CROQ - Vol. 1, Number 2, 2016

CROQ

Clinical Refractive & Optometry Quebec EDITION

VOLUME 1, NUMBER 2, 2016

CLICK HERE TO DOWNLOAD AND PRINT THIS ISSUE

All articles are accredited by the OOQ for Category A UFC credits

Treating and Managing Dry Eye Chronic Central Serous Choroidopathy Blink Mechanics: Viscoadaptive Technology for the Ocular Surface Dragged Fovea Diplopia Syndrome

Clinical

&Refractive Optometry Quebec

Editorial Board • Volume 1, Number 2, 2016 Editor-in-Chief

Associate Editor

Yvon Rhéaume, OD Montreal, Quebec

Richard Maharaj, OD Toronto, Ontario

Contributing Editors Brad Almond, OD Calgary, Alberta

Louis Catania, OD Philadelphia, Pennsylvania

Guy Julien, OD Montreal, Quebec

Rodger Pace, OD Waterloo, Ontario

Jean Bélanger, OD Montreal, Quebec

Paul Dame, OD Calgary, Alberta

Gerald Komarnicky, OD Vancouver, British Columbia

Maynard Pohl, OD Bellevue, Washington

Scott D. Brisbin, OD Edmonton, Alberta

Danielle DeGuise, OD Montreal, Quebec

Bart McRoberts, OD Vancouver, British Columbia

Barbara Robinson, OD Waterloo, Ontario

Lorance Bumgarner, OD Pinehurst, North Carolina

Pierre Forcier, OD Montreal, Quebec

Ron Melton, OD Charlotte, North Carolina

Jacob Sivak, OD, PhD Waterloo, Ontario

Barbara Caffery, OD Toronto, Ontario

John Jantzi, OD Vancouver, British Columbia

Langis Michaud, OD Montreal, Quebec

Randall Thomas, OD Concord, North Carolina

Publication Staff Publisher Lawrence Goldstein

Managing Editor Mary Di Lemme

Senior Medical Editor Evra Taylor

Layout Editor Colin MacPherson

Graphics & Design Mediconcept Inc.

Mission Statement Clinical & Refractive Optometry Quebec is an online, quarterly, peer-reviewed, professional journal dedicated to publishing and distributing clinical and scientific COPE approved articles which have been accredited by the OOQ as Category A, UFC-credit courses. The contents of the journal are composed of articles that will be of particular use and interest to practicing eye care professionals. Test participants who score 50% or more on the UFC test questionnaires will receive a printed UFC-credit certificate by return email.

Why are these UFC-credit articles published in English?

Recently the regulations governing continuing education credits in Quebec have been amended so that COPE approved CE-credit articles, which have been written by some of the most noted and influential optometric opinion leaders in North America, can now be offered to Quebec ODs as Category A, UFC-credit distance learning courses.

In this regard it’s important to note that these articles, which were written in English, require a letter from their authors authorizing both their publication and accreditation. And it would be unrealistic to ask a US doctor to sign off on and approve a paper that has been rewritten in French. For this reason the re-accredited COPE approved articles in this journal are presented here in English.

Clinical

&Refractive Optometry Quebec

Contents • Volume 1, Number 2, 2016 44

PUBLISHER’S PAGE

UFC CREDIT ARTICLES

46

Treating and Managing Dry Eye Shachar Tauber, MD ABSTRACT: Much has been learned about the tear film (and its impact on dry eye) over the years, from the discovery of its multi-level properties, increased understanding on the role of mucin, through to the interaction between the surface and the tear film. From an epidemiological standpoint, dry eye prevalence is in the range of between 6% and 14%, although most people have experienced dry eye in one of its many forms.

52

Chronic Central Serous Choroidopathy David C. Kung, OD; Pauline F. Ilsen, OD ABSTRACT: Chronic central serous retinopathy (CCSR) is a lesser known variant of central serous retinopathy (CSR), with clinical features characterized by multifocal serous detachments associated with diffuse decompensation of the retinal pigment epithelium (RPE). The disease tends to be bilateral and typically affects individuals over the age of 50.

Due to the chronic nature of the disease, permanently reduced visual acuity is often observed.

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Blink Mechanics: Viscoadaptive Technology for the Ocular Surface Richard Maharaj, OD, FAAO INTRODUCTION: While the body of Dr. Maharaj’s work is in Meibomian Gland Dysfunction, he noted that this presentation topic was focused on blink metrics in mild to moderate dry eye patients. There are two components in the discussion of the mechanics of blinking and viscoadaptive technologies.

The first is what the eyelid does on a given blink. The second is the microanatomy involved in the blink at the inner and outer eyelid surface. Dr. Maharaj has observed that a blanket approach to treatment with artificial tears isn’t an effective model of care for the multifactorial dry eye patient.

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Clinical & Refractive Optometry Quebec is published 4 times per year

by Mediconcept.

The Journal is made available to all practicing optometrists in Quebec on www.crojournal.com.

Advertising insertion orders and copy must be received before the first day of the preceding month for which the advertising is scheduled.

While the editorial staff of Clinical & Refractive Optometry Quebec exercises great care to ensure accuracy, we suggest that the reader consult the manufacturer’s instructions before using products mentioned in this publication. The views contained in the Journal are those of the respective authors and not of the Publisher.

Please direct all correspondence to: Mediconcept Editorial & Sales Office 3484 Sources Blvd., Suite 518 Dollard-des-Ormeaux, Quebec Canada H9B 1Z9 Tel.: (514) 245-9717 E-mail: info@mediconcept.ca Printed in Canada. All rights reserved.

Copyright © 2016 Mediconcept.

The contents of the publication may not be mechanically or electronically reproduced in whole or in part without the written permission of the publisher.

All drug advertisements have been cleared by the Pharmaceutical Advertising Advisory Board.

Dragged Fovea Diplopia Syndrome After Epiretinal Membrane Peel Surgery Adam T. Gorner, OD; Leonid Skorin Jr., OD, DO, MS ABSTRACT: Dragged fovea diplopia can be extremely frustrating for both patients and doctors. An understanding of this condition will allow practitioners to detect it and treat the symptoms in order to allow patients to function normally.

ISSN: 2369-498X; Date of Issue: March 2016

Cover Image: Epiretinal membrane with macular pucker Courtesy of: Dr. Adam T. Gorner and Dr. Leonid Skorin Jr.

Clinical

&Refractive Optometry Quebec Volume 1, Number 2, 2016

Publisher’s Page Yes, its official. The Order of Optometrists of Quebec (OOQ) has officially amended the regulations regarding how optometrists in Quebec can acquire their annual requirement of continuing education credits in order to maintain their optometric licences. More specifically, the OOQ will now accept COPE accredited journal articles for Category A, UFC credit. This means that Quebec ODs now have the choice of either attending UFC accredited meetings and/or reading UFC accredited COPE journal articles and successfully completing their associated test questionnaires.

In response to this change in the regulations, the publishers of CRO (Clinical & Refractive Optometry) Canada’s leading all COPE approved CE-credit journal, have launched this new peer reviewed, UFC accredited journal, entitled CROQ (Clinical & Refractive Optometry Quebec Edition) which is being made available both online at no charge and in print by paid subscription. Each issue of CROQ will feature four OOQ approved, Category A, UFC credit articles, as they were written and approved by COPE, in English, by some of North America’s leading and most recognized optometric experts.

In order to distribute this journal to optometrists across Quebec, complimentary online subscriptions are being offered with issues being forwarded directly to the reader’s email account. These online issues are fully downloadable for immediate viewing and they can also be saved (either in whole or in part) for later use. Each article in the journal will have an accompanying Category A, UFC test questionnaire that can be completed and returned for grading at a cost of $25 per test. Upon successfully completing each test, a UFC credit certificate will be emailed to each applicant. Please note that we are also offering a printed version of the journal by paid subscription which will include all the UFC test charges at no additional cost. For more details about the print version, please see the Subscription Upgrade Form on the facing page.

We hope that you will enjoy reading the journal, and that you will come to rely on this publication as a valued resource for your annual UFC credit requirements. We would also like to hear from you with your thoughts and impressions about this new journal, and most importantly what you would like to see included in future issues.

Lawrence Goldstein Publisher lgoldstein@mediconcept.ca

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Clinical & Refractive Optometry Quebec 1:2, 2016

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now with 4 prepaid UFC tests per issue Subscribe to the Print Edition and you will automatically receive four consecutive printed issues by direct mail, Each of those 4 issues will contain at least four OOQ approved Catagory A UFC-credit articles in every issue, each with prepaid UFC test questionnaires. For those of you doing the math, this means that you will receive the printed issues and $400 worth of Category A UFC-credit tests, for a one-time price of $280 plus tax, a savings of over $100.

Subscription Form Clinical & Refractive Optometry Quebec: Print Edition Yes, please enter my subscription for 4 consecutive issues of the Print Edition of Clinical & Refractive Optometry Quebec to be delivered by direct mail. Your subscription will include a total of sixteen prepaid Category A UFC-credit tests which have been approved by the OOQ all for a total of $321.30 including GST & QST. Registration Information Title ______ First Name ___________________ Last Name _______________________________ Number __________ Street _____________________________________________ Suite ________ City ______________________________________________________ Postal Code ______________ Office Phone (_____) _______________________ E-mail _________________________________ Professional License ________________________________________________________________ Please forward a cheque made payable to Mediconcept Communications, and mail it today to:

3484 Sources Blvd., Suite 518, Dollard-des-Ormeaux, Quebec, Canada H9B 1Z9

CLICK HERE TO PRINT THIS UFC CREDIT ARTICLE AND TEST

Clinical & Refractive Optometry Quebec is pleased to present this continuing education (CE) article by Dr. Shachar Tauber, Cornea and Refractive Surgeon at Mercy Clinic Eye Specialists, Springfield, MO. This article has been approved for 1 Category A, UFC credit in Ocular Health by the Ordre des Optométristes du Québec. In order to obtain your credit, please refer to page 50 for complete instructions.

Treating and Managing Dry Eye Shachar Tauber, MD Springfield, Missouri

ABSTRACT Much has been learned about the tear film (and its impact on dry eye) over the years, from the discovery of its multi-level properties,1 increased understanding on the role of mucin,2 through to the interaction between the surface and the tear film.3 From an epidemiological standpoint, dry eye prevalence is in the range of between 6% and 14%, although most people have experienced dry eye in one of its many forms.

INTRODUCTION This article reviews dry eye, its epidemiology, etiology, prevalence, and therapeutic options.

TEAR FILM STRUCTURE For many years, ophthalmology taught that the tear film was comprised of three distinct layers. What has been found is that it is actually an indistinct transition where the mucins are dissolved within the aqueous in a gradient (Fig. 1). The lipid layer is the thinnest of the layers and acts to prevent the evaporation produced by the meibomian glands. The aqueous layer is the thickest layer, and its role is to transport oxygen, enzymes, proteins, and other matter. The mucin layer is the innermost layer closest to the cornea, and it serves as a coating for the hydrophobic cornea regulating surface tension; it is produced by goblet cells and is composed of 21 different mucins.

ETIOLOGY Dry eye worsens with age and can be due to numerous causes. Therefore, it is important to regard dry eye not as a disease but as a multi-factorial disorder; and because of this, treatment has been extremely difficult to develop and S. Tauber — Section Chair Ophthalmology, Director of Ophthalmic Research and Telemedicine, Cornea and Refractive Surgeon, Mercy Eye Specialists, Springfield, MO Correspondence to: Dr. Shachar Tauber, Mercy Clinic Eye Specialists Ophthalmology - Surgery Center, 1229 E. Seminole, Suite 420, Springfield, MO 65804; E-mail: Shachar.Tauber@Mercy.Net This article has been peer-reviewed.

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be proven as effective. Other than such environmental factors as air-conditioning and cold or dry weather, there are many other factors including different surgeries and disease entities that can cause dry eye.

Medication-Induced Dry Eye Many patients present to us on multiple medications including beta-blockers, antihistamines, diuretics, chemotherapy, and anti-depressants. In fact, more patients on anti-depressants seek refractive surgery, which is an interesting relationship worthy of further investigation.

Glycocalyx The glycocalyx is where the mucin attaches to the corneal epithelium and this interdigitation is quite important: when it fails, clinical dry eye develops (Fig. 2). The glycocalyx is a cotton-candy-like substance that grabs the mucin layer of the tear and allows it to adhere to the microvilli or the surface epithelium. Thus the ocular surface is made up of stroma matrix and fibroblasts, the epithelial cell membrane, the aqueous, the glycocalyx, and the mucin.

Innervations Innervations are important as they are the sensory component going from the cornea to the lacrimal nucleus (Fig. 3). If those nerves are interfered with, outgoing messages to different parts of the lacrimal system will be affected. This is a problem often encountered in laser in-situ keratomileusis (LASIK), where it interferes with the corneal nerves.

DRY EYE CLASSIFICATION The National Eye Institute has classified dry eye into two general categories: tear deficient and evaporative; and within each main category are subcategories. Under “tear deficient” we find such conditions as Sjögren’s and auto-antibodies, and non-Sjögren’s and lacrimal deficiency, lacrimal obstruction, and reflex. Under “evaporative” we find the subcategories oil deficient lid-related, contact lenses, and surface changes.

TEAR FILM DEFICIENCIES Various dry eye disorders can be placed under one of three areas of tear film insufficiency: lipid, aqueous, and mucin.

Fig. 1 The traditional tear film model compared to the updated tear film model

Fig. 2 Glycocalyx helps mucin adhere to corneal epithelial cells; any damage to the glycocalyx means mucin deficiency, causing tear film destabilization and break up

eye symptoms, and begins a downward spiral. If we operate on these people, there is a risk of wound healing issues, infection, and chronic inflammation, whether performing LASIK, cataract surgery, transplant surgery, or glaucoma surgery. Therefore, treating the dry eye prior to surgery is indicated.

Fig. 3 Nerve distribution in a normal eye

Lipid Layer Deficiency Under this category we find a diverse group of disorders that lead to changes in meibomian gland secretions, including blepharitis.

Aqueous Layer Deficiency As with lipid layer deficiency, there are many disorders that can lead to aqueous layer insufficiency and dry eye.

These include: inflammation, trauma, neurological defects, and congenital absence, among others.

Mucins Again, there are many potential causes of disruption to this tear film layer, including: Stevens-Johnson syndrome, pemphigoid, vitamin A deficiency, trachoma, and radiationinduced issues.

DRY EYE CYCLE Typically, a patient will present complaining of discomfort, which is actually environmental or contact lens intolerance.

This creates surface changes that further worsen the dry

Tear Film Instability The tear film instability cycle (Fig. 4) begins with surface desiccation and leads to a hydrophobic cornea to which the mucin is unable to attach. This exposes the epithelial cells to evaporation, resulting in an inflamed cornea. Regardless of the original causal factor(s), the cycle remains the same: tear production decreases or tear evaporation increases; there is an increase in tear osmolarity and toxin concentrations; and goblet cell density decreases and epithelial desquamation increases. This leads to a breakdown of the cornea-tear interface and leads to an increase in such inflammatory mediators as cytokines and leukotrienes. The last step of this cycle is permanent surface stem cell, stromal matrix, and neurotrophic damage. Patients are then very susceptible to infection, inflammation, and ulceration of the cornea. When metaplasia is encountered in the lid margin, it becomes difficult for the ophthalmologist to separate the concomitant blepharitis and dry eye. Due to the advanced progression of the disease at this point, there are now overlapping issues with oil release, tear film evaporation, and dry eye exacerbation.

Unprotected Surface What are the consequences of an unprotected surface?

At time zero, when the blink occurs, the tear protects the ocular surface until that tear breaks up. If the tear breaks up prior to the subsequent blink, it results in ocular staining of the now unprotected surface. When repeated

Treating and Managing Dry Eye — Tauber

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Fig. 4 The process of tear film destabilization and the resulting corneal cell damage

Fig. 5 The OPI measures TFBUT as related to blink interval to determine whether the ocular surface has adequate tear film protection

PREVALENCE The prevalence of diagnostic dry eye must not be underestimated; because it is so common, it tends to be ignored.

The symptoms can be extremely confusing; patients may present with decreased vision, and it is difficult to determine whether one is dealing with an early cataract, early Fuchs, or indeed an ocular surface issue.

TESTING TOOLS

Fig. 6 An evaluation (in seconds) of tear film break up elapsed time

over the course of a day, this can result in 4,000 to 8,000 seconds where the surface is unprotected and causes epithelial desiccation.

OCULAR PROTECTION INDEX (OPI) The OPI (Fig. 5) measures the tear film break up time (TFBUT). We then divide that time by the interval between blinks (IBI). Simply, if the patient blinks prior to TFBUT, then the ratio is >1 and the ocular surface is protected. Conversely, if the TFBUT occurs prior to the blink the ratio is <1, and the ocular surface is unprotected.

There is a host of conditions that affect an individual’s blink rate. For example: hormonal changes, mental disorders, menstrual phase, muscular fatigue, drug interactions, computer use, and talking. It is recommended that clinicians watch their patients while taking their history to determine their blink rate.

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In addition to observation of TFBUT, there are many diagnostic tools at our disposal for dry eye evaluation.

Multiple dyes will stain the cornea and tear including Rose Bengal (which stings significantly), Lissamine Green, and fluorescein staining (frequently used).

Fluorophotometry and osmolarity testing are quite complex and have not yet been sufficiently standardized to be used clinically.

TFBUT TFBUT is diagnostically helpful, but must also be standardized. Improved tear-film evaluation techniques include using ≤ 5µl of sodium fluorescein and Wratten filters for optimal imaging. Figure 6 shows one such tear-film evaluation in action. Another method to evaluate TFBUT is to ask patients to blink twice and look straight ahead. Using a stopwatch, time the seconds until they say they have ocular awareness. One second following ocular awareness equals the symptomatic tear break up time.

THERAPEUTIC OPTIONS Patient education is tantamount in helping them take a proactive role in the treatment process. Patients must be taught awareness of TFBUT, drying medications (i.e., oral antihistamines and antidepressants), adverse environments (i.e., dry, windy places), and visual tasking (i.e., computer usage, reading).

Artificial Tears There is a lengthy list of tear substitutes. The optimal artificial tear characteristics have increased dwell time and long-lasting protection. It must have minimal blurring and lid-caking, offer improved comfort, and it should contain non-irritating preservatives. However, rather than simply managing dry eye by flooding it, future therapy is going to involve treating dry eye via targeting the different tear film layers.

Secretagogues Secretagogues will soon treat production of essential tear components at all three levels: there is the 15(S)-HETE that stimulates mucin production, as well as the INS-365 that stimulates all three tear-film layers.

Anti-Evaporatives This upcoming therapeutic category stimulates lipid secretion to enhance and optimize the barrier function of the lipid layer. Anti-evaporatives include topical androgens that regulate the quality and quantity of lipid secretions, as well as lipid component replacements such as lipocalin, phosphatidylcholine, and castor oil.

Anti-Inflammatories Anti-inflammatories target the inflammation component of dry eye at the lacrimal gland. It has been demonstrated that reducing the inflammatory response of the dry eye

is an effective treatment option; Restasis® is one such anti-inflammatory that has received FDA approval and is used widely in the United States. Other anti-inflammatories include low-dose steroids and tetracyclines.

Mucomimetics The mucomimetics, as the name implies, mimic the functions of naturally occurring mucins; by stabilizing the tear film, they actually result in a healthier ocular surface.

MILCIN™ is one mucomimetic that is on the horizon as a treatment option.

CONCLUSION To reach our collective goal of ocular surface protection, we must heal the damage and reduce inflammation and irritation. This will likely be accomplished by a line of products rather than one “cure-all”. With the many causes of dry eye and nearly as many therapeutic approaches, we will certainly be looking at combination therapy, with different treatments for different ideologies. ❏

REFERENCES 1.

2.

3.

Wolf. Normal Physiology of the Ocular Surface. Section 8 Basic and Clinical Sciences Course, American Academy of Ophthalmology 2002-2003, page 49.

Holly FJ. Formation and stability of the tear film. Int Ophthalmol Clin 1973; 13(1): 73-96.

Tseng SC, Tsubota K. Important concepts for treating ocular surface and tear disorders. Am J Ophthalmol 1997; 124: 825-835.

Treating and Managing Dry Eye — Tauber

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CATEGORY A UFC C REDIT A PPLICATION F ORM

1:2, 16

INSTRUCTIONS

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FOR

1 CATEGORY A, UFC CREDIT

This course has been approved for 1 Category A, UFC credit in Ocular Health by the Ordre des Optométristes du Québec. Please complete and submit this test questionnaire for grading before March 31, 2018.

In order to obtain 1 Category A, UFC credit, please follow these steps: • Fill in the identification section and answer the 10 multiple choice questions in this UFC credit application form • Prepare a cheque payable to Mediconcept for $25.00 • Mail your completed UFC credit application form along with your cheque to: CRO Quebec, 3484 Sources Blvd, Suite 518, Dollard-des-Ormeaux, QC H9B 1Z9 Your answers will be graded by Clinical & Refractive Optometry. If you score 50% or more, a UFC Credit Certificate approved by the Ordre des Optométristes du Québec will be issued to you for your records.

CLICK HERE TO PRINT THIS UFC CREDIT TEST AND ARTICLE Name: First______________________________ Last___________________________________ Address:________________________________________________________________________ Number

Street

Suite

_______________________________________________________________________________ City

Office Phone: (

Province

) _____________ Fax: (

Postal Code

) ______________ e-mail: __________________

Registration Number:_____________________________________________________________

QUESTIONNAIRE Treating and Managing Dry Eye Shachar Tauber, MD 1. ❑ ❑ ❑ ❑

According to the paper, what is the prevalence of dry eye?

6%-14% 10% 20% 25%

2. ❑ ❑ ❑ ❑

Which of the following is the thinnest tear film layer?

Mucin Aqueous Lipid They all are of equal thickness

3. ❑ ❑ ❑ ❑

Aqueous layer deficiency can be caused by all of the following, EXCEPT: Trauma Inflammation Neurological defects Heredity

Clinical & Refractive Optometry Quebec 1:2, 2016

CATEGORY A UFC C REDIT A PPLICATION F ORM

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4. ❑ ❑ ❑ ❑

Mucin layer deficiency can be caused by all of the following, EXCEPT: Pemphigoid Vitamin A deficiency Scleroderma Trachoma

5. ❑ ❑ ❑ ❑

All of the following can affect an individual’s blink rate, EXCEPT: Computer use Age Talking Drug interactions

6. ❑ ❑ ❑ ❑

All of the following are important characteristics of artificial tears, EXCEPT: Comfort Minimal blurring Long-lasting protection Rapid runoff

7. ❑ ❑ ❑ ❑

All of the following elements can cause dry eye, EXCEPT: Eye strain due to prolonged computer use Cold weather Air conditioning Certain types of surgery

8. ❑ ❑ ❑ ❑

In the last step of the tear film instability cycle, patients are vulnerable to all of the following, EXCEPT: Ulceration of the cornea Sjögren’s syndrome Inflammation Infection

9. ❑ ❑ ❑ ❑

Which of the following is the optimal treatment approach for dry eye?

Anti-inflammatories Anti-evaporatives Combination therapy Mucomimetics

10. ❑ ❑ ❑ ❑

Which of the following is the thickest tear film layer?

Aqueous layer Mucin layer Lipid layer They are all of equal thickness

Treating and Managing Dry Eye — Tauber

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CLICK HERE TO PRINT THIS UFC CREDIT ARTICLE AND TEST

Clinical & Refractive Optometry Quebec is pleased to present this continuing education (CE) article by Dr. Davis C. Kung, Resident at the West Los Angeles Healthcare Center, Los Angeles, CA, and Dr. Pauline F. Ilsen, Professor at Marshall B. Ketchum University, Los Angeles, CA. This article has been approved for 1 Category A, UFC credit in Ocular Health by the Ordre des Optométristes du Québec. In order to obtain your credit, please refer to page 63 for complete instructions.

Chronic Central Serous Choroidopathy

INTRODUCTION

David C. Kung, OD; Pauline F. Ilsen, OD Los Angeles, California

Central serous retinopathy (CSR) is characterized by serous neurosensory retinal detachment with associated leaks at the level of the retinal pigment epithelium (RPE).

It was first described in 1866 by Von Graefe1 as “central recurrent retinitis” and reported under a variety of names until the term “idiopathic central serous chorioretinopathy” was coined in 1967 by Gass.2 A more severe variant of the disease, chronic CSR, was described in 1977 by Frederick.3 Chronic central serous retinopathy, also referred to as diffuse retinal pigment epitheliopathy (DRPE), is defined

by Yanuzzi as neurosensory detachment of the macula for more than 6 months, or the presence of multifocal recurrent detachments with widespread decompensation of the retinal pigment epithelium (RPE).4 The fluorescein angiography (FA) is characterized by uneven areas of granular hyperfluorescence containing one or more subtle leaks.

Individuals with chronic CSR tend to be in their 50s or older, and bilateral involvement is observed in the majority of cases.5,6 It is estimated that a third to a half of patients with classic CSR end up developing a chronic or recurrent form of CSR.7,8 Photoreceptor layer disruption9,10 along with cystoid degeneration of the macula11,12 can result in poor visual outcomes.

Two cases of patients with chronic CSR are discussed.

They present with different clinical presentations and final best-corrected visual acuities. Diagnosis and management are reviewed in detail.

ABSTRACT Background: Chronic central serous retinopathy (CCSR) is a lesser known variant of central serous retinopathy (CSR), with clinical features characterized by multifocal serous detachments associated with diffuse decompensation of the retinal pigment epithelium (RPE). The disease tends to be bilateral and typically affects individuals over the age of 50.

Due to the chronic nature of the disease, permanently reduced visual acuity is often observed. Case Reports: Two patients with CCSR are discussed. The first patient was a 38-year-old Caucasian male presenting for a routine eye exam, with a history of chronic CSR in the right eye diagnosed four years prior by an outside provider. Fluorescein angiography (FA) and OCT revealed diffuse RPE decompensation with a gravitational tract in both eyes, with foveal thinning in the right eye. The second patient was a 56-year-old African-American male who presented for a routine eye exam, with a history of a “grey spot” in his left eye for over three decades. OCT revealed small areas of RPE atrophy as well as pigment epithelial detachments in both eyes. Conclusion: Chronic CSR has a wide variety of clinical presentations. In individuals with suspected chronic CSR, the optometrist should inquire about systemic conditions and medications associated with CSR. Macular line scans on OCT and FA should be performed to assist with diagnosis. A referral to a retina specialist for possible treatment should be considered. Due to poor visual prognosis, individuals with a history of chronic CSR should be evaluated on a yearly basis.

D.C. Kung — Resident, West Los Angeles VA Healthcare Center, Los Angeles, CA; P.F. Ilsen — Professor, Marshall B. Ketchum University, Los Angeles, CA. Correspondence to: Dr. Pauline F. Ilsen, Marshall B. Ketchum University, Los Angeles, CA. West Los Angeles Veterans Affairs Healthcare Center, Optometry Clinic (123) Bldg. 304, Room 2-123, 11301 Wilshire Blvd., Los Angeles, CA 90073; E-mail: Pauline.Ilsen@va.gov This article has been peer reviewed.

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CASE REPORTS Case One A 38-year-old Caucasian male presented for a routine eye exam with no particular complaints. His ocular history was significant for longstanding serous retinopathy in the right eye diagnosed 4 years prior by an outside provider.

The patient reported poor vision in the right eye for 8 years. He reported being hit in the right eye with a baseball at age 8, with no subsequent ocular injuries or surgeries. His medical history was significant for post-traumatic stress disorder (PTSD), alcohol dependence, cocaine dependence, and substance abuse disorder.

Medications included multivitamin, folic acid, thiamine, cephalexin, ranitidine, antacid, citalopram, and trazodone, with a remote history of corticosteroid usage 20 years prior.

Pinhole visual acuities were 6/30 (20/100) OD, and 6/7.5 (20/25) OS. Pupils were equal, round, and reactive to light, with no afferent pupillary defect. Refraction was not performed with ophthalmology. Intraocular pressures

by Goldmann applanation tonometry were 16 mmHg in both eyes. Anterior segment revealed healthy lashes, cornea, conjunctiva, and lenses in both eyes. Examination of the posterior segment revealed clear media, with healthy optic nerve heads with cup-to-disc ratios of 0.30 in each eye, with a central area of RPE change in the macula of the right eye, and a solitary cotton wool spot (CWS) inferior to the optic disc of the left eye. The tentative diagnosis of chronic CSR OD was made, and further investigation of the CWS was deferred until fundus photography, fluorescein angiogram and OCT could be obtained.

One month later the patient returned for ophthalmic imaging. OCT revealed foveal thinning in the right eye (Fig. 1). Fluorescein angiography revealed extensive RPE decompensation throughout the macula and in a linear pattern nasal to the macula (Fig. 1). The diagnosis of chronic CSR OD was confirmed, and follow-up visits to determine etiology of the CWS were made. HIV AB testing a month prior was negative and glucose was 100 mg/dL. ANA and CBC were ordered, which revealed slight anemia. However, a thorough review of his blood pressure revealed poor control within the past 6 months, reaching 148/112 mmHg just a month before the initial eye exam. The hypertensive episode was ultimately deemed to be the cause of the CWS. At follow-examination a month later, the CWS had resolved and blood pressure was well-controlled.

The patient was lost to follow-up and returned to the optometry clinic 3 years later, with increased metamorphopsia described as a “blurry spiral in his vision with everything around it melding in.” Best-corrected vision was 6/18 (20/60) OD and 6/4.5- (20/15-) OS with a mild myopic correction. Recent blood pressure readings revealed consistent spikes, with BP as high as 192/120 mmHg a month prior. Amsler grid revealed a large central scotoma OD extending to all four corners of grid, sparing 2-3 boxes in each corner. A polycarbonate glasses prescription was released, and referral to ophthalmology for further management was made. At the latest exam, the patient’s visual acuity was 6/60 (20/200) OD and 6/4.5-2 (20/15-2) OS. He was followed for another 5 months before being lost to follow-up.

Case Two A 56-year-old African-American male presented for a routine eye exam, reporting that he had recently lost his glasses. His ocular history was significant for a traumatic

glass injury to right eye 25 years prior, as well as a gray “spot” in his left eye for around 35 years. He reported no history of eye surgery. His medical history was significant for hypertension, chronic obstructive pulmonary disease (COPD), chronic low back pain, and tobacco use. Blood pressure was poorly controlled, with a high of 165/121 mmHg a month prior. Medications included albuterol, budesonide/formoter, omeprazole, tiatropium, amlodipine, and artificial tears.

Best-corrected visual acuities were 6/7.5 (20/25) in each eye, with refraction of -1.00 -1.00 x 150 OD and PL -1.00 x 055 OS. Pupils were equal, round, and reactive to light, with no afferent pupillary defect. Intraocular pressures by Goldmann applanation were 12 mmHg in the right eye and 13 mmHg in the left. Anterior segment was remarkable for focal corneal endothelial pigment in the right eye with two anterior stromal scars, as well as mild lenticular cortical changes in both eyes. Examination of the posterior segment revealed clear media, with healthy optic nerve heads and cup-to-disc ratios of 0.20 in each eye. Mild RPE mottling within both maculae with trace epiretinal membranes in both eyes were present, along with two vitreoretinal tufts peripherally in the right eye.

The patient was prescribed new glasses and asked to return in a year for another comprehensive exam.

The patient did not return until 4 years later, again reporting that he had lost his glasses. Blood pressure remained under poor control, measured at 150/100 mmHg two weeks prior. Best-corrected visual acuities were 6/9-2 (20/30-2) in the right eye and 6/15-2 (20/50-2) in the left. Anterior segment had remained unchanged from the previous exam. Examination of the posterior segment revealed mild macular RPE mottling in the right eye and extensive macular grey RPE mottling within the left eye, with 1-2 soft drusen temporal to the left macula. Spectraldomain OCT revealed multiple patches of RPE atrophy in the right macula, with few PEDs and extensive RPE atrophy in the left eye (Fig. 2). Any evidence of drusen or ERM was minimal on OCT and likely non-contributory to the reduction in best-corrected acuity. A fluorescein angiogram was ordered but the patient never returned for the procedure despite numerous attempts at follow-up.

DISCUSSION Epidemiology Short-term studies of up to 5 years in length report that 10% to 41% of patients with CSR end up developing the chronic form of central serous retinopathy.7,13-15 Long-term actuarial calculus predicts that the number of patients with a chronic or recurrent form of CSR reaches as high as 50% after 12 years.7 However, recurrent forms of CSR can have short-lived episodes and do not truly represent the chronic form of CSR. Kim et al make a clear distinction

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A

B

C

D

E

D

Fig. 1 Case 1. (A,B) Fundus photograph of patient showing RPE mottling and few subretinal deposits in the macula of the right eye.

Left eye is unremarkable. (C) Early and (D) Medium stage fluorescein angiograph showing mottling in the macula and decompensation of the RPE in a â&#x20AC;&#x153;gravitational tractâ&#x20AC;? fashion. The linear pattern of RPE decompensation is a representative of previous persistent subretinal fluid.

(E) Time-domain OCT showing thinning of the fovea with disruption of the photoreceptor layer.

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A

B

C

D

Fig. 2 Case 2. (A,B) Spectral-domain OCT of the right eye demonstrating multiple small areas of photoreceptor disruption. (C) Spectral-domain OCT of the left eye demonstrating focal area of photoreceptor dropout. (D) Spectral-domain OCT of the left eye demonstrating small PED nasally, few areas of photoreceptor disruption, and thickened choroid.

between the two, defining recurrent CSR as a repeated history of CSR with a leakage pattern consistent with acute CSR, without severe RPE changes on FA.16 Patients with chronic CSR are likely to be older than age 50, with a higher incidence of chronic CSR in Hispanics and Asians.13,17 Unlike with classic CSR, gender does not appear to be a predictor of developing chronic CSR,13 especially when related to exogenous corticosteroid use.18 Lafaut reported that ICG findings were bilateral in 95% of both active and chronic cases of CSR, while FA only detected bilateral changes in 68% of eyes.19 It is possible that studies using only FA may be underestimating the true extent of bilateral involvement in this disease.

Signs and Symptoms If serous detachment occurs away from the fovea or in the non-dominant eye, the patient may be asymptomatic.20 When the macula is affected, patients typically present with metamorphopsia, relative central scotoma, micropsia, reduced contrast sensitivity, and altered color perception.

Due to recurrent detachments and RPE changes which may shift according to gravity, there may be additional loss of field and worsened dark adaptation.21 Biomicroscopy typically reveals RPE mottling within the macular region, with possible subretinal granular or fibrinous deposits.22,23 Wang et al suggested that

these early granular deposits could be fragments of the disrupted outer photoreceptor layer.24 With long-term serous detachment, subretinal fibrosis can occur, either as a result of persistent fibrin deposition from the choroid or as sequelae of choroidal neovascularization (CNV).25 Optical coherence tomography will demonstrate extensive RPE alteration and atrophy, with pigment epithelial detachments in 53% to 66% of cases.22,26 Serous retinal detachments are usually shallow, persistent, and multifocal in nature.6 Significantly increased choroidal thickness is also evident on high-definition OCT, often presenting bilaterally even if only one eye is symptomatic.27,28 Indocyanine green angiography will demonstrate initial choroidal filling delay,29 with later multifocal zones of increased choroidal hyperpermeability, with a distribution that may shift or diminish with time.4,30,31 Fluorescein angiography will reveal areas of granular hyperfluorescence with variable patches of leakage, often corresponding to areas of ICG leakage.31 RPE gravitational tracts, a linear representative of previous persistent severe subretinal fluid located below the macula, may also be present on FA.6,16 Etiology, Pathogenesis While numerous hypotheses have been proposed for the pathophysiology of CSR, the exact mechanism remains unclear. Focal injury to the RPE alone is not enough to

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Table I Risk factors for chronic CSR - Type A behavior - Diagnosis of psychiatric illnesses - Exogenous corticosteroid use - High endogenous cortisol levels

- PDE-5 inhibitors - Hypertension - Obstructive sleep apnea - Helicobacter pylori

cause serous detachment; an underlying source of fluid pressure and impaired fluid transport beyond the site of leakage must also be present in order for serous detachment to occur.32 The increased usage of indocyanine green angiography (ICGA) has allowed for detailed examination of hemodynamic disturbances within the choroid, which may ultimately be the culprit.29,33 Prunte et al proposed that choroidal hyperpermeability in CSR was caused by capillary and venous congestion after ischemia of the choroidal lobules.34 More recent OCT imaging studies demonstrate areas of increased choroidal thickness corresponding to these areas of hyperpermeability,27,28 along with focally increased hydrostatic pressure of the choroid.35 Even in patients with unilateral complaints, choroidal vascular hyperpermeability was commonly present in the other eye, with fellow involvement in 55% to 97% of patients.5,33 These findings suggest that chronic CSR does not simply involve local vascular anomalies, but is a diffuse and pervasive choroidal disease with underlying systemic etiology.

It is likely that cortisol plays a significant role in the pathogenesis of CSR. Sharma et al proposed that cortisol increases the permeability of the choriocapillaris by potentiating the effect of epinephrine.36 Tewari et al reported that individuals with CSR tend to have overall significantly increased sympathetic activity,37 which has classically been associated with increased blood cortisol levels.

Furthermore, central serous retinopathy in patients with Cushingâ&#x20AC;&#x2122;s syndrome secondary to pituitary or adrenocortical adenomas have been documented.38-40 Based on high endogenous levels of cortisol found in individuals with chronic CSR, Caccavale et al derived that hypercoagulability and platelet aggregation may contribute to pathogenesis.41,42 Treatment of CSR with aspirin resulted in quick recovery of visual acuity and reduced the number of recurrences,41 lending support to this hypothesis.

Few other case reports have hinted at a possible association with elevated levels of testosterone and CSR,43,44 but correlation remains weak at best.

Risk Factors CSR has classically been has associated with Type A behavior45 and highly distressed individuals.46-48 Tittl et al reported that usage of psychopharmacologic medications was a predictor of chronic CSR,13 suggesting that these individuals have more difficulty adapting to demands or coping with stress. A diagnosis of psychiatric illnesses has been strongly linked to recurrence of episodes (Table I).49

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There exists a particularly strong association between exogenous corticosteroid use and chronic central serous retinopathy.13,20,36,50-53 The amount of time to develop maculopathy and dosage of steroid necessary for retinal detachment has not been established, though complete discontinuation of the steroids has resulted in rapid reattachment of the macula and improvement of symptoms in these studies. Oral, intravenous and topical usage appeared to be the most common routes of steroid administration. Acute cases of CSR developing from inhaled and intranasal steroid usage have been reported in the literature,54 but association remains weak.

Association of chronic CSR has also been made with certain systemic conditions, especially hypertension13,15,55 and obstructive sleep apnea.56 Chronic CSR as a result of post-organ and bone marrow transplants have also been documented,20,52,57-59 but often in the setting of hypertensive patients with prolonged corticosteroid usage or other immunosuppressive drugs. When adjusting for systemic steroid usage, post-organ transplants was statistically insignificant as a risk factor for CSR.60 The presence of H. pylori as a risk factor has also been reported.61,62 Case reports of CSR as a result of phosphodiesterase-5 (PDE-5) inhibitor usage, in particular sildenafil citrate, have been reported.63-65 Sildenafil is known to alter the retrobulbar and choroidal circulation by increasing blood flow velocity.66 A recent study by Vance et al demonstrated that choroidal thickness temporarily increases after ingestion of sildenafil.67 However, a recent post-marketing surveillance study did not support an association between PDE-5 inhibitors and CSR.68 Interestingly, Tsai et al recently reported that a diagnosis of CSR was independently associated with an increased risk of being subsequently diagnosed with erectile dysfunction.69 It is possible that underlying systemic factors such as stress remain as contributing factors to CSR in these cases.

Nonetheless, cessation should be considered in chronic cases of CSR. In a small study of 27 patients with progressive, largely bilateral chronic CSR, 52% of patients had 1 or more relatives who were affected. While the inheritance pattern could not be established, these findings suggest a possible genetic disposition toward chronic CSR.70 Differential Diagnoses A diagnosis of chronic central serous retinopathy must involve excluding other causes of macular detachment or edema, as well as any disease that may cause multiple shallow detachments and/or PEDs. As chronic CSR tends to occur in an older population, these patients will likely present with numerous systemic and ocular co-morbidities, such as hypertension, diabetes, age-related macular degeneration (AMD) or glaucoma. Optic nerve pit, diabetic macular edema, cystoid macular edema, choroidal

Table II Management and treatment of CSR Management options - Focal laser - Transpupillary Thermotherapy - Photodynamic Therapy - Anti-VEGF (Bevacizumab)

Oral alternatives - Rifampin - Finasteride - Eplerenone - Low-dose aspirin - Acetazolamide

melanoma, hypertensive retinopathy, and choroidal neovascular membrane (CNVM) are a few differentials to consider. The tendency of chronic CSR to be bilateral6,71 helps to exclude several differentials on this list.

Accelerated hypertension, defined by the World Health Organization (WHO) as diastolic blood pressure >120 mmHg associated with retinal hemorrhages and soft exudates without papilledema, can cause RPE lesions called Elschnig spots. These spots represent focal areas of RPE infarction resulting from underlying choriocapillaris necrosis.72 In the acute phase these lesions are yellowwhite and leak fluorescein, but with time they become pigmented centrally and block fluorescein.73,74 In chronic CSR, the lesions demonstrate persistent, confined low grade leakage irrespective of time course.

Due to its bilateral nature and tendency to affect the older population, chronic CSR can be misdiagnosed as AMD with underlying choroidal neovascularization. It is also likely that both diseases may occur simultaneously.

Gajdzik-Gajdecka reported the presence of CNV in 11.8% of patients with chronic CSR, in patients with aged 48 to 67.26 In patients 64 years and older with chronic CSR, Lafaut reported CNV in as many as 33% of 1 9 p a t i e n t s .

Yet the presence of signs such as retinal precipitates, gravitational tracts, and missing drusen should clue in to proper diagnosis of CSR.75 OCT can be utilized to confirm the presence or absence of subretinal fluid, and leakage patterns on FA and ICG can greatly assist to distinguish between the two diseases.19 Vogt-Kayanagi-Harada (VKH) disease, an autoimmune disease with ocular manifestations of bilateral uveitis and multifocal serous detachments,76 can present similarly to chronic CSR especially when prodromal central nervous system symptoms are not yet present.

Kunavisurat described a case when individuals with chronic CSR were misdiagnosed with Harada disease and consequently treated with steroids, resulting in worsened vision.53 Yet the multifocal RPE lesions in VKH are often more numerous and more leaky, and will respond favorably to steroid treatment.6 There are a number of other posterior pole inflammatory diseases that mimic the appearance of chronic CSR. Multifocal choroiditis is typically characterized by bilateral multiple choroidal inflammatory lesions, but has a predilection for young myopic females.77 Other diseases such as birdshot retinochoroidopathy or other white dot

syndromes can resemble chronic CSR, but will often have systemic manifestations. The lesions in choroiditis are typically fluffy, elevated, and leak fluorescein, while the lesions in chronic CSR are primarily flat (except for PEDs) and do not expand on fluorescein.6 Special care must be taken when initiating systemic corticosteroid treatment in these patients to avoid exacerbating a mistaken case of chronic CSR. Management and Treatment In patients with reduced vision, polycarbonate or Trivex® (PPG Optical products), lenses should be prescribed to protect the better-seeing eye. With severe cases of vision loss or bilateral vision loss, a low vision exam or low vision rehabilitation referral may be warranted.

The clinician should work closely with the patient’s primary care provider (PCP) to ensure that hypertension and other systemic risk factors are addressed. An important initial step in management should involve removing or replacing systemic medications that are risk factors for exacerbating CSR. Sharma et al reported that discontinuation of systemic steroids in chronic CSR has shown to stop RPE leakage and aid in retinal reattachment in 87.5% of cases, though final visual acuity is typically better in patients younger than 40.36 Discontinuation of a PDE-5 inhibitor should be considered when possible.63 When the patient remains overtly symptomatic or in cases of non-resolving CSR, other treatment options should be considered.

Focal laser photocoagulation has been demonstrated to shorten the duration of symptoms and reduce the rate of recurrence of episodes, but studies differ on whether the procedure can improve final best-corrected acuities (Table II).78-81 Focal laser has limited indications in chronic CSR due to the large number of leaks present and proximity of leakage to the fovea. Complications can involve accidental photocoagulation of the macula, scotomas, dramatic loss of contrast sensitivity, and most significantly, an increased risk for developing CNV several months after treatment.82-84 In fact, newer treatments have been used to “rescue” cases of secondary CNV as a result of focal laser.85-87 More recently, transpupillary thermotherapy (TTT), which involves using lower power laser photocoagulation for a longer period of time, has shown ability to induce retinal re-attachment and improve best-corrected visual acuities in more than 90% of eyes.88,89 Originally developed to treat choroidal metastases,90 TTT is gaining increased acceptance as a possible treatment modality.

Numerous studies have shown the effectiveness of photodynamic therapy (PDT) with chronic CSR.4,21,91 In a recent study, anatomic and visual success was achieved for up to 4 years with standard fluence PDT, with only 8.6% of eyes requiring retreatment.92 Due to its ability to treat multiple areas of leakage without compromising Chronic Central Serous Choroidopathy — Kung, Ilsen

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retinal integrity, PDT has a large advantage over focal laser. However, cases of secondary CNV have also been reported with this modality.8,30 Half-dose (or half-fluence) PDT has demonstrated success with a reduced side effect profile, showing complete resolution of serous detachment in 89.6% of eyes over the course of one year, versus 83% for full-dose PDT.93 In another study, at 12-month follow-up, subretinal fluid resorption was observed in 79% of full fluence PDT eyes versus 91% of half-fluence eyes.94 However, most of the studies mentioned above utilized time-domain OCT in their analyses. Using spectral-domain OCT to analyze half-fluence treated eyes, Shinojima et al observed an initial recurrence of PEDs and consequent retinal detachment on 1-year follow-up, suggesting the effectiveness of this treatment is likely short term.95 Patients with higher initial visual acuity may benefit greater from PDT, and earlier treatment is likely to produce better visual results.21 Patients older than age 55 were less likely to respond to PDT due to persistent serous detachment, and presence of PED also resulted in less favorable response to treatment.93,94 A study comparing PDT and focal laser reveals that half dose PDT facilitates earlier resolution of macular detachment and recovery of central retinal function, but after 3 months there was no significant difference between the two modalities.81 Anti-VEGF factors have been attempted in treatment of this disease due to the moleculeâ&#x20AC;&#x2122;s profound effects on altering vascular permeability.96,97 Anti-VEGF agents are able to restore occludin proteins in the blood-retinal barrier,97 reducing leakage of fluid into the subretinal space. With respect to chronic CSR, intravitreal bevacizumab (IVB) has demonstrated initial success in improving mean acuity and reducing foveal thickness, presumably by its ability to penetrate the retina and affect choroidal hyperpermeability.98,99 The injection is well tolerated at 1-year follow-up.100 Compared to the effectiveness of low-dose PDT, IVB has little to no edge in improving mean visual acuity.101 Less invasive oral alternatives have also demonstrated promise for visual improvement. Rifampin, thought to improve chronic CSR by way of altering the production of endogenous steroids, has initially demonstrated successful resolution of multifocal CSR and presents a cost-effective method of treatment.102 By way of similar mechanism, promising results have been achieved with finasteride,103 mifepristone,104 and eplerenone, a specific mineralocorticoid receptor (MR) antagonist.105 Azetazolamide treatment appears effective in shortening the time for subjective and objective clinical resolution, but has no bearing on final visual outcome or recurrence rate of the disease.106 As mentioned previously, low-dose aspirin has also been a potential form of treatment.41

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Prognosis Chronic CSR tends to have poor visual outcomes due to the pervasive and recurrent nature of the disease.6 A negative correlation between duration of symptoms and best-corrected visual acuities has been reported,16 with progressive atrophy of the outer plexiform layer (OPL) and degeneration of the photoreceptors explaining the severe reduction in visual acuity.9 If the OPL remains intact and the inner segment/outer segment (IS/OS) junction undisrupted, final visual acuity of 6/12 (20/40) or more is likely after macular reattachment.16 Piccollino et al reported that granulation of the OPL begins after several months of detachment, but severe atrophy does not occur until at least 1 year later, after which the visual prognosis deteriorates.9 Wang et al reported that foveal attenuation can occur as early as 4 months of symptoms, but severe reduction of foveal thickness resulting in best-corrected visual acuity of 6/12 (20/40) or less was most associated with more than 10 years duration of symptoms.107 These studies warrant close follow-up of these patients, and early treatment should be considered.

Location and size of RPE atrophy are also important prognostic factors in predicting final best-corrected visual acuity. Bandello et al followed 51 patients for 35.7 months without treatment, and reported that approximately 15% of patients decreased in mean best-corrected visual acuity by 3 lines from baseline. The decrease in acuity was strongly associated with disease duration of >7 years or the presence of confluent areas of RPE atrophy at least 2 disk diameters in size on ICG.108 Kim et al reported that the presence of an abnormal hyperfluorescent area within 1 macular photocoagulation study disc area on FA was correlated with final visual acuity of 6/12 (20/40) or less.16 Long-term increased choriocapillaris permeability can cause fibrin to accumulate beneath the retina, resulting in subretinal fibrosis and decreased best-corrected visual acuity.25,109 Prolonged and recurrent macular detachment can also cause cystoid macular degeneration (CMD), characterized by cystoid changes on OCT with no fluorescein leakage in the macula. CMD tends to have a preferential distribution in the papillomacular bundle and has been reported in patients with as little as 3.5 years of symptoms.11 When the fovea is involved, it is usually correlated with final visual acuity 6/60 (20/200) or less.11,16 In certain cases, cystoid changes can present in an extrafoveal pattern called posterior cystoid retinal degeneration, sparing central vision and resulting in final visual acuity of 6/12 (20/40) or better.12 Final visual acuity in chronic CSR appears to be independent of gender, initial visual acuity, the number of areas of RPE atrophy, or the presence of gravitational tracts.15,16,108,110 More recent studies are suggesting that the presence of CSR with associated PEDs is not associated

with poorer visual prognosis, although PEDs in these studies were largely extrafoveal.16,111 The presence of persistent or central PEDs appears to be associated with visual prognosis of <6/12 (<20/40) and poorer response to PDT treatment.93,110 While significant and most clinically relevant, bestcorrected acuities are only a measure of foveal function and do not represent structural changes outside the foveal region.112 Increased usage of microperimetry to measure macular function has demonstrated that low dose PDT can improve retinal sensitivity in short-term cases of follow-up even when best-corrected acuities remain unchanged.112,113 Measuring retinal sensitivity may give better insight to factors such as contrast sensitivity, dark adaptation, and color perception in cases of chronic retinal detachment. As these can significantly affect quality of life, a low vision consult in long-term cases of CSR should be considered.

5.

6.

7.

8.

9.

10.

11.

Complications Secondary CNVM is a known complication of chronic CSR.5 It occurs in around 4% of eyes with chronic CSR108 and occurs more commonly in patients with vision worse than <6/12 (<20/40).110

12.

13.

CONCLUSION Optometrists should be aware of systemic associations and medications known to cause CSR or initiate recurrence of episodes. We should be aware that CSR has numerous atypical manifestations and can take on a chronic course that results in poor visual prognosis if not managed properly. Optometrists need to be monitoring medications regularly for steroids and working closely with the patient’s primary care provider in ensuring control of blood pressure. Alternatives to PDE-5 inhibitors should be considered when possible.

Referral to ophthalmology for a baseline FA should be obtained in patients to assess the full extent of damage to RPE and underlying structures. Due to the progressive nature of the disease, referral for treatment should be considered in early stages of the disease. As patients with acute CSR can end up developing the chronic form of the disease, close follow-up is warranted especially with acute cases. ❏

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15.

16.

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19.

20.

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64. Fraunfelder FW, Fraunfelder FT. Central serous chorioretinopathy associated with sildenafil. Retina 2008; 28(4): 606-609.

65. Aliferis K, Petropoulos IK, Farpour B, et al. Should central serous chorioretinopathy be added to the list of ocular side effects of phosphodiesterase 5 inhibitors? Ophthalmologica 2012; 227(2): 85-89. doi: 10.1159/000333824. Epub 2011 Dec 7.

66. Harris A, Kagemann L, Ehrlich R, et al. The effect of sildenafil on ocular blood flow. Br J Ophthalmol 2008; 92(4): 469-473.

67. Vance SK, Imamura Y, Freund KB. The effects of sildenafil citrate on choroidal thickness as determined by enhanced depth imaging optical coherence tomography. Retina 2011; 31(2): 332-335.

68. French DD, Margo CE. Central serous chorioretinopathy and phosphodiesterase-5 inhibitors: a case-control postmarketing surveillance study. Retina 2010; 30(2): 271-274.

69. Tsai DC, Huang CC, Chen SJ, et al. Increased risk of erectile dysfunction among males with central serous chorioretinopathy - a retrospective cohort study. Acta Ophthalmol 2012 Sep 23. doi: 10.1111/j.17553768.2012.02528.x. [Epub ahead of print] 70. Weenink AC, Borsje RA, Oosterhuis JA. Familial chronic central serous chorioretinopathy. Ophthalmologica 2001; 215: 183-187.

71. Ross A, Ross AH, Mohamed Q. Review and update of central serous chorioretinopathy. Curr Opin Ophthalmol 2011; 22(3): 166-173. doi: 10.1097/ICU.0b013e3283459826.

72. Kishi S, Tso MO, Hayreh SS. Fundus lesions in malignant hypertension. I. A pathologic study of experimental hypertensive choroidopathy. Arch Ophthalmol 1985; 103(8): 1189-1197.

73. de Venecia G, Jampol LM. The eye in accelerated hypertension. II. Localized serous detachments of the retina in patients. Arch Ophthalmol 1984; 102(1): 68-73.

74. Lafaut BA, De Vriese AS, Stulting AA. Fundus fluorescein angiography of patients with severe hypertensive nephropathy. Graefes Arch Clin Exp Ophthalmol 1997; 235(12): 749-754.

75. Inhoffen W, Ziemssen F, Bartz-Schmidt KU. [Chronic central serous chorioretinopathy (cCSC): differential diagnosis to choroidal neovascularisation (CNV) secondary to age-related macular degeneration (AMD)]. Klin Monbl Augenheilkd 2012; 229(9): 889-896. Epub 2012 Aug 28.

[Article in German]

76. Sachdev N, Gupta V, Gupta A, Singh R. Posterior segment recurrences in Vogt-Koyanagi-Harada disease. Int Ophthalmol 2008; 28(5): 339-345. Epub 2007 Sep 26.

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79. Burumcek E, Mudun A, Karacorlu S, Arslan MO. Laser photocoagulation for persistent central serous retinopathy: results of long-term follow-up. Ophthalmology 1997; 104(4): 616-622.

80. Ladas ID, Rouvas AA, Apostolopoulos M, Brouzas D, Karagiannis DA, Georgalas I, Baltatzis S. Diffuse retinal pigment epitheliopathy: treatment with laser photocoagulation. Eur J Ophthalmol 2004; 14(4): 315-320.

81. Lim JW, Kang SW, Kim YT, Chung SE, Lee SW. Comparative study of patients with central serous chorioretinopathy undergoing focal laser photocoagulation or photodynamic therapy. Br J Ophthalmol 2011; 95(4): 514-517. Epub 2010 Jul 19.

82. Matsunaga H, Nangoh K, Uyama M, Nanbu H, Fujiseki Y, Takahashi K. [Occurrence of choroidal neovascularization following photocoagulation treatment for central serous retinopathy]. Nihon Ganka Gakkai Zasshi 1995; 99(4): 460-468. [Article in Japanese] 83. Simon P, Glacet-Bernard A, Binaghi M, Coscas G, Soubrane G. [Choroidal neovascularization as a complication following laser treatment of central serous chorioretinopathy]. J Fr Ophtalmol 2001; 24(1): 64-68. [Article in French] 84. Ha TW, Ham DI, Kang SW. Management of choroidal neovascularization following laser photocoagulation for central serous chorioretinopathy. Korean J Ophthalmol 2002; 16(2): 88-92.

85. Cakir M, Cekiç O, Yilmaz OF. Photodynamic therapy for iatrogenic CNV due to laser photocoagulation in central serous chorioretinopathy. Ophthalmic Surg Lasers Imaging 2009; 40(4): 405-408.

86. Pikkel J, Rumelt S. Intravitreal bevacizumab for choroidal neovascularization secondary to laser photocoagulation for central serous chorioretinopathy. Eur J Ophthalmol 2012; 22(3): 488-491.

87. Nomura Y, Obata R, Yanagi Y. Intravitreal bevacizumab for iatrogenic choroidal neovascularization due to laser photocoagulation in central serous chorioretinopathy. Jpn J Ophthalmol 2012; 56(3): 245-249. Epub 2012 Apr 20.

88. Shukla D, Kolluru C, Vignesh TP, et al. Transpupillary thermotherapy for subfoveal leaks in central serous chorioretinopathy. Eye (Lond). 2008; 22(1): 100-106. Epub 2006 May 26.

89. Kawamura R, Ideta H, Hori H, et al. Transpupillary thermotherapy for atypical central serous chorioretinopathy. Clin Ophthalmol 2012; 6: 175-179. Epub 2012 Jan 25.

90. Journée-de Korver JG, Oosterhuis JA, Kakebeeke-Kemme HM, de Wolff-Rouendaal D. Transpupillary thermotherapy (TTT) by infrared irradiation of choroidal melanoma. Doc Ophthalmol 1992; 82(3): 185-191.

91. Cardillo Piccolino F, Eandi CM, Ventre L, et al.

Photodynamic therapy for chronic central serous chorioretinopathy. Retina 2003; 23(6): 752-763.

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92. Silva RM, Ruiz-Moreno JM, Gomez-Ulla F, et al.

Photodynamic therapy for chronic central serous chorioretinopathy: a 4-year follow-up study. Retina 2012 Oct 22. [Epub ahead of print] 93. Chan WM, Lai TY, Lai RY, et al. Safety enhanced photodynamic therapy for chronic central serous chorioretinopathy: one-year results of a prospective study.

Retina 2008; 28(1): 85-93.

94. Reibaldi M, Cardascia N, Longo A, Standard-fluence versus low-fluence photodynamic therapy in chronic central serous chorioretinopathy: a nonrandomized clinical trial. Am J Ophthalmol 2010; 149(2): 307-315.e2. Epub 2009 Nov 6.

95. Shinojima A, Kawamura A, Mori R, et al. Detection of morphologic alterations by spectral-domain optical coherence tomography before and after half-dose verteporfin photodynamic therapy in chronic central serous chorioretinopathy. Retina 2011; 31(9): 1912-1920.

96. Harhaj NS, Felinski EA, Wolpert EB, et al. VEGF activation of protein kinase C stimulates occludin phosphorylation and contributes to endothelial permeability. Invest Ophthalmol Vis Sci 2006; 47(11): 5106-5115.

97. Wolfensberger TJ, Gregor ZJ. Macular edema — rationale for therapy. Dev Ophthalmol 2010; 47: 49-58. Epub 2010 Aug 10.

98. Schaal KB, Hoeh AE, Scheuerle A, et al. Intravitreal bevacizumab for treatment of chronic central serous chorioretinopathy. Eur J Ophthalmol 2009; 19(4): 613-617.

99. Artunay O, Yuzbasioglu E, Rasier R, et al. Intravitreal bevacizumab in treatment of idiopathic persistent central serous chorioretinopathy: a prospective, controlled clinical study. Curr Eye Res 2010; 35(2): 91-98.

100. Inoue M, Kadonosono K, Watanabe Y, et al. Results of oneyear follow-up examinations after intravitreal bevacizumab administration for chronic central serous chorioretinopathy.

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101. Semeraro F, Romano MR, Danzi P, et al. Intravitreal bevacizumab versus low-fluence photodynamic therapy for treatment of chronic central serous chorioretinopathy. Jpn J Ophthalmol 2012 Aug 23. [Epub ahead of print] 102. Steinle NC, Gupta N, Yuan A, Singh RP. Oral rifampin utilization for the treatment of chronic multifocal central serous retinopathy. Br J Ophthalmol 2012; 96(1): 10-13.

Epub 2011 Nov 3.

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103. Forooghian F, Meleth AD, Cukras C, et al. Finasteride for chronic central serous chorioretinopathy. Retina 2011; 31(4): 766-771.

104. Nielsen JS, Jampol LM. Oral mifepristone for chronic central serous chorioretinopathy. Retina 2011; 31(9): 1928-1936.

105. Zhao M, Célérier I, Bousquet E, et al. Mineralocorticoid receptor is involved in rat and human ocular chorioretinopathy. J Clin Invest. 2012; 122(7): 2672-2679. doi: 10.1172/JCI61427. Epub 2012 Jun 11. PubMed PMID: 22684104; 106. Pikkel J, Beiran I, Ophir A, Miller B. Acetazolamide for central serous chorioretinopathy. Ophthalmology 2002; 109: 1723-1725.

107. Wang MS, Sander B, Larsen M. Retinal atrophy in idiopathic central serous chorioretinopathy. Am J Ophthalmol 2002; 133(6): 787-793.

108. Bandello F, Virgili G, Lanzetta P, et al. [ICG angiography and retinal pigment epithelial decompensation (CRSC and epitheliopathy)]. J Fr Ophtalmol 2001; 24(4): 448-451.

[Article in French] 109. Schatz H, McDonald HR, Johnson RN, et al. Subretinal fibrosis in central serous chorioretinopathy. Ophthalmology 1995; 102(7): 1077-1088.

110. Loo RH, Scott IU, Flynn HW Jr, et al. Factors associated with reduced visual acuity during long-term follow-up of patients with idiopathic central serous chorioretinopathy.

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111. Mudvari SS, Goff MJ, Fu AD, et al. The natural history of pigment epithelial detachment associated with central serous chorioretinopathy. Retina 2007; 27(9): 1168-1173.

112. Reibaldi M, Boscia F, Avitabile T, et al. Functional retinal changes measured by microperimetry in standard-fluence vs low-fluence photodynamic therapy in chronic central serous chorioretinopathy. Am J Ophthalmol 2011; 151(6): 953-960.e2. Epub 2011 Mar 31.

113. Senturk F, Karacorlu M, Ozdemir H, et al. Microperimetric changes after photodynamic therapy for central serous chorioretinopathy. Am J Ophthalmol 2011; 151(2): 303-309.e1. Epub 2010 Dec 18.

CATEGORY A UFC C REDIT A PPLICATION F ORM

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INSTRUCTIONS

FOR

1 CATEGORY A, UFC CREDIT

This course has been approved for 1 Category A, UFC credit in Ocular Health by the Ordre des Optométristes du Québec. Please complete and submit this test questionnaire for grading before March 31, 2018.

In order to obtain 1 Category A, UFC credit, please follow these steps: • Fill in the identification section and answer the 10 multiple choice questions in this UFC credit application form • Prepare a cheque payable to Mediconcept for $25.00 • Mail your completed UFC credit application form along with your cheque to: CRO Quebec, 3484 Sources Blvd, Suite 518, Dollard-des-Ormeaux, QC H9B 1Z9 Your answers will be graded by Clinical & Refractive Optometry. If you score 50% or more, a UFC Credit Certificate approved by the Ordre des Optométristes du Québec will be issued to you for your records.

CLICK HERE TO PRINT THIS UFC CREDIT TEST AND ARTICLE Name: First______________________________ Last___________________________________ Address:________________________________________________________________________ Number

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_______________________________________________________________________________ City

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Province

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Registration Number:_____________________________________________________________

QUESTIONNAIRE Chronic Central Serous Choroidopathy David C. Kung, OD; Pauline F. Ilsen, OD 1. ❑ ❑ ❑ ❑

All of the following statements about central serous retinopathy (CSR), EXCEPT: Typically it is bilateral It usually occurs in individuals over age 50 Permanently reduced visual acuity is often observed It occurs more frequently in males than in females

2. ❑ ❑ ❑ ❑

At initial presentation the patient in Case 1 initially reported all of the following, EXCEPT: No surgeries Substance abuse disorder Suicidal tendencies Post-traumatic stress disorder (PTSD)

3. ❑ ❑ ❑ ❑

The patient in Case 1 was found to have all of the following, EXCEPT: Pupils reactive to light Healthy cornea Healthy optic nerve heads Elevated intraocular pressure OS

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CATEGORY A UFC C REDIT A PPLICATION F ORM 64

4. ❑ ❑ ❑ ❑

At the 3-year point following the initial exam, what was the visual acuity of the patient in Case 1?

6/120 (20/400) OD and 6/4.5 (20/15) OS 6/4.5-2 (20/15-2) OD and 6/60 (20/200) OS 6/60 (20/200) OD and 6/4.5-2 (20/15-2) OS 6/36 (20/120) OD and 6/4.5-2 (20/15-2) OS

5. ❑ ❑ ❑ ❑

The patient in Case 2 was found to have all of the following, EXCEPT: Mild lenticular cortical changes in the left eye No afferent pupillary defect Healthy optic nerve heads Normal intraocular pressures

6. ❑ ❑ ❑ ❑

According to short-term studies, what percentage of patient with CSR develop the chronic form of the condition?

5% to 10% 10% to 41% 50% 65% to 75%

7. ❑ ❑ ❑ ❑

In which ethnic groups is chronic CSR predominant?

Caucasians African Americans and Asians Hispanics Hispanics and Asians

8. ❑ ❑ ❑ ❑

All of the following are risk factors for CSR, EXCEPT: Lupus Type A behavior Psychopharmacologic medications Psychiatric illnesses

9.

All of the following are important prognostic factors in predicting best-corrected visual acuity (BCVA), EXCEPT: Etiology of RPE atrophy Duration of symptoms Location of retinal pigment epithelium (RPE) Size of RPE atrophy

❑ ❑ ❑ ❑

10. Secondary choroidal neovascular membrane (CNVM) occurs in approximately what percentage of eyes with chronic CSR? ❑ 1% ❑ 4% ❑ 6% ❑ 8%

Clinical & Refractive Optometry Quebec 1:2, 2016

CLICK HERE TO PRINT THIS UFC CREDIT ARTICLE AND TEST

Clinical & Refractive Optometry Quebec is pleased to present this continuing education (CE) article by Dr. Richard Maharaj, Clinical Director at eyeLABS, Brampton, ON. This article has been approved for 1 Category A, UFC credit in Ocular Health by the Ordre des Optométristes du Québec. In order to obtain your credit, please refer to page 70 for complete instructions.

Blink Mechanics: Viscoadaptive Technology for the Ocular Surface Richard Maharaj, OD, FAAO Brampton, Ontario

20-20-20 rule. When one looks at dry eye and ocular |surface disease, one realizes the role that the blink plays in it. Dr. Maharaj stated that understanding blink mechanics makes it easier to understand the mechanisms involved in the development of the dry eye.

INTRODUCTION While the body of Dr. Maharaj’s work is in Meibomian Gland Dysfunction, he noted that this presentation topic was focused on blink metrics in mild to moderate dry eye patients. There are two components in the discussion of the mechanics of blinking and viscoadaptive technologies. The first is what the eyelid does on a given blink. The second is the microanatomy involved in the blink at the inner and outer eyelid surface. Dr. Maharaj has observed that a blanket approach to treatment with artificial tears isn’t an effective model of care for the multifactorial dry eye patient.

Following the artificial tear evolution and consideration of the chemical properties of various artificial tear products, industry has moved toward meibomian gland driven therapies with specific focus on lipid layer supplementation.

BLINK MECHANICS AND VISCOADAPTIVE DEVICES In a normal functioning eye, the eyelid closes as the superior eyelid comes down and meets the bottom eyelid, grabs onto the lipid layer and the oil film rises with the upper lid to coat the tear film. This is clearly shown on video imaging with the Oculus keratograph 5M and looks very clear under slit lamp. The human body has evolved in such a way that this mechanism of action is responsible for achieving comfort, and in fact can be the source of discomfort, said Dr. Maharaj. He noted that one of the current focuses of the Tear Film & Ocular Surface Society (TFOS) is the mechanics and metrics of blinking.

Computer vision syndrome is not surprisingly on the rise. A common at home tip for patients involves blinking 20 times every 20 seconds by looking 20 feet away or the R. Maharaj — Clinic Director, eyeLABS, Brampton, Ontario; Staff Optometrist, Humber River Regional Hospital - York/Finch Eye Associates, Toronto, Ontario Correspondence to: Dr. Richard Maharaj, 7900 Hurontario, Suite 406 Brampton, ON L6Y0P6; E-mail: rmaharaj@eyelabs.ca This article has been peer-reviewed.

MECHANICS OF DRY EYE DISEASE Dr. Maharaj described rheology, the behavior of fluids in response to applied forces, which is different from Newtonian physics; fluids respond differently than solids.

An appreciation of this difference is crucial in reviewing viscoadaptive technology and pseudoelastic viscoadaptive tears.

While dry eye is a chronic condition for which there is no cure, ECPs can manage it. Dr. Maharaj counsels patients that they can be treated and progress to a point where they are more comfortable, where they may not notice their eyes on any given day or any given week, but by no means is it a cure.

According to various worldwide studies over the past decade, the prevalence of dry eye ranges from 7 percent up to close to 50 percent, depending on the study. In Dr. Maharaj’s dry eye clinic, more than 90 percent of patients actually exhibit the condition in itself; however, in general eye care practices, dry eye as a condition is second only to cataracts. Pre-identification of the dry eye patient undergoing surgery and pretreatment is far more likely to result in patients having a better postoperative experience.

When considering sending a 65-year-old patient to a cataract surgeon for cataract surgery, for instance, preparing the patient’s ocular surface has been shown to contribute to their postoperative success. Patients that lack preoperative treatment have a four times greater risk of their dry eye worsening following surgery. In the next two to ten years, stated Dr. Maharaj, practitioners will see their role in the perioperative arena growing, and rightfully so. Based on current trends, he predicted greater discussion and use of triglyceride omega 3s for added systemic impact on meibomian gland disease.

Dr. Maharaj discussed osmolarity as a dry eye metric that is important to understand in a general setting. Tear osmolarity is a valuable tool, relative to the Ocular Surface Disease Index (OSDI), corneal staining and Schirmer tear test and has been shown to be more sensitive and more specific than these other measures.

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Fig. 1 Mechanics of blinking.

Fig. 2 Breakdown of blinking process.

When examining the correlation to the severity of the condition, osmolarity has the strongest correlation.

To identify existing dry eye patients in a general practice, it is extremely relevant for patients that may not be symptomatic but are silently suffering. Those are the ones who may, in fact, have a hyperosmolar tear film, which means that they do have a higher component of salt and proteins like MMP-9 and other inflammatory cytokines in their tear film. If this inflammation is elevated and the patient is not symptomatic, the chronic inflammatory environment will eventually produce symptoms.

together, the gland orifice isn’t receiving any negative pressure to draw oil out of it, and if it’s not used, obstruction begins, prompting a cascade of events.

Figure 2 depicts a breakdown of the blinking process, showing a superior component and a torsional component of the upper eyelid moving mainly up and down and slightly, with a minor rotation. However, the inner eyelid barely moves vertically; it actually has a nasal movement.

This is an extremely complex movement with the forces being applied to the cornea and to the ocular surface, in addition to the forces being applied to the fluid between the eyelid and the cornea.

Dr. Maharaj expressed his opinion that there are some more effective solutions for dry eye than artificial tears.

Regardless of ethnicity or the shape of the eye, there is slight vertical movement on the superior eyelid; there is nasal and torsional movement of the superior eyelid; the inferior eyelid margin typically makes lateral movements.

This produces a type of shearing force. What occurs is that rather than the front surface closing, it is the posterior lid margin that closes. The mucocutaneous junction otherwise known as the Line of Marx (LOM) forms a ridge that is not meeting up. There’s no seal of the superior and inferior LOM on lid. A quick test for this is the light test using a transilluminator (Fig. 3). With retroillumination similar to what is being depicted in the figure, a slight gap becomes apparent.

Even in those patients who, under a microscope, appear to be blinking completely, they may, in fact, have inadequate lid seal which will exacerbate the condition.

This will lead to increased friction, causing the lid wiper to become inflamed. In this case, the posterior lid surface is in direct opposition to the cornea with a thin pre-corneal tear film acting as a buffer between the two surfaces. The result is tissue with repetitive microtrauma causing eventual, epitheliopathy and lid inflammation. The meibomian glands are very closely associated to the lid wiper and this

BLINK MECHANICS Under a slit lamp, it is quite common for the lower eyelid to hang slightly lower than the iris, which is very common and produces infrequent, incomplete blinking. There are, however, some patients who don’t have this characteristic; they have a neat palpebral fissure, but the eyelid still doesn’t drop all the way down. In terms of blink mechanics, said Dr. Maharaj, what most patients think happens is that their lower eyelid and upper eyelid come together, touch and then move away. However, when one starts to examine the mechanics of a blink, one sees that this is, in fact, the opposite of what occurs (Fig. 1). The lower eyelid makes very little vertical movement; however, the superior eyelid does most of the travel and there’s actually a torsional component to it. That’s not even taking into consideration ethnicity, the thickness of the tear, the inner eyelid surface, or the lid wiper itself, the band of tissue that also impacts the way eyelids move.

In Dr. Maharaj’s experience, examining the asymmetry between one eye and the other, one often sees anatomical and morphological changes in the meibomian gland of the eye that has a decreased blink rate and decreased blink completeness. In patients whose eyelids come together, there is a correlation with meibomian gland atrophy or truncation: if the eyelids are not coming completely

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Fig. 3 Transilluminator test.

Fig. 4 Components of the TFOS DEWS algorithm.

is where Meibomian Gland Dysfunction (MGD) can start in some patients. Dr. Maharaj stated that while it is important to distinguish between aqueous deficiency and evaporative dry eye, he does not view the situation as one or the other.

This condition is very much a spectrum disease.

At some point, MGD will lead to up-regulation of the lacrimal gland, eventually causing it to become inflamed, resulting in aqueous deficiency. All dry eye patients appear at some point on this spectrum.

forces previously discussed, and whether or not it stabilizes the tear film.

MECHANICS OF DYSFUNCTIONAL BLINKING In terms of the MGD cycle, Dr. Maharaj stated that the TFOS DEWS algorithm is extremely complex; therefore, he has extracted some of the elements he feels are most relevant (Fig. 4). He suggests that practitioners examine the eyelid aperture of the blink first, looking for the lid seal.

When the blink becomes dysfunctional, it results in lid wiper microtrauma due to friction. The resulting symptoms can include extreme pain, mild to severe contact lens intolerance and visual instability. This will lead to hyperosmolarity with an up-regulation in MMP-9 (Matrix metallopeptidase 9), salts and other proteins. Tear hyperosmolarity drives the tear solutes toward the lid margin and meibomian glands and thus the evaporative and aqueous cycle begins. This process applies to the vast majority of mild to moderate dry eye patients and is therefore a good starting point in determining the goal of an artificial tear.

Looking at the problems created by that cycle, the first thing that occurs is decreased blink rate and poor closure. Therefore, said Dr. Maharaj, the goal in tear film therapeutics should be aimed at increased residence time on the cornea with minimal effect on vision stability.

Examining the attributes of a topical treatment that allows it to last longer on the eye is essential. For instance, how it interacts with the eyelid surfaces with the shearing

CURRENT DRY EYE TREATMENTS The goal of therapy is long-term stability, which is a very important part of the tear chemistry — an essential element. As an immunomodulator — a targeted antiinflammatory therapy — Restasis® (cyclosporine ophthalmic emulsion, Allergan Canada, Markham, ON), is extremely effective, noted Dr. Maharaj, at addressing aqueous deficient dry eye.

At the 2011 MGD workshop, MGD became defined as perhaps the leading cause of dry eye disease around the globe. With this, replacing the lipid layer became the utmost priority.

The term “viscoadaptive” was introduced; Dr. Maharaj remarked that it appears to be a confusing term. When doctors refer to the viscosity of a solution, they know what it means in terms of thicker or thinner.

Intraoperatively, it has a different meaning than viscoadaptive on the external eye.

In rheology, the study of forces on fluids is very different when compared to forces on solids because fluids are very much like air; the forces are more or less Newtonian. One can pass one’s hands through it without resistance. However, with a fluid like glass, the forces that need to be applied to get it to move like a liquid are very, very high. The three tenets are understanding viscosity, understanding elasticity, and then examining the cohesive and dispersive nature of fluids.

Dr. Maharaj stated that there are four patterns of rheometric behavior of fluids (Fig. 5); namely Newtonian, pseudoplastic, plastic and dilatant. In Figure 5 the further to the left on the x axis, the lower the shear forces being applied; the further to the right, the higher the shear force.

The y axis relates to viscosity. The solution can be a

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Rheometric Patterns of Fluid Behaviour: Viscosity

Intraocular OVD Pseudoplasticity Curves

Fig. 5 Variations in applied force.

Fig. 6 Pseudoplastic curves of viscoelastic devices.

liquid which will be lower down on the graph or, it can behave like glass or a fractureable solid which will appear higher on the graph.

of this type of fluid is hyaluronic acid (HA). In order to make it a dispersive substance, one can add a short-chain branched molecule that is not bound to the HA that can actually separate from the HA by force. What happens with an artificial tear with HA and a short-chain branched polymer is exposed to blink forces, the HA separates — it binds with the water found in the aqueous component of tears — and it excludes the short branched polymer present.

A hyaluronate and glycerin solution during the blinking process will almost behave like a contact lens — a fractureable solid — in the eye when the eyelid closes because it is applying a high amount of shear force. When the eyelid opens, the solution returns to a fluid state.

In terms of applying these forces to an artificial tear, consideration needs to be given to the way the eyelid moves with a HA-based eye drop compared to a Newtonian solution like methylcellulose, for example.

In the surgical context, the pseudoplastic curves of some of the ophthalmic viscoadaptive devices used in intraocular surgery are shown in Figure 6. The curves vary depending on the device used. Dr. Maharaj noted that some examples currently used in surgery were actually used to derive hyaluronic-based eye drops. Healon® 5 (sodium hyaluronate, AMO, Markham, ON) and iVisc® (sodium hyaluronate, I-Med Pharma, Montreal, QC), for instance, are commonly used. Depending on the shear forces applied, the liquid will eventually reach a certain viscosity and not go past that point. Artificial tears such as Tears Naturale® (ocular lubricant, Alcon Canada, Mississauga, ON), Systane® (lubricant eye drops, Alcon Canada, Mississauga, ON), GenTeal® (lubricant eye drops, Alcon Canada, Mississauga, ON), all have a very simple linear Newtonian movement on the eye regardless of the eye’s blink mechanics.

NEWTONIAN TEAR SOLUTIONS Many fluids are pseudo-Newtonian; they’re not quite Newtonian; however, they possess more or less these same characteristics. On the other hand, plastics when exposed to a great force can carry liquid-like characteristics.

As shown in Figure 5, fluid-like behaviors or low viscosity behaviors at a certain force will become more viscous. The term for this is zero shear rate. Past the zero shear rate it becomes a fractureable solid. The zero shear rate of a pseudoplastic material is important in surgery (intraoperative surgery is really where it all evolved from) because there has to be a point at which it doesn’t become more viscous. If it did, it would harden in the anterior chamber making surgery very difficult. Pseudoplastics have evolved and have been adapted to the ocular surface specifically because of this fact.

Dr. Maharaj stated that this is particularly important when considering artificial tears: The eyelid moves around and applies shear forces. Viscous solutions that still have Newtonian-like behavior with long and short branched polymers behave in more or less a Newtonian fashion. Pseudoplastic or viscoadaptive solutions will behave differently to the various moments in a blink.

NON-NEWTONIAN TEAR SOLUTIONS Regarding blink forces, instead of a tear solution progressing from a cohesive fluid to a hard solid, it actually moves from a cohesive fluid to an elastic material.

In the process of blinking, the eyelid comes down and compresses. It squeezes the material down. One example

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FEATURES OF PSEUDOPLASTIC ELASTOVICOUS TEARS The first Canadian pseudoplastic elastoviscous tear is known as i-drop® (I-Med Pharma, Montreal, QC). It is distinguished by its high molecular weight sodium hyaluronate combined with a short-chain branched polymer, glycerin. The interesting feature of HA is that all the cells in the body, including those of the cornea, have hyaluronic binding sites. The HA in the eye drop binds to these binding sites, anchoring the tear onto the ocular surface. The HA actually combines with the water found in the tears.

It excludes the glycerin which rises to the surface as the eyelid blinks. The glycerin provides a lubricating surface to the blink, decreasing friction on the ocular surface. Once the eyelid reaches down to the bottom, and the eyelid comes up and the solution returns to its original low viscosity. As a result of this process, the residence time is high. The tear mimics all three layers of the tear film simply by virtue of its physical properties.

Dr. Maharaj uses this approach in his general patients, in order to prolong residence time, decrease evaporation and create visual stability. A high molecular weight hyaluronic-based drop allows this. From a rheological perspective, pseudoplastic elastoviscous tears, or PETs, produce the desired effect, mimicking naturally occurring tears.

The problem of decreased blink rate and closure requires that a topical tear increases the residence time on the eye, which i-drop achieves. This is accomplished through decreasing friction on the ocular surface with unbound glycerin and stabilization of the tear film via HA. This decreases evaporation and stabilizes the tear film, providing patients substantially greater comfort.

Dr. Maharaj stated that the last benefit of some of the new drops coming to market, i-drop being one of them, is that they are packaged in a multi-dose, non-preserved bottle. He views the lack of preservatives as an important

benefit. The bottle form may make it more convenient for patients.

The first clinical study of hyaluronan eye drops was undertaken in 1982. At the time, HA was found to have a much longer residence time. This led to the Hylan™ Surgical Shield (Elastoviscous Hylan Surgical Shield, 0.45%) which surgeons were using during surgery to coat and protect the ocular surface.

Dr. Maharaj suggested that when addressing the ocular surface, practitioners ought to carefully consider the true etiology of the condition and all available solutions. With an abundance of products on the market and patients not knowing which to choose, Dr. Maharaj suggested that eye care professionals make very specific patient recommendations.

It is now known that patients are blinking less frequently and less completely, which Dr. Maharaj noted are facts that need to be addressed when weighing treatment options for dry eye. He stated that the best way to achieve this is to provide patients the most successful available products, rather than simply telling them to modify their blink behavior and to use the nearest artificial tear.

In Dr. Maharaj’s Dry Eye Clinic, a very discrete and direct protocol is used. He instructs his patients, “Follow my specific instructions or you won’t feel better. That’s why I’m being specific.” He takes this approach because if one tells patients to use any artificial tear, they will.

This leaves the decision of choosing the topical up to the patient. As a health provider is it imperative to educate patients to make an informed decision.

CONCLUSION Dr. Maharaj concluded his presentation by emphasizing the importance of providing patients a specific recommendation to their individual dry eye problem. The tear film ought to be addressed as a mechanism, as opposed to an element that must be supplemented. ❏

Blink Mechanics: Viscoadaptive Technology for the Ocular Surface — Maharaj

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In order to obtain 1 Category A, UFC credit, please follow these steps: • Fill in the identification section and answer the 10 multiple choice questions in this UFC credit application form • Prepare a cheque payable to Mediconcept for $25.00 • Mail your completed UFC credit application form along with your cheque to: CRO Quebec, 3484 Sources Blvd, Suite 518, Dollard-des-Ormeaux, QC H9B 1Z9 Your answers will be graded by Clinical & Refractive Optometry. If you score 50% or more, a UFC Credit Certificate approved by the Ordre des Optométristes du Québec will be issued to you for your records.

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QUESTIONNAIRE Blink Mechanics: Viscoadaptive Technology for the Ocular Surface Richard Maharaj, OD, FAAO 1. ❑ ❑ ❑ ❑

According to worldwide studies, what is the estimated prevalence of dry eye?

7 percent to 20 percent 7 percent to 30 percent 7 percent to 40 percent 7 percent to 50 percent

2. ❑ ❑ ❑ ❑

What is the rate of risk for patients who lack preoperative treatment having their dry eye worsen following surgery?

Two times greater Three times greater Four times greater Five times greater

3. ❑ ❑ ❑ ❑

Which of the following is a risk factor for dry eye?

Dysfunctional blink Patient age Blink rate Heredity

Clinical & Refractive Optometry Quebec 1:2, 2016

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4. ❑ ❑ ❑ ❑

How common is the phenomenon of the lower eyelid hanging slightly lower than the iris?

Rare Very common More common in the Asian population Occurs in approximately 50 percent of the overall population

5. ❑ ❑ ❑ ❑

All of the following can affect blink mechanics, EXCEPT: Recent episode of conjunctivitis Thickness of the tear The inner eyelid surface Ethnicity

6. ❑ ❑ ❑ ❑

All of the following statements regarding blink mechanics are false, EXCEPT: Blink frequency and completeness have not changed over the last decade People are blinking less frequently and less completely People are blinking more frequently due to computer vision syndrome People are blinking more frequently and less completely

7. ❑ ❑ ❑ ❑

All of the following are clinical signs/symptoms of dysfunctional blinking, EXCEPT: Extreme ocular pain Visual instability Foreign body sensation Contact lens intolerance

8. ❑ ❑ ❑ ❑

In Dr. Maharaj’s dry eye clinic, what percentage of patients exhibit dry eye?

25% 50% 70% 90%

9. ❑ ❑ ❑ ❑

All of the following statements about dry eye are false, EXCEPT: It can be managed but not cured In the earliest stage of the disease, it can be cured Various studies have shown cure rates of 5 percent to 20 percent It can be cured if patients comply with strict medication protocols

10. ❑ ❑ ❑ ❑

Which of the following is the most accurate measure of dry eye severity?

Schirmer tear test Ocular Surface Disease Index (OSDI) Tear osmolarity Corneal staining

Blink Mechanics: Viscoadaptive Technology for the Ocular Surface — Maharaj

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Clinical & Refractive Optometry Quebec is pleased to present this continuing education (CE) article by Dr. Adam Gorner, Optometrist in Private Practice, Dawson Creek, BC and Dr. Leonid Skorin, Jr., Senior Staff Ophthalmologist, Mayo Clinic Health System, Albert Lea, MN. This article has been approved for 1 Category A, UFC credit in Ocular Health by the Ordre des Optométristes du Québec. In order to obtain your credit, please refer to page 80 for complete instructions.

Dragged Fovea Diplopia Syndrome After Epiretinal Membrane Peel Surgery Adam T. Gorner, OD, Dawsan Creek, BC Leonid Skorin Jr., OD, DO, MS, Albert Lea, MN

ABSTRACT Background: Dragged fovea diplopia syndrome is a condition involving intractable binocular diplopia associated with macular pathology often involving epiretinal membrane and macular pucker. The prevalence of this condition is unknown. There is no known cure for this condition but effective treatment for the symptoms is available. Case Reports: Two cases of intractable central binocular diplopia of 2 to 3 years’ duration that were not correctable with prism are presented. Both patients had a history of epiretinal membrane and had undergone membrane peel with vitrectomy. No extraocular muscle dysfunction or paresis was evident in either patient. Both responded favorably to partial monocular occlusion with semitransparent tape. Conclusion: Dragged fovea diplopia can be extremely frustrating for both patients and doctors. An understanding of this condition will allow practitioners to detect it and treat the symptoms in order to allow patients to function normally.

INTRODUCTION Binocular diplopia is most often due to a defect of the ocular motor system, involving the muscles, nerves or supranuclear pathways.1 Less commonly, binocular diplopia can be caused by retinal pathology at or near the macula.

Some of the reported retinal pathologies known to cause diplopia are epiretinal membrane (ERM), choroidal neovascular membrane, and central serous retinopathy.2 In the case of ERM, diplopia can occur due to wrinkling of the macula1 or following surgical intervention such as vitrectomy A.T. Gorner — Private Practice, Dawson Creek, BC; L. Skorin, Jr. — Senior Staff Ophthalmologist, Mayo Clinic Health System, Albert Lea, MN Correspondence to: Dr. Adam T. Gorner, Kadziolka & Smart, 1100 103rd Avenue, Dawson Creek, BC, V1G 2G7; E-mail: manotheredearth@ gmail.com This article has been peer-reviewed.

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and membrane peel.3 Dragged fovea diplopia syndrome is a

condition in which the fovea in one or both eyes is displaced causing a loss of correspondence between foveas and thus diplopia which is not correctable with prism.2 We present two cases of intractable diplopia following vitrectomy and epiretinal membrane peel along with their treatment. We also propose ocular coherence tomography as a means of visualizing the dragged fovea and suggest that further investigation into this technique is warranted.

CASE REPORTS Case 1 EN is an 83-year-old white male. He presented to our clinic after seeing numerous doctors in the past 4 to 5 years. He claimed to be experiencing double vision that was worse in the distance and none of the treatments he had received involving prism provided any lasting relief. EN had been suffering from intractable binocular diplopia since his first epiretinal membrane peel surgery on the right eye 5 years earlier. He had since undergone the same surgery on the left eye as well but the diplopia persisted despite many variations of prism correction. He denied any dizziness, pain, or monocular diplopia but was having trouble judging distances. He was not taking any ocular medications or culpable systemic medications. He denied any allergies and had not endured injury to either eye. He had a history of cataract extraction with posterior chamber intraocular lens (PCIOL) implantation on both eyes. Family history was unremarkable but EN had a history of hypertension.

Distance visual acuity was 6/12-1 (20/40-1) in the right eye (OD) and 6/15+2 (20/50+2) in the left eye (OS) with habitual correction of pl-1.00 x 060 2 base down OD, and -0.75-1.00 x 094 3 base up OS. Pinhole acuities over habitual spectacles were 6/9-1 (20/30-1) OD and 6/9-2 (20/30-2) OS. Near acuity was 6/6-1 (20/20-1) OD and 6/9+1 (20/30+1) OS through a near add of +3.50 in both eyes (OU). Pupils were round and reactive without relative afferent pupillary defect, motilities were full and unrestricted OU, and confrontation fields were full to finger counting. Cover test with habitual correction revealed a 4 prism diopter (PD) exophoria and a 3 PD intermittent left hypertropia at distance and a 14 PD

De Pool et al3 by shining a target from a direct ophthalmoscope onto a black background and comparing fusion ability with the lights on and off. While wearing his habitual glasses EN was unable to fuse while looking at the target with the lights on but when the lights were turned off he reported that the targets would come closer together and he would almost see singly but then they would break further apart. We concluded that his habitual spectacles contained enough prism power to make fusion impossible.

We performed a few trials of differing prism strengths but none of the variations produced acceptable results. We tried monovision in spectacles with a +2.50 D addition over the left eye and the distance correction in the right eye but this was not comfortable for EN. Finally, we placed a piece of semitransparent plastic tape on the center of the left spectacle lens and EN reported single vision. He elected to keep the tape on his glasses lens as the form of treatment for his condition.

Fig. 1 Ocular coherence tomography scan of the left macula in Case 1 possibly showing foveal displacement.

exophoria at near. The vertical prism in his spectacles appeared to be too strong since the patient’s left hypertropia with correction converted to a left hypotropia when tested without correction. On Amsler grid, EN reported a missing area on the far nasal field of the right eye but no metamorphopsia or scotoma on the left eye’s field. Manifest refraction was +0.75-1.00 x 162 6/9 (20/30) OD and -0.25-1.25 x 098 6/9 (20/30) OS.

External appearance and adnexa were unremarkable.

Biomicroscopy revealed corneal arcus OU, normal conjunctiva, deep and quiet anterior chambers with flat irides and stable PCIOLs OU with clear or opened posterior capsule. Intraocular pressures were 13 mmHg OD and 8 mmHg OS by applanation. Both optic nerve heads exhibited deep cups with visible lamina and cup to disc ratios of 0.6 and 0.5 OD and OS respectively with healthy pink neuroretinal rim. An epiretinal membrane was present in each eye with a slightly darker area over the macula that resembled a pseudohole. Watzke-Allen sign was negative in both eyes. Otherwise the maculae were flat. Retinal periphery was flat without holes, tears, or retinal detachments OU. Optical coherence tomography (Stratus OCT, Carl Zeiss Meditec, Inc.) was performed on both maculae. The scan for the right eye showed a normal flat macula, but the scan of the left macula appeared displaced with areas of thickening and thinning (Fig. 1). We also performed a modified version of the lights on-off test as described by

Case 2 JS is a 64-year-old white male. He first presented complaining of a blurred crescent shape obstructing his vision in the right eye for 6 or 7 months and that he would drive with his right eye closed. Best-corrected visual acuity was 6/12+2 (20/40+2) OD and 6/6 (20/20) OS. He had a history of a retinal bleed and a posterior vitreous detachment in the right eye. Amsler grid testing showed central metamorphopsia OD and normal OS. Wrinkling of the right macula was evident on ophthalmoscopy and he was diagnosed with an epiretinal membrane for which he underwent a vitrectomy and a membrane peel. Following the surgery he reported some residual blur as well as double vision with images separated vertically. Vertical diplopia was caused by a phoria which over time became an intermittent tropia. He received a prescription with vertical prism which would be altered numerous times over the next year without providing lasting relief from diplopia. His symptoms decreased for a short time after each change to the prism but would soon return. He reported that his peripheral vision appeared single but his central vision was double and still distorted, despite the surgery. One year after the vitrectomy he had a cataract removed from the right eye with implantation of a PCIOL. Following the surgery his best-corrected visual acuity was 6/7.5 (20/25) OD. He still noted metamorphopsia on Amsler grid testing OD and residual macular wrinkling could be observed on ophthalmoscopy. After a number of visits he was referred back to the surgeon who performed the membrane peel. The retinal surgeon assured JS that the surgery was a success, but she found that one of his spectacle lenses was decentered and tilted. She recommended that a new refraction be performed and his frames adjusted. Changes were again made to his glasses

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Fig. 3 White illuminated 6/21 (20/70) Snellen optotype on a black background used to perform the lights on-off test).

Fig. 2 Optical coherence tomography scan of the right macula in Case 2 possibly showing foveal displacement.

including altered vertical prism without improvement.

Finally, he was sent to a strabismus specialist who diagnosed him with dragged fovea diplopia and placed a piece of semitransparent tape on the center of his right lens to partially occlude the eye and eliminate his central diplopia. When he returned to our clinic in follow-up about 3 years after the initial presentation he was relieved to have single vision. We gave him a new prescription without prism and he continues to wear tape on his right lens. Both maculae appear normal without obvious wrinkling. OCT of the right eye showed a displaced fovea with normal thickness (Fig. 2). We performed the lights on-off test as described by De Pool et al.3 We presented an illuminated white 6/21 (20/70) optotype on a black background (Fig. 3) with the room lights on and JS reported central diplopia with single vision in the periphery.

The room lights were then extinguished and a single white optotype was reported within 1 to 2 seconds.

DISCUSSION Binocular diplopia in association with central retinal pathology has been reported in the past.4,5 The dragged fovea diplopia syndrome was coined by De Pool et al3 to describe a condition in which a person experiences central double vision that is not correctable with prism. Often when a patient with this condition is given prism in their glasses they will initially respond favorably but ultimately the diplopia will return. Sometimes the diplopia returns almost immediately, or it may take hours to days for symptoms

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to appear again.3 Usually a comitant, smallangle hyperdeviation is present without evidence of extraocular muscle dysfunction or paresis. The explanation for this intractable diplopia is a mechanical displacement of the fovea in one or both eyes disrupting the normal foveal correspondence and creating rival2,4-6 ry between central and peripheral fusional mechanisms. A small correcting movement of one or both eyes is made to allow central fusion, thus placing the peripheral retina of each eye in conflict. It is thought that the peripheral drive for fusion overrides the central drive because Panumâ&#x20AC;&#x2122;s 7,8 fusional area is greater peripherally than centrally. Thus, central diplopia is manifest and since prism cannot exclusively influence the central retina, the diplopia remains despite prism treatment. Another possible contributing factor to diplopia, either solely or in conjunction with foveal displacement, is aniseikonia. Benegas et al6 proposed that separation or compression of the photoreceptors from macular disease may produce a difference in retinal image size significant enough to cause diplopia. This is another reason why prism does not relieve symptoms in these patients. We did not perform any tests to detect aniseikonia in our patients.

Some of the reported causes of binocular diplopia from macular pathology are: epiretinal membrane, choroidal neovascularization, central serous retinopathy, paramacular scars, and localized macular detachments.2-5 Both of our patients had a history of epiretinal membrane with subsequent vitrectomy and membrane peel. Diplopia did not ensue until after the surgery was performed.

Silverberg et al2 also found this to be the case in 4 out of 7 patients they reviewed and attributed it to improved vision in the operated eye which previously was reduced enough to preclude diplopia. The prevalence of this condition is not known but epiretinal membrane appears to be one of the more common causes. De Pool et al3 reported it as the cause in more than half of the 87 patients they reviewed with dragged fovea diplopia.

Fig. 4 (A) Epiretinal membrane with macular pucker. (B) Note the radial striations from contraction of the membrane.

PATHOPHYSIOLOGY OF EPIRETINAL MEMBRANES Epiretinal membranes (ERMs) are most commonly found in individuals over the age of 50 and are usually bilateral but often asymmetrical.9,10 ERMs are sometimes found in children, although this is rare. If an ERM is present in a child, it is commonly associated with trauma.11 Population-based studies of different demographics show an overall prevalence ranging from 2.2% to 18.5% and age-related prevalence of 2% in the 6th decade and up to 35% in the 8th decade.9,10,12-16 They can be classified clinically into an early, usually asymptomatic type called cellophane maculopathy caused purely by glial cell proliferation along the internal limiting membrane (ILM).

There is also a more advanced type called preretinal macular fibrosis or macular pucker (Fig. 4A,B). The advanced type is usually more severe and is also caused by glial cells but with a fibrous component that causes traction and wrinkling of the retina.9,15 These membranes can also be classified as either primary or secondary depending on their underlying cause. Primary epiretinal membranes occur idiopathically or following posterior vitreous detachment (PVD). Secondary epiretinal membranes are associated with some kind of pathology or intraocular surgery; usually proliferative diabetic retinopathy, retinal tears or holes, macular holes, retinal detachment, or after cataract surgery.17 The histocytology of epiretinal membranes differs depending on the underlying pathology. Simple primary epiretinal membranes are formed when glial cells migrate through breaks in the ILM of the retina and begin to proliferate along the retinal surface.

18 Snead et al classified ERMs into three types: simple laminocyte ERMs, tissue repair ERMs, and neovascular ERMs. Simple ERMs form after PVD or idiopathically.

18

Snead et al described the glial cells in a simple ERM as laminocytes because they form a monolayer on the ILM as they proliferate and migrate along the vitreoretinal junction.

The ILM in these membranes may become hyperconvoluted as the ERM contracts causing distortion of the retina and subsequent metamorphopsia and reduced visual acuity.

Tissue repair ERMs develop after retinal tear, trauma, infection, or blunt injury. This membrane differs slightly from the simple type in that it also contains retinal pigment epithelial 18,19 (RPE) cells, fibroblasts, and macrophages. RPE cells may be liberated when a retinal tear or break occurs, forming the characteristic tobacco dust in the anterior vitreous. Over time these cells settle onto the retina to cause a pigmented 19 epiretinal membrane. Neovascular ERMs develop as a consequence of proliferative diabetic retinopathy, radiotherapy, or vasoformative tumors. This type of membrane is very different because it contains capillaries and acellular 18 20 stromal tissue. Kampik et al found that ERMs also contained collagen and myofibroblasts and concluded that these features may account for the contractile properties of the membranes.

Epiretinal membrane can be treated by surgical removal.

Vitrectomy and membrane peel can achieve an increase in visual acuity of 2 Snellen lines or more in up to 90% of 21,22 patients and can significantly reduce metamorphopsia. This reduction in metamorphopsia may be an important benefit even 23 if visual acuity is not noticeably improved.

DIAGNOSIS AND TREATMENT ERMs can be seen as a glistening sheen on the surface of the retina different from that seen in a healthy young fundus. This sheen appears less regular, like sunlight reflecting off disturbed water. The membrane may be clear or may have a greenish-grey appearance depending

Dragged Fovea Diplopia Syndrome After Epiretinal Membrane Peel Surgery â&#x20AC;&#x201D; Gorner, Skorin

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on the etiology. If macular pucker is present, radiating folds from one or more retinal contraction foci may be visible (Fig. 4A,B).24 After a membrane peel is performed, some residual retinal wrinkling may be evident and/or an apparent pseudohole may be seen. Alternatively, the retina may appear normal with no evidence of macular pathology on funduscopic examination. Case 1 had a visible remnant of epiretinal membrane and a pseudohole over the macula in each eye with a negative Watzke-Allen sign. In Case 2 some residual wrinkling was apparent in the operated eye.

It is not possible to visualize the displacement of the fovea on funduscopy so this condition must be confirmed in other ways. The lights on-off test described by De Pool et al3 is a simple test that we have found very useful. A white illuminated optotype of about 6/21 (20/70) Snellen equivalent is presented on a black background (Fig. 3). In a positive result the patient reports central diplopia with the lights on but when the lights are extinguished and all peripheral cues to fusion are eliminated a single object is reported. Both of our patients responded positively to this test. When we attempted this test in Case 1, we did not have the setup exactly as described but we arranged a modified version with an illuminated target from an ophthalmoscope on a black background. Case 1 reported that the objects came closer together and almost became single but then broke further apart. We attribute this to his glasses which contained vertical prism of sufficient quantity to prevent fusion. In Case 2 we had an LCD screen with a black background and a white optotype as described which produced a definitive positive result. The synoptophore has been used in the past to confirm the disparity between central and peripheral fusion, but the lights on-off test seems to be a valid substitute.2 With the increasing availability of computerized visual acuity charts, the lights on-off test may be more readily available than the synoptophore.

We performed OCT (Stratus OCT, Carl Zeiss Meditec, Inc.) of the macula on both patients with interesting results. The image showed the foveal area displaced from the center of the reference lines (Figs. 1, 2). This was instructive because such a displacement is not generally seen when performing macular scans. We wondered if the image produced by the OCT was actually showing the displaced fovea. We recognize that there are inherent flaws in this assumption since fixation cannot be accurately monitored while performing the scans. Gupta et al24 were able to visualize the foci of contraction on the retina with macular pucker using OCT with scanning laser ophthalmoscopy (SLO). This instrument allowed coronal plane images from the OCT to be superimposed on the SLO image with point to point registration. This combined image revealed multiple centers of retinal contraction with retinal folds and areas of thickening easily referenced with

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the anatomical location on the retina. One wonders if it would be possible to measure the displacement of the fovea with this method in dragged fovea diplopia syndrome.

There is no known cure for dragged fovea diplopia, only palliative treatment. There is no way to align the foveas without causing peripheral diplopia or vice versa.

Others have reported on the success of placing Bangerter foils of different densities over the affected eye in order to degrade the image for that eye and eliminate diplopia.2,3 The foil is cut down so it only affects the central vision and can be placed on the inside center of the spectacle lens. This allows the patient to fixate with the other eye and use peripheral retina to maintain fusion. Patients tend to find this acceptable. Another option described by De Pool et al3 is Scotch Satin tape (3M Co., St. Paul, MN).

They found that this was more cosmetically appealing than the more opaque Scotch Magic tape (3M Co., St. Paul, MN) and less expensive than Bangerter foil. Both our patients responded very favorably to tape placed on the center of one lens. The patient in Case 2 has been wearing this tape for almost 2 years. We also attempted monovision in the patient in Case 1; however, he found this uncomfortable and was not able to tolerate it.

CONCLUSION Dragged fovea diplopia syndrome may be more common than we currently realize. It can be very frustrating for both patients and doctors to encounter this condition if it is not understood. There is a simple subjective way to test for it using the lights on-off test. As technology advances perhaps an objective means of detecting this condition will become available. We suggest that further testing should be done with OCT to determine if the actual foveal displacement can be objectively quantified. This condition cannot be cured but the symptoms can be treated very inexpensively and with relatively good success by partially occluding one eye with semitransparent tape or Bangerter foil. ❏

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Bixenman WW, Joffe L. Binocular diplopia associated with retinal wrinkling. J Pediatr Ophthalmol Strabismus 1984; 21: 215-219.

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Burian HM. Fusional movements: role of peripheral retinal stimuli. Arch Ophthalmol 1939; 21: 486-491.

FraserBell S, YingLai M, Klein R, Varma R, Los Angeles Latino Eye Study. Prevalence and associations of epiretinal membranes in latinos: the Los Angeles Latino Eye Study.

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McCarty DJ, Mukesh BN, Chikani V, Wang JJ, et al.

Prevalence and associations of epiretinal membranes in the visual impairment project. Am J Ophthalmol 2005; 140: 288-294.

Khaja HA, McCannel CA, Diehl NN, Mohney BG. Incidence and clinical characteristics of epiretinal membranes in children. Arch Ophthalmol 2008; 126: 632-636.

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Dragged Fovea Diplopia Syndrome After Epiretinal Membrane Peel Surgery â&#x20AC;&#x201D; Gorner, Skorin

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INSTRUCTIONS

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FOR

1 CATEGORY A, UFC CREDIT

This course has been approved for 1 Category A, UFC credit in Ocular Health by the Ordre des Optométristes du Québec. Please complete and submit this test questionnaire for grading before March 31, 2018.

In order to obtain 1 Category A, UFC credit, please follow these steps: • Fill in the identification section and answer the 10 multiple choice questions in this UFC credit application form • Prepare a cheque payable to Mediconcept for $25.00 • Mail your completed UFC credit application form along with your cheque to: CRO Quebec, 3484 Sources Blvd, Suite 518, Dollard-des-Ormeaux, QC H9B 1Z9 Your answers will be graded by Clinical & Refractive Optometry. If you score 50% or more, a UFC Credit Certificate approved by the Ordre des Optométristes du Québec will be issued to you for your records.

CLICK HERE TO PRINT THIS UFC CREDIT TEST AND ARTICLE Name: First______________________________ Last___________________________________ Address:________________________________________________________________________ Number

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QUESTIONNAIRE Dragged Fovea Diplopia Syndrome After Epiretinal Membrane Peel Surgery Adam T. Gorner, OD, and Leonid Skorin Jr., OD, DO, MS 1. ❑ ❑ ❑ ❑

The patient in Case 1 had an absence of the following clinical signs and symptoms, EXCEPT: Ocular pain Difficulty judging distances Dizziness Sudden loss of visual acuity

2. ❑ ❑ ❑ ❑

The patient in Case 2 presented with which of the following signs or symptoms?

Decreased left-sided visual field A floater Blurred shape obstructing his vision in the right eye Reduced vision at night

3. ❑ ❑ ❑ ❑

All of the following statements about dragged fovea diplopia syndrome are true, EXCEPT: Diplopia may disappear and appear again It is not correctable by prism OCT is effective in determining if the foveal displacement can be objectively quantified Prism is usually effective in curing the condition

Clinical & Refractive Optometry Quebec 1:2, 2016

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4. ❑ ❑ ❑ ❑

Which of the following best describes an individual with epiretinal membranes (ERMs)?

55-year-old female 60-year-old Caucasian male 65-year-old African-American male 76-year-old Asian female

5. ❑ ❑ ❑ ❑

What is the prevalence of ERMs according to population-basic studies?

1.2% to 4.5% 2.2% to 18.5% 5.3% to 9.4% 3.6% to 20.5%

6. ❑ ❑ ❑ ❑

Secondary epiretinal membranes are associated with all of the following, EXCEPT: Cystoid macular degeneration Macular holes Retinal tears Retinal detachment

7. ❑ ❑ ❑ ❑

Surgery is effective in achieving an increase of visual acuity of 2 Snellen lines in what percentage of patients?

60% 75% 90% 95%

8. ❑ ❑ ❑ ❑

Which of the following is the most likely cause of dragged fovea diplopia syndrome?

Cataract extraction Vitreous detachment Membrane peel Family history of the condition

9. ❑ ❑ ❑ ❑

In what number of patients did diplopia occur after vitrectomy and membrane peel?

2 out of 3 4 out of 7 6 out of 9 8 out of 10

10. ❑ ❑ ❑ ❑

Which of the following treatments was effective in the two Case Reports presented in the paper?

Partial monocular occlusion with semitransparent tape Care and regular patient monitoring Prism correction Monovision in spectacles

Dragged Fovea Diplopia Syndrome After Epiretinal Membrane Peel Surgery — Gorner, Skorin

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