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This continuing medical education activity is supported through anunrestricted educational grant from Bausch + Lomb Incorporated.

New Evidence and Insights on the

CME Monograph

Jointly sponsored by The New York Eye and Ear Infirmary

and MedEdicus LLC

Highlights from a Continuing Medical Education Symposium heldduring the American Academy of Ophthalmology 2012 Meeting*

InflammationPanorama

From Ocular Surface Disorders to Surgery

ORIGINAL RELEASE: March 15, 2013

LAST REVIEW: February 22, 2013

EXPIRATION: March 31, 2014

*This CME symposium was not affiliated with the official program of the AAO/APAO Joint Meeting.

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Learning Method and Medium

This educational activity consists of a supplement and ten (10) study questions.The participant should, in order, read the learning objectives contained at thebeginning of this supplement, read the supplement, answer all questions inthe post test, and complete the Activity Evaluation/Credit Request form. Toreceive credit for this activity, please follow the instructions provided on thepost test and Activity Evaluation/Credit Request form. This educationalactivity should take a maximum of 1.5 hours to complete.

Content Source

This continuing medical education (CME) activity captures content from aCME symposium held on November 10, 2012, in Chicago, Illinois.

Target Audience

This activity intends to educate ophthalmologists.

Learning Objectives

Upon completion of this activity, participants will be better able to:• Summarize key efficacy and safety attributes of new anti-inflammatory

agents• Demonstrate best-practice regimens for reducing inflammation risk for

patients undergoing cataract, refractive, or glaucoma procedures• Demonstrate best-practice regimens for the management of inflammation in

patients with inflammatory conditions such as dry eye, blepharitis, allergy,and/or anterior uveitis• List anti-inflammatory therapies in development

Accreditation Statement

This activity has been planned and implemented in accordance with theEssential Areas and Policies of the Accreditation Council for ContinuingMedical Education (ACCME) through the joint sponsorship of The New York

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Richard L. Lindstrom, MD (Program Chair and Moderator)

Founder and Attending SurgeonMinnesota Eye Consultants, PABloomington, MinnesotaAdjunct Professor EmeritusDepartment of Ophthalmology and Visual NeurosciencesUniversity of MinnesotaMinneapolis, Minnesota

Eric D. Donnenfeld, MDOphthalmic Consultants of Long IslandRockville Centre, New YorkClinical Professor of OphthalmologyNew York UniversityNew York, New YorkTrusteeGeisel School of Medicine at DartmouthHanover, New Hampshire

Stephen S. Lane, MDMedical DirectorAssociated Eye CareStillwater, MinnesotaAdjunct ProfessorUniversity of MinnesotaSt. Paul, Minnesota

Terrence P. O’Brien, MDProfessor of OphthalmologyCharlotte Breyer Rodgers Distinguished Chair in OphthalmologyDirector, Refractive Surgery ServiceBascom Palmer Eye InstitutePalm Beach Gardens, Florida

Eye and Ear Infirmary and MedEdicus LLC. The New York Eye and Ear

Infirmary is accredited by the ACCME to provide continuing medicaleducation for physicians.

AMA Credit Designation Statement

The New York Eye and Ear Infirmary designates this enduring material fora maximum of 1.5 AMA PRA Category 1 Credits™. Physicians should claimonly the credit commensurate with the extent of their participation in the activity.

Grantor Statement

This continuing medical education activity is supported through anunrestricted educational grant from Bausch + Lomb Incorporated.

Disclosure Policy Statement

It is the policy of The New York Eye and Ear Infirmary that the faculty andanyone in a position to control activity content disclose any real or apparentconflicts of interest relating to the topics of this educational activity, and alsodisclose discussions of unlabeled/unapproved uses of drugs or devices duringtheir presentation(s). The New York Eye and Ear Infirmary has establishedpolicies in place that will identify and resolve all conflicts of interest prior tothis educational activity. Full disclosure of faculty/planners and theircommercial relationships, if any, follows.

Faculty Disclosures

Eric D. Donnenfeld, MD, had a financial agreement or affiliation during thepast year with the following commercial interests in the form of Consultant/

Advisory Board: Abbott Medical Optics; AcuFocus, Inc; Alcon, Inc; Allergan, Inc;AqueSys, Inc; Bausch + Lomb Incorporated; Better Vision Network; Cataractand Refractive Surgery Today; ELENZA, Inc; Glaukos Corporation;LacriPen/LacriSciences LLP; LenSx Lasers/Alcon Inc; Merck & Co, Inc;NovaBay Pharmaceuticals; Odyssey Pharmaceuticals; Pfizer Inc; PRN PhysicianRecommended Nutriceuticals; QLT Inc; SARcode Bioscience, Inc; TearLabCorporation; TLC Laser Eye Centers; TrueVision; and WaveTec Vision.

Richard L. Lindstrom, MD, had a financial agreement or affiliation duringthe past year with the following commercial interests in the form ofConsultant/Advisory Board: Abbott Medical Optics; AcuFocus, Inc; Adoptics;Advanced Refractive Technologies; Alcon, Inc; AqueSys, Inc; Bausch + LombIncorporated; Bio Syntrx, Inc; Calhoun Vision, Inc; Clarity Ophthalmics;Clear-Sight Inc; CoDa Therapeutics, Inc; EBV Partners; EGG BasketVentures; ELENZA, Inc; Encore; e-Vision Photography, Inc; Eyemaginations,Inc; Foresight Venture Fund #3; ForSight Labs; Glaukos Corporation; HighPerformance Optics; Hoya Surgical Optics; Improve Your Vision, LLC; ISTAPharmaceuticals, Inc; LensAR; LenSx Lasers, Inc; LifeGuard Health LLC;Lumineyes, Inc; Minnesota Eye Consultants, PA; NuLens Ltd; Ocular OpticsCo, Ltd; Ocular Surgery News/Slack Inc; Ocular Therapeutix, Inc; OmegaEyeHealth; Omeros Corporation; PixelOptics, Inc; Quest; Refractec, Inc;RevitalVision, LLC; Schroder Life Science Venture Fund; Seros Medical, LLC;Sightpath Medical; Strategic Pharmaceutical Advisors; Surgijet/Visijet; 3DVision Systems LLC; TLC Vision Corporation; TearLab Corporation; TraceyTechnologies; Transcend Medical, Inc; TrueVision Systems, Inc; VersantCorporation; and Vision Solutions Technologies; Ownership Interest: AbbottMedical Optics; AcuFocus, Inc; AqueSys, Inc; Bausch + Lomb Incorporated;Bio Syntrx, Inc; Calhoun Vision, Inc; Clarity Ophthalmics; Clear-Sight Inc;CoDa Therapeutics, Inc; Confluence Acquisition Partners I, Inc; CurveRightLLC; Cxl Ophthalmics, LLC; EBV Partners; EGG Basket Ventures; Encore; e-Vision Photography, Inc; Evision Medical Laser; Eyemaginations, Inc;Foresight Venture Fund #3; FzioMed; Glaukos Corporation; HealthcareTransaction Services; HEAVEN Fund; High Performance Optics; ImproveYour Vision, LLC; LensAR; LenSx Lasers, Inc; LifeGuard Health LLC;Minnesota Eye Consultants, PA; Nisco; NuLens Ltd; Ocular Optics Co, Ltd;Ocular Therapeutix, Inc; OmegaEye Health; OnPoint Medical Diagnostics,Inc; One Focus Ventures; PixelOptics, Inc; Quest; Rainwater Healthcare, Inc;Refractec, Inc; ReVision Optics, Inc; RevitalVision, LLC; Sarbox NP, Inc;SARcode Bioscience, Inc; Schroder Life Science Venture Fund; SightpathMedical; SolBeam, Inc; Surgijet/Visijet; 3D Vision Systems LLC; TLC VisionCorporation; TearLab Corporation; Tracey Technologies; Transcend Medical,Inc; TriPrima Inc; TrueVision Systems, Inc; Viridax Corporation; VisionSolutions Technologies; and Wavefront Systems Ltd; Medical Director:

Refractec, Inc; Sightpath Medical; and TLC Vision Corporation.

Stephen S. Lane, MD, had a financial agreement or affiliation during thepast year with the following commercial interests in the form of Honoraria:Alcon, Inc; and Bausch + Lomb Incorporated; Fees for promotional, advertising

or non-CME services received directly from commercial interest or their Agents

(eg, Speakers Bureaus): Alcon, Inc; and Bausch + Lomb Incorporated.

Faculty


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Terrence P. O’Brien, MD, had a financial agreement or affiliation during the past year with the following commercial interests in the form ofConsultant/Advisory Board: Alcon, Inc; Allergan, Inc; Abbott Medical Optics; Bausch + Lomb Incorporated; and ISTA Pharmaceuticals, Inc.

Peer Review Disclosure

Ted Gerszberg, MD, has no relevant commercial relationships to disclose.

Editorial Support Disclosures

Cheryl Krader Guttman; Cynthia Tornallyay, RD, MBA, CCMEP;

Kimberly Corbin, CCMEP; Barbara Aubel; and Vivian Fransen, MPA,

have no relevant commercial relationships to disclose.

Disclosure Attestation

The contributing physicians listed above have attested to the following:1) that the relationships/affiliations noted will not bias or otherwise influencetheir involvement in this activity; 2) that practice recommendations givenrelevant to the companies with whom they have relationships/affiliations willbe supported by the best available evidence or, absent evidence, will beconsistent with generally accepted medical practice; and 3) that all reasonableclinical alternatives will be discussed when making practice recommendations.

Off-Label Discussion

This educational activity includes off-label discussion of topical azithromycinfor meibomian gland dysfunction (MGD), loteprednol etabonate gel andointment for inflammation other than that related to cataract surgery, anddoxycycline for MGD.

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For questions about this activity, call 212-979-4383.

To Obtain AMA PRA Category1 Credit™

To obtain AMA PRA Category 1 Credit™ for this activity, read the material inits entirety and consult referenced sources as necessary. Complete theevaluation form along with the post test answer box within this supplement.Remove the Activity Evaluation/Credit Request page from the printedsupplement or print the Activity Evaluation/Credit Request page from theDigital Edition. Return via mail or fax to Kim Corbin, Director, ICME, The

New York Eye and Ear Infirmary, 310 East 14th Street, New York, NY10003 or fax to 212-353-5703. Your certificate will be mailed to the addressthat you provide on the evaluation form. Please allow 3 weeks for mailed/faxed forms to be processed.There are no fees for participating in andreceiving CME credit for this activity.

Alternatively, we offer instant certificate processing and support Green CME. Please take this post test and evaluation online by going towww.MedEdicus.com, Educational Activities tab, and clicking the Post-Test & CME Certificate button. Upon passing, you will receive yourcertificate immediately. You must score 70% or higher to receive credit for thisactivity, and may take the test up to 2 times. Upon registering and successfullycompleting the post test, your certificate will be made available online and youcan print it or file it.

Disclaimer

The views and opinions expressed in this educational activity are those of thefaculty and do not necessarily represent the views of The New York Eye

and Ear Infirmary, MedEdicus LLC, Bausch + Lomb Incorporated, orOphthalmology Times. Please refer to the official prescribing information for each product for discussion of approved indications, contraindications, and warnings.

This continuing medical education activity is copyrighted to MedEdicus LLC ©2013.

All rights reserved.

Introduction

A recent case-based continuing medical education

symposium focused on a spectrum of inflammatory

disorders that can compromise the success of cataract and

laser vision correction surgery. This continuing medical

education monograph includes the cases presented and

highlights from the faculty’s discussions covering the

diagnosis, treatment, and prevention of various

inflammatory disorders. We hope the information it

contains will be helpful to clinicians as they strive to

minimize surgical complications and optimize outcomes

for their patients.

—Richard L. Lindstrom, MD

Case 1: Cystoid Macular Edema Prophylaxis

—Richard L. Lindstrom, MD

A 73-year-old male presents with a chief complaint of decreasedvisual acuity and vision difficulty while driving and reading. Hehas an 18-year history of diabetes that is controlled with oralmedication. Best corrected visual acuity (BCVA) is 20/60 OU,and ophthalmic examination shows bilateral 3+ nuclear scleroticcataracts and 1+ background diabetic retinopathy.

The patient undergoes uneventful cataract surgery and isprescribed a topical fluoroquinolone for 2 weeks plusprednisolone acetate 1% 4 times a day for 2 weeks, thenprednisolone acetate 1% twice a day until gone. BCVA improvesinitially to 20/25, but at 1 month postoperatively, the patientpresents with BCVA of 20/40 and reports he ran out of hismedication 1 week earlier. Central foveal thickness on opticalcoherence tomography (OCT) is 543 microns (Figure 1).

Dr Lindstrom: Is fluorescein angiography needed to diagnosecystoid macular edema (CME) in this patient?

Dr Lane: The risk of postcataract surgery CME is increased inpatients with diabetes. So, in this case, the patient’s history andOCT seem sufficient for diagnosing CME.

Dr Lindstrom: What about the differential diagnosis? Is thereanything that might have been missed preoperatively?

Figure 1. Case 1: Optical coherence tomography image with readily apparentmacular thickening.

Photo courtesy of Richard L. Lindstrom, MD


Dr O’Brien: Surgeons should maintain suspicion for subtlevitreomacular interface abnormalities, including epiretinalmembrane and vitreomacular traction, in patients with diabetes.Since the cataract can obscure visualization, it is useful toperform OCT prior to surgery.

Dr Lindstrom: This patient may have had edema from diabetic macular edema or possibly an epiretinal membranepreoperatively. Possible causes for decreased or blurry visionafter cataract surgery include ocular surface disease, regular andirregular astigmatism, and age-related macular degeneration.Since this patient ran out of his steroid early, postcataractsurgery CME was diagnosed and treated as such.

Do you modify your medication regimen for cataract surgerypatients at high risk for CME?

Dr O’Brien: Yes. These individuals at higher risk for CME need a longer duration of treatment with a nonsteroidal anti-inflammatory drug (NSAID) preoperatively andpostoperatively.1,2 I instruct the patient at higher risk for CME toinitiate the NSAID 1 week preoperatively and continue it for atleast 6 to 8 weeks after surgery and sometimes, when indicated,even as long as 3 months.

Dr Lindstrom: My bias is that if we are going to give theantibiotic plus NSAID preoperatively, there is no reason not tostart the steroid at the same time. I think it helps clean up theocular surface, and the more anti-inflammatory therapy onboard at the time of the surgical insult, the better. The steroidalso seems to protect the corneal endothelium. Dr Donnenfeld,please tell us about your research in that area.

Dr Donnenfeld: Traditionally, NSAIDs are used preoperativelyand steroids are used postoperatively. However, based in parton evidence from randomized controlled clinical trials of patientsundergoing various major surgical procedures that preoperativeadministration of a steroid has benefits for reducing edema andpain,3 we conducted a study comparing difluprednate 0.05%and prednisolone acetate 1% in which both medications werestarted 2 hours prior to cataract surgery, pulse dosed in theperioperative period, and then tapered.4 The steroid was started2 hours preoperatively since its mechanism is to inhibit therelease of arachidonic acid that only occurs after there has beentissue damage. The pulse dosing regimen was used because theeffect of the steroid is dose-dependent, and then it is taperedquickly after surgery.

Eyes treated with difluprednate had clearer corneas on day 1postoperatively, less CME at 2 and 4 weeks, and higherendothelial cell density at 4 weeks, as compared to eyes nottreated with difluprednate.

A topical corticosteroid also helps control pain after cataractsurgery.5 Patients can have 20/20 vision on day 1postoperatively, but if they are uncomfortable, they view thesurgery as a failure.

Dr Lindstrom: The difluprednate-treated patients in your studyalso had better vision on the first day postoperatively, andanecdotally, I think the preoperative use of a steroid with anNSAID helps to maintain pupillary dilation intraoperatively.

We agree that patients at high risk for CME should be treatedwith a steroid preoperatively and be treated for a longer durationwith an NSAID. My short list of patients at high risk for CME

includes those with diabetes, vascular occlusion, epiretinalmembranes, a history of uveitis, CME in the same or fellow eye,previous ocular surgery, prolonged operating time, and vitreousloss. However, sometimes you do not know preoperatively whois at high risk for CME. So, do you use an NSAID in all patients?

Dr Lane: You can get an idea about the risk for CME from thepatient’s history, but in the United States, most cataractsurgeons are routinely using an NSAID.

It is useful to have 2 regimens—1 for “routine patients” andanother for the group of patients at high risk for CME who use thesame medications, but more intensively. Since you do not alwaysknow who the patient at high risk for CME is, having somecoverage with both the NSAID and steroid makes good sense.

I use difluprednate with an NSAID for controlling inflammationafter cataract surgery in the eyes of patients at high risk forCME, but loteprednol combined with an NSAID is my treatmentof choice in routine cases. In a study we conducted with EdwardJ. Holland, MD, in which patients who were having routinecataract surgery received an NSAID postoperatively and wererandomized to prednisolone acetate 1% or loteprednoletabonate 0.5% suspension, inflammation control wasequivalent in the 2 groups, but the loteprednol-treated grouphad less intraocular pressure (IOP) fluctuation than theprednisolone-treated group.6

Dr Lindstrom: If you see a patient who had CME after his orher first eye cataract surgery, what will you do differently whenoperating on the second eye?

Dr Donnenfeld: Patients are counseled about their risk for CMEand told what will be done to try to give them the best possiblesurgical outcome. I would obtain a preoperative OCT, and ifthere is significant macular edema, I would refer the patient to aretinal surgeon for possible intravitreal steroid injection prior to surgery.

If the CME was not significant, I would treat the patient beforesurgery with an NSAID plus a steroid. I use bromfenac 0.09%,which is recommended for once-daily dosing, but I wouldprescribe it for use twice a day in a patient with diabetes,starting 1 week preoperatively and continuing it for 2 to 3 months postoperatively. I would also have the patient startdifluprednate 1 day before surgery and, importantly, begin pulsedosing difluprednate right before surgery. The patient should befollowed closely postoperatively.

If there is any intraoperative complication, I like to useintracameral triamcinolone acetonide, not only to recognizevitreous loss, but also to reduce inflammation. I am veryaggressive with the use of steroids in these patients.

Dr O’Brien: I would agree and also have a low threshold forintraocular corticosteroid therapy. I use intracameral preservative-free dexamethasone in patients at risk for CME and intravitrealpreservative-free triamcinolone acetonide in patients who havecomplications or are at high risk for CME. Perhaps in the nearfuture, we will have sustained-delivery vehicles for the longer-termrelease of corticosteroids with zero-order pharmacokinetics tocontrol inflammation for an extended period.

Dr Lindstrom: The point here is that steroids worksynergistically with NSAIDs to minimize postoperativeinflammation and thus can be used aggressively.

4


CME is more common than people think. If postcataract surgeryCME is defined as any leakage or thickening of the retina onOCT, its rate is near 90% in patients having uneventful cataractsurgery, according to a study by Lobo and colleagues.7 Amongthe 32 eyes included in the trial, 88% of the eyes had evidenceof retinal vascular leakage at 12 weeks postoperatively.

If the goal of cataract surgery is to provide patients with the bestpossible visual acuity, surgeons need to focus on preventingCME. OCT is becoming a critical tool for identifying patients athigh risk for CME, and we have drugs that work synergisticallyto help prevent CME.

Dr Lane: Something I have come to realize in treating patientswith CME is that while visual acuity usually comes back to20/20, visual quality may still be reduced. Since we do notknow who is going to develop CME, the use of medications toprevent CME makes good sense.

Dr Donnenfeld: My partner, John Wittpenn, MD, was the leadauthor of a paper that provided evidence-based information inthis area.8 He and his colleagues randomized approximately550 cataract surgery patients to receive a steroid alone orcombined with an NSAID postoperatively. Retinal thickening ofmore than 10 microns occurred in twice as many eyes in thesteroid-only group than in the NSAID-plus-steroid group, andhaving more than 10 microns of retinal thickening wasassociated with lower contrast sensitivity.

Extrapolating these data to the more than 3 million cataractsurgeries performed in the United States annually suggestsabout 150,000 patients would suffer a visual deficit if they werenot treated with this combination of an NSAID plus steroid.That is a staggering number.

Dr Lindstrom: Indeed, we must think about the prevention ofCME, and today we have more effective steroid options than inthe past for controlling postoperative inflammation withdifluprednate 0.5% emulsion as well as loteprednol 0.5%, whichnow includes preservative-free ointment and a gel formulation inaddition to the suspension. Our NSAID options have also beenexpanding with the development of formulations that havereduced dosing frequency relative to their predecessors. Inaddition to once-daily bromfenac 0.09%, there has been theintroduction of ketorolac tromethamine 0.45% solution, whichis preservative-free and has a dosing frequency of twice-dailyadministration. Nepafenac 0.3% suspension was very recentlyapproved by the US Food and Drug Administration with a once-daily regimen for the treatment of pain and inflammationassociated with cataract surgery, and it received approval inEurope for the prevention of CME in patients with diabetes. Inaddition, a New Drug Application has been filed for a lower-concentration preparation of bromfenac that was showneffective as a once-daily treatment for pain and inflammationassociated with cataract surgery.9

Case 2: Preoperative Managementof Comorbidities in CataractSurgery—Blepharitis and Dry Eye

ÑStephen S. Lane, MD

A 75-year-old female who had been using artificial tears 5 timesa day for comfort presents with a complaint of decreased visualacuity. BCVA is 20/80 OD and 20/70 OS. Examination at the

slit-lamp reveals trace collarettes and scales on the lashes. Shehas a clear cornea, rapid tear break-up time (TBUT), and foamytear film (Figure 2), along with a 2+/3+ nuclear scleroticcataract and 1+ posterior capsular cataract OU. The fundusexamination is unremarkable, and the patient wants apresbyopia-correcting intraocular lens (IOL).

What are the striking findings in her slit-lamp images?

Dr OÕBrien: She exhibits typical signs of combined anteriorblepharitis and posterior blepharitis with inflammation at theanterior lid margin, collarettes, and crusting, along with aglistening from oil reflection of light off the lid skin and lidmargin telangiectatic vessels.

Dr Donnenfeld: The soap-like material along the lid margin isthe result of saponification. It is caused by lipase hydrolysis ofthe meibomian gland lipids to soaps and fatty acids, and thosebreakdown products cause burning and tear film instability witha shortened TBUT. Inspissation of the glands is also present andis pathognomonic for meibomian gland dysfunction (MGD).Normally, the meibum has an olive oil-like appearance, but withMGD, the thickened secretions block the glands.

Dr Lane: We do corneal topography routinely for patientsreceiving advanced technology IOLs to check the ocular surface.This patient has irregular astigmatism secondary to an irregularocular surface (Figure 3).

Dr Donnenfeld: There are a few things that can account for thetype of topographic irregularity seen in this patient, but it isimportant not to operate in this situation because thekeratometry will be irregular and result in IOL power selectionerror. The black areas seen at the bottom of the topographicimage represent frank dropout because of the surface

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Figure 2. Case 2: Slit-lamp findings in a patient with combined anterior andposterior blepharitis show scurf at the base of the lashes (A), inspissation andplugging of the meibomian glands (B), foam in the tear film (C), and irregulartear film break-up (D).

Photos courtesy of Stephen S. Lane, MD

Figure 3. Case 2: Corneal topography with irregular astigmatism.

Photo courtesy of Stephen S. Lane, MD

A B

C D


irregularity. That should tell a surgeon there is a problem thatneeds to be rectified before operating.

Dr OÕBrien: The quality of the topographic image is adverselyimpacted in this patient by the film instability and overall poorquality of the tear lake, and the use of the information obtainedwill lead to spurious keratometry and inaccurate IOL powerselection. This is a clear case of the Ògarbage in will yieldgarbage outÓ principle in terms of IOL power selection andrefractive outcome.

Dr Lane: Yes. Implanting a multifocal IOL in this patient is aformula for disastrous results. Not only will the IOL power bewrong, but the image quality will be reduced postoperativelybecause of the tear film irregularity (Figure 4). MGD needs tobe treated aggressively prior to surgery.

Do patients present with pure MGD, pure aqueous deficient dryeye, or pure anterior blepharitis?

Dr Lindstrom: There certainly are cases of true aqueousdeficient dry eye, as in patients with SjšgrenÕs syndrome.However, according to a study by Lemp and colleagues,10 86%of dry eye is evaporative, and it is also my impression that morepatients have MGD with secondary evaporative dry eye thantrue aqueous deficient dry eye, especially seniors.

Dr OÕBrien: With respect to the lid margin disease, somepatients have a clearly defined clinical picture where the anteriorlid margin is principally involved, and others have involvementthat is more exclusively limited to the posterior lid margin.However, the majority of the patients have a combination ofanterior and posterior lid margin involvement, and bothcomponents need to be addressed for effective control. Theinvolvement of the posterior lid margin adds to the poor qualityof meibum, an unstable lipid layer, and accelerated evaporativetear loss with resultant aqueous tear layer insufficiency.

Dr Donnenfeld: I have found an overwhelming associationbetween a chief complaint of tired eyes and MGD or dry eyedisease. The reason is that as these patients attempt to maintainimage quality, they may double or triple their blink rate.Consequently, the levator muscles tire. Other than a slightlyshortened TBUT, they may have no other signs of dry eye.However, their borderline condition may be converted to anacute dry eye state after surgery. Then, they might be very upsetand blame the surgery for a preexisting problem that wasmarginally compensated.

Dr Lane: I think we would all agree to postpone surgery inthese patients. How should they be managed?

Dr Lindstrom: Because MGD is so common, all patients deservewhat I call Òocular surface preparation.Ó The regimen I use isinfluenced by a study in which Dr Lane was an investigator thatshowed improvements were achieved in patients with moderate-to-severe blepharitis/blepharoconjunctivitis after 1 week oftreatment with a fixed combination of topical antibiotic-corticosteroid.11 My approach is to use a fixed combinationantibiotic-corticosteroid, tobramycin-loteprednol, or tobramycin-dexamethasone, together with lid hygiene and artificial tears for1 week prior to surgery.

I think these eyes remain more vulnerable to intraoperativetrauma, and so I put some dispersive viscoelastic on the eye forprotection during surgery. For long-term maintenance therapy, Iam a big advocate of omega-3 fatty acids, but there is no reasonnot to start that preoperatively.

Dr. OÕBrien: I certainly agree that particular attention to andproper preparation of the ocular surface preoperatively can leadto less instability and faster recovery postoperatively from thestress that cataract surgery inevitably poses to any ocularsurface. One cautionary note about viscous surface protectantsis to be certain to apply the antiseptic and antibiotic agents forantimicrobial prophylaxis prior to placing the viscous agent.This order of use allows sufficient time for effective antimicrobialaction that can be blocked by the viscous lubricant substance.

Ocular nutriceuticals, including sources of essential omega-3fatty acids and related nutrients, play an important role in ocularsurface management, but may require a more extended courseto achieve significant and lasting improvements of the tear filmand ocular surface. Cyclosporine may also take several weeks tomonths to gain control of ocular surface inflammation. Thus, acorticosteroid preparation that is ocular surface friendly,effective, and safe provides a tool to rapidly reduce ocularsurface inflammation preoperatively.

Dr Lane: Many patients are already taking omega-3 fatty acids,but often it is not the right kind or enough. The preparationneeds to contain the triglyceride form to assure goodabsorption.12 Results of a randomized clinical trial of patientswith blepharitis and MGD showed improvements in objectiveand subjective measures after 1 year of treatment withapproximately 3 g/d of omega-3 fatty acids.13

To treat MGD and ocular surface disease prior to surgery, I liketo use a fixed combination of loteprednol-tobramycin because ofthe safety of loteprednol. Loteprednol ointment might also beconsidered to decrease inflammation when initiating treatmentfor more severe inflammatory anterior blepharitis and MGD. It is a nice formulation because it is not greasy and contains no preservatives.

To decrease inflammation related to MGD, cyclosporine mightalso be considered.

Dr Donnenfeld: Patients coming for surgery want somethingthat is rapidly effective, and they do not want to wait 3 monthsfor the benefit from omega-3 fatty acids. For these patients,loteprednol rapidly optimizes the ocular surface,14 has a goodsafety profile, and works synergistically with cyclosporine, whichalso has a delayed onset of efficacy and causes irritation. Wefound starting loteprednol first and initiating cyclosporine after

6

Figure 4. Reduction in visual quality due to tear film abnormality.

Photo courtesy of Stephen S. Lane, MD


1 to 2 weeks increases the patient’s comfort and tolerability withcyclosporine.15 I start loteprednol 4 times a day for 2 weeks,then twice a day for 2 weeks.

Dr Lindstrom: A lot of patients are unhappy if they are startedon cyclosporine alone. I tell my patients that if we startcyclosporine, it is a lifetime treatment, but I find I can sometimesgo from twice-a-day to once-a-day administration after 6 to 12months. In a randomized study, Su and colleagues reported thatmost patients with dry eye disease treated with cyclosporinetwice a day for a year could maintain control when switched toonce-daily dosing.16

Dr Donnenfeld: We also decrease the dosing frequency ofcyclosporine to once a day for some patients with dry eye.However, it depends on the underlying etiology, and patientshave to be monitored for potential worsening that wouldnecessitate a return to twice-daily dosing.

Dr Lane: In terms of the patient in this case, surgery waspostponed, and the patient was instructed to perform lidhygiene and to start omega-3 fatty acids at 3 g/d. Treatmentalso included loteprednol 0.5% ointment since the inflammatorycomponent of the mixed blepharitis was significant enough tonecessitate a steroid, and she started taking doxycycline. Therewas a significant improvement after 2 weeks. The patient hadsurgery and did well. For long-term control, she was started onmaintenance therapy with topical azithromycin every othermonth and continued oral omega-3 fatty acids supplementationand lid hygiene.

Dr Lindstrom: I also find topical azithromycin effective for long-term maintenance therapy in patients with MGD.

Dr O’Brien: Azithromycin, an advanced macrolide agent, is well-suited for MGD management because it has bothimmunomodulatory properties conferring anti-inflammatoryactivity and is antimicrobial. Anterior blepharitis is not aninfectious process, but it is associated with excessive bacterial colonization.

For lid hygiene, I like to use a foaming lid scrub that containslinalool, a tea tree oil derivative that has some anti-inflammatoryand antimicrobial properties, including activity against methicillin-resistant Staphylococcus aureus and Staphylococcus epidermidis.17

We also caution the sometimes obsessive-compulsive patientswith MGD blepharitis to not use detergent-containing lid scrubsexcessively as this may result in further breakdown of abnormalmeibum into free fatty acids, and triglyceride soaps may also addto the ocular surface irritation.

Case 3: Ocular Allergy and Ocular Surgery

—Terrence P. O’Brien, MD

A 61-year-old male presents with IOPs of 36 mm Hg OD and38 mm Hg OS as well as early glaucomatous changes in hisvisual field and retinal nerve fiber layer. Previously, he had beena suspect for primary open-angle glaucoma with a cup-to-discratio of 0.7 OU, borderline high IOP, and a family history ofglaucoma. He is a patient with a moderately high degree ofmyopia who has worn rigid gas-permeable contact lensessuccessfully for many years.

He was placed on a prostaglandin analogue once nightly. IOPdecreased only to the mid-20s, and an alpha adrenergic agent(brimonidine) was added twice a day. The patient complained ofitching, occasional redness, and episodic mucus discharge, andhe was developing contact lens intolerance. Photographs fromhis external examination are shown in Figure 5. What is yourdiagnosis?

Dr Donnenfeld: Given the appearance and history of contactlens wear, I would diagnose giant papillary conjunctivitis.

Dr O’Brien: Talking in general about patients with glaucomaplus ocular surface disease, what are the issues to consider whenusing topical medications?

Dr Lane: IOP-lowering agents can be a double-edged swordbecause of the risks for an allergic reaction to some medicationsand for toxicity from the medications themselves or frompreservatives, especially benzalkonium chloride.18,19 In thispatient who needs a steroid to treat inflammation, the potentialfor an IOP response also needs to be considered.

Dr O’Brien: How do you differentiate whether the conjunctivalredness in this patient is a sign of allergy or irritation?

Dr Donnenfeld: With a prostaglandin analogue, there can beirritation from the preservative or from the active ingredient.

Switching to a preservative-free medication might be a reasonablething to try. Sometimes I prescribe an oral glaucoma medicationfor a few weeks to treat the IOP and leave such patients on 1topical medication in 1 eye only. If the redness in the fellow eyeimproves, I know which topical medication was the cause.

Brimonidine can cause allergic reactions.20 Patients with anallergic reaction to brimonidine tend to rub their eyes a lot. Therubbing perpetuates the redness by causing mast celldegranulation, and the rubbing is also detrimental in patientswith glaucoma because the rubbing increases IOP.

Dr Lindstrom: When a patient has an allergic reaction, there isitching, often right over the caruncle, and there might be someerythema of the skin as well. Blepharitis burns, and dry eyestypically are associated with a foreign body gritty sensation.

Dr O’Brien: To manage this patient, we suspended the contactlens wear and treated him with a pulse dosing regimen ofloteprednol etabonate 0.5%. Loteprednol has a safetyadvantage in the patient with glaucoma because it has a reducedpotential for IOP elevations relative to other steroids,21 and thiscase was managed using the suspension formulation. Now,

7

Figure 5. Case 3: Clinical findings of giant papillary conjunctivitis with tarsalhyperemia in a patient with long-term rigid gas-permeable contact lens wear.Fluorescein sodium outlines the giant papillae on the upper eyelid.

Photos courtesy of Terrence P. O’Brien, MD


however, loteprednol gel 0.5% is available and would have beena good choice because it contains 70% less preservative thanthe suspension, 0.003% vs 0.01%. Therefore, it is friendlier tothe ocular surface. The vehicle is a “smart” polymer andcontains the demulcents polyethylene glycol and glycerin. Itdispenses as a liquid and converts to a gel on the eye, but causesminimal blur.

Dr Lane: I think gel formulations are going to bring a paradigmshift in treating ocular surface disease because of their potentialfor increased dwell time on the ocular surface.

Dr Lindstrom: The gel formulation of loteprednol etabonate isalso a non-settling suspension so that a uniform dose isdelivered with each drop and without a need for shaking.

Dr O’Brien: That is an excellent point as, despite frequentinstruction, few patients properly agitate the eyedrop bottle toachieve a uniform suspension of the active ingredient with drop delivery.22

In addition to loteprednol etabonate 0.5%, this particular patientwas also started on a dual-acting anti-allergy agent (olopatadine)twice daily and was switched to daily disposable soft contactlenses. Brimonidine was stopped. The patient’s IOP increasedto above 30 mm Hg, but was controlled with the addition of abeta-blocker. The patient did well but returned 14 months laterwith even worse dryness, irritation, itching, hyperemia, andmucus discharge.

We referred this patient for consultations with both therefractive surgery and glaucoma services, hoping that refractivesurgery would eliminate his need for contact lenses and theglaucoma surgery would minimize the need for topicalmedications. He was also restarted on a pulse dosing regimen ofloteprednol 0.5%. He continued the anti-allergy agent, usedpreservative-free artificial tears, and returned for a refractivesurgery evaluation after 6 weeks.

At the Bascom Palmer Eye Institute, we developed analgorithmic approach to rationally manage the candidate forLASIK (laser-assisted in situ keratomileusis) who has comorbidallergy (Figure 6).23 Just as it is important to controlinflammatory conditions prior to performing cataract surgery, itis important to have ocular allergy under control prior to LASIK.

Dual action anti-allergy agents have become our mainstay fortreating ocular allergy. However, it is important to realize thatthey may differ in their effects on the tear film due to differencesin histamine receptor binding affinity profiles.24

Dr Lindstrom: In a contact lens wearer or patient with knowndry eye, I am using bepotastine besilate 1.5%. Bepotastine is ahighly selective H1 receptor antagonist with low binding affinityfor muscarinic receptors,24 and therefore it has a low likelihoodfor exacerbating dry eye.

Loteprednol etabonate 0.2% is also an effective option for ocularallergy management,25 and it has been reported to be safe whenused on a long-term basis in patients with chronic allergy.26

Dr O’Brien: This patient had LASIK performed in 2 stages.First, the flap was created with a femtosecond laser, but theexcimer laser photoablation was delayed for 6 weeks after

trabeculectomy with mitomycin-C so that it would correct anyastigmatism induced by the glaucoma surgery.

Postoperatively, the patient had excellent unaided visual acuity,20/20 OD and 20/15 OS, with very little residual refractive errorand no need for contact lenses. He continued the preservative-free artificial tears for 6 months and the dual action anti-allergyagent as needed. The hyperemia and papillae in this patientgradually improved, although it took about a year, and thepersistence of the papillae can be associated with exacerbationsand recurrences. However, the patient was delighted to no longerneed contact lenses, IOP was controlled in the low teens, and thevisual field and nerve fiber layer were stable.

Dr Donnenfeld: Dr Lindstrom has published on the benefit ofcataract surgery for glaucoma control.27,28 Therefore,phacoemulsification, perhaps combined with a trabecular micro-bypass stent, might have been an alternative to trabeculectomyin this patient.

In patients with milder glaucoma who have ocular irritationassociated with their topical medication, laser trabeculoplasty isalso a reasonable procedure for trying to eliminate topicalmedication use.

Dr Lindstrom: Most 60-year-olds have early cataracts. If a patienthas what I call the 3G syndrome—glare from cataract, glasses,and glaucoma—I often think of a refractive lens exchange.

8

Figure 6. Preoperative workup for LASIK candidates with a history of allergy.23

Reprinted with permission from Lippincott Williams & Wilkins.

Crosstalk

Diagnosis

KCS TFD VKC GPC AKC PAC SAC

Optimization of Ocular Surface

Severity-based treatment

Lubricants

Antihistamines

Multiple-action agents

Mast cell stabilizers

Immunomodulators

Steroids/CyAImmunotherapy

Re-evaluate Ocular Surface (4 weeks)

OphthalmologistAllergist/

Immunologist

Red eye

Tear film

dysfunction

Infectious

Autoimmune

Vasomotor

Suspected

allergy

Schirmertest

Tear film osmolarity

RPS inflammatory dry eye

Detector

Tear IgE

Conjunctival cytology

Visual disturbance

Ocular pain

Photophobia

Chronic contact lens wearer

Rhinitis

Asthma

Sinusitis

Atopic dermatitis

Urticaria/Angioedema

Slit lamp exam

Tear breakup time

Vital staining

(fluorescein, lissamine

green, rose bengal)

Skin test

Atopic evaluation

Rhinoscopy

Peak flow spirometry

History


Case 4: Inflammation andSurviving a Toxic AnteriorSegment Syndrome Epidemic

—Eric D. Donnenfeld, MD

A 71-year-old female underwent uneventful cataract surgery in2005 and received the standard postoperative medicationregimen that included a fourth-generation fluoroquinolone, anNSAID, and prednisolone acetate 1%. She presents on the firstpostoperative day without pain, minimal lid swelling, and arelatively quiet eye, but complains about decreased vision. A slit-lamp photo of her eye is shown (Figure 7). What are theimportant findings?

Dr O’Brien: The corneal edema is diffuse. It is not just adjacentto the incision, but is limbal to limbal, horizontally and vertically.That suggests a toxic response.

Dr Lane: However, unless you have a reason to suspect toxicanterior segment syndrome (TASS) because of an ongoingoutbreak, your first obligation is to rule out infectiousendophthalmitis.

Dr O’Brien: The time course also provides diagnostic clues.Significant hypopyon within 24 hours of surgery suggests it maybe triggered by a toxic response rather than infection. Despitethese suggestive clues, I certainly agree that it is incumbent uponthe surgeon to perform the requisite diagnostic tests to rule out infection.

Dr Donnenfeld: TASS was suspected in this patient because Ilearned a TASS epidemic had started the day before. Otherpatients seen by other surgeons had a similar presentation, andsome had an anterior chamber tap with nothing found on Gramstain. How do you manage TASS?

Dr Lane: I would do an anterior chamber washout, prescribe anintracameral antibiotic, and treat TASS with an aggressive anti-inflammatory regimen.

Dr O’Brien: The possible sequelae of TASS include CME,endothelial damage, and damage to the trabecular meshworkleading to uncontrollable glaucoma. The pupil may also beaffected by the toxins and become permanently mydriatic and nonreactive.

Based on my experience with TASS cases seen on referral, I thinkearly anterior chamber irrigation plus washout is an importantmaneuver to prevent permanent intraocular damage, especially inthis case where the inflammation is so severe. TASS is a toxicinsult to the intraocular milieu, and the solution to pollution is

dilution. We need to be aggressive in irrigating the toxins awayand then start the patient on high-dose corticosteroids.

Dr Lindstrom: I think of TASS in much the same way as I thinkof diffuse lamellar keratitis (DLK). If I see DLK on the first dayafter LASIK, I do not immediately lift the flap and irrigate, butusually give patients an opportunity to respond to aggressivetopical steroids while monitoring them very closely.

Dr Donnenfeld: Nick Mamalis, MD, a professor ofophthalmology at the John A. Moran Eye Center, University ofUtah, Salt Lake City, and co-chairman of the American Societyof Cataract and Refractive Surgery TASS Task Force, is againstusing antibiotics, and I think washout is also controversial.

For a mild case, I start treatment for the patient with a potenttopical steroid, but when there is severe corneal edema, I washout the eye and inject steroid intracamerally. I use preservative-free dexamethasone sodium phosphate because it works morequickly than triamcinolone and does not stay around as long.Then I start the use of topical difluprednate because of itspotency. In a study of patients with severe anterior uveitis, theuse of difluprednate 4 times a day was more effective thanbrand-name prednisolone acetate 1% 8 times a day.29

This case was part of a nationwide epidemic that included 37 cases at our surgery center over 6 weeks. An investigationled by Dr Mamalis identified endotoxin in one manufacturer’sbalanced salt solution as the cause. What are some other causesof TASS?

Dr Lane: Residue in inadequately cleaned reusable cannulas is abig culprit.

Dr O’Brien: Some detergent residues used in processingsurgical instruments are also a cause.

Dr Donnenfeld: The lessons we learned from this TASSoutbreak were that you have to scrupulously examine theprocess of cleaning and processing instruments; document lotnumbers for all products coming in contact with the eye; keeprecords of all staff and equipment used; communicate earlywithin and outside your facility; and identify TASS early, treataggressively with steroids, and avoid vitreous taps andintravitreal antibiotics.

The first 9 cases at our center were sent to a retinal specialistfor evaluation, and the 2 most severe cases had a vitreous tapwith intravitreal antibiotics, but you do not want to do thosemaneuvers if you know it is TASS. These patients need to bewatched very carefully, and you have to certainly be willing tosee them every 4 to 5 hours until you know what is going on.

The patient was treated with cyclopentolate 1% andprednisolone acetate because difluprednate was not available atthe time. She did well with the clearing of her corneal edema,fibrin, and hypopyon over 3 weeks, but she had low-gradeinflammation with chronic iritis, CME, and photophobia, andwas maintained on a long-term basis with loteprednol.

TASS can be associated with long-term smolderinginflammation. How would you manage this patient whopresents 2 months later with low-grade iritis?

9

Figure 7. Case 4: Sterile hypopyonin a patient with TASS.

Photo courtesy of

Eric D. Donnenfeld, MD


Dr Lane: The goal for long-term treatment for low-grade iritis is to use an agent that is potent enough to control theinflammation, but has a high enough safety margin so that youdo not have to be concerned about adverse effects of chronictreatment. Loteprednol fits that description and would be anappropriate choice. I would start treatment for low-grade iritiswith the gel formulation, taper it to once or twice a day, andinstead of discontinuing the steroid altogether, switch toloteprednol 0.2% for longer-term use.

There are published reports of patients using loteprednol 0.2%daily for up to 3 years without developing cataracts or IOPelevation.26 I find it is very helpful for managing mildinflammation for the long term.

Dr Donnenfeld: Loteprednol is a strong steroid with minimal

side effects, and it is my corticosteroid of choice for long-term

maintenance treatment, such as following a penetrating

keratoplasty. I also use loteprednol for everything anterior to

Descemet membrane—anything involving the ocular surface,

anterior cornea, conjunctiva, pterygia, or lid margin. My early

experience with loteprednol gel is that it is even more potent

than the suspension and may be used for intraocular

inflammation. I use difluprednate when I need a potent steroid

for rapid inflammation control. I use it in pulse dosing for TASS,

for acute graft rejection, and in cataract surgery when I want to

completely suppress inflammation.

10

1. Heier JS. Preventing post-cataract extraction CME: early identification of

patients at risk and prophylactic treatment may avert vision loss. Ophthalmol

Manage. October 2004:63-72.

2. O’Brien TP. Emerging guidelines for use of NSAID therapy to optimize cataract

surgery patient care. Curr Med Res Opin. 2005;21(7):1131-1137.

3. Holte K, Kehlet H. Perioperative single-dose glucocorticoid administration:

pathophysiologic effects and clinical implications. J Am Coll Surg. 2002;195(5):

694-712.

4. Donnenfeld ED, Holland EJ, Solomon KD, et al. A multicenter randomized

controlled fellow eye trial of pulse-dosed difluprednate 0.05% versus

prednisolone acetate 1% in cataract surgery. Am J Ophthalmol. 2011;152(4):

609-617.

5. Korenfeld MS, Silverstein SM, Cooke DL, Vogel R, Crockett RS; Difluprednate

Ophthalmic Emulsion 0.05% (Durezol) Study Group. Difluprednate ophthalmic

emulsion 0.05% for postoperative inflammation and pain. J Cataract Refract

Surg. 2009;35(1):26-34.

6. Lane SS, Holland EJ. Loteprednol etabonate 0.5% versus prednisolone acetate

1.0% for the treatment of inflammation after cataract surgery. J Cataract Refract

Surg. 2013;39(2):168-173.

7. Lobo CL, Faria PM, Soares MA, Bernardes RC, Cunha-Vaz JG. Macular

alterations after small-incision cataract surgery. J Cataract Refract Surg.

2004;30(4):752-760.

8. Wittpenn JR, Silverstein S, Heier J, et al. A randomized, masked comparison of

topical ketorolac 0.4% plus steroid vs steroid alone in low-risk cataract surgery

patients. Am J Ophthalmol. 2008;146(4):554-560.

9. Klier SM, Pearce JH, Goldberg DF, Gow JA, McNamara TR, Low-

Concentration, Modified Bromfenac Ophthalmic Solution Once Daily Study

Group. Efficacy of low-concentration, modified bromfenac ophthalmic solution

administered once daily for ocular inflammation and pain associated with

cataract surgery. Poster presented at: Association for Research in Vision and

Ophthalmology Annual Meeting; May 10, 2012; Fort Lauderdale, FL.

Abstract 6684.

10. Lemp MA, Crews LA, Bron AJ, Foulks GN, Sullivan BD. Distribution of

aqueous-deficient and evaporative dry eye in a clinic-based patient cohort: a

retrospective study. Cornea. 2012;31(5):472-478.

11. Torkildsen GL, Cockrum P, Meier E, Hammonds WM, Silverstein B, Silverstein

S. Evaluation of clinical efficacy and safety of tobramycin/dexamethasone

ophthalmic suspension 0.3%/0.05% compared to azithromycin ophthalmic

solution 1% in the treatment of moderate to severe acute blepharitis/

blepharoconjunctivitis. Curr Med Res Opin. 2011;27(1):171-178.

12. Dyerberg J, Madsen P, Møller JM, Aardestrup I, Schmidt EB. Bioavailability of

marine n-3 fatty acid formulations. Prostalgandins Leukot Essent Fatty Acids.

2010;83(3):137-141.

13. Macsai MS. The role of omega-3 dietary supplementation in blepharitis and

meibomian gland dysfunction (an AOS thesis). Trans Am Ophthalmol Soc. 2008;

106:336-356.

14. Pflugfelder SC, Maskin SL, Anderson B, et al. A randomized, double-masked,

placebo-controlled, multicenter comparison of loteprednol etabonate ophthalmic

suspension, 0.5%, and placebo for treatment of keratoconjunctivitis sicca in

patients with delayed tear clearance. Am J Ophthalmol. 2004;138(3):444-457.

15. Donnenfeld E, Sheppard JD, Holland EJ. Prospective, multicenter, randomized

controlled study on the effect of loteprednol etabonate on initiating therapy with

cyclosporine A. Presented at: American Academy of Ophthalmology Annual

Meeting; November 2007; New Orleans, LA.

16. Su MY, Perry HD, Barsam A, et al. The effect of decreasing the dosage of

cyclosporine A 0.05% on dry eye disease after 1 year of twice-daily therapy.

Cornea. 2011;30(10):1098-1104.

17. Gilbard JP, Douyon Y, Huson RB. Time-kill assay results for a linalool-

hinokitiol-based eyelid cleanser for lid hygiene. Cornea. 2010;29(5):559-563.

18. Epstein SP, Chen D, Asbell PA. Inflammatory response by ocular surface

epithelia upon exposure to prostaglandin analogs. Invest Ophthalmol Vis Sci.

2008;49:E-abstract 3820.

19. Baudouin C. Labbé A, Liang H, Pauly A, Brignole-Baudouin F. Preservatives in

eyedrops: the good, the bad and the ugly. Prog Retin Eye Res. 2010;29(4):

312-334.

20. Blondeau P, Rousseau JA. Allergic reactions to brimonidine in patients treated

for glaucoma. Can J Ophthalmol. 2002;37(1):21-26.

21. Comstock TL, Decory HH. Advances in corticosteroid therapy for ocular

inflammation: loteprednol etabonate. Int J Inflam. 2012;2012:789623.

22. Apt L, Henrick A, Silverman LM. Patient compliance with use of topical

ophthalmic corticosteroid suspensions. Am J Ophthalmol. 1979;87(2):

210-214.

23. Bielory BP, O’Brien TP. Allergic complications with laser-assisted in situ

keratomileusis. Curr Opin Allergy Clin Immunol. 2011;11(6):483-491.

24. Wade L. Bielory L, Rudner S. Ophthalmic antihistamines and H1-H4 receptors.

Curr Opin Allergy Clin Immunol. 2012;12(5):510-516.

25. Elion-Mboussa A, Gong L, Roy L, Zhu B, DeCory H, Chu E. Loteprednol

etabonate ophthalmic suspension, 0.2% is as safe as olopatadine hydrochloride

ophthalmic solution, 0.1% with superior relief of signs and symptoms in the

treatment of seasonal allergic conjunctivitis. Presented at: Proceedings of the

Annual Meeting of the American Academy of Allergy Asthma and Immunology;

March 2012; Orlando, FL.

26. Ilyas H, Slonim CB, Braswell GR, Favetta JR, Schulman M. Long-term safety of

loteprednol etabonate 0.2% in the treatment of seasonal and perennial allergic

conjunctivitis. Eye Contact Lens. 2004;30(1):10-13.

27. Poley BJ, Lindstrom RL, Samuelson TW, Schulze R Jr. Intraocular pressure

reduction after phacoemulsification with intraocular lens implantation in

glaucomatous and nonglaucomatous eyes: evaluation of a causal relationship

between the natural lens and open-angle glaucoma. J Cataract Refract Surg.

2009;35(11):1946-1955.

28. Poley BJ, Lindstrom RL, Samuelson TW. Long-term effects of

phacoemulsification with intraocular lens implantation in normotensive and

ocular hypertensive eyes. J Cataract Refract Surg. 2008;34(5):735-742.

29. Foster CS, Davanzo R, Flynn TE, McLeod K, Vogel R, Crockett RS. Durezol®

(difluprednate ophthalmic emulsion 0.05%) compared with Pred Forte®

Ophthalmic Suspension in the treatment of endogenous anterior uveitis.

J Ocul Pharmacol Ther. 2010;26(5):475-483.

References


1. All of the following are risk factors for postcataract surgerycystoid macular edema, except:

A. DiabetesB. Vitreous lossC. History of LASIK (laser-assisted in situ keratomileusis)D. Epiretinal membrane

2. In a published study by Lobo and colleagues of patientsundergoing uneventful cataract surgery, the percentage ofeyes found to have evidence of retinal vascular leakage after12 weeks was near:

A. 25%B. 50%C. 75%D. 90%

3. In a study by Wittpenn and colleagues comparing postcataractsurgery treatment with a steroid alone or combined with anNSAID, retinal thickening of more than 10 microns:

A. Occurred more often in the combination treatmentgroup

B. Was associated with reduced contrast sensitivityC. Was prevented by combination treatmentD. Was associated with reduced uncorrected visual acuity

4. Depending on the intraocular pressure and other ocularfindings, all of the following might be a reasonable surgicalstrategy for minimizing medication use in patients withglaucoma plus ocular surface disease, except:

A. TrabeculectomyB. PhacoemulsificationC. Laser trabeculoplastyD. Any of the above might be reasonable, depending on

individual circumstances

5. All of the following may be signs of meibomian glanddysfunction, except:

A. Low Schirmer test scoreB. Rapid tear break-up timeC. Lid margin telangiectasiaD. Foamy tear film

6. Initial treatment for dry eye associated with meibomian glanddysfunction might include all of the following, except:

A. DoxycyclineB. Punctal plugsC. Topical corticosteroid-antibiotic combinationD. Lid hygiene

7. A benefit of using bepotastine besilate to treat ocular allergyin contact lens wearers is:

A. Its receptor selectivity profile confers a reducedlikelihood of exacerbating dry eye

B. It is recommended for once-daily dosingC. It contains no preservativesD. It can be instilled without removing the contact lenses

8. Adverse sequelae of toxic anterior segment syndrome (TASS)may include all of the following, except:

A. Cystoid macular edemaB. Permanent miosisC. GlaucomaD. Endothelial damage

9. Which of the following should be absolutely avoided in an eyewith TASS?

A. Vitreous tapB. Topical corticosteroid treatmentC. Anterior chamber washoutD. Cyclopentolate

All of the following ophthalmic nonsteroidal anti-inflammatory drugs are recommended for once-daily dosing, except:

A. Bromfenac 0.09%B. Ketorolac tromethamine 0.45%C. Nepafenac 0.3%D. All 3 products are recommended for once-daily dosing

11

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Activity Evaluation/Credit RequestNew Evidence and Insights on the Inflammation Panorama: From Ocular Surface Disorders to Surgery

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