several surgical advances such as high-speedcutting, perfluorocarbons (PFCL), and wide angleviewing have been helpful, we cannot avoid PVR. Wecan, however, minimize PVR. Several papers have shownthat we can minimize PVR with the use of steroids.

Triamcinolone acetonide decreases inflammation, stabi-lizes the ocular-blood barrier, and may have some directinhibitory action on cellular proliferation. A small studywas performed studying adjunctive intraocular triamci-nolone acetonide in vitreoretinal surgery for retinaldetachment with PVR. 29 eyes with retinal detachmentand PVR grade C1-D2 were included. Group 1 receivedtriamcinolone and Group 2 was the control. The surgicaltechnique was vitrectomy with membrane peelingfollowed by a fluid air exchange. Right after the fluid airexchange, the eyes receiving triamcinolone acetonidehad the fluid aspirated so that only the crystals remained.The silicone oil was then injected on top of that.

The results showed a 92.9% rate of retinal reattachmentwithout reoperation in group A compared to 60.7% inthe control group. This was not statistically significant,however. The eyes in group A were more complex casesand more retinotomies were performed but still had alower reoperation rate.

Retinotomy was first described by Machemer in 1979. Itis common sense among retinal specialists that retino-tomies are helpful especially in cases of retinal shrinkage.The rationale for retinotomy comes from maculartranslocation surgery, where there were relatively goodvisual acuity results and low complication rates eventhough the techniques were difficult. Fluorescein angiog-raphy studies have shown nearly normal RPE and retinaat the edges of the retinotomy. Some problems associatedwith retinotomy are retinal atrophy and photoreceptorloss at the edges of the retinotomy on histopathologicstudies. Other studies have shown an association betweenlarge retinotomies and worse functional outcome.However, this may reflect the severity of PVR, whichmay account for the less favorable visual results, and notthe effect of the retinotomy per se.

The surgical techniques include a good vitrectomy,including extensive vitreous shaving. A thoroughdissection of membranes should be done, especially priorto using PFCL. Diathermy should be performed at themargin of the retinotomy, as peripheral as possible.Removing the anterior retinal remnants may be helpfulin preventing post operative hypotony. Silicone oil isthen injected after a fluid air exchange.

VIDEOS

A video of a large retinotomy with removal of subretinalmembranes. The retina was flattened with PFCL and theedges lasered. The anterior remnants of the retina werethen removed.

Video of a taut retina. A 270 degree retinotomy wasperformed due to residual traction. Pan retinal photo -coagulation was performed. The rationale of panretinalphotocoagulation (PRP) is to distribute the tractionalforces evenly. In some of Dr. Gomes’ cases, the edges of the retinotomy and the posterior retina would beattached but the retina in between would not. PRP may prevent this problem.

Video of creating radial retinotomies, using scissors,forming a clover leaf configuration. PRP was applied.The patient maintained 10/400 vision.

Video of severe PVR. The membranes were peeledfollowed by creation of a 360 degree retinotomy.Bleeding was kept to a minimum. Once flat, PRP wasapplied. Triamcinolone acetonide was injected and thefluid aspirated so that the crystals rest on the retinalsurface under silicone oil.


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In the literature, the anatomical results for PVR surgeryare not bad, ranging from 61-85%. However, there is asignificant range of complications. The visual acuityresults are not very good. Even if visual acuity improves,the mean final visual acuity is 20/400 to count fingers.

In a retrospective analysis of 38 eyes, most eyes had a180 degree retinotomy, although 10 eyes had a 360degree retinotomy. The retina was reattached in 95% ofcases. However, 63% needed a reoperation. More thanhalf of these cases had a visual acuity ranging from20/100 to 20/200, but 21% had only hand motionsvision. Visual acuity improved in 79% but decreased in13%. Hypotony was the most common complication. Ina silicone filled eye, a difference in IOP between the eyes>2 mmHg should raise concern for phthisis after removalof the silicone oil. Other complications includedprogressive PVR, corneal decompensation, bleeding atthe margins, hyphema and phthisis. 6 eyes had hypotonyand 1 eye developed neovascular glaucoma.

IN CONCLUSION

• Retinotomy in PVR cases shows reasonable results.

• Studies are very difficult to compare.

• Early intervention seems to favor better outcomes. We tend to add retinotomies after the second or thirdoperation. Maybe after one operation, if there is someretina forshortening, it may be better to do a retinotomyearly rather than trying to force the retina flat again.

• Although anatomic outcomes are good, final visualacuities are limited.

• In the future, early intervention may be better.

• Sometimes, a buckle can be in the way and facilitateslippage.

• Radial retinotomies, as opposed to large circum -ferential retinotomies, can minimize RPE exposure.

DISCUSSION

Q: Under what situations would you go straight toretinotomy without a scleral buckle first?

A: I would not place a buckle and would just do avitrectomy. I also do not usually revise buckles in thesecases.

Comment: If I do less than 270 degrees of retinectomy, I add a buckle to each of these eyes.

Q: Who would place a scleral buckle in a recurrentretinal detachment with PVR?

A: By hands, most of those in the audience stated theywould.

Q: There is a concern for retinal toxicity with placingundiluted triamcinolone acetonide directly on the foveaunder silicone oil. If it is going to used in this way, apreservative free formulation should be utilized.

A: I use a preservative free steroid preparation in thesecases.

Q: Is anyone interested in using 5FU in high-risk casessuch as trauma?

A: No one had any experience using it in this setting.

Q: Our group is doing a pilot study of retinoic acid forPVR. Do you have comments? Also, in a case where theprimary repair fails with an inferior retinal detachmentand retinal forshortening, I would do a vitrectomy and abuckle, and not necessarily a retinectomy, since thebuckle will essentially decrease the length the retinaneeds to drape over to stay flat.

A: I find that it is difficult to just get away with a bucklein the cases I see where there is severe PVR. That is whyI go to retinotomy early on.

Q: What techniques do you use to avoid slippage in casesof large retinectomies and also, do you have anyexperience using direct silicone oil-PFCL exchange?

A: I do not do direct exchange. To minimize slippage, Imake sure to remove all the fluid over the dome shapedPFCL first, staying at the anterior margin of the breaks,prior to removing the PFCL.


Q: On a recurrent case of retinal detachment with PVR do you:

Try to revise the buckle and peel more membranes . . . . . . . . . . . . . . . . . . . . . 3.8%Do not revise the buckle, peel membranes and avoid retinotomies . . . . . 39.6%Tend to do retinotomies as well as extensive membrane peeling . . . . . . . . . . . . . . 56.6%Refer the patient to another physician . . . . . . . 0.0%

Q: When performing retinotomy do you mostly use:

Scissors . . . . . . . . . 11%Vitreous cutter . . . 89%

Q: Do you think that diathermy before retinotomyshould be done?

Yes . . . . . . . . . . . . 74%No . . . . . . . . . . . . 26%

See Gomes PowerPoint presentation, A.94


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IV. Ocular Trauma Surgery: Surgical Video Review/PresentationCarl Claes, MD

PRESENTATION

Videos on Combined Surgery Complications of heavy silicone oil Pigment epithelium transplantation Trauma cases

NOTES

Video: Removal of subretinal blood in macular degener-ation. A large blood clot was removed. These patientsusually are LP. There is a large atrophic zone underneath,and even if the retina could be replaced over the area,the visual acuity results are bad. To try to improve visualoutcomes, a flap of pigment epithelium was placed underthe fovea. However, the pigment transplant can becomevery fibrotic. So, in these very large atrophic zones, thepigment epithelium transplant may not have a goodchance to survive.

Case Presentation: A patient who at the time of siliconeoil removal had poor results.

Angiography of this patient was shown who developed aRPE tear after injection with ranibizumab. A large RPEtransplant was placed under the fovea. Post operativeangiography was shown. The patient recovered 20/25vision for 2 years.

Case Presentation: A case of contusion trauma with arupture of Bruch’s membrane involving the fovea. AnRPE flap was placed.

Case Presentation: A case of serpiginous chorioretinopathy.The patient was losing visual acuity from atrophy. AnRPE flap was placed under the fovea. Visual acuity wasstabilized. Survival of the RPE flap was shown withfluorescein angiography.

Case Presentation: A case of a myopic patient was thenshown. Macular translocation was done on the eye 5years prior. The patient had recovered good visual acuity,but over time the atrophy progressed to involve thefovea with loss of central vision. A second maculartranslocation could not be done, so an RPE transplan-tation was done in this case. The technique is similar toa macular translocation but is shorter and easier.

Video: The retina is detached. In this case, there is aprior retinotomy area from the macular translocation sothat the retinotomy is made more posteriorly. Thescissors are used to make the retinotomy in this case. TheRPE flap is prepared with diathermy and a full thicknessRPE-Bruch’s membrane flap is removed with verticalscissors. The flap shrinks immediately. It is graspedbimanually and then placed under a PFCL bubble that is

preplaced in the subretinal space after the retinotomy isflipped over nasally. PFCL is then used to push out thesubretinal PFCL bubble. Silicone oil is left in the eye for3 months. In this patient vision was stabilized.

Q: Is it possible to tell if the RPE flap has flipped over?

A: The bottom side has a different color and you can tell.

VIDEOS

There is an in-the-bag dislocation of a PCIOL alongwith a capsular tension ring in the vitreous. The capsulartension ring is brought up to the anterior chamber andremoved through a limbal incision. The PCIOL issutured onto the iris using 10-0 prolene suture. Thepupil can still be dilated after the procedure for otherretinal procedures.

Phacovitrectomy. A suture is not placed across thecorneal incision. The corneal incision is made at the 12o’clock position. Make sure the intraocular pressure isnot low after cataract surgery to insert the trocars. In orerto prevent leak, don’t make the trocar incision at thelevel of the corneal incision. Scleral indentation isshown in the area of the corneal incision. Indentation isdone posterior to the corneal incision and there is noleakage from the incision.

Phacovitrectomy in the presence of a dense vitreoushemorrhage, where there is no red reflex. Vision blue isplaced in the anterior chamber. A trocar is placed and achandelier is inserted. The phaco is then performed withretroillumination.

A case of trauma. Vitreous is in the anterior chamber. A25g cutter is used after the infusion is placed through thepars plana. The 25g forceps is used to make a capsulor-rhexis and the cutter is used to remove the lens withinthe capsule. A capsular tension ring is then placed afterwhich the IOL is inserted. The vitrectomy can then beperformed to remove the vitreous hemorrhage undergood visualization.

Pediatric trauma case of a pencil into the eye. There is acentral corneal scar. 2-3 months after primary repair thepatient presents with a giant retinal tear and a closedfunnel retinal detachment. Visualization is good througha wide angle viewing system and the corneal scar is not aproblem. In the past, a PKP would have been necessary.The scar tissue is dissected from the periphery and fromthe perforation site. It is important to remove all scartissue from the periphery in these cases. A direct PFCLto silicone oil exchange is performed. While directlyinjecting the silicone oil, the peripheral fluid is removedfirst, before the PFCL is removed. This prevents slippage.

Bilateral retinal detachment in a child. There is a closedfunnel RD with anterior membranes in contact with the


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lens. The lens is removed. The anterior membranes aredissected from the periphery with curved scissors.Traction of the ciliary body by these membranes can beappreciated. Relieving this traction is important for pre -venting hypotony and for normal anatomic developmentof the eye. A stalk is then visualized, leading to adiagnosis of PFV (or PHPV).

A child with anterior synechiae and a small pupil. Thepupillary membrane is removed first. The vitreous isorganized and there is a complete retinal detachment.There is no PVD. It is important to remove the hyaloid.The vitreous is very fibrotic. A good cutter is needed toremove this tissue without causing too much traction onthe retina and creating iatrogenic breaks. Bilateraldelamination is done to the vitreous base as far peripheralas possible and retinotomy is performed only if thereremains significant retinal stiffness or traction. Other -wise, he injects silicone oil and observes. Dr. Claesavoids making retinotomies in children. In this case, theposterior membranes are removed and a large colobomais now appreciated. Silicone oil is introduced. It can bedifficult to keep the retina over the coloboma flattened if there is a break in this area.

DISCUSSION

Q: Have you seen PVR after RPE translocation surgery?

A: I do not see PVR. I have had a 1% incidence of PVRin the last 100 cases with macular translocation. It isimportant to completely dissect the vitreous base beforemaking the retinotomy.

Comment. Dr. Claes’ results are different than what isreported. He is much more aggressive about anteriordissection. Other series have shown rates of late PVRafter 360 degree macular translocation to be in the 20%range. The Europeans have perfected this techniquewhile we have moved away from it in the US. Theproblem was not the technique itself but the compli-cation after surgery, so it is interesting to see that thecomplication rates out of Europe are much different fromwhat was expected from our early experience in the USwith 360 degree translocation.

A: In our first 30 cases, there was a 30% incidence ofPVR. So, there is a learning curve.

Q: In the context of complex pediatric cases involvingthe macula, have you had any experience using amacular plomb?

A: I have not used the macular plomb. I’m not in favorof its use. Rather, I use standard vitrectomy techniquesfor these cases and for macular holes in high myopes.

Comment. Recent series have shown complications withmacular plombs such as RPE alteration. Most in the UShave not advocated its use and have used standardvitrectomy techniques for these cases.

Q: How many have used macular buckling?

A: Very few in the room indicated that they have.

Comment. With iris sutured IOLs, a lot of iridodenesishas been observed with the IOL moving with every eyemovement. The patient is asymptomatic, however.

A: In Europe there is a lot of experience with iris clawlenses. These eyes also have the same phenomenon of IOLmovement with eye movement, but are asymptomatic.

V. Retinoblastoma: Unique Diagnosis and Treatment Paradigms in 2011Timothy G. Murray, MD, MBA

PRESENTATION

Retinoblastoma remains the mostcommon primary intraocular malignancyin childhood. Over the last century, dramatic declines in mortality have

occurred reducing mortality from 100% to essentiallyzero in developed countries. This dramatic reduction inmortality has been accomplished through early diagnosis,enhanced understanding of molecular tumor genetics,and evolving aggressive therapies.

Understanding of the implications of RB-1 genetic alter-ations enabled the recognition of treatment impact onsecond malignancies and effected a shift from externalbeam radiotherapy to chemotherapy. Improved survivalof the child transitioned to a focus on globe retentiontherapies and commitment to visual preservation.Systemic treatment related morbidities, particularlymyelosuppression and immunosuppression, spurred aninterest in focal treatment (uniquely suited to anintraocular malignancy) and a shift from systemicchemotherapy to focal chemotherapy.

Over the last two years, a significant move to selectiveophthalmic artery chemotherapy has generated a newtreatment paradigm that has required understanding ofdifferential pharmacokinetics, impact of combined lasertreatments and use of a previously discounted chemo -therapeutic agent (Melphalan).

In this presentation, the participants will identify newdiagnostic imaging modalities and their impact onretinoblastoma tumor imaging and treatment, will under-


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stand the impact of evolving treatment shifting fromsystemic chemotherapy to intra-arterial chemotherapy,and will appreciate the impact of long-term screeningprotocols on detection of new and recurrentretinoblastoma.

HIGHLIGHTS

• Multidrug chemotherapy is the mainstay of treatmentof retinoblastoma, but must be coupled with laser to be curative.

• Systemic chemotheraphy is limited by systemic sideeffects.

• Focal delivery of treatment is important since the eyeis the nidus of tumor activity.

• Periocular chemotherapy is effective but can haveorbital complications.

• Intra-ophthalmic artery chemotherapy with melphalanis effective as both salvage and primary treatment forretinoblastoma.

• Unique complications are seen with this newtreatment.

• Follow-up is critical after treatment with intra-arterialchemotherapy to monitor for late tumor recurrence.

INTERACTIVE QUESTIONS:

Q: The most common pediatric intraocular malignancy is:

Uveal melanoma. . . . . . . . . . . . . 0.0%Choroidal hemangioma . . . . . . . 0.0%Astrocytic hamartoma . . . . . . . . 9.5%Retinoblastoma . . . . . . . . . . . . 90.5%

Internationally, the most common intraocular malignancy is retinoblastoma.

Q: Retinoblastoma presents with:

Pain . . . . . . . . . . . . . . . . . . . . . . . 0.0%Cellulitis . . . . . . . . . . . . . . . . . . . 0.0%Leukocoria. . . . . . . . . . . . . . . . . . 2.2%Strabismus . . . . . . . . . . . . . . . . . . 0.0%All of the above . . . . . . . . . . . 97.8%

Leukocoria occurs in 60%, strabismus in 30-40%,cellulitis in 10% and pain in <1%.

Q: Retinoblastoma treatment most commonly includes:

External beam radiotherapy . . . . . . . . . . . . . . . . 6.7%Systemic monodrug chemotherapy . . . . . . . . . . 0.0%Systemic multidrug chemotherapy . . . . . . . . . . 24.4%Periocular chemotherapy . . . . . . . . . . . . . . . . . . 0.0%Laser tumor ablation. . . . . . . . . . . . . . . . . . . . . . 0.0%Chemotherapy plus laser ablation . . . . . . . . . 68.9%

NOTES

Multidrug chemotherapy is a mainstay of therapy, but itis not curative for retinoblastoma. If you don’t consoli -date with laser, the failure rate approaches 100%. Thebest study performed was out of St. Jude’s where that wasexactly done. Their failure rate was 100%. They wereable to rescue those eyes with external beam radiationand enucleation, but those eyes would have had a 100%response rate if they had been treated with chemo -therapy plus concomitant laser.

There have been huge advances in the treatment ofretinoblastoma. The idea is to move away from systemicchemotherapy to treat the eye directly and thereforelimit complications. The most interesting advance hasbeen supraselective intra-ophthalmic artery chemo -therapy. It was pioneered by the Japanese and modifiedby Dr. Abramson’s group at Memorial Sloan Kettering.

Case Presentation: 7 year old girl with stage 5b retino -blastoma. No family history. Presented with decreasedvisual acuity. She was 20/25 in the right eye and 20/20 in the left eye. The anterior segment examination wasbenign. The posterior segments look excellent, but there is an endophytic/exophytic tumor nasally with fine vitreous seeding. What is not seen in the photo isanother tumor in the far periphery. B-scan shows intra-tumor calcification and no extraocular extension.

Remember that the goals are to save the life first, savethe eye and then salvage the vision.

Systemic chemotherapy reduces tumor volume to allowconsolidation with laser.

It’s the laser that destroys the intraocular tumor andprevents expansion and metastasis.

Dr. Murray typically uses 6 cycles of 3 drug chemo -therapy (carboplatin, vincristine and etoposide) formoderate disease and 9 cycles of 4 drug chemotherapy(carboplatin, vincristine, etoposide and cyclosporine) foradvanced disease. Incredible reduction in tumor volumeis seen even with the first cycle of treatment.

The most important component is to couple chemo -therapy with laser, directly ablating and confluentlytreating the intraocular tumor. This has been demon-strated in multiple studies, both in the laboratory and inclinical practice.

Case Presentation: A child with a large macular retino -blastoma. Four months into chemoreduction, the tumorvolume has reduced significantly. However, there is also asmall additional focus of disease. Unilateral, multifocaldisease has a clear RB1 germline mutation and is asdefinitive as if the child had bilateral disease.


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Case Presentation: Another example of a child afterchemotherapy, followed up after 7 years was shown. Theeye has 20/60 vision.

The issue with systemic chemotherapy is systemiccomplications. The major concern is myelosuppressionleading to fever of unknown origin. These childrenrequire hospitalization. Ototoxicity was a commonconcern with cisplatin, and is less frequently seen withcarboplatin, but is still a concern. There is also concernthat etoposide is associated with secondary malignancy.

Novel delivery methods can reduce the systemicchemotherapy risks and include injection of drug aroundthe eye with depots, polymers and miniature catheters.Focal delivery is important because the eye is the nidusfor tumor. Significantly lower doses can be delivered.

The problem with periocular chemotherapy is thatcarboplatin in the periorbital space is toxic and a portionof these eyes develop significant fibrosis and enoph-thalmos.

Case Presentation: A child with advanced disease onlytreated with periocular carboplatin was shown. The eyeis 20/20 5 years after last treatment.

Abramson modified the Japanese technique of intra-arterial delivery of chemotherapy to use microcannulainsertion into the ophthalmic artery. We have used thisas both salvage and primary therapy.

Presentation: Angiography of cannulation of theophthalmic artery was shown. The agent used ismelphlan. The drug infusion is micropulsed over a 30minute period. One of the concerns is vascular perfusionto the brain.

The results of the first 12 patients treated at BascomPalmer were presented. Since it was a new treatment, thepatients selected for treatment were those destined forenucleation. 75% of these eyes, destined for enucleation,were able to be salvaged. The initial reports stated thatthere were no complications. In this series, there was oneunique complication after another. Complications thatwere seen include periocular inflammation of the orbitaltissue and the rectus muscles, post procedure vitreoushemorrhage, microembolic phenomenon (Purtscher’s like retinopathy) and systemic neutropenia. The compli-cation profile is significant and differs from othertreatments for retinoblastoma. In contrast, Dr. Abramsondid not report any complications. Every other programthat has used this treatment has seen the complicationsjust described.

Follow-up is critical since there can be late tumor recur-rence. This is different from external beam radiation,where there was no new retinoblastoma tumor seen aftertreatment. Therefore, radiation therapy alters theanatomy and prevents further development ofretinoblastoma, whereas chemotheraphy does not.

Case Presentation: A case of an eye 4 days after intra-arterial chemotherapy was shown with a purtscher’s likeretinopathy and alterations in the deep choroidalperfusion pattern.

Case Presentation: Another example of a child treatedprimarily with intra-arterial chemotherapy coupled withlaser was shown. The tumor involuted after a secondtreatment of intra-arterial chemotherapy. Dr. Murraypointed out areas of choroidal infarction and markedpigment epithelial alterations, but the tumor showedinvolution and visual acuity was 20/20.

Dr. Murray’s new treatment approach for unilateral andbilateral disease is to treat the patient in a single session.Both eyes are done at a single session. The dose rangesfrom 5 mg to 7 mg, which is much higher than the dosesinitially advocated by Dr. Abramson. Most patients aregetting 3 repetitive treatments of intraarterial chemo -therapy. A new clinical trial will evaluate 3 initialtreatments with intra-arterial chemotherapy with 5 mg of melphalan coupled with laser tumor ablation.

In conclusion, intra-ophthalmic arterial infusion ofmelphalan chemotherapy appears to be an effective tool in the management of both primary and salvageadvanced retinoblastoma with lower morbidity thansystemic chemotherapy.

DISCUSSION

Q: What laser do you use and how extensively do you treat?

A: I use a large spot size diode laser, but I don’t thinkwavelength makes a difference. I apply a confluence oftreatment over the tumor looking, not to whiten thetumor, but to gray the surface. This is easier to do with adiode laser than with another wavelength, but it is okayto use whatever wavelength is available.

See Murray PowerPoint presentation, A.98


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APPENDIX

POWERPOINT PRESENTATIONS

from the 39th Annual

Aspen Retinal Detachment

Society Meeting

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A.2 APPENDIX

The New Paradigm for Treatment of DME in the Anti-VEGF Era Harry W. Flynn, Jr., MD

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The New Paradigm for Treatment of DME in the Anti-VEGF Era Flynn

APPENDIX A.3

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A.4 APPENDIX


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APPENDIX A.5

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A.6 APPENDIX


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APPENDIX A.7

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A.8 APPENDIX


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APPENDIX A.9

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A.10 APPENDIX


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Familial Exudative Vitreoretinopathy Mina Chung, MD

APPENDIX A.11

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A.12 APPENDIX

Familial Exudative Vitreoretinopathy Chung

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APPENDIX A.13

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A.14 APPENDIX


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APPENDIX A.15

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A.16 APPENDIX


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APPENDIX A.17

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A.18 APPENDIX


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APPENDIX A.19

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A.20 APPENDIX

Retinal Detachment Repair: To Buckle or Not Robert L. Avery, MD

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Retinal Detachment Repair: To Buckle or Not Avery

APPENDIX A.21

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A.22 APPENDIX


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APPENDIX A.23

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A.24 APPENDIX


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APPENDIX A.25

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A.26 APPENDIX

Surgery for Complex Retinal Detachment and Proliferative Vitreoretinopathy Allen C. Ho, MD

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Surgery for Complex Retinal Detachment and Proliferative Vitreoretinopathy Ho

APPENDIX A.27

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A.28 APPENDIX


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APPENDIX A.29

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A.30 APPENDIX


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APPENDIX A.31

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A.32 APPENDIX


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Acquired Vitelliform Lesions K. Bailey Freund, MD

APPENDIX A.33

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A.34 APPENDIX

Acquired Vitelliform Lesions Freund

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APPENDIX A.35

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A.36 APPENDIX


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APPENDIX A.37

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A.38 APPENDIX


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Surgical Management of Idiopathic Macular Holes Andre V. Gomes, MD, PhD

APPENDIX A.39

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A.40 APPENDIX

Surgical Management of Idiopathic Macular Holes Gomes

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APPENDIX A.41

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A.42 APPENDIX


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Vitrectomy and Pars Plana Baerveldt Glaucoma Implants Robert L. Avery, MD

APPENDIX A.43

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A.44 APPENDIX

Vitrectomy and Pars Plana Baerveldt Glaucoma Implants Avery

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APPENDIX A.45

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A.46 APPENDIX


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APPENDIX A.47

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A.48 APPENDIX

Panel Discussion: Complex Surgical Case Management

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APPENDIX A.49

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A.50 APPENDIX


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APPENDIX A.51

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A.52 APPENDIX


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Do We Need a New Classification for CNV in AMD? K. Bailey Freund, MD

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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . APPENDIX A.53

Do We Need a New Classification for CNV in AMD? Freund

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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .A.54 APPENDIX


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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . APPENDIX A.55


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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .A.56 APPENDIX


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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . APPENDIX A.57


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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .A.58 APPENDIX

Retinal Complications of the Dohlman Keratoprosthesis Mina Chung, MD

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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . APPENDIX A.59

Retinal Complications of the Dohlman Keratoprosthesis Chung

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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .A.60 APPENDIX


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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . APPENDIX A.61


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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .A.62 APPENDIX


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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . APPENDIX A.63

Endophthalmitis after Intravitreal Anti-VEGF Injections Harry W. Flynn, Jr., MD

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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .A.64 APPENDIX

Endophthalmitis after Intravitreal Anti-VEGF Injections Flynn

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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . APPENDIX A.65


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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .A.66 APPENDIX


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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . APPENDIX A.67


. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .A.68 APPENDIX


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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . APPENDIX A.69


. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .A.70 APPENDIX

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . APPENDIX A.71

Allergy to Povidone Iodine and Cephalosporins Wykoff, Flynn, Han

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Allergy to Povidone Iodine and Cephalosporins Wykoff, Flynn, Han

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . APPENDIX A.73

Taylor Smith Lecture: The Practice Environment of Retina in 2015 David W. Parke, II, MD

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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .A.74 APPENDIX

Taylor Smith Lecture: The Practice Environment of Retina in 2015 Parke, II

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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . APPENDIX A.75


. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .A.76 APPENDIX


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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . APPENDIX A.77


. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .A.78 APPENDIX


. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . APPENDIX A.79


. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .A.80 APPENDIX

Microincision Vitrectomy 2011 Allen C. Ho, MD

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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . APPENDIX A.81

Microincision Vitrectomy 2011 Ho

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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .A.82 APPENDIX


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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . APPENDIX A.83


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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .A.84 APPENDIX


. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . APPENDIX A.85


. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .A.86 APPENDIX


. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . APPENDIX A.87

Management of Anterior Segment Complications Gregg T. Kokame, MD, MMM

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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .A.88 APPENDIX

Management of Anterior Segment Complications Kokame

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . APPENDIX A.89


. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .A.90 APPENDIX


. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . APPENDIX A.91


. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .A.92 APPENDIX


. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . APPENDIX A.93

PVR and Retinotomies: How Far Should We Go? Andre V. Gomes, MD, PhD

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PVR and Retinotomies: How Far Should We Go? Gomes

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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .A.96 APPENDIX


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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . APPENDIX A.97

Retinoblastoma: Unique Diagnosis and Treatment Paradigms Timothy G. Murray, MD, MBA

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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .A.98 APPENDIX

Retinoblastoma: Unique Diagnosis and Treatment Paradigms Murray

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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .A.100 APPENDIX


. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . APPENDIX A.101


. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .A.102 APPENDIX


. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . APPENDIX A.103

Dear Aspen Retinal Detachment Society Meeting Participant,

Once again, we are delighted to offer you this booklet of notes, supplemented by the

majority of slide presentations (edited), from our recent meeting. The notes were taken

and assembled by two young, talented, rising retinal stars – Drs. Minhee Cho and

Kevin Suk – who attended every talk and captured the essence of the vigorous

post-talk discussion, for which the ARDS is deservedly famous. We would also like to

acknowledge the editorial assistance of Dr. R.V. Paul Chan.

This work was made possible by a generous contribution provided by Genentech, Inc.

We are grateful to Drs. Cho, Suk and Chan and to all of you for contributing to the

intellectual vibrancy of ARDS. We hope you will find this booklet interesting, and also

of value to you in the care of your patients.

Please join us March 3-7, 2012 for the 40th Annual ARDS Meeting.

Sincerely,

Organizing Committee

Timothy G. Murray, MD, MBA Donald J. D’Amico, MD William O. Edward, MD Ottiwell W. Jones, MD Jerry E. Leclaire, MD

39thAnnual


MeetingMARCH 5–9, 2011 • SNOWMASS, COLORADO

40thAnnual


Meeting

March 3-7,2012The Viceroy Snowmass

MEDICAL CONFERENCE PLANNERS, INC.1251 Post Road, Scarsdale, NY10583

914-722-0664

[email protected]

www.medconfs.com

For information

SAVETHE

DATE

JOINTLY SPONSORED BY THE FLORIDA MEDICAL ASSOCIATION AND THE ASPEN RETINAL DETACHMENT SOCIETY

This activity has been planned and implemented in accordance with the Essential Areas and policiesof the Accreditation Council for Continuing Medical Education through the joint sponsorship ofthe Florida Medical Association and the Aspen Retinal Detachment Society. The Florida MedicalAssociation is accredited by the ACCME to provide continuing medical education for physicians.

The Florida Medical Association designates this educational activity for a maximum of twelve (12.0) AMA PRA Category 1 Credits.™ Physicians should only claim credit commensurate with the extent of their participation in the activity.


M A R C H 5 – 9, 2 0 11 • S N O W M A S S, C O L O R A D O


Meeting Notes

ARDS

39thAnnual

MEDICAL CONFERENCE PLANNERS, INC.

1251Post Road, Scarsdale, NY10583

914-722-0664

[email protected]

www.medconfs.com

The Aspen Retinal Detachment Society

gratefully acknowledges Genentech, Inc.

for their generous contribution toward

the production of this booklet.

Aspen R

etinal Detachm

ent Society Meeting N

otes 2011

2011


Documents

ARDS Notes Cover 11