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*High Oxygen Transmissible Lenses: Dk/t = 138 @ -3.00D. **Compared to ACUVUE^ ADVANCE^, ACUVUE^ OASYS^, PureVision^, Biofi nity^ and Avaira^ contact lenses. †Lotrafi lcon B contact lenses tested include AIR OPTIX® AQUA, AIR OPTIX® AQUA Multifocal and

AIR OPTIX® for Astigmatism contact lenses.^Trademarks are the property of their respective owners.Important information for AIR OPTIX® COLORS (lotrafi lcon B) contact lenses: For daily wear only for near/farsightedness. Contact lenses, even if worn for cosmetic reasons, are prescription medical devices that must only be worn under the prescription, direction, and supervision of an eye care professional. Serious eye health problems may occur as a result of sharing contact lenses. Although rare, serious eye problems can develop while wearing contact lenses. Side effects like discomfort, mild burning, or stinging may occur. To help avoid these problems, patients must follow the wear and replacement schedule and the lens care instructions provided by their eye doctor. References: 1. Based on ratio of lens oxygen transmissibilities; Alcon data on fi le, 2013. 2. Based on in vitro measurement of contactangles of unworn lenses; signifi cance demonstrated at 0.05 level. Alcon data on fi le, 2013. 3. Eiden SB, Davis R, Bergenske P. Prospectivestudy of lotrafi lcon B lenses comparing 2 versus 4 weeks of wear for objective and subjective measures of health, comfort, and vision. Eye & Contact Lens. 2013;39(4):290-294.© 2014 Novartis 2/14 AOC14003JAD-B See product instructions for complete wear, care and safety information.

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NEW

Scleritis: When a Red Eye Raises a Red Flag, Page 26

www.revoptom.com

July 15, 2014

Plotting the Path of Progression

2

Tailor Your Approach to PXG Management

Page 38

The Changing and Challenging Epidemiology of Glaucoma

Page 44

Earn 2 CE Credits: Glaucoma on Trial:

Clinical Implications of the Landmark Glaucoma Studies

Page 50

20th Annual GLAUCOMA Report

Help protect their eyes.Your patients protect their skin.

* UV-blocking percentages are based on an average across the wavelength spectrum.

ACUVUE® Brand Contact Lenses are indicated for vision correction. As with any contact lens, eye problems, including corneal ulcers, can develop. Some wearers may experience mild irritation, itching or discomfort. Lenses should not be prescribed if patients have any eye infection, or experience eye discomfort, excessive tearing, vision changes, redness or other eye problems. Consult the package insert for complete information. Complete information is also available from VISTAKON® Division of Johnson & Johnson Vision Care, Inc., by calling 1-800-843-2020 or by visiting acuvueprofessional.com.

Many patients are unaware of the long-term implications that may be associated with cumulative day-to-day ultraviolet (UV) exposure to eye health.1

UV-blocking contact lenses worn in addition to sunglasses and a wide-brim hat can provide an additional layer of protection against UV radiation.2

†Helps protect against transmission of harmful UV radiation to the cornea and into the eye.

WARNING: UV-absorbing contact lenses are NOT substitutes for protective UV-absorbing eyewear such as UV-absorbing goggles or sunglasses, because they do not completely cover the eye and surrounding area. You should continue to use UV-absorbing eyewear as directed. NOTE: Long-term exposure to UV radiation is one of the risk factors associated with cataracts. Exposure is based on a number of factors such as environmental conditions (altitude, geography, cloud cover) and personal factors (extent and nature of outdoor activities). UV-blocking contact lenses help provide protection against harmful UV radiation. However, clinical studies have not been done to demonstrate that wearing UV-blocking contact lenses reduces the risk of developing cataracts or other eye disorders. Consult your eye care practitioner for more information.

References: 1. The big picture: eye protection is always in season. The Vision Council Web site. http://www.thevisioncouncil.org/sites/default/files/VCUVReport2013FINAL.pdf. Accessed May 7, 2014. 2. Chandler H. Ultraviolet absorption by contact lenses and the significance on the ocular anterior segment. Eye Contact Lens. 2011;37(4):259-266.

ACUVUE®, 1-DAY ACUVUE® MOIST®, 1-DAY ACUVUE® TruEye®, ACUVUE® OASYS®, HYDRACLEAR®, INNOVATION FOR HEALTHY VISION™, and VISTAKON® are trademarks of Johnson & Johnson Vision Care, Inc.

© Johnson & Johnson Vision Care, Inc. 2014 ACU-43878G May 2014

Educate your patients about ACUVUE® Brand Contact Lenses— the only major brand to block at least 97% of UVB and 81% of UVA rays as standard across the entire line.*†

To learn more, visit acuvueprofessional.com.

N e w s R e v i e w

4 REVIEW OF OPTOMETRY JULY 15, 2014

Omega-3s Suppress CNV

Omega-3 fatty acid supple-mentation can slow or inhibit choroidal neovas-

cularization (CNV) caused by wet age-related macular degeneration, according to research published in the June 16 Proceedings of the Na-tional Academy of Sciences Online Early Edition.

In this study, a team from Schepens Eye Research Institute at Harvard Medical School evaluated whether omega-3 or omega-6 long-chain polyunsaturated fatty acids could retard CNV proliferation. Researchers randomized groups of mice to receive an experimental diet enriched with either omega-3s or omega-6s, or a control diet, for two weeks. Then, the mice under-went laser photocoagulation to precipitate CNV development.

The researchers determined that

those in the omega-3 group exhib-ited markedly smaller CNV lesions and less vascular leakage than those in the omega-6 or control groups.

“These are the fi rst results showing that omega-3 long-chain polyunsaturated fatty acids and their cytochrome P450-derived metabolites can regulate choroidal angiogenesis in vivo,” says senior author Kip Connor, PhD, assistant professor of ophthalmology at Harvard Medical School. “Our fi ndings not only show promising therapeutic potential for resolution of neovascular AMD, but also for other conditions or diseases that involve pathologic angiogenesis and infl ammation.” Yanai R, Mulki L, Hasegawa E, et al. Cytochrome P450-generated metabolites derived from omega-3 fatty acids attenuate neovascularization. PNAS. 2014 Jun 16. [Epub ahead of print]

IN THE NEWS

The FDA has approved Afrezza Inhala-tion Powder (insulin human, MannKind Corporation) to improve glycemic control for adults with diabetes. The new treat-ment option is a rapid-acting inhaled insulin that is administered before each meal. A 24-week study evaluating the

effi cacy of the drug in a total of 3,017 patients with both type 1 and type 2 dia-betes demonstrated its ability to reduce HbA1c. The drug is not a substitute for long-acting insulin and must be used in combination with one.

Researchers have determined that telemedicine screening for retinopa-thy of prematurity (ROP) is valid when conducted by trained nonphysicians. The study, published in the June 26 online edition of JAMA Ophthalmology, enrolled 1,257 premature infants weigh-ing less than 1,251 grams (2lbs. 12oz.) and born at 27 weeks of gestational age on average. Trained nonphysicians took standard sets of six images in both eyes and graded them using a standard pro-tocol. When compared to examinations conducted by ophthalmologists, the telemedicine readers correctly identifi ed 90% of infants with referral-warranted ROP. Telemedicine could make treating ROP easier and increase the frequency of screening for the condition, which currently depends on the schedule of physicians, the study concludes.

V O L . 1 5 1 N O . 7 ■ J U L Y 1 5 , 2 0 1 4

For the first time, omega-3 fatty acids were shown to inhibit choroidal angiogenesis. By Michael Hoster, Managing Editor

Researchers have identifi ed a way to enhance regrowth of human corneal tissue to restore vision, using a molecule known as ABCB5 that acts as a marker for hard-to-fi nd limbal stem cells. The research, published online in Nature, is also one of the fi rst successes in constructing a tissue from an adult-derived human stem cell.

This breakthrough development—a collaboration among the Massachusetts Eye

and Ear/Schepens Eye Research Institute, Boston Children’s Hospital, Brigham and Women’s Hospital and the VA Boston Healthcare System—offers promise to patients with ocular burn, chemical injury and damaging eye diseases, the researchers say.

Ksander BR, Kolovou PE, Wilson BJ, et al. ABCB5 is a limbal stem cell gene required for corneal development and repair. Nature. 2014 Jul 2. [Epub ahead of print]

Scientists Grow First Human Cornea Using Limbal Stem Cells

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News Review

New research shows that the brain—not the eye—con-trols the cellular process

that leads to glaucoma. The results may not only spur treatments for glaucoma, but also help develop future therapies for preserving brain function in other age-related disorders, such as Alzheimer’s.

In glaucoma, loss of the visual field in each eye appears to be hap-hazard. Conversely, neural damage in the brain caused by strokes or tumors produces visual field loss that is almost identical for each eye, which supports the idea that the entire degenerative process in glaucoma must occur at random in the individual eye—without brain involvement.

However, as previously disabled optic nerve axons recover, the remaining areas of permanent visu-al loss in one eye coincide with the areas that remain functional in the other eye. That is, the team found that the visual field of the two eyes fit together like a jigsaw puzzle, resulting in much better vision with both eyes open than could possibly arise by chance.

“The extent and statistical

strength of the jigsaw effect in conserving the binocular visual field among the clinical popula-tion turned out to be remarkably strong,” says author William Eric Sponsel, MD, of the University of Texas at San Antonio. “The entire phenomenon appears to be under the meticulous control of the brain.”

Dr. Sponsel further explains: “As age and other insults to ocular health take their toll on each eye, discrete bundles of the small axons within the larger optic nerve are sacrificed so the rest of the axons can continue to carry sight infor-mation to the brain. This quiet, intentional sacrifice of some wires to save the rest, when there are decreasing resources to support them all, is analogous to pruning some of the limbs on a stressed fruit tree so the other branches can continue to bear healthy fruit.”

This research is the first evidence in humans that the brain plays a part in “pruning” optic nerve axon cells. According to the researchers, this process in glaucoma—apop-tosis—is remarkably similar to the apoptotic mechanism that oper-

ates in the brains of people with Alzheimer’s disease.

“If the brain is actively trying to maintain the best binocular field, and not just producing the jigsaw effect accidentally, that would imply some neuroprotec-tive substance is at work prevent-ing unwanted pruning,” says the study’s coauthor Ted Maddess, PhD, of the ARC Centre of Excel-lence in Vision Science, Australian National University. “Since glau-coma has much in common with other important neurodegenerative disorders, our research may say something generally about con-nections of other nerves within the brain and what controls their main-tenance.”

Dr. Sponsel foresees how this research can soon translate to clinical use. “It would be relatively straightforward to modify existing equipment to allow for the perfor-mance of simultaneous binocular visual fields, in addition to stan-dard right eye and left eye testing,” he says. Sponsel WE, Groth SL, Satsangi N, et al. Refi ned data analy-sis provides clinical evidence for central nervous system control of chronic glaucomatous neurodegeneration. Transl Vis Sci Technol. 2014 May 6;3(3):1.

Is Glaucoma a Brain Disease?

Compared with sleeping in the supine position, sleeping in the 20-degree head-up position results in a lower IOP (an average reduction of 1.56mm Hg, or 9.33%, in glaucoma patients), and may prove to be an effective, inexpensive and noninvasive adjunct in IOP reduction for glaucoma care, according to a new study in the Journal of Glaucoma.

“If sleeping at a ... 20-degree angle could decrease the IOP by almost 10%, it may be of therapeutic benefi t to recommend,” the authors conclude.

Further research is needed to determine the optimal head position to provide the greatest decrease in IOP while maintaining patient comfort, and whether it alters the progression of disc damage and visual fi eld deterioration over time.

Lazzaro EC, Mallick A, Singh M, et al. The effect of positional changes on intraocular pressure during sleep in patients with and without glaucoma. J Glaucoma. 2014 Jun-Jul;23(5):282-7.

Sleeping Up Brings IOP Down by Almost 10%

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News Review

There will be enough optom-etrists—and perhaps an oversupply—into the year

2025, according to a new study of the number of US eye care provid-ers.

The Eye Care Workforce Study was jointly initiated by the AOA and the Association of Schools and Colleges of Optometry (ASCO) and performed by The Lewin Group, a health care policy con-sulting fi rm. The study considered a complex mix of both supply and demand factors in all of eye care—optometrists and ophthalmologists included.

On the supply side, the study factored in retiring eye doctors, the stagnant supply of ophthal-mologists, the rising numbers of female optometrists (and how their workload could affect supply) and a potential increase of optometrists with the opening of more OD schools. The study also took into account that many optometrists have open appointments in their schedules that could be fi lled with

additional patients—an “excess ca-pacity” of 20 patient visits a week without adding practice hours.

On the demand side, the study factored in the growth of the US population. It also estimated an increased number of adults and children covered under the Afford-able Care Act, as well as a need for more eye care services due to the growing prevalence of diabetes in America.

“If these sources of demand are realized, then excess capacity in the [eye care] workforce will be substantially reduced, but not eliminated,” concluded the execu-tive summary of the study.

Some specifi c points from the study:

• An estimated 40,484 ODs are in active practice in 2014.

• Male optometrists (22,809) currently make up 56% of the workforce and female optometrists (17,675) account for 44%. How-ever, the average female OD is sig-nifi cantly younger (40.2 years old) than the average male OD (50.9),

which suggests a growing propor-tion of women in the workforce.

A Starting PointAt a press conference held dur-

ing June’s AOA meeting in Phila-delphia, AOA and ASCO offi cials underscored that this study is merely a start—a working model from which to begin to continu-ously assess eye care supply and demand as factors change.

“What we’ve got is a great start-ing point,” said ASCO representa-tive David Heath, OD, MEd. The study will be updated on a yet-to-be determined intermittent basis.

For now, people can use the study in several ways. Optometry schools—or universities interested in opening an optometry school—can use the data to consider that expanding class size or opening a new school may not be necessary, Dr. Heath said.

Also, it may help point out to current students the importance of practice location. “We do know that there are huge underserved [rural] areas in the United States,” Dr. Heath said. But opening a new practice down the street from your optometry school alma mater? Not a smart idea.

The study also corroborates optometry’s expansion of scope of practice and the removal of insur-ance barriers to providing care, not to mention greater involvement in health policy decisions, said AOA’s Randy Brooks, OD, who chaired the study project.

“Most of the new demand [predicted by the study] is coming from the medical side,” Dr. Brooks said. “So it shows there’s a greater opportunity for ODs to provide full-scope eye care.”

Enough ODs, Workforce Study Says

Engineers at the University of Washington have designed a low-power sensor that can be permanently placed in a glaucoma patient’s eye to measure even the small-est changes in intraocular pressure.

The sensor would be embedded within an intraocular lens implanted during cata-ract surgery and could detect changes instantly. These changes would then be

transmitted wirelessly using radio frequency waves. The engineers have fi led patents on an initial prototype, which they admit is “radical,” as no one has ever put electronics inside the lens of an eye—yet. The current prototype is too large to fi t in an artifi cial lens, but the team says it’s confi dent that they can downscale it to a workable size.

Varel Ç, Shih Y, Otis BP, et al. A wireless intraocular pressure monitoring device with a solder-fi lled microchannel antenna. J Micromech Microeng. Published online March 13, 2014.

Monitoring IOP with an IOL

Imag

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News Review

Costs related to eye disease are expected to skyrocket 376% by 2050 as a result

of changing US demographics, ac-cording to “The Future of Vision: Forecasting the Prevalence and Costs of Vision Problems,” a new report from Prevent Blindness.

The shifting American land-scape includes aging baby boomers, an increase in minor-ity populations and a growing number of women living past age 90—all of which will contribute to an upward climb in cases of eye disease and vision problems, with a price tag of $717 billion by 2050 when adjusted for infl ation, the study says.

“We cannot stand by and passively accept vision loss as an inevitable condition of grow-ing old,” Prevent Blindness CEO Hugh R. Parry said in a statement. “The sheer numbers of those who are and will be personally and

fi nancially impacted by vision im-pairment and blindness is far too great to ignore. The time to plan and develop a national strategy for saving sight is now.”

The report, commissioned from researchers at the National Opin-ion Research Center at the Uni-versity of Chicago, predicts that eye disease and vision problems will cost more than $384 billion by 2032.

Researchers further predict that costs will shift from patients and private insurance to government as the baby-boomer generation ages into the Medicare program. Based on researchers’ predictions, the government will pay more than 41% of costs by 2050, while the burden paid by patients will drop to 44% and that paid by private insurers to 16%.

For more information or to view the report, visit www.preventblindness.org. ■

Eye Disease Costs to Skyrocket by 2050

$1,000900800700600500400300200100

Total Economic Burden of Vision Loss and Eye Disorders by 2050

2050 in the United States, $ billions

$ real (2014) $ nominal

$ 716.93

$ 373.22

Source: Prevent Blindness

By 2050, the US cost of eye disease and vision problems is expected to reach $373 billion in real dollars, which translates to $717 billion when adjusted for inflation.

See product instructions for complete wear, care and safety information.

© 2014 Novartis 1/14 WIC14001JAD

PERFORMANCE DRIVEN BY SCIENCETM

Important information for AIR OPTIX® AQUA (lotrafilcon B), AIR OPTIX® AQUA Multifocal (lotrafilcon B), and AIR OPTIX® for Astigmatism (lotrafilcon B) contact lenses: For daily

wear or extended wear up to 6 nights for near/far-sightedness, presbyopia and/or astigmatism. Risk of serious eye problems (i.e. corneal ulcer) is greater for extended wear.

In rare cases, loss of vision may result. Side effects like discomfort, mild burning or stinging may occur.

Important information for AIR OPTIX® NIGHT & DAY® AQUA (lotrafilcon A) contact lenses: Indicated for vision correction for daily wear (worn only while awake) or extended wear

(worn while awake and asleep) for up to 30 nights. Relevant Warnings: A corneal ulcer may develop rapidly and cause eye pain, redness or blurry vision as it progresses. If left

untreated, a scar, and in rare cases loss of vision, may result. The risk of serious problems is greater for extended wear vs daily wear and smoking increases this risk. A one-year

postmarket study found 0.18% (18 out of 10,000) of wearers developed a severe corneal infection, with 0.04% (4 out of 10,000) of wearers experiencing a permanent reduction

in vision by two or more rows of letters on an eye chart. Relevant Precautions: Not everyone can wear for 30 nights. Approximately 80% of wearers can wear the lenses for

extended wear. About two-thirds of wearers achieve the full 30 nights continuous wear. Side Effects: In clinical trials, approximately 3-5% of wearers experience at least one

episode of infiltrative keratitis, a localized inflammation of the cornea which may be accompanied by mild to severe pain and may require the use of antibiotic eye drops for

up to one week. Other less serious side effects were conjunctivitis, lid irritation or lens discomfort including dryness, mild burning or stinging. Contraindications: Contact lenses

should not be worn if you have: eye infection or inflammation (redness and/or swelling); eye disease, injury or dryness that interferes with contact lens wear; systemic disease

that may be affected by or impact lens wear; certain allergic conditions or using certain medications (ex. some eye medications). Additional Information: Lenses should be

replaced every month. If removed before then, lenses should be cleaned and disinfected before wearing again. Always follow the eye care professional’s recommended lens

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REVIEW OF OPTOMETRY JULY 15, 2014 13

50 Why Dry Eye TrialsOften Fail

From disease variability to confounding underlying conditions, there are countless reasons why new dry eye drugs have come up short in FDA testing. By Paul M. Karpecki, OD, Co-Chief Clinical Editor

61 A Lifetime ofDry Eye

Dry eye can strike patients of any age. Do you know the subtle signs and symptoms to look for, and the particular treatments to provide, among patients of different ages?By Cheryl G. Murphy, OD, Contributing Editor

ContentsReview of Optometry July 2014

This painful inflammation is often an indicator of more serious health concerns. By Michael Trottini, OD, and Candice Tolud, OD

Scleritis: When a Red Eye Raises a Red Flag 26

20th Annual Glaucoma Report

Treatment without evidence is like taking a shot in the dark. These major studies provide proof to apprehend the ‘sneak thief of sight.’ By David Lynne, OD, Maria Mandese, OD, and Erica Walker, OD

Earn 2 CE Credits: Glaucoma on Trial: Clinical Implications of the Landmark Glaucoma Studies

50

Patients with pseudoexfoliative glaucoma often require a more thorough diagnostic work-up and earlier intervention than those with POAG. So how do these conditions differ, and why? By Anupam Laul, OD, and Marta Fabrykowski, OD

Tailor Your Approach to PXG Management38

Our success in managing glaucoma hinges on our ability to recognize—and make sense of—both structural and functional changes. By Scott Anthony, OD

As the aging population doubles and minority groups skyrocket, we face increased challenges in tailoring our glaucoma care to each patient. By Mark Swanson, OD, MSPH

Plotting the Path of Progression

The Changing and Challenging Epidemiology of Glaucoma

32

44

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Review of Optometry July 2014

4 News Review

18 Outlook Rise and Shine JACK PERSICO

20 Chairside iPhone Refraction? iLove it! MONTGOMERY VICKERS, OD

22 Coding Abstract No More ‘Glaucoma Checks’ JOHN RUMPAKIS, OD, MBA

60 Cornea + Contact Lens Q+A Fresh Ink JOSEPH P. SHOVLIN, OD

62 Comanagement Q+A Steroid Adds to the Pressure PAUL C. AJAMIAN, OD

64 Review of Systems The Tangled Web We Weave CARLO J. PELINO, OD JOSEPH J. PIZZIMENTI, OD

69 Retina Quiz Pale in Comparison MARK T. DUNBAR, OD

73 Therapeutic Review A Hole-in-One? JOSEPH W. SOWKA, OD ALAN G. KABAT, OD

77 Product Review

80 Meetings + Conferences

81 Advertisers Index

84 Classifieds

88 Surgical Minute ASP: Take a Bite Out of RCE DEREK N. CUNNINGHAM, OD WALTER O. WHITLEY, OD, MBA

90 Diagnostic Quiz A 50-50 Split ANDREW S. GURWOOD, OD

90

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CONTRIBUTING EDITORSPAUL C. AJAMIAN, OD, ATLANTA

AARON BRONNER, OD, KENNEWICK, WASH.MILE BRUJIC, OD, BOWLING GREEN, OHIO

DEREK N. CUNNINGHAM, OD, AUSTIN, TEXAS

MARK T. DUNBAR, OD, MIAMI

ARTHUR B. EPSTEIN, OD, PHOENIX

JAMES L. FANELLI, OD, WILMINGTON, NCFRANK FONTANA, OD, ST. LOUIS

GARY S. GERBER, OD, HAWTHORNE, NJANDREW S. GURWOOD, OD, PHILADELPHIA

ALAN G. KABAT, OD, MEMPHIS, TENN.DAVID KADING, OD, SEATTLE

PAUL M. KARPECKI, OD, LEXINGTON, KY.JEROME A. LEGERTON, OD, MBA, SAN DIEGO

JASON R. MILLER, OD, MBA, POWELL, OHIO

CHERYL G. MURPHY, OD, HOLBROOK, NYCARLO J. PELINO, OD, JENKINTOWN, PA.

JOSEPH PIZZIMENTI, OD, FORT LAUDERDALE, FLA.JOHN RUMPAKIS, OD, MBA, PORTLAND, ORE.

DIANA L. SHECHTMAN, OD, FORT LAUDERDALE, FLA.JEROME SHERMAN, OD, NEW YORK

JOSEPH P. SHOVLIN, OD, SCRANTON, PA.JOSEPH W. SOWKA, OD, FORT LAUDERDALE, FLA.MONTGOMERY VICKERS, OD, ST. ALBANS, W.VA.

WALTER O. WHITLEY, OD, MBA, VIRGINIA BEACH, VA.

EDITORIAL REVIEW BOARDJEFFREY R. ANSHEL, OD, CARLSBAD, CALIF.

JILL AUTRY, OD, RPH, HOUSTON

SHERRY J. BASS, OD, NEW YORK EDWARD S. BENNETT, OD, ST. LOUIS

MARC R. BLOOMENSTEIN, OD, SCOTTSDALE, ARIZ.

CHRIS J. CAKANAC, OD, MURRYSVILLE, PA.JERRY CAVALLERANO, OD, PHD, BOSTON

WALTER L. CHOATE, OD, MADISON, TENN. BRIAN CHOU, OD, SAN DIEGO

A. PAUL CHOUS, MA, OD, TACOMA, WASH.ROBERT M. COLE, III, OD, BRIDGETON, NJGLENN S. CORBIN, OD, WYOMISSING, PA.

ANTHONY S. DIECIDUE, OD, STROUDSBURG, PA.S. BARRY EIDEN, OD, DEERFIELD, ILL.

STEVEN FERRUCCI, OD, SEPULVEDA, CALIF.MURRAY FINGERET, OD, HEWLETT, NYIAN BEN GADDIE, OD, LOUISVILLE, KY.

MILTON HOM, OD, AZUSA, CALIF.BLAIR B. LONSBERRY, MS, OD, MED, PORTLAND, ORE.

THOMAS L. LEWIS, OD, PHD, PHILADELPHIA

DOMINICK MAINO, OD, MED, CHICAGO

KELLY A. MALLOY, OD, PHILADELPHIA

RICHARD B. MANGAN, OD, LEXINGTON, KY.RON MELTON, OD, CHARLOTTE, NC

PAMELA J. MILLER, OD, JD, HIGHLAND, CALIF.BRUCE MUCHNICK, OD, COATESVILLE, PA.

MARC MYERS, OD, COATESVILLE, PA.WILLIAM B. POTTER, OD, FREEHOLD, NJCHRISTOPHER J. QUINN, OD, ISELIN, NJ

JACK SCHAEFFER, OD, BIRMINGHAM, ALA.MICHAEL C. RADOIU, OD, STAUNTON, VA.

KIMBERLY K. REED, OD, FORT LAUDERDALE, FLA.LEO P. SEMES, OD, BIRMINGHAM, ALA.

LEONID SKORIN, JR., OD, DO, ROCHESTER, MINN.BRAD M. SUTTON, OD, INDIANAPOLIS

LORETTA B. SZCZOTKA, OD, PHD, CLEVELAND

TAMMY P. THAN, MS, OD, BIRMINGHAM, ALA.RANDALL THOMAS, OD, CONCORD, NC

KATHY C. WILLIAMS, OD, SEATTLE

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Patients look to optometrists for expertise, knowledge, and direction, not a goody bag. Lens care makes a difference in the comfort and safety of a patient’s wearing experience, and most of us have a preferred product. It is up to the eye care professional to invest the time to properly educate and direct patients’ choices. Lens care is too essential to be diminished to a “trick or treat” equivalent.

ESTABLISHING A PRODUCTIVE RELATIONSHIP WITH PATIENTS Whereas about 95% of optometrists in a recent survey said they handed out a sample lens care kit for every contact lens patient, only 31% of patients said they received an actual recommenda-tion for a specifi c product.1 This is an excellent reminder that distributing free sample kits does not always translate into a recommendation. In reality, free samples have not impacted pa-tient compliance or pa-tients’ decisions about what to purchase.

Instead, patients want direction. In a recent survey, patients had to choose between receiving a free sample of solution or a recom-mendation for a specifi c product. The majority of patients surveyed chose the doctor’s recommendation, saying they would forgo a free sample in exchange for doctor-driven direction.2

Optometrists should compare the ocular products on the market and de-termine which ones they would prefer patients to use—both prescription and OTC products. It is critical to effec-tively communicate a specifi c product recommendation and proper lens

care protocol to the patient. Using a small tear-off pad that de-tails your suggestions for the lens’ care, wear time, and disposal schedule could be use-ful for disseminating this information.

Sample solution kits are good for fi rst-time wearers, who are receptive to taking direction in both what

to use and how to properly care for their lenses. These individuals have nothing at home to use, and we want to start them off on the right track with the right habits.

Patients who have been in contact lenses for years are typically older and likely experiencing decreased tear production and dryer eyes, meaning they have higher demands to keep their lenses wet and comfortable. Unfortu-nately, the established wearers are the least loyal to branded solutions,3 and their propensity to move toward store-branded solutions may not provide the desired comfort they need.

Discomfort is the number-one reason patients discontinue lens wear, and contact lens care infl uences comfort.4 In a recent global survey of over 10,000 patients, 58% of contact lens wearers reported end-of-day dryness after using their current lens care protocol, but only 19% continued to have issues after switching to OPTI-FREE® PureMoist® MPDS for two weeks.5 These data highlight the importance of spending time to educate patients on using the recommended solution in the correct manner.

CONCLUSION The doctor’s recommendation is the key to infl uencing patient behavior. If it is true that there is a difference in lens care products—and it is true—then our advice on what product to use should not change according to our supply of sample kits. It is our responsibility to research and decide which products are best for our patients, and it is our duty to relay that information to our patients in a manner that translates the importance of compliance.

Crystal Brimer, OD, has a private practice in Wilmington, North Caro-lina, and serves as a primary clinical investigator, with special interests in contact lenses, dry eye disease, and practice management. She is a paid consultant to Alcon.

Dr. Brimer may be reached at [email protected].

Free is Not Always EffectiveHow do we ensure patients use the ocular products we think are best? For prescription products, the answer is simple; but in the over-the-counter (OTC) realm, it is much more complex. For decades, we have handed out free samples and coupons, but do they affect patients’ decision making, or does defi nitive direction from the doctor have a greater impact on patient purchases?

ADVERTORIAL

© 2014 Novartis 6/14 OPM14033AD

By Crystal M. Brimer, OD

WHAT’S THE SOLUTION?

KEY POINTS• Patients look to their eye care provider

for expertise, knowledge, and specifi c direction.

• Patients in a recent survey indicated they would forgo a free sample in exchange for a specifi c recommendation from their eye care provider.2

• Giving patients clear advice about what products to use—and how to use them—may be the key to ensuring better compliance with lens protocols.

1. Alcon data on file, 2012. 2. In a survey of 353 contact lens wearers; Alcon data on file, 2012. 3. Alcon data on file, 2010. 4. Rumpakis JMB. New data on contact lens dropouts: an international perspective. Rev Optom. 2010:1-4. 5. Lemp J, Kern JR. Results from a global survey of contact lens-wearer satisfaction with OPTI-FREE® PureMoist® Multi-Purpose Disinfecting Solution. Clinical Optometry. 2013;5:39-46.

It is critical to effectively communicate a specifi c product recommendation and proper lens care protocol to the patient.

Outlook


Even if the annual glaucoma incidence numbers were declining, the prospects for

making headway against this insidi-ous disease could be described as abysmal. “Current estimates are that 60% to 70% of glaucoma in the US population is undiagnosed,” notes Mark Swanson, OD, MSPH, in his article on epidemiology on page 44 of this issue, our 20th Annual Glaucoma Report. “When taking into account the low levels of adherence to glaucoma medica-tion regimens,” he goes on, “as much as 80% of glaucoma in the US population may be untreated.”

But we all know the numbers aren’t declining—they’re increas-ing, both in the aggregate and in the lifetime exposure per patient. Because the population is aging, and average lifespan has length-ened, we have more elderly people than ever, and they live longer nowadays. If it’s true that only one in five glaucoma patients is ade-quately maintained on therapy, the challenge to eye doctors seeking to reverse those trends is formidable.

For minority patients, the future looks especially grim. Various racial and ethnic subgroups have higher rates of glaucoma, higher rates of poverty and higher rates of popula-tion growth than the country as a whole. Put all those together and they point to a crisis in the making: more patients in need of care, with a disproportionate lack of access to routine medical services, and cultural and financial obstacles to contend with too.

For patients, it’s the perfect storm; for ODs, the perfect oppor-tunity to rise to the challenge.

With its chronic, slowly progres-sive nature, glaucoma is best suited for doctors who can invest the time to document its course over a long time span. The battery of standard tests—visual fields, OCTs, optic nerve exams—can make patient visits time consuming for the prac-tice. The clinical decision-making responsibilities—though potentially life-changing for the individual—are typically non-urgent, allowing time for careful analysis and con-sideration, including consultation with specialists when needed. And the doctor/patient rapport must be strong enough to break through the barriers to medication adherence.

Every one of those aligns exactly with the strengths of optometric practice (and, not coincidentally, with deficits in ophthalmology), as ODs cultivate relationships with patients through years or often decades of routine care. With MD practices fewer in number com-pared to optometry’s footprint, and their practitioners so overwhelmed with surgical case loads, glaucoma is an inherently poor fit for most busy ophthalmology practices.

Put another way, glaucoma care won’t improve until ODs take charge of it. Now’s your chance to shine.

ODs: We’re Up to the TaskFortunately, optometrists seem

both willing and able to take on the extra work. In the recently released AOA manpower study of eye care

supply and demand in the US, optometrists said that they could fit in an additional 19.8 patient visits per week even if they already had a full schedule, without adding more hours to their clinic time.

The manpower study cites a previous AOA research effort, the 2012 National Eye Care Workforce Survey of Optometrists, in which “responding optometrists indicated that, if they were able to operate at their full capacity without increas-ing their current patient care hours, they could provide about 32% more patient visits per year than they were actually providing.”

“If we take this excess capacity into account and compare supply including excess capacity to the baseline demand, there is no longer excess demand,” the manpower report states. “In fact, our estimates indicate that there is significant excess supply when this excess capacity is included.”

There’s no shortage of patients in need of care to take up that excess capacity, of course. The AOA report cites the often-mentioned increase in pediatric patient visits in the wake of the ACA, and also the need for more diabetic eye health screenings. Without diminishing those pressing needs, glaucoma might be the ideal place to start.

Fitting in lots of extra patient visits won’t be easy. Relating to the increasingly diverse population will pose challenges too. But glaucoma is a public health crisis in the mak-ing—and optometrists are ideally positioned to conquer it. ■

ODs are in prime position to address the growing needs of under-served glaucoma patients, elevating the profession with distinction. By Jack Persico, Editor-in-Chief

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OF THE INDEPENDENT

Cha i r Side

iPhone Refraction? iLove It!An app that refracts is like having an OD in your pocket—which begs the question: Is that an OD in your pocket or are you just happy to see me? By Montgomery Vickers, OD

Ihear there’s now a smartphone app that can perfectly refract a patient in the comfort of his or

her own car in between texts. This is awesome, as I have been refract-ing old-school for 34+ years and have never reached perfection.

One advantage is that the phone won’t have to put up with patients saying they like “number one” when they really like “number two.”

In those inevitable cases when a patient has trouble adapting to their glasses Rx, and they inevitably ask, “Why did this happen?” I inevita-bly smile my most benevolent smile and inevitably say, “Because you said you liked number one when you really liked number two!”

They think I’m joking. But, now, through the wonderful

power of our phones, this conversa-tion will never take place! And who will they complain to when they can’t see through their “phony” glasses? Us. I cannot wait to see the look on their faces when I explain that I charge $413.34 to recheck a phone-induced Rx. Should be a hoot. Perhaps I’ll film it on MY phone for YouTube.

Amazing, life-changing technolo-gies are all around us these days. Just look at Google. Do you realize that Ryan Seacrest is the same exact height as I am? That’s right! 6’4”! (If you dig deep enough, there must be at least one website that will say he’s not 5’8”.) The bad news is my right leg outweighs him. These smartphones are awesome!

The power in this little device is just amazing. For example:

• I recently used my phone to photograph a lady’s anterior seg-ment. (I’ll just leave the joke on the table there.)

• I recently used my phone to trace a rectangle for my grandkids.

• I recently used my phone to keep my napkin from blowing away at a picnic.

And to think this $500 paper-weight can replace my need to refract? I have died and gone to heaven! Now the world won’t come to an end because opticians won’t have any reason to politick to refract. Heck, any idiot with an app can refract now, right? And, lazy ophthalmologists will finally stop using Donders’ Table to decide what seg power a patient needs! The phone will decide! Sweet! Power to the people!

But now that we’ve learned how the government uses our phones to track and control us, what really happens when you stick your eye up there to get your new glasses prescription? Could they really be shooting rays into our brains that make us dumb enough to keep voting for them? How else could you explain

it? Must be the phones.As technology moves forward, I

can envision a time when we won’t really need to see at all. We’ll just dangle two smartphones in front of our eyes from a designer frame. Your car will drive itself so you’ll be free to watch “Game of Thrones” on one side and “Jeopardy!” on the other.

Daily Double? “What are naked dragons?”

How long will it take until you can get the newest DangleGlasses for nothing at the mall? Every street corner will be full of begging bums, formerly known as eye doctors, who scramble for a buck now that their services are no longer needed, thank you very much.

That may sound crazy but once the smartphones put all the eye problems behind us, what else is behind us?

“iColonoscopy”? I can’t wait! ■

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Coding Abstract

One of the biggest reasons for failing an insurance audit is not being specific

enough when performing services for a patient. A perfect example of this is what many doctors call a “glaucoma check.” I see it in patient records quite frequently when I’m doing an internal audit for a practice. The chief complaint (CC) might say, “Patient returning for glaucoma check,” or sometimes nothing more than “IOP check.”

Simple phrases mean different things to different people. Just what is a “glaucoma check”? To some, it may be only measuring IOP. To others, it’s a dilated evaluation of

the optic nerve, a visual field and an OCT of the optic disc. Some may like to include gonioscopy, while others prefer anterior segment OCT.

Because there’s so much variation in services provided, avoid all-pur-pose phrases in the medical record. Rather, describe exactly why the patient is returning to the office.

Patient care—and our medical record—need to be specific to the individual patient. We don’t per-form services based on an ICD-9 or ICD-10 code, nor do we bundle

care just because we don’t want to miss something. We should evaluate each patient as an individual, and our assessment of their individual risk is based upon their history and physical findings. Some patients may require more or less testing than others.

For that matter, the same patient may require different levels of examination and testing on differ-ent visits; our records need to prop-erly reflect that.

State Your ReasonsKeep in mind that medical care

today is based on medical neces-sity—meaning that the level of the

office visit performed and the addi-tional testing ordered must be nec-essary for that individual patient.

Also, remember that the CC requirement can be fulfilled prop-erly if you direct the patient to return to the office for a specific reason at an appropriate interval. So, perhaps the plan section of our medical record should include a statement such as: “Patient to return to clinic for evaluation of IOP and optic nerve Q3 months or PRN should additional symptoms arise,” rather than: “RTC three

months for glaucoma check.” The former statement tells the record what I want the patient to do and why I want him to do it, while the latter provides no explicit reasoning or medical strategy.

Then, when the patient returns, the CC should read: “Patient returning to clinic per doctor-directed order for evaluation of IOP and optic nerve.” And, if you have orders pending for special ophthalmic testing, those could also be listed in both the plan and the reason for the visit.

Last but not least, be aware of current Correct Coding Initiative edits, which stipulate whether you can perform specific ophthalmic tests on the same day. For example, you cannot do both an anterior seg-ment OCT (92132) and a posterior OCT (either 92133 or 92134) on the same date of service.

Creating a medical record that is both specific and individualized for the patient is critical. Your medical record is your greatest weakness and your most powerful weapon—it’s the only thing that a carrier can use against you in an audit, and it is the only thing you can use in your defense. Most importantly, it’s one of the few things that you, as a phy-sician, have total control over.

So, try to make your medical record perfect; not only will it help you pinpoint your patient care, but help protect you, too. ■

Please send your questions and comments to [email protected].

Avoid vague, stock phrases in your medical record. Get down to specifics. By John Rumpakis, OD, MBA, Clinical Coding Editor

No More ‘Glaucoma Checks’

Just what is a “glaucoma check”? To some, it may be only

measuring IOP. To others, it’s a dilated evaluation of the optic

nerve, a visual field, and an OCT of the optic disc.

Better to avoid such all-purpose phrases in the medical record.

THIS IS WHY OPTI-FREE® PureMoist® Solution allows patients to wear contact lenses MORE COMFORTABLY1 AND LONGER each day.2

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References: 1. Campbell R, Kame G, Leach N, et al. Clinical benefits of a new multipurpose disinfecting solution in silicone hydrogel and soft contact lens users. Eye & Contact Lens. 2012;38(2):93-101. 2. Alcon data on file, 2011. 3. Lally J, Ketelson H, Borazjani R, et al. A new lens care solution provide moisture and comfort with today’s contact lenses. Optician. 2011;241:42-46. 4. Davis J, Ketelson HA, Shows A, Meadows DL, A lens care solution designed for wetting silicone hydrogel materials. ARVO Meeting Abstracts. 2012;38(2):93-101. 5. Lemp J, Kern JR. Results from global survey of contact lens-wearer satisfaction with OPTI-FREE® PureMoist® MPDS. Clinical Optometry. 2013:5 39-46. © 2014 Novartis 4/14 OPM14001JAD

The HydraGlyde® Moisture Matrix attaches and forms a hydrophilic environment across the surface of the lens—providing moisture from

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Sequenom and RetnaGene are trademarks of Sequenom, Inc. and are used with permission by Sequenom Center for Molecular Medicine, LLC, dba Sequenom Laboratories.

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Clinical Care

Scleritis: When a Red Eye Raises a Red Flag

Scleritis manifests as a very painful red eye—but it sometimes suggests that some-

thing deeper than the eye is involved. It’s often, but not always, associated with an underlying autoimmune dis-order. So, it’s vitally impor-tant to get to the bottom of this uncommon but aggravat-ing condition.

Scleritis can be classified as either anterior or posterior, where anterior scleritis can be further cat-egorized into four different types:

• Diffuse scleritis is widespread inflammation of the sclera, and the most common type.1

• Nodular scleritis is character-ized by a localized area of inflam-mation where a distinct nodule can be seen.

• Necrotizing scleritis with inflammation is frequently associ-ated with collagen vascular dis-orders causing destruction of the sclera.

• Necrotizing scleritis without

inflammation, also known as scle-romalacia perforans, is a very rare form of scleritis presenting with no symptoms. It can be seen in patients with rheumatoid arthritis, granulomatosis with polyangiitis (formerly known as Wegener’s granulomatosis) and relapsing polychondritis.2

Posterior scleritis can also be nodular or diffuse and necrotizing, and involves the sclera posterior to the insertion of the rectus muscles.2

In this article, we present a few challenging cases of scleritis to highlight various treatment

approaches and learning points.

Case 1. Red Eye, Cough and Weight Loss

• History. A 66-year-old Indian male presented with bilateral red and mildly painful eyes. He said his eyes had been getting red on and off, but this episode was much worse.

• Diagnostic data. Slit-lamp exam showed bilateral sectoral nodular scleritis. Although it was mostly superficial, there was some deeper episcleral inflammation noted. His vision was correctable to 20/25- OD and OS, and his intraocular pressures were 18mm Hg OD and 19mm Hg OS.

Upon questioning, he reported chronic respiratory issues with a persistent cough for the past four to six months. He had been diagnosed with recurring bronchi-tis and was treated with several courses of antibiotics as well as oral steroids. He had also lost an unexplained 20 lbs. during the past four months and was reporting

This painful inflammation is often an indicator of more serious health concerns. By Michael Trottini, OD, and Candice Tolud, OD

Case 1. Sectoral nodular scleritis.


generalized muscular pain. He was already taking a course

of prednisone for his respiratory issues, so started him on Durezol (difluprednate 0.05%, Alcon) QID. Given his bilateral scleral inflammation along with his sys-temic issues, we ordered additional lab testing, which included: RF, ANA, HLAB27, Lyme, PPD, FTA-ABS, ACE, C-ANCA, P-ANCA, ESR, CRP. (See “Common Labo-ratory Tests for Patients with Scle-ritis,” right.)

When he returned one week later, his eyes were white and quiet. We reviewed his lab results, which showed significantly ele-vated ANCA and CRP levels. We contacted his pulmonologist due to a high concern for granuloma-tosis with polyangiitis (GPA, aka Wegener’s granulomatosis); imag-ing studies and a lung tissue biopsy later confirmed the diagnosis. Our patient was sent to a GPA special-ist for further evaluation and treat-ment.

• Discussion. Half of all scleritis cases have an underlying systemic cause.2 So, a thorough history and review of systems are very impor-tant to help identify any underly-ing etiologies and guide laboratory studies or further medical evalua-tion.

GPA is often overlooked due to its rare incidence—just three cases per 100,000 people.3 Approxi-mately 10% of patients with GPA develop scleritis, so ANCA testing should be included in the workup of these patients.4

In addition to GPA, rheumatoid arthritis, relapsing polychondri-tis, polyarteritis nodosa, systemic lupus erythematosus, sarcoidosis, anklyosing spondylitis herpes zos-ter, syphilis and tuberculosis are associated with scleritis and should

be tested as causative factors.2

Our patient returned for follow-up six months later. He was taper-ing prednisone and had started methotrexate for the GPA. The overall improvement in his health was remarkable. He had gained back 20 lbs., and was feeling significantly better with no more breathing or coughing issues. His scleral inflammation has been quiet since.

Case 2. Angle Closure or Inflamed Sclera?

• History. A 47-year-old white female presented for a second opinion with a very painful, red left eye with decreased vision. She had been diagnosed with primary angle-closure glaucoma and had undergone a YAG peripheral iri-dotomy a few days prior to this visit. However, after the proce-dure, she was still in a moderate amount of pain, which was wors-ening.

She was taking Pred Forte (prednisolone 1%, Allergan) QID, Azopt (brinzolamide 1%, Alcon)

BID and Combigan (brimonidine 0.2%/timolol 0.5%, Allergan) BID.

• Diagnostic data. Her visual acuity was 20/20 with plano cor-rection in the right eye and 20/100 in the left eye, which improved to 20/30 with a -2.00D correc-tion. Her corneas were clear. Left anterior segment showed moderate conjunctival/scleral erythema, a 2+ anterior chamber cell and a very shallow anterior chamber with a

Case 2. Scleral inflammation in a patient who had recent angle-closure glaucoma.

Common Laboratory Tests for Patients with ScleritisLaboratory Test Systemic ConditionACE (angiotensin-converting enzyme)Chest X-ray Sarcoidosis

ANA (antinuclear antibody) Lupus

c-ANCA (cytoplasmic antineutrophil cytoplasmic antibody) Wegener’s granulomatosis

p-ANCA (perinuclear antineutrophil cytoplasmic antibody) Vasculitis, polyarteritis nodosa

FTA-ABS (fluorescent treponemal antibody absorption)RPR/VDRL (rapid plasma reagin/venereal disease reference laboratory)

Syphillis

ELISA (enzyme-linked immunosorbent assay)Western blot Lyme disease

RF (Rheumatoid factor) Rheumatoid arthritis

CRP (C-reactive protein)ESR (erythrocyte sedimentation rate)

Nonspecific systemic inflammation


patent peripheral iridotomy. Goni-oscopy in the left eye showed no visible angle structures. Her right anterior segment was normal with a deep anterior chamber and goni-oscopy open to her ciliary body. Her intraocular pressure measured 18mm Hg OD and 42mm Hg OS. Her retinal exam showed an annu-lar choroidal detachment.

• Discussion. Given the open angle in her right eye, absence of risk factors for angle closure (such as hyperopia or a denser cataract), poor response to YAG PI, myopic shift and choroidal detachment, we determined that her primary issue was posterior scleral inflammation causing a ciliochoroidal effusion syndrome and not pupillary block angle closure.

Posterior scleritis with ciliary body inflammation can initiate cili-ary body rotation, which causes an anterior displacement of the lens iris diaphragm resulting in second-ary angle closure.5 Additionally, ciliary body edema relaxes the lens zonules, which causes thickening of the crystalline lens and a myopic shift, as in this patient.6

Ciliochoroidal effusion syn-drome, although rare, can often be

mistaken for pupillary block angle closure. It is incredibly important to be able to distinguish the two conditions because the treatments are vastly different. Pupillary block glaucoma is typically seen in older individuals who have denser cata-racts.7 Hyperopes are at a greater risk due their shorter axial length and shallower anterior chamber depth.7 Pilocarpine, steroid drops and IOP-lowering agents, along with a peripheral iridotomy, help resolve pupillary block glaucoma. In contrast, ciliochoroidal effu-sion syndrome can be reversed by cycloplegia along with anti-inflam-matories and IOP-lowering agents. The anti-inflammatories reduce ciliary body edema and cycloplegia induces posterior rotation of the ciliary body, deepening the ante-rior chamber.6,8

We cyclopleged the patient in office, discontinued Pred Forte and started her on Durezol QID, hom-atropine 5% BID, oral prednisone 60mg, and continued Combigan and Azopt.

At one-day follow-up, there was a significant improvement of inflammation, and examination revealed a deepening of the ante-

rior chamber. The patient’s vision improved to 20/30+ OS and the IOP reduced to 16mm Hg. We continued to manage her on anti-inflammatories and slowly tapered them as well as her IOP meds.

Laboratory testing showed an elevated antinuclear antibody, which prompted us to send the patient for rheumatologic evalu-ation. The rheumatologist diag-nosed her with lupus.

At her last follow-up, her inflammation had resolved, IOP was stable, anterior chamber was deep and the choroidal detachment had resolved.

Case 3. Cancer Med is a Confounder

• History. A 42-year-old white male presented with an acute, painful, red right eye that had started the day before. He had a systemic history of melanoma with brain metastasis for which the primary lesion had not been identi-fied. Previous ocular examinations were negative for choroidal or iris malignancies. The patient recently underwent removal of a metastatic

Case 3. A similar patient who presented with nodular, non-necrotizing scleritis. Treatment involved Durezol QID and a Medrol Dosepak PO. At one-week fol-low up, the scleral inflammation had resolved.

Clinical Care

Case 2. A very shallow anterior chamber due to posterior scleritis. Inflammation has caused the ciliary body to rotate, creating anterior displacement of the lens iris diaphragm.

After cycloplegia, the ciliary body has re-rotated back to its original position, and the anterior chamber and the angle have deepened. Also, anti-inflammato-ries have reduced ciliary body edema.


brain lesion and was started on Zelboraf (vemurafenib, Genentech) a protein kinase inhibitor used to treat late-stage melanoma.9

• Diagnostic data. Entering visual acuity was 20/25 OD and 20/20 OS. IOPs were within nor-mal limits at 15mm Hg OD and 16mm Hg OS. There was a moder-ate nodular, non-necrotizing scleri-tis in the right eye. After instilling phenylephrine drops, moderate scleral inflammation was still noted temporally and inferiorly. There was a trace anterior cham-ber cell in that eye as well. The left eye was unremarkable.

We started the patient on Durezol QID and a Medrol Dosepak (methylprednisolone 4mg, Pfizer) PO. At one-week fol-low up, the scleral inflammation had resolved. We instructed the patient to taper the Durezol over the next two weeks.

• Discussion. Be aware of pos-sible ocular effects from systemic medications. A thorough review of current medications is just as important as a review of symp-toms. Although a rare side effect, ocular inflammation associated with Zelboraf has been docu-mented and should be considered because it is being used more com-monly for treatment of late-stage melanoma.9,10 In one report, Zel-boraf was associated with a case of severe sclerouveitis.9 The drug has also been reported to cause uveitis in up to 4.5% of patients.10

In addition to Zelboraf, bisphos-phonates—commonly used for treatment of osteoporosis—can also be associated with scleritis.11

In this patient’s case, coman-agement with oncology was critical. We kept in close contact with the oncologist and, because of the patient’s good response to treatment with no additional

recurrences, he continues to take Zelboraf and is monitored closely.

We did order a rheumatologic evaluation as well, just to rule out the possibility of underlying sys-temic etiologies, which was nega-tive.

Case 4. Hit This Patient Hard and Fast (with Steroids)

• History. A 42-year-old His-panic male was referred to our office for a painful, red right eye for the past three weeks that was unresponsive to treatment and was developing elevated intraocular pressure. The patient had been treated with Lotemax (loteprednol 0.5%, Bausch + Lomb) QID dur-ing this time but had no improve-ment.

• Diagnostic data. Entering visual acuity was 20/30 OD and 20/20 OS. Intraocular pressure

was 25mm Hg OD and 15mm Hg OS. Slit-lamp examination showed a moderate nodular anterior scle-ritis in the right eye. Retinal exam was unremarkable in both eyes.

We switched the treatment to Durezol QID and a Medrol Dosepak. We also prescribed Com-bigan and Azopt to treat the ste-roid-induced ocular hypertension.

One week later, the patient returned for follow-up with a significant reduction in scleral inflammation and improvement of symptoms. Intraocular pressure was reduced to 20mm Hg in the affected eye. The patient finished taking the methylprednisolone and was switched from Durezol to Pred Forte for taper over the next 10 days.

At the following visit one week later, his scleral inflammation had completely resolved and his

Scleritis vs. EpiscleritisScleritis can be differentiated from episcleritis both by history and clinical examination.

• Episcleritis typically presents with little to no pain and is most often idiopathic. It is generally a self-limiting inflammatory process affecting only the conjunctival and superficial episcleral vascular plexuses.2

• Scleritis patients, by contrast, present with moderate to severe pain and the inflam-mation extends into the deep episcleral plexus. Phenylephrine can be instilled in the eye to determine the depth of the inflammation. The conjunctival and superficial vessels will blanch or constrict from phenylephrine administration, but the deeper episcleral vessels will not.

Treatment of both episcleritis and scleritis is aimed toward controlling inflammation. Episcleritis can be treated with topical steroids or oral NSAIDs along with lubricants, while scleritis is managed with both topical and oral anti-inflammatories.

To help differentiate episcleritis from scleritis, use phenylephrine to blanch the superficial vessels—the deeper, episcleral vessels won’t blanch.


intraocular pressure was stable at 18mm Hg in the affected eye. We discontinued all drops at that time.

• Discussion. Although lotepre-dnol can be used to treat milder cases of episcleritis (especially if there is a concern with a patient’s intraocular pressure), more potent steroid drops should be used for treating scleritis. (See “Scleritis vs. Episcleritis,” page 29.)

Clearly, one of the advantages of loteprednol over prednisolone, dexamethasone and difluprednate is the lower incidence of steroid-induced ocular hypertension. As prednisolone and difluprednate are ketone-based steroids, the molecules will linger in the eye lon-ger.12 Loteprednol is an ester-based steroid, so any unbound molecules become metabolized by the natu-ral esterases within the eye.12 As a result, loteprednol has a lower incidence of steroid-induced glau-coma; however, the risk still exists,

as seen in our patient. When treating scleritis, we typi-

cally take the “hit ’em hard, hit ’em fast” approach. This gener-ally minimizes the duration of steroid therapy. We find it better to start off with a more potent corticosteroid drop and switch to a milder one, if needed, after a good amount of the inflammation has resolved.

Steroid drops administered for four to six weeks can cause an IOP rise of 6mm to 15mm Hg in 30% of patients and more than 16mm Hg in 5% of patients.13,14 Our goal of treating aggressively from the start is to have most patients off steroid therapy before this time frame. Even with moderate scleritis in a patient who is a known ste-roid responder, we will still treat aggressively and pre-treat with IOP drops in anticipation of the steroid response.

The diagnosis, treatment and

management of scleritis can vary based on presenting signs, symp-toms and associated factors. Anti-inflammatory agents are key in treatment of this condition, and should be used quickly and appropriately to maximize patient response. Also, be sure to consider all aspects of the patient’s medi-cal history and review of systems in order to initiate appropriate therapy. Good communication between optometrists, internists and other medical specialists help to facilitate prompt diagnosis and adequate care of any underlying disease. ■

Dr. Trottini is in practice at Outlook Eyecare, in Monroe Township, NJ.

Dr. Tolud is in practice at South Jersey Eye Physicians, in Colum-bus, NJ.

1. Sims J. Scleritis: presentations, disease associations and management. Postgrad Med J. 2012 Dec;88(1046):713-8.2. Okhravi N, Odufuwa B, McCluskey P, Lightman S. Scleri-tis. Surv Ophthalmol. 2005 Jul-Aug;50(4):351-63. 3. Tarabishy AB, Schulte M, Papaliodis GN, Hoffman GS. Wegener’s granulomatosis: clinical manifestations, dif-ferential diagnosis, and management of ocular and systemic disease. Surv Ophthalmol. 2010 Sep-Oct;55(5):429-44.4. Hoffman GS, Kerr GS, Leavitt RY, et al. Wegener’s granu-lomatosis: an analysis of 158 patients. Ann Intern Med. 1992 Mar 15;116(6):488-98. 5. Ugurbas SH, Alpay A, Ugurbas SC. Posterior scleritis presenting with angle closure glaucoma. Ocul Immunol Inflamm. 2012 Jun;20(3):218-20.6. Litwak AB. Posterior scleritis with secondary ciliochoroidal effusion. J Am Optom Assoc. 1989 Apr;60(4):300-6.7. Lee JW, Lai JS, Lam RF, et al. Retrospective analysis of the risk factors for developing phacomorphic glaucoma. Indian J Ophthalmol. 2011 Nov-Dec;59(6):471-4.8. Ikeda N, Ikeda T, Nomura C, Mimura O. Ciliochoroidal effusion syndrome associated with posterior scleritis. Jpn J Ophthalmol. 2007 Jan-Feb;51(1):49-52.9. Wolf SE, Meenken C, Moll AC, et al. Severe pan-uveitis in a patient treated with vemurafenib for metastatic melanoma. BMC Cancer. 2013 Dec 1;13:561.10. Sandhu S, Ling C, Lim L, et al. Vemurafenib (B-RAF inhibitor) associated uveitis in patients with metastatic cuta-neous melanoma. Clin Exp Ophth. 2012;40(S1):118.11. Leung S, Ashar BH, Miller RG. Bisphosphonate-associ-ated scleritis: a case report and review. South Med J. 2005 Jul;98(7):733-5.12. Comstock TL, Decory HH. Advances in corticosteroid therapy for ocular inflammation: loteprednol etabonate. Int J Inflam. 2012;2012:789623.13. Armaly MF. Statistical attributes of the steroid hyperten-sive response in the clinically normal eye. I. The demonstra-tion of three levels of response. Invest Ophthalmol Vis Sci. 1965 Apr;4:187-97.14. Becker B. Intraocular pressure response to topical corti-costeroids. Invest Ophthalmol Vis Sci. 1965 Apr;4:198-205.

This patient presented with a moderate nodular anterior scleritis, which was unresponsive to Lotemax, as well as elevated intraocular pressure.

Clinical Care

After one week of treatment with Durezol QID and a Medrol Dosepak, as well as aqueous suppressants for the IOP, the inflammation had significantly improved.

Scleritis Responds to Oral Anti-inflammatoriesIn addition to topical steroid drops, oral NSAIDs or oral steroids are indicated for treating scleritis. Ibuprofen and indomethacin are often used initially for treating anterior diffuse and nodular scleritis. For mild scleritis cases, consider also prescribing a 4mg Medrol Dosepak (methylprednisolone, Pfizer). The self-tapering schedule helps with ease of use and patient compliance. For more moderate to severe cases, start with 60mg to 80mg of prednisone, and taper accordingly.

Smoothing the Surface: a Biomimetic Approach to Contact Lens Comfort

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resembles the structure of the cornea itself.The water gradient structure of DAILIES TOTAL1®

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exceptionally high surface lubricity.7,8

A NEW OPPORTUNITYWearers of DAILIES TOTAL1® contact lenses report all-day

comfort and clear vision.9 Having this lens available offers us a new way to address contact lens discomfort—which is often challenging to discuss with patients. Many wearers brush off contact lens discomfort because they assume there is no alternative. Others hesitate for fear that admitting discomfort will exclude them from lens wear.

Acknowledging that patients might experience contact lens discomfort—and letting them know that we may be able to address it—works well. When I introduce DAILIES TOTAL1® water gradient contact lenses, I explain that the lens surface is moist, lubricious, and very smooth—so smooth that they may not feel the lens at all.10 Patients appreciate learning about new technology and, even if they do not opt for DAILIES TOTAL1® contact lenses right away, are reassured to know that a new level of contact lens comfort is available.

Paul Karpecki, OD, FAAO, works in Corneal Services and is Clinical Research Director at the Koffler Vision Group in Lexington, KY.

REFERENCES 1. Craig JP, Willcox MDP, Argüeso P, et al. The TFOS international workshop on

contact lens discomfort: report of the contact lens interactions with the tear film subcommittee. Invest Ophthalmol Vis Sci. 2013;54:TFOS123-6.

2. Cruz AAV, Garcia DM, Pinto CT, Cechetti SP. Spontaneous eyeblink activity. Ocul Surf. 2011;9(1):29-41.

3. Coles C. Coefficient of friction and contact lens comfort. OptomVis Sci. 2012;89. E-abstract 125603.

4. Korb DR, Greiner JV, Herman JP, et al. Lid-wiper epitheliopathy and dry-eye symptoms in contact lens wearers. CLAO J. 2002;28(4):211-6.

5. Thekveli S, Qui Y, Kapoor Y, et al. Structure-property relationship of delefilcon A lenses. Contact Lens Anterior Eye. 2012;35(Supp 1):e14.

6. Alcon data on file, 2011. 7. Angelini T, Nixon R, Dunn At, et al. Viscoelasticity and mesh-size at the surface

of hydrogels characterized with microrheology. Invest Ophthalmol Vis Sci. 2013;54:E-abstract 500.

8. Sawyer WG, Dunn AC, Uruena JM, et al. Robust contact lens lubricity using surface gels. Invest Ophthalmol Vis Sci. 2012;53: e-abstract 6095.

9. Pérez-gómez I, Giles T. European survey of contact lens wearers and eye care professionals on satisfaction with a new water gradient daily disposable contact lens. Clinical Optometry. 2014;6:17-23.

10. In a clinical study with 80 patients. Alcon data on file, 2011.

*In vitro measurement of unworn lenses.

When placed on the eye, a contact lens alters the structure of the tear film and reduces its stability.1 Depending on lens material, tear evaporation can lead to the formation of dry spots on the lens surface and to increased friction during blink.1 Ideally, soft contact lens materials should minimize impact on tear film stability and friction during blink.

But the surface of most soft contact lenses lacks the cornea’s ability to bind mucus, which aids in the formation of the normal tear film. In lieu of the cornea’s mucin glycocalyx, a moist and lubricious contact lens surface can create an appropriate environment for tear film stability and for the eyelids to pass over smoothly.

LUBRICITY: THE CONCEPTLubricity is defined as the inverse of friction, the resistance

between two surfaces when one moves over the other. When the eyelid slides across a contact lens surface during blink, the lubricity of that surface determines how smooth the movement is. Considering that a normal eye blinks more than 1,000 times per waking hour, the importance of lens surface lubricity is clear.2

Indeed, recent studies have found that a low coefficient of friction (high lubricity) is a principal factor in predicting contact lens comfort.3 Further, lens wearers with dryness symptoms are significantly more likely to exhibit lid wiper epitheliopathy than asymptomatic wearers, suggesting a connection between ocular surface dryness, friction, and epithelial cell damage.4

IMPROVING LUBRICITY: THE CHALLENGEThough high surface lubricity is desirable, balancing it with

other material properties has been challenging, particularly with silicone hydrogels. Silicone hydrogel lenses are highly oxygen permeable, but because silicone is hydrophobic, they require modification for enhanced surface hydrophilicity.

Silicone hydrogel lenses have been modified using plasma surface coatings and wetting agents in the lens matrix and/or the packaging solution. But with the introduction of DAILIES TOTAL1® water gradient contact lenses, the approach to contact lens surface wettability has been fundamentally transformed, ushering in a new era of contact lens technology.

A NOVEL SOLUTIONUnlike other soft contact lenses, DAILIES TOTAL1® contact

lenses are not composed of a single, uniform bulk material. Rather, the core of DAILIES TOTAL1® contact lenses is a highly breathable silicone hydrogel of 33% water content, which transitions to an ultra-hydrophilic surface gel exceeding 80% water content.5,6* This material innovation resolves the challenge of silicone hydrogel surface wettability, and it

PAUL KARPECKI, OD, FAAO Help patients understand the significance of contact lens surface lubricity, and let them experience it firsthand with DAILIES TOTAL1® water gradient contact lenses.

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Plotting the Path of ProgressionW

ith just one health sta-tus variable that yields to medical or surgical intervention, glaucoma

management at its core is very fun-damental—lower the intraocular pressure (IOP) to a level that reins in visual field loss. In this clinical model, detecting glaucoma progres-sion becomes paramount for suc-cessful management outcomes.

Serial optical coherence tomogra-phy (OCT) of the retinal nerve fiber layer (RNFL) and threshold visual field analysis, herein referred to as glaucoma progression tests, com-prise much of our ability to achieve this task. Both are complemented by statistical software packages designed to enhance this ability. Tonometry, though unsophisticated in what it tells us about the patient, remains essential. As such, treating glaucoma in 2014 requires clinicians to effectively navigate a variety of testing modalities and analytical software that must be logically inte-grated into a comprehensive, mean-ingful clinical picture.

This article looks at practical

approaches to reconciling three com-plex and interrelated components of glaucoma care: IOP assessment, serial RNFL OCT analysis and serial threshold visual field analysis.

Organize IOP ReadingsGlaucoma progression tests are

only relevant if we can do some-thing about the findings; namely, adjusting the patient’s IOP range through either medical or surgical means. Therefore, it is important to compare any changes in your glau-coma progression tests with the IOP levels during the period in which the changes occurred.

In a busy practice, it is easy to only look at the last couple of IOP readings to gauge the treatment effi-cacy. However, to successfully treat glaucoma, it is imperative to dem-onstrate a real IOP lowering effect from the treatments that you have prescribed, and this often requires gathering all IOP data for analysis. Quantifying the IOP reduction from your baseline values will provide context for any changes seen on glaucoma progression tests. This is

best achieved by taking the average IOP for each treatment or combina-tion of treatments prescribed.

Calculating average IOP when analyzing therapeutic response is advantageous in that it has been shown to correlate with the extent

Our success in managing glaucoma hinges on our ability to recognize—and make sense of—both structural and functional changes. By Scott Anthony, OD

Figure 1 (at right). This patient with moder-ate POAG OS demonstrates the complexity of contemporary glaucoma management. It can take years to establish enough visual fields to accurately determine if progres-sion has occurred. In that time, treatments are added or adjusted, and technologies change, requiring updating of the base-line exams to determine if the therapy is adequate.

Each treatment is demarcated by a block of time to coordinate IOP findings, RNFL OCT scans and GPA for visual fields. Because this patient required multiple medication changes in a relatively short period of time, it was best to use only the pretreatment block and an all-treatments block.

Despite a variety of treatments with vary-ing reductions in IOP, this patient’s RNFL OCT and GPA revealed no progression over a seven-year period, thereby meeting the overall management goal.



pret

reat

men

t gro

uptr

avop

rost

gro

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avop

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+

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ine

grou

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t + b

rimon

idin

e gr

oup

all

tr

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ents

IOP Average 20.7mm Hg Standard deviation 1.15mm Hg

IOP Average 16.2mm Hg Baseline reduction: -22%



IOP Average 15.2mm Hg Baseline reduction: -27%Standard deviation 2.7mm Hg

RNFL OCT NO PROGRESSION all scans within expected test-retest variability

HVF glaucoma progression analysis NO PROGRESSION FROM BASELINE SCANS

RNFL time-domain OCT BASELINE average RNFL: 68µm

RNFL time-domain OCT FOLLOW-UP 1 average RNFL: Δ+4µm

RNFL spectral-domain OCT BASELINE [JAN. 2010] average RNFL: 57µm

BASELINE [JAN. 2010] average RNFL: 57µm

FOLLOW-UP 2 [FEB. 2011] average RNFL: Δ0µm

FOLLOW-UP 3 [MAY 2012] average RNFL: Δ-3µm

FOLLOW-UP 4 [SEPT. 2013] average RNFL: Δ-2µm

BASELINE 1 JUNE 2006

BASELINE 2 JULY 2006

FOLLOW-UP 1 SEPT. 2007

FOLLOW-UP 2 MARCH 2008

FOLLOW-UP 3 JUNE 2009

FOLLOW-UP 4 MAY 2010

FOLLOW-UP 5 FEB. 2011

FOLLOW-UP 6 MAY 2012


of glaucoma progression.1 You may also consider calculating the degree of IOP fluctuation—thought to be a factor in glaucoma progression, although this has been contested.2 It can be estimated using the standard deviation (SD) of IOP (free SD cal-culators are readily available online) or taking the difference between maximum and minimum values. In studies that did find fluctuating IOP to be a risk factor for glaucoma progression, the SD values were typically greater than 2mm Hg to 3mm Hg. Statistically, estimating the average IOP and SD of IOP becomes more powerful as you accumulate additional IOP measurements.

The process of cataloging IOP readings is very straightforward

and only requires that you group all measurements according to the treatments prescribed at that time, if any. For instance, if a patient has been on travoprost monotherapy for four years and I notice they are progressing and add dorzolamide in response, I will establish two treat-ment groups from which to analyze all of my clinical data (e.g., IOP, RNFL OCT, visual fields): a travo-prost group and a travoprost/dorzol-amide group. Once this is done, you can calculate the average IOP for each treatment group to assess the extent of IOP lowering.

The pretreatment block of time is the most critical, as this establishes the IOP range that is known to result in a glaucomatous outcome.

Therefore, it is recommended that multiple IOPs be taken at different times of day prior to initiating any glaucoma treatments. As a reference, the Early Manifest Glaucoma Trial and Ocular Hypertension Treatment Study, both highly regarded clinical trials, used just two pretreatment IOP measurements from which to judge the efficacy of the treatments studied.3,4

Ideally, recording diurnal IOP measurements on different days is best for assessing the true IOP, as IOP has been shown to fluctuate both spontaneously over time and asymmetrically between the eyes.2,5 Realistically, two to three IOP mea-surements at different times of day may be sufficient.

2009

2010

2012

A B C D E

Average RNFL: 108µm

Average RNFL: 109µm Δ+1µm

Average RNFL: 92µm Δ-16µm

Right Eye



Because patient compliance can vary considerably, attempt to grossly quantify the compliance level for each treatment group whenever pos-sible. For instance, if a patient tells me he misses his latanoprost drops about twice a week because he falls asleep prior to instilling the drops, I estimate his compliance to be approximately 70%.

Estimating compliance can be helpful when glaucoma progression tests worsen despite the average IOP meeting the target range. This may suggest that your patient is compli-ant in the days leading up to their examination, but noncompliant otherwise. Also, when analyzing each treatment group it is important to look for any trending of the IOP

values to avoid averaging out poten-tial problems, such as therapeutic tachyphylaxis (i.e., a loss of treat-ment efficacy over time) or a change in compliance. Always keep in mind that IOP-independent mechanisms may contribute to glaucoma pro-gression, even in the face of low IOP levels.

By grouping and then averaging IOP readings for your various treat-ments, you will be better prepared to correlate any changes that you encounter in your glaucoma pro-gression tests (see figure 1).

Reconciling OCT Findings The approach to detecting pro-

gressive thinning of the RNFL differs among OCT devices, particularly in

the use of software modules to help identify progressive RNFL thinning. Most, if not all, OCT devices assess the RNFL thickness based upon a ring scan centered on the optic disc. In addition to the parapapillary circle scan, some OCT devices also scan the entire area immediately sur-rounding the optic disc. Irrespective of your OCT’s acquisition and ana-lytical capabilities, it will be impor-tant to match the RNFL data with the IOP groups you have established for each glaucoma treatment.

Here are a few ideas on how serial RNFL evaluation can help detect progression as early as possible.

As we move out of the time-domain (TD) and into the spectral-domain (SD) era of OCT

F

A B C D E

Average RNFL: 99µm



Figure 2. A non-compliant patient had rapid RNFL progres-sion detected by SD-OCT: (A) Optic nerve photo. (B) Infrared reflectance image showing parapapillary ring scan. (C) Red-free reflectance image showing RNFL wedge defects OU.(D) Volumetric RNFL thickness map and (E) RNFL deviation map of the parapapillary region showing RNFL defects detected with SD-OCT. (F) The RNFL OCT changes are consistent with a step-wise pro-gressive pattern, with a period of stability in 2009 and 2010 followed by a dramatic drop in the average RNFL thickness.

Left Eye


acquisition, our ability to produce highly repeatable measurements is vastly improved, as is the ability to detect microstructural changes evident in glaucoma progression.6

With TD-OCT, measurement of the RNFL was limited to the circular line-scan mentioned above. Alterna-tively, volumetric RNFL assessment of the entire parapapillary region (not capable with a parapapillary circle scan) is now possible with SD-OCT. This method of RNFL analy-sis yields topographical maps that can assist in defining areas of RNFL depression in the form of wedge defects or generalized thinning—fea-tures that are technically difficult to appreciate using funduscopy or photography.7 Figure 2 provides an example of this.

In fact, Leung et al. demonstrated that measuring RNFL thickness using a 3.46mm circumpapillary ring is not as sensitive in identifying progression as using a 6mm x 6mm volumetric grid pattern centered over the optic disc, the acquisition protocol used by the Cirrus HD-OCT (Carl Zeiss Meditec). The usefulness of constructing an RNFL topographical map around the disc is that it expands the ability to iden-tify widening, deepening or the for-mation of new RNFL wedge defects, all classic signs of glaucoma progres-sion.7 Although the parapapillary ring scan is still the most commonly used method to assess RNFL thick-ness, volumetric scans can provide complementary data for detecting glaucoma progression.

Regardless of the RNFL scan type used, detecting RNFL thinning requires good intratest repeatability and point-to-point retinal registra-tion to ensure accurate comparisons between scans, thereby giving you the best chance to determine if progression is occurring.8 Clinical studies show that the average RNFL

thickness parameter is useful for demonstrating glaucoma progres-sion.9 This metric is used in guided progression analysis (GPA) software available with Cirrus HD-OCT.

In healthy eyes, the average RNFL thickness should show minimal change over time due to age. Typi-cally, test-to-test repeatability for SD-OCT ranges from 1µm to 5µm for average RNFL thickness. There-fore, if the average RNFL OCT indices are reduced by greater than 5µm from the baseline values, the clinician should be alerted to pos-sible glaucomatous progression. Evaluating RNFL thickness change by sector and quadrant is also fea-sible, with the inferior temporal sector and inferior quadrant having greater predictive value for identify-ing progression.9

Tracking RNFL measurement changes that fall outside the range of expected test-retest variability is termed event analysis.9,10 Simply put, with event analysis you establish two baseline scans at the start of your treatment period; for instance, when starting a patient on a glau-coma medication or switching from monotherapy to combination ther-apy. You then judge all future RNFL scans to the baseline scans taken at the beginning of the treatment period, knowing that the RNFL values should change minimally if the therapy is effective. This type of analysis can help you determine if progression is present, but does not tell you how fast it is occurring.

To assess the rate of RNFL pro-gression you must perform trend analysis, which can be estimated using OCT GPA. Always be cau-tious when RNFL thickness mea-surements change, as they may not always indicate glaucoma progres-sion. Instead, it may be secondary to poor signal strength, misaligned scan, or errors in automated seg-

mentation line placement. To rule out false progression due to artifact in the OCT scan, carefully examine all the parapapillary cross-sectional OCT images and look for areas where the retinal layers appear ill-defined or blurred. These are areas of poor signal strength and can result in deviation of the segmen-tation lines from the anatomical boundaries of the RNFL, which can influence the average RNFL thick-ness values.

If the RNFL is progressively thin-ning based on your serial RNFL OCT analysis, close inspection of the IOP treatment blocks may shed light on the range of IOP that resulted in the changes seen. Although RNFL thinning has been known to be a precursor to functional loss, there may be no concordant change in the visual field status.

Also keep in mind that glaucoma progression can take on different rate patterns, with both a continu-ous and step-wise pattern having been previously described.9 The former will demonstrate a slow-steady decline, whereas the step-wise pattern will have periods of stability interrupted by periods of progres-sion, typically during intermittent glaucomatous events such as angle closure or compliance issues (see figure 2).

The RNFL is not the only inner retinal structure that shows attenua-tion commensurate with glaucoma-tous damage. The ganglion cell layer and inner plexiform layer are also affected, making this a target for assessing glaucoma progression, spe-cifically in the macula. For instance, RTVue (Optovue) OCT assesses the combined thickness of these two layers along with the RNFL, known collectively as the ganglion cell com-plex (GCC), whereas Cirrus OCT analyzes exclusively the ganglion cell layer and inner plexiform layer.



The utility of ganglion cell OCT imaging in the macula is emerging as a viable clinical tool for assessing glaucoma progression, with some recent evidence suggesting greater sensitivity than RNFL OCT analy-sis. Specifically, Naghizadeh et al. found that the pattern-based param-eters of GCC imaging using the RTVue OCT—which include focal loss volume and global loss volume measurements—may be more effec-tive at this task.11

Although ganglion cell layer OCT analysis adds yet another dimension to glaucoma management, many of the principles used for RNFL OCT analysis also apply. Notably, the test-retest variability ranges from 2µm to 5µm, providing some basis for event analysis.12,13

Visual Field Interpretation The presence of visual field

progression can be detected using a combination of methods, all of which rely on statistical analysis (e.g., glaucoma change analysis, visual field index, GPA). Both GPA and visual field index require customization of the baseline and follow-up visual fields to improve their ability to detect progression and evaluate the success of therapy. Otherwise, the GPA program auto-matically selects the baseline scans.

Just as in your RNFL OCT progression analysis, visual field analysis also requires that you appropriately set the baseline visual fields according to events that occur during management, such as add-ing or changing glaucoma drops, recommending glaucoma surgery or the presence of a sustained period of noncompliance.

Despite its ability to recognize visual field progression, GPA can produce misleading results if the baseline visual fields do not correlate with treatment groups, are unreli-

able, or if the time between the two baseline exams is too long, as this introduces the potential for progres-sion to occur between visual fields.

Choosing the most appropriate baseline visual field is imperative to reveal the effectiveness of the treat-ments being prescribed. Although resetting the baseline visual field is important to monitor glaucoma pro-gression following a change in treat-ment, it is not always required. For example, in patients with multiple medication changes, resetting the baselines may actually preclude your ability to accumulate enough follow-up exams to provide meaningful results, as it becomes time prohibi-tive. In such cases, it can be better to divide your IOP, RNFL and VF data into a pretreatment group and treatment group, without assessing each individual treatment type (see figure 1). This is usually necessary in patients who have multiple treat-ment changes over a shorter period of time.

Discordance between structural and functional glaucoma progres-sion is well-recognized. Surprisingly, despite stable OCT RNFL thick-ness values, up to 35% of patients were shown to develop progressive threshold visual field loss in a study that used TD-OCT.14 Although these results may not correlate directly with the performance of SD-OCT technology, it should be a reminder to the clinician that stable RNFL OCT readings do not always rule out glaucoma progression. As would be expected, progressive OCT RNFL thinning significantly increases the likelihood of future visual field loss.

As such, if a change in glaucoma therapy is made in light of serial RNFL OCT thinning, despite stable visual fields, you should factor in the possibility of a delayed onset of visual field progression when

evaluating the efficacy of your new therapy.

The Big PictureIt is easy to become mired in the

nuances of glaucoma progression tests and snapshot views of IOP recordings. However, an appropri-ate analysis of IOP and its relation to glaucoma progression testing can be maintained to preserve the sim-plicity of glaucoma management. ■

Scott Anthony, OD, is on staff at the Louis Stokes VA Medical Center in Cleveland, Ohio.

1. The AGIS investigators. Am J Ophthalmol 2000;130:429-440.2. Leidl M, Choi C, Syed Z, Melki S. Intraocular pressure fluctuation and glaucoma progression: what do we know? Br J Ophthalmol 2014;Epub ahead of print.3. Leske C, Heijl A, Hyman L, Bengtsson B, et al. Ophthalmo-lol 1999;106:2144-2153.4. Gordon M, Beiser J, Brandt J, et al. The Ocular Hyper-tension Treatment Study: Baseline factors that predict the onset of primary open-angle glaucoma. Arch Ophthalmol 2002;120:714-720.5. Realini T. A prospective, randomized, investigator-masked evaluation of the monocular trial in ocular hypertension or open-angle glaucoma. Ophthalmol 2009;116:1237-1242.6. Leung C, Chiu V, Weinreb R, et al. Evaluation of retinal nerve fiber layer progression in glaucoma: A comparison between spectral-domain and time-domain optical coherence tomography. Ophthalmol 2011;118:1558-1562.7. Leung C, Yu M, Weinreb R, et al. Retinal nerve fiber layer imaging with spectral-domain optical coherence tomography: Patterns of retinal nerve fiber layer progression. Ophthalmol 2012;119:1858-1866. 8. Sehi M, Iverson S. Glaucoma diagnosis and monitoring using advanced imaging technologies. US Ophthalmic Rev 2013;6:15-25.9. Kotowski J, Wollstein G, Ishikawa H, Schuman J. Imaging of the optic nerve and retinal nerve fiber layer: An essential part of glaucoma diagnosis and monitoring. Surv Ophthalmol 2013: Epub ahead of print.10. Leung, C. Diagnosing glaucoma progression with optical coherence tomography. Curr Opin Ophthalmol 2014;25:104-111.11. Naghizadeh F, Garas A, Vargha P, Hollo G. Detection of early glaucomatous progression with different parameters of the RTVue optical coherence tomograph. J Glaucoma 2014;23:195-198.12. Kotowski J, Wollstein G, Folio L, Ishikawa H, Schuman J. Clinical use of OCT in assessing glaucoma progression. Ophthalmic Surg Lasers Imaging 2011;42:S6-S14.13. Francoz M, Fenolland J, Giraud J, et al. Reproducibility of macular ganglion cell-inner plexiform layer thickness measurement with Cirrus HD-OCT in normal, hypertensive and glaucomatous eyes. Br J Ophthalmol 2014;98:322-328.14.Sehi M, Zhang X, Greenfield D, et al. Retinal nerve fiber layer atrophy is associated with visual field loss over time in glaucoma suspect and glaucomatous eyes. Am J Ophthalmol 2013;155:73-82.


Tailor Your Approach To PXG Management

Pseudoexfoliation syndrome refers to an abnormal accu-mulation of extracellular exfoliative material in the

anterior segment structures of the eye.1,2 Although the condition was first described in 1917, we now know that the exfoliative material isn’t isolated to the eye. In fact, this composite of elastic microfibrillar-associated glycoproteins also is found in the skin, lung, heart, kidney, abdomen and blood vessel walls.1,3

Although pseudoexfoliation syn-drome is the most common identifi-able cause of open-angle glaucoma (OAG) worldwide, the condition has many unique qualities that merit review.

For example, pseudoexfoliative glaucoma (PXG) is much more aggressive than conventional OAG––intraocular pressure (IOP) may fluctuate widely, it presents more asymmetrically and it could be less responsive to topical medi-cal therapy. Further, PXG patients often require early detection and close, careful monitoring.

EpidemiologyExtensive population studies

have shown a marked difference in pseudoexfoliation syndrome incidence based on geographic loca-tion, which is highly suggestive of a racial predilection.3 The Framing-ham Eye Study in Massachusetts and the Blue Mountains Eye Study in Australia, for example, showed a disease prevalence of 1.8% and 2.3%, respectively; however, some European studies report up to a 50% incidence in some Scandina-vian countries.3,4 It is important to note that psuedoexfoliation is most commonly found in whites over age 50 with a slight female predilec-tion.2,3,5

Recent studies have implicated the lysyl oxidase-like 1 (LOXL1) gene in pseudoexfoliation syn-drome, and showed that individuals with two specific LOXL1 variants were more likely to develop the condition.5 LOXL1 is responsible for the biogenesis of connective tis-sue, so any genetic alteration could potentially result in increased pro-duction of extracellular material.5

Additionally, genetic variants of contactin-associated protein-like 2 (CNTNAP2) and clusterin (CLU) are being evaluated as potential catalysts for PXG.5

Outside of genetic predilection, one research group postulated in 1979 that sunlight exposure might contribute to the expression of psuedoexfoliation; however, this association has not been further evaluated in recent studies.3,6 Addi-tionally, the Nurses’ Health Study and Health Professionals Follow-up Study found an increased risk of pseudoexfoliation secondary to increased caffeine intake.5

Glaucoma RiskAs previously mentioned, pseu-

doexfoliation is the most common identifiable risk factor associated with open-angle glaucoma.7 His-tological and electron microscope studies have documented unique pathological and structural changes to the cornea, iris, trabecular meshwork and zonules in affected individuals––all of which increase glaucoma risk.1

Patients with pseudoexfoliative glaucoma often require a more thorough diagnostic work-up and earlier intervention than those with POAG. So how do these conditions differ, and why? By Anupam Laul, OD, and Marta Fabrykowski, OD



The primary mechanism of glau-comatous damage in pseudoexfolia-tion syndrome is the impedance of aqueous outflow.1 The accumula-tion of pseudoexfoliative material in the trabecular meshwork and subsequent degenerative changes to the tissue pose the greatest resis-tance to proper drainage. Addition-ally, it has been shown that active, localized production of pseudoex-foliative material by the endothe-lium of Schlemm’s canal can cause lumen narrowing.1 Proliferation of psuedoexfoliative material by the corneal endothelial cells, as well as secondary migration posteriorly over the trabecular meshwork, may further lead to increased intraocular pressure.1

The mean intraocular pressure (IOP) of patients with PXG is up to 1.7mm Hg higher than those without it.3 The Olmsted County Study––which monitored the natural course of PXG––found that 44% of patients required glaucoma medications over a 15-year period.8

Further, glaucoma patients with pseudoexfoliation have more vari-able IOPs, higher rates of treatment failure and faster progression of optic nerve damage.8,9

Systemic AssociationsUnlike primary open-angle glau-

coma (POAG), pseudoexfoliation has a systemic component. Post-mortem electron microscope exami-nation of several visceral organs showed evidence of pseudoexfolia-tive material, suggesting systemic involvement.1

As in the eye, pseudoexfolia-tion can cause ultrastructural and immunohistochemical changes in affected organ systems. This can precipitate a variety of systemic complications, including abdominal aneurysms and an increased risk of coronary artery disease.1,10,11 Addi-

tionally, secondary pathological alterations to the tunica intima can cause vascular fibrosis and elas-tosis, which often increase blood flow resistance.10,11 Interestingly, a 30-year epidemiological study showed no increased risk of mortal-ity in those with PXF.12

It is also worth noting that those with pseudoexfoliation are more likely to experience sensorineural hearing loss.13 Although not com-pletely understood, extracellular fibrils likely accumulate in the structures of the inner ear, resulting in decreased sensitivity.13

Clinical AspectsPhysiologic ocular findings of

this aggressive disease may be subtle. The ocular presentation generally is bilateral, but not neces-sarily symmetrical. Corneal findings in pseudoexfoliation syndrome are fairly rare; however, careful examination of the endothelium may show flakes of bright white fibrillar material.14,15 These deposits often appear as irregularly spaced aggregates, reminiscent of small filaments. The flakes can vary in shape and size, and––due to con-vection currents of the aqueous in the anterior chamber––may evolve over time.

The corneal endothelial cells often are affected dramatically in pseudoexfoliation syndrome patients. Most individuals exhibit fewer total endothelial cells with morphological alterations. Such endothelial changes are also seen in Fuchs’ dystrophy––although they do not present in conjunction with other pseudoexfoliative changes observed in the eye.

In certain instances, these changes are accompanied by increased central corneal thick-ness.14 Fine measurements via specular microscopy can show a measureable decrease in the number of endothelial cells, as well as poly-morphism.15 Clinically, these cell alterations may appear as a light paracentral area of pigmentation on the corneal endothelium that’s occasionally organized in the pat-tern of a Krukenberg spindle.

Further evaluation should include a 360° assessment of ante-rior chamber depth, in addition to a measurement comparison between both eyes. Although there are many direct indications of lens dislocation, one indirect sign is an alteration in chamber depth. A lens can subluxate forward, leading to a shallow anterior chamber, or may fall backward towards the vitreous, resulting in a hyper-deep chamber.16

Examine trabecular meshwork pigementation via gonioscopy, looking specifically for pigment located anterior to Schwalbe’s line.17,18 Pseudoexfoliation patients often have an abnormally high volume of angle pigmentation, even without any other syndrome findings. Pseudoexfoliation is also classically associated with pigment loss––both at the pupillary margin and around the iris sphincter.

On iris transillumination, the margin may exhibit a “moth-eaten appearance.”15 Gray-white flakes

1. Telltale clinical sign of peripupillary accumulation of fibrillar material on a patient with dark irides.


may be present at the pupillary margin, and frequently are the only overt sign of disease (figure 1).15,16

Several researchers have linked deposition of this material with changes in iris function.15,16 Because the iris sphincter may be compro-mised, there may be a reduced response to mydriatics. Iris flutter is another indirect sign of weak zon-ules, which hold the lens in place; however, sometimes the iris may be more rigid in pseudoexfoliation patients, so this clinical sign may not be evident.15,16

Iris changes in psuedoexfoliation syndrome closely correlate with lenticular findings. Most often, exfoliative material presents on the anterior capsule of the lens. This finding commonly manifests in a “target” or “bull’s eye” pattern, which consists of three zones after dilation: the central disk (approxi-mately the diameter of the pupil), the clear zone and a peripheral band of fibrillar material (figure 2).14,15 This is another sign that clas-sically presents asymmetrically.

A definitive indication of zonular damage is phacodonesis, or lens flutter.15,16 Although crude, jolt-ing the slit lamp table during lens examination can produce a subtle vibration or movement indicative of zonular weakness. A loose or subluxated lens is best viewed after dilation––although looking for a decentered fetal nucleus may be helpful in poorly dilating eyes.14

Individuals with pseudoexfo-liative glaucoma exhibit a similar optic nerve appearance to that observed in POAG patients, includ-ing axonal loss, increased central cupping and disc rim thinning at both the superior and inferior poles.19 In advanced cases, a Drance hemorrhage may be seen.

As with other glaucomatous presentations, optical coherence

tomography or Heidelberg Retinal Tomography (Heidelberg Engineer-ing) will help you assess retinal nerve fiber layer thinning. The standard of care for visual field evaluation in all glaucoma patients is a Humphrey 24-2, which remains true for patients suspected of, or already diagnosed with, PXG.

Although the general appearance of a nerve with PXG is similar to one with open-angle glaucoma, asymmetrical presentation often helps you differentiate accurately. Interestingly, recent studies have indicated that, similar characteris-tics aside, nerves with pseudoex-foliation are histopathologically unique––with higher capillary den-sity, despite axonal loss.20

Because pseudoexfoliative material can potentially rest in a multitude of anatomical locations, intraocular pressure may vary widely. A patient’s diurnal and daily IOPs can spike dramatically. Further, depending on the extent of pseudoexfoliative asymmetry, IOP varies significantly between eyes. This can make PXG treatment difficult, because establishing the patient’s baseline pressure can be a challenge. Multiple IOP measure-ments over a series of visits may be necessary to determine an accept-able pressure range.

There is no specific algorithm for quantifying IOP oscilation––although one report indicated that patients with PXG fluctuate the highest outside office hours, mak-ing diurnal mapping even more difficult.21 In some studies, patients’ IOPs were measured six times over a 24-hour period, which is impractical and unrealistic.22 From experience, however, it seems that a minimum of two measurements per day (i.e., one in the morning, and one in the afternoon) is both ade-quate and relatively easy to obtain.

Topical Hypotensive Treatment

Managing cases of pseudoex-foliative glaucoma with topical hypotensive therapy may require increased vigilance and a certain element of creativity. In 2013, Murray Fingeret, OD, indicated that 16% of PXG patients require therapeutic intervention upon ini-tial presentation.17 So, a treatment decision may need to be made early or even immediately in the manage-ment process.

Traditional medications are less effective for PXG than POAG, but are still often used as first-line ther-apy because they are more effective than carbonic anhydrase inhibi-tors or alpha agonists.23 Both beta blockers and prostaglandin ana-logs are ideal places to start, with carbonic anhydrase inhibitors and alpha adrenergic agonists following as likely adjunctive medications.

Similar to the management of pigmentary glaucoma, the use of miotics has some theoreti-cal advantage for PXG patients. Miotic agents forcefully open the trabecular meshwork and increase drainage, as well as limit pupillary movement.18,24 By reducing pupil motion, less pigment and pseudoex-foliative material are released from their respective locations.18 Take note that miotics should be used with discretion in individuals with cardiac risk factors, and may pre-cipitate retinal detachments in some patients.25

Typically, the managing clinician will begin dosing with one class of ocular hypotensive agents, and then add secondary medications as needed. Because PXG has a higher incidence of progression and is more likely to be resistant to medi-cal management than POAG, fur-ther therapeutic intervention often is required.26



Surgical InterventionThe Early Manifest Glaucoma

Trial showed us that PXG is more rapidly progressive and is more likely to require surgical interven-tion than POAG.27 When topical treatment fails, or if maximum medical therapy is inadequate in achieving the desired IOP, surgical management should be considered.

• Non-incisional. Laser trabecu-loplasty is a commonly performed procedure that increases aqueous outflow in eyes with POAG.28 Argon laser trabeculoplasty (ALT) was once thought to yield trabecu-lar meshwork contraction and sub-sequent aqueous collector channel widening.

However, a histological study published in 2007 indicated that ALT’s effect actually causes a remodeling of the juxtacanalicular region of the meshwork.29,30 Selec-tive laser trabeculoplasty (SLT), on the other hand, uses a Q-switched frequency-doubled Nd:YAG laser to selectively target pigmented cells within the trabecular meshwork and increase aqueous outflow.31

Use of either ALT or SLT on eyes with POAG or PXG has been found to yield comparable levels of IOP reduction across the board.28 In a series of studies, POAG eyes exhibited nearly a 22% IOP reduc-tion one day following surgery, compared to a 29% IOP reduction in PXG eyes.28 However, at three-year follow-up, POAG eyes main-tained an average IOP reduction of 34%, whereas PXG eyes remained just 21% below baseline.28 Because PXG tends to be more aggressive than POAG, pseudoexfoliative patients often require additional management once the pressure-lowering effect from ALT or SLT subsides.

• Cataract removal. It is well documented that oxidative stress in

pseudoexfoliation syndrome leads to early cataract formation.32 In many cases, patients with PXG will require cataract surgery. A retro-spective study of more than 1,000 patients with pseudoexfoliation showed a significant improvement in IOP after uncomplicated phaco-emulsification.33 Those with PXG had a more significant and sus-tained IOP reduction than patients without PXG.33 Further, only about 3% of eyes with early evidence of pseudoexfoliation syndrome progressed to PXG over a 10-year postoperative period.33

• Trabeculectomy. In cases of more advanced glaucoma, tra-beculectomy is one of the most commonly indicated surgical inter-ventions.34 The procedure involves scleral flap formation and ostium creation, which allows aqueous dis-sipation into the subconjunctival space.34-36

Trabeculectomy for PXG patients is a successful means of reducing intraocular pressure; how-ever, some clinicians believe there might be a higher incidence of post-operative pressure spikes compared to POAG patients who undergo the procedure.36 Combined cataract removal and trabeculectomy often yields fewer pressure spikes than trabeculectomy alone.35,37

• Minimally invasive glaucoma surgery (MIGS). These surgical procedures are relatively new, and are intended to increase aqueous drainage through the trabecular meshwork.38-40 The two most com-mon MIGS procedures are the Tra-bectome (NeoMedix) and the iStent (Glaukos). Take note that only the Trabectome has been studied in a large pseudoexfoliation study sample.40

In a Trabectome procedure, the surgeon removes the trabecular meshwork through a clear corneal

approach, which exposes the col-lector channels of Schlemm’s canal. In the study mentioned above, 173 PXG eyes underwent Trabectome surgery.40 Of these, 34% were pha-kic, 25% were pseudophakic and 41% underwent combined cataract and Trabectome surgery.40 At one-year follow-up, the entire patient population exhibited a mean IOP reduction of 30%.40

Although not thoroughly studied in the pseudoexfoliation popula-tion, the iStent is placed into the angle via a clear corneal incision.38 The stent is a 1.0mm nonferro-magnetic, L-shaped device that is inserted into Schlemm’s canal.38 Because the iStent facilitates bypass of the trabecular meshwork, the resultant IOP is based on the cir-cumferential flow of Schlemm’s canal, the collector ducts and the episcleral venous pressure.38 Fol-lowing the procedure, IOPs typi-cally range in the high teens.38

• Endocyclophotocoagulation (ECP). Cyclodestruction of the ciliary body as a treatment for glaucoma was first attempted in the 1970s.41 Historically, the procedure

2. Apparent “bull’s eye” pattern of fibrillar material on a dilated, lightly pigmented patient. Looking closely, there’s also a peripupillary accumulation of material.

Photo: Stephen A. Obstbaum, M

D


was performed transsclerally with cryotherapy, an Nd:YAG laser or a diode laser, and was reserved for eyes with severe disease and/or little potential for visual gain.41 Because the target is not visible to the sur-geon transsclerally, there is risk of adjacent tissue damage and resul-tant inflammation, decreased visual acuity, hypotony and phthisis.42

ECP is performed intraocularly with the aid of an endoscope (usu-ally in conjunction with cataract extraction), which permits direct visualization of the targeted ciliary body tissue.41 In a case series of 68 patients (including those with PXG), researchers documented a 34% mean IOP reduction following ECP.41 Although a large prospective study of ECP in eyes with pseudo-exfoliation has not been performed, this seems like a promising therapy going forward.

Pseudoexfoliative glaucoma, a well-known member of the OAG family, is a fairly unique clinical entity. While PXG’s signs can be subtle, its impact can be visually devastating––so we are tasked with identifying the condition as early as possible.

In comparison to those with pri-mary open-angle glaucoma, PXG patients often need topical ocular hypotensive agents earlier in the disease process. Additionally, they require more frequent follow-ups and testing, as well as adjunctive therapy, to reduce the likelihood of irreversible vision loss. ■

Dr. Fabrykowski is on staff at the Manhattan Eye, Ear and Throat Hospital Faculty Ophthalmology Practice, operated by Lenox Hill Hospital, in New York.

Dr. Laul is an instructor of ophthalmology at the Wilmer Eye Institute, Johns Hopkins School of Medicine, in Baltimore.

They thank Harry A. Quigley, MD, professor of ophthalmology at Wilmer Eye Institute, and Bradford J. Shingleton, MD, Ophthalmic Consultants of Boston and associate clinical professor of ophthalmology at Harvard School of Medicine for their research guidance.

1. Naumann GO, Schlötzer-Schrehardt U, Küchle M. Pseudo-exfoliation syndrome for the comprehensive ophthalmologist. Intraocular and systemic manifestations. Ophthalmology. 1998 Jun;105(6):951-68.2. Cashwell LF, Shields MB. Exfoliation syndrome. Preva-lence in a southeastern United States population. Arch Ophthalmol. 1988 Mar;106(3):335-6.3. Mitchell P, Wang JJ, Hourihan F. The relationship between glaucoma and pseudoexfoliation: the Blue Mountains Eye Study. Arch Ophthalmol. 1999 Oct;117(10):1319-24.4. Hiller R, Sperduto RD. Pseudoexfoliation, intraocular pres-sure, and senile lens changes in a population-based survey. Arch Ophthalmol. 1982 Jul;100(7):1080-2.5. Sein J, Galor A, Sheth A, et al. Exfoliation syndrome: new genetic and pathophysiologic insights. Curr Opin Ophthal-mol. 2013 Mar;24(2):167-74.6. Taylor HR. Pseudoexfoliation, an environmental disease? Trans Ophthalmol Soc UK. 1979 Jul;99(2):302-7.7. Ritch R. Exfoliation syndrome-the most common identifi-able cause of open-angle glaucoma. J Glaucoma. 1994 Summer;3(2):176-7.8. Jeng SM, Karger RA, Hodge DO, et al. The risk of glau-coma in pseudoexfoliation syndrome. J Glaucoma. 2007 Jan;16(1):117-21.9. Leske MC, Connell AM, Wu SY, et al. Risk factors for open-angle glaucoma. The Barbados Eye Study. Arch Oph-thalmol. 1995 Jul;113(7):918-24.10. Schumacher S, Schlötzer-Schrehardt U, Martus P, et al. Pseudoexfoliation syndrome and aneurysms of the abdomi-nal aorta. Lancet. 2001 Feb 3;357(9253):359-60.11. Citirik M, Acaroglu G, Batman C, et al. A possible link between the pseudoexfoliation syndrome and coronary artery disease. Eye (Lond). 2007 Jan;21(1):11-5.12. Svensson R, Ekström C. Pseudoexfoliation and mortality: a population-based 30-year follow-up study. Acta Ophthal-mol. 2014 Mar 26. [Epub ahead of print]13. Cahill M, Early A, Stack S, et al. Pseudoexfo-liation and sensorineural hearing loss. Eye (Lond). 2002 May;16(3):261-6.14. Crista AR. Pseudoexfoliation syndrome and cataract sur-gery in pseudoexfoliation syndrome. Clinic of Ophthalmol-ogy: Timisoara Medical Journal. Available at: www.tmj.ro/article.php?art=237564682127339. Accessed June 10, 2014. 15. Drolsum L, Ringvold A, Nicolaissen B. Cataract and glau-coma surgery in pseudoexfoliation syndrome: A review. Acta Ophthalmol Scand. 2007 Dec;85(8):810-21.16. Shingleton BJ, Crandall AS, Ahmed II. Pseudoexfolia-tion and the cataract surgeon: preoperative, intraoperative, and postoperative issues related to intraocular pressure, cataract, andintraocular lenses. J Cataract Refract Surg. 2009 Jun;35(6):1101-20.17. Fingeret M. Exfoliation glaucoma. Optometric Glaucoma Society Residency Education Meeting. Fort Worth, Texas. August 5, 2013.18. Susanna R, Weinreb R Answers in Glaucoma. Rio de Janeiro, Brazil: Cultura Medica; 2005.19. Gottanka J, Kuhlmann A, Scholz M, et al. Pathophysi-ologic changes in the optic nerves of eyes with primary open angle and pseudoexfoliation glaucoma. Invest Ophthalmol Vis Sci. 2005 Nov;46(11):4170-81.20. Gottanka J, Flügel-Koch C, Martus P, et al. Correla-tion of pseudoexfoliative material and optic nerve damage inpseudoexfoliation syndrome. Invest Ophthalmol Vis Sci. 1997Nov;38(12):2435-46.

21. Majka CP, Pratap C. Ophthalmic pearls: glaucoma; diagnosis and management of pseudoexfoliation glaucoma. EyeNet Magazine Online. Available at: www.aao.org/publica-tions/eyenet/200606/pearls.cfm. Accessed June 10, 2014. 22. Dul MW. Ocular and systemic pseudoexfoliation syn-drome. Optometric Management. Available at: www.optometricmanagement.com/articleviewer.aspx?articleid=71827. Accessed June 10, 2014. 23. Konstas AG, Mantziris DA, Stewart WC. Diurnal intra-ocular pressure in untreated exfoliation and primary open-angle glaucoma. Arch Ophthalmol. 1997 Feb;115(2):182-5.24. Altinta O, Yüksel N, Karaba VL, Qalar Y. Diurnal intra-ocular pressure variation in pseudoexfoliation syndrome. Eur J Ophthalmol. 2004 Nov-Dec;14(6):495-500.25. Bartlett J. Ophthalmic Drug Facts, 2006. Philadelphia: Wolter Kluwer Health, Inc.; 2006.26. Desai MA, Lee RK. The medical and surgical manage-ment of pseudoexfoliation glaucoma. Int Ophthalmol Clin. 2008 Fall;48(4):95-113.27. Leske MC, Heijl A, Hussein M, et al. Factors for glaucoma progression and the effect of treatment: the early manifest glaucoma trial. Arch Ophthalmol. 2003 Jan;121(1):48-56.28. Gracner T. Intraocular pressure response of capsular glaucoma and primary open-angle glaucoma to selective Nd:YAG laser trabeculoplasty: a prospective, comparative clinical trial. Eur J Ophthalmol. 2002 Jul-Aug;12(4):287-92.29. Cvenkel B, Hvala A, Drnovsek-Olup B, Gale N. Acute ultrastructural changes of the trabecular meshwork after selective laser trabeculoplasty and low power argon laser trabeculoplasty. Lasers Surg Med. 2003;33(3):204-8.30. Johnson DH. Histologic findings after argon laser trabeculoplasty in glaucomatous eyes. Exp Eye Res. 2007 Oct;85(4):557-62.31. Realini T. Selective laser trabeculoplasty: a review. J Glaucoma. 2008 Sep;17(6):497-502.32. Schlötzer-Schrehardt U, Naumann GO. Ocular and sys-temic pseudoexfoliation syndrome. Am J Ophthalmol. 2006 May;141(5):921-37.33. Shingleton BJ, Laul A, Nagao K, et al. Effect of phaco-emulsification on intraocular pressure in eyes withpseudo-exfoliation: single-surgeon series. J Cataract Refract Surg. 2008 Nov;34(11):1834-4134. Jea SY, Francis BA, Vakili G, et al. Ab interno trabecu-lectomy versus trabeculectomy for open-angle glaucoma. Ophthalmology. 2012 Jan;119(1):36-42.35. Shingleton BJ, Wooler KB, Bourne CI, O’Donoghue MW. Combined cataract and trabeculectomy surgery in eyes with pseudoexfoloation glaucoma. J Cataract Refract Surg. 2011 Nov;37(11):1961-70.36. Landers J, Martin K, Sarkies N, et al. A twenty-year fol-low-up study of trabeculectomy: risk factors and outcomes. Ophthalmology. 2012 Apr;119(4):694-702.37. Jacobi PC, Dietlein TS, Krieglstein GK. Comparative study of trabecular aspiration vs trabeculectomy in glaucom-atriple procedure to treat pseudoexfoliation glaucoma. Arch Ophthalmol. 1999 Oct;117(10):1311-8.38. Traverso CE, Bagnis A, Papadia M, Scotto R. Current and emerging medical therapies in the treatment of glau-coma. Expert Opin Emerg Drugs. 2011 Jun;16(2):293-30739. Lankaranian D, Razeghinejad MR, Prasad A, et al. Inter-mediate-term results of the Ex-PRESS miniature glaucoma implant under a scleral flap in previously operated eyes. Clin Experiment Ophthalmol. 2011 Jul;39(5):421-8.40. Jordan JF, Wecker T, van Oterendorp C, et al. Tra-bectome surgery for primary and secondary open angle glaucomas. Graefes Arch Clin Exp Ophthalmol. 2013 Dec;251(12):2753-60.41. Lin SC. Endoscopic and transscleral cyclophotocoagula-tion for the treatment of refractory glaucoma. J Glaucoma. 2008 Apr-May;17(3):238-47.42. Lima FE, Magacho L, Carvalho DM, et al. A prospective, comparative study between endoscopic cyclophotocoagula-tion and the Ahmed drainage implant in refractory glaucoma. J Glaucoma. 2004 Jun;13(3):233-7.


wettability and lipid deposit resistance compared to other silicone hydrogel lenses.4

CLINICAL RELEVANCEThe lipid deposits and lens changes

induced by cosmetics may interfere with contact lens shape and optical performance.1,2

One obvious way to reduce buildup of cosmetic residues is to use daily disposable lenses. But when this is not an option, selecting a lens material that maintains wettability and resists deposits—of both tear film lipids and of cosmetic products—may increase the likelihood of successful lens wear.

In addition to appropriate lens selection, contact lens exposure to cosmetics can be further minimized by giving patients clear instructions about cosmetic application and removal. In addition to thoroughly washing and drying hands prior to handling their lenses, patients should insert lenses before applying eye makeup and remove lenses before using makeup remover. Patients who believe their lenses have been damaged due to cosmetics exposure should be instructed to replace their lenses with a new pair.

Gina Wesley, OD, MS, FAAO, practices at Complete Eye Care of Medina, in Medina, MN.

REFERENCES 1. Srinivasan S, Luensmann D, Otchere H, et al. The impact

of cosmetics on the surface appearance and wettability of silicone hydrogel contact lenses. Presented at the American Academy of Optometry Meeting; October 24-27, 2012; Phoenix, AZ. Abstract 120317.

2. Luensmann D, Srinivasan S, Yu M, et al. The impact of cosmetics on the physical dimension and optical performance of silicone hydrogel contact lenses. Presented at the British Contact Lens Association Meeting; May 25-27, 2012; Birmingham, UK.

3. Keir N, Jones L. Wettability and silicone hydrogel lenses: a review. Eye Contact Lens. 2013;39:100-8.

4. Carney FP, Nash WL, Sentell KB. The adsorption of major tear film lipids in vitro to various silicone hydrogels over time. Invest Ophthalmol Vis Sci. 2008;49:120-4.

The Makeup Factor: Expanding the Definition of “Deposit Resistance”

Cosmetics on the surface of a soft contact lens can affect wettability, fit, and, ultimately, comfort—

but in vitro testing shows that not all lenses are equally affected. Gina Wesley, OD, MS, FAAO

Important information for AIR OPTIX® AQUA (lotrafilcon B) contact lenses: For daily wear or extended wear up to 6 nights for near/far-sightedness. Risk of serious eye problems (i.e., corneal ulcer) is greater for extended wear. In rare cases, loss of vision may result. Side effects like discomfort, mild burning or stinging may occur.

See product instructions for complete wear, care and safety information.

©2014 Novartis 1/14 AOA14003AD-C

Many contact lens wearers use cosmetics on and around the eye, but the impact of these products on contact lenses has received little attention. Recent in vitro research, however, has shown that hand creams, mascaras, and makeup removers can alter contact lens shape and optics and, over time, interfere with lens comfort and performance.

EFFECTS OF COSMETICS Investigators at the University

of Waterloo Centre for Contact Lens Research measured the effect of commonly used cosmetic products on silicone hydrogel contact lenses.1,2 Following in vitro exposure to test products (hand cream, mascara, and eye makeup remover), lenses were assessed for change in surface appearance and physical and optical parameters. Lenses were then cleaned with a commercially available hydrogen peroxide contact lens solution and reevaluated.

Among the products tested, mascara was associated with the greatest degree of surface deposition, as observed by researchers and quantified by mean pixel brightness using darkfield microscopy.1 Cleaning with hydrogen peroxide only partially removed these deposits, with those left by waterproof mascara least responsive to cleaning. Liquid makeup removers induced the greatest changes to lens diameter, sagittal depth, and base curve.2

Of the seven lens materials tested, AIR OPTIX® AQUA (lotrafilcon B) contact lenses demonstrated the greatest resistance to surface deposition from mascara.1 The same lenses underwent the least conformational change when exposed to makeup remover.2 Furthermore, these lenses demonstrated the fewest changes in optical performance metrics (lens power and image quality index).2

Rx only

THE AIR OPTIX® DIFFERENCE The hydrophobic domains in

silicone hydrogel lenses attract tear film lipids as well as the oil components of cosmetic products used on the eye.3 Because of this, developers of silicone hydrogel lenses have employed various strategies to render them more water-loving.4 Some lenses are made more wettable by embedding hydrophilic polymers within the lens material or in the soaking solution, others by surface modification.3

AIR OPTIX® is the only family of lenses with a unique, permanently bonded plasma coating that creates a uniform and uninterrupted hydrophilic surface. Both the chemical composition of the plasma coating and its uniformity across the lens surface are likely contributors to these lenses’ greater

» Cosmetic products can deposit onto and affect silicone hydrogel contact lens performance

»Mascara—especially waterproof—and eye makeup removers are particularly prone to lens deposition

»In in vitro studies, cleaning with hydrogen peroxide removes some, but not all, cosmetic deposits, and AIR OPTIX® contact lenses were least affected by tested cosmetic products

»The uniform plasma surface treatment keeps AIR OPTIX® contact lenses wettable and deposit resistant

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Glaucoma The Changing and Challenging

Epidemiology of

When asked to think about the prototypical glau-coma patient, most eye care providers would

likely picture an older African-American patient. While African Americans and Hispanics have a higher risk of developing glaucoma than do whites, the overwhelm-ing majority (75%) of current glaucoma patients within the US population are in fact white.1 This stems from the fact that, at this point in time, the preponderance of US population at risk for glaucoma is white. About 85% of all adults over 65 in the US population are white; for the population over age 75, whites make up an even larger percentage of the total population (90%).1

However, shifts that are occur-ring in the demographics of the US population are going to markedly change the make-up and prevalence of glaucoma in the coming decades. Two major population trends are

affecting, and will continue to affect, the prevalence of glaucoma for decades. Those are the aging of US society and the growth of minority populations.

An Aging PopulationThe prevalence of glaucoma

is believed to be about 2% (with estimates ranging between 1.6% and 2.7%) in adults over the age of 40.1,3 In the year 2000, an estimated 2.2 million Americans had glau-coma, including those either diag-nosed or unknown.1,3 This number is expected to reach 3.3 million by the year 2020.3 The rapid growth in glaucoma is due to the aging of baby boomer population.

Various definitions for baby boomers exist, but it is generally regarded as the cohort born from 1946 to 1964. The first of the baby boom population turned 65 in 2011, and by 2034 all of the baby boom population will be over 65. Based on 2012 census data, 41 mil-

lion Americans are over the age of 65. Population predictions indicate that from 2010 to 2050 the number of adults over 65 will more than double, to 88.5 million.4 The cur-rent aging of the US population has been accompanied by phenomenal growth in the number of the “old-est-old.” The single-fastest growing segment of the US population cur-rently is the group over the age of 90.4 The number of the oldest-old population will continue to grow in the coming decades, with the num-bers of Americans reaching age 90 accelerating rapidly after 2030.

Numerous studies have shown that the prevalence of glaucoma increases with age. The Eye Dis-ease Prevalence Research Group developed estimates of glaucoma prevalence from data that included multiple US-based and international studies. The group estimated that open-angle glaucoma prevalence increased from 0.7% at age 40 to 7.7% for those over age 80.3 Self-

As the aging population doubles and minority groups skyrocket, we face increased challenges in tailoring our glaucoma care to each patient. By Mark Swanson, OD, MSPH



reported epidemiologic data from the National Health Interview Survey found glaucoma prevalence increasing from 0.2% at age 18 to over 10.7% for those over 75.3 The growth in the oldest-old is impor-tant, as the prevalence of glaucoma triples in those over 75 compared to those aged 65.3

While data is limited, there is no indication that new cases of glaucoma decline in those who reach very advanced age. As such, the number of people who develop glaucoma can be expected to increase throughout the lifespan. The growth of early glaucoma in octogenarians and nonagenarians will present both logistical chal-lenges in caring for adults who may have multi-morbidity, cognitive impairment and frailty, and ethical ones in balancing the benefits of treatment of a disease with a long-

term course to impairment with the remaining life expectancy.

Growth of Minority Populations

A second significant contribu-tor to the increasing prevalence of glaucoma is the growth of the non-Caucasian older adult population. It is well known that race plays a role in glaucoma development, with minorities over-burdened by the disease. Over the next several decades, growth in the minority population will be most rapid in those under 65, but by 2050 minor-ities will make up 42% of the adult population over 65 and 33% of the population over age 85.4 Based on this, the number of minorities with glaucoma will exceed the number of non-Hispanic whites with the disease by the year 2035.5

Among adults over 40, African

Americans and Hispanics have between 50% and 300% higher odds of having glaucoma than do whites, at all ages.3 Glaucoma will be particularly significant among older Hispanics due to the exponential growth of this group. Hispanics accounted for 50% of the total growth in the entire US population between the 2000 and 2010 Census reports.6 This rapid growth will continue—the Hispanic population is expected to make up 20% of adults over 65 and 15% of adults over 85 by 2050.6

Other minority populations (Asians, Pacific Islanders, Ameri-can Indians, Native Alaskans) are expected to increase in numbers rel-ative to whites as well. Among this group, glaucoma risk is most well defined among Asian Americans. Older Asian populations have a risk of open-angle glaucoma estimated

100

90

80

70

60

50

40

30

20

10

02010 2015 2020 2025 2030 2035 2040 2045 2050

Projected Population Aged 65 and Over by Race for the United States: 2010 to 2050

White

Millions

Black AsianAmerican Indian and Alaska Native

Native Hawaiian and Other Pacific Islander

Two or More Races

Unless otherwise specified, data refer to population who reported a race alone. Populations for each race group include both Hispanics and non-Hispanics, as those of Hispanic ethnicity may be of any race. Source: US Census Bureau.


to be 6.6% for those over the age of 40. This rate is slightly higher than that seen among Latinos and much higher than that seen in non-Hispanic whites.7

In assessing glaucoma risk among the growing minority older adult population, it’s important to rec-ognize the difference between race and ethnicity. For purposes of the US Census, Hispanic is considered an ethnicity, not a race. The terms Hispanic and Latino are frequently used interchangeably. More specifi-cally, Latino refers to individuals with geographic ties to the Carib-bean and Central or South Amer-ica. Hispanic refers more broadly to those with Spanish ancestry or who are Spanish speakers. Latino ethnicity would include Portuguese-speaking Brazilians, whereas His-panic ethnicity would not.

When filing out Census forms, individuals may self-identify in a yes/no format as Hispanic/Latino or not Hispanic/Latino. A follow-up question allows individuals who answered yes to identify themselves among one of 23 subgroups largely based on country of origin.

There is a separate race question in the Census, where individual Hispanics may identify themselves as white, black, multiracial or other race. This leads to groups of Ameri-cans who identify themselves as Hispanic-whites, Hispanic-blacks or Hispanic of multiracial origin, among several other possibilities. The growth in the racial group identified as white in the US has largely been driven by Hispan-ics who self-identify their race as white.6

Importantly, the risk of devel-oping glaucoma is not the same among all Hispanic subgroups. Latinos have been found to have higher rates than other Hispanics.3 Among Latinos, Mexican-Ameri-

cans have generally been found to have a higher risk of open-angle glaucoma than do others who iden-tify themselves as Hispanic. It has been speculated that these differ-ences may be due to the degree of Native American ancestry among Hispanic subgroups.

The two major studies that looked at glaucoma among Hispan-ics (Proyecto VER) and Latinos (LALES) had significant differences in Native American admixture in their study cohorts. In Proyecto VER, 40% of participants had Native American ancestry, while just 5% of LALES participants did.8 The Mexican-American ethnic group is a key demographic, given that it is the largest among the growing US Hispanic/Latino popu-lation.

A similar issue is found among the population of older Asian Americans. While not as numerous as Hispanics and African Ameri-cans in the population, the number of older Asians is expected to triple in the US by 2050. Asians of Viet-namese and Chinese descent have a much higher risk of narrow-angle glaucoma than do other ethnic Asians.7 Americans of Japanese descent have a 10-fold higher risk of normal tension glaucoma than do other Asian subgroups.7

Why ethnicity and race impact glaucoma is unclear. There are a variety of anatomical, biochemical and genetic associations with the glaucomas that have been found to segregate by race and ethnicity without being exclusive to a single race. African Americans are known to have a greater likelihood of having thinner corneas, anatomi-cally larger optic discs and variant lamina cribrosa configurations compared to other ethnic groups.9 Mongolians, Indians and Chinese have been found to have differ-

ences in anterior chamber angle depth and configuration compared to other ethnic Asian groups and non-Asians.10 The ability to man-age ocular oxidative stress appears lower among African Americans.11

Latinos may have an inherently lower tolerance to factors relating intraocular pressure to blood pres-sure.8,9

Gene-wide association studies have identified a number of single nucleotide polymorphisms associ-ated with open-angle glaucoma, angle closure and normal tension that seem to segregate by race.12 It is entirely possible that race and ethnicity are simply markers for these and other, as-yet unknown biomarkers of glaucoma. Under-standing the race-based risk of glaucoma will become even more complex in the future as the num-ber people identified as multiracial grows.

A secondary effect of the increase in the number of minority glau-coma patients will be an increase in the number of years these indi-viduals will likely suffer from the disease. In addition to having a higher risk of glaucoma, African Americans and Hispanics begin to develop glaucoma at earlier ages than do whites.3 The prevalence of glaucoma in African Americans and Latinos is about 2% for those in their early 50s. It does not reach 2% for whites until age reaches the late 60s to early 70s.

At the other end of the glaucoma age continuum, life expectancy is longer for Hispanics and Asians than for other ethnic groups. Among those in the US population who live to 65, Hispanics have the longest remaining life expectancy of any ethnic group, at more than 20 years.4 At younger ages, African Americans have lower life expec-tancy than other ethnic groups;



however, among the oldest Ameri-cans—those 85 and older—there is a shift and African Americans have a slightly longer life expectancy than other racial groups.4 The end result will be a longer required treatment period.

Gender DistinctionsThe expected time course of the

disease is also impacted by gender. In studies done across the world, the absolute number of women with glaucoma exceeds that of men with the disease (a 60:40 ratio).13 The gender gap in glaucoma is largely due to the differential sur-vival of women and men.

At birth, across all racial and ethnic groups in the US population, women are expected to live about four to five years longer than men. The gap in the life expectancy of men compared to women narrows with advancing age over 65, but men never quite catch up in terms of expected survival, even among those men over 90.4

In terms of absolute risk, women have higher odds of developing narrow-angle glaucoma than do men. There is variation among ethnic groups, but most estimates place the gender risk at two to four times higher for women than men. The excess risk is largely attributed to the anatomically smaller anterior chambers found in women.13 The evidence for gender differences in open-angle glaucoma risk is less clear. Studies of gender differences in POAG when stratified by age and race or ethnicity produce rela-tively small numbers. This leads to wide estimate intervals, making interpretation of the exact gender impact difficult. Studies do indicate that women are more likely than men to become visually impaired from glaucoma.

The differential survival of

women gives them more years of disease exposure. Life expectancy alone does not account for all of the gender disparity in visual impair-ment associated with glaucoma, however. Socioeconomic and edu-cational opportunity is thought to play a role in this disparity, particu-larly outside of the US population.

Poverty StatusPoverty is associated with the

development of myriad health conditions. The question, “Does poverty lead to glaucoma?” has not been fully answered, but has had some study. The US govern-ment uses a metric the poverty-to-income ratio (PIR) as a measure of socioeconomic status. The PIR is a continuous measure that takes into account the income, expenses and family size. Those with PIR <1.0 have income below the federal poverty level for families, whereas those with PIR >4 are considered to have high income.

Elongation of the vertical cup/disc (CD) ratio is a hallmark sign of glaucoma. Many studies use the vertical cup/disc ratio at the 97.5th population percentile as

the cut point for a disc defined as glaucomatous. Within the overall US population, this level is a verti-cal CD ratio of 0.63.1 One study has compared the 97.5th percentile of vertical CD ratio among the US population at various PIR catego-ries. No differences in the vertical CD ratio size that defined glaucoma were found between PIR categories. This indicates that socioeconomic status does not seem to be related to early glaucoma.

This same study showed that PIR did have an impact on the vertical CD ratio at the 99.5th popula-tion percentile.1 As PIR category changed from high income to middle income to the poverty level, the vertical cup/disc ratio increased. This change is likely representative of an overall delay in the diagnosis of glaucoma or higher numbers of treatment failures for those in lower socioeconomic classes producing larger vertical CD ratios even at the most extreme range found within the population.

Studies in the United Kingdom and Canada have shown that those in lower socioeconomic classes are more likely to present with more

Percent Female for Older Population by Age for the United States: 2010, 2030 and 2050

2010

57 55 55 54 53 5258 56 55

6762 61

2030 2050

65 years and over 65 to 74 years 75 to 84 years 85 years and over

Source: US Census Bureau


advanced glaucoma at the time of the initial diagnosis.14 Lower socioeconomic status within the US population has been associated with lower medication adherence in studies using electronic drop monitoring.15 Race and age also appear to play a role with adher-ence, with African Americans and older adults showing lower adher-ence compared to younger adults and people of European ancestry.15

Insurance claims data monitoring in the US population has shown that half of all patients stop glaucoma medications within six months of initiating therapy and less than 40% fill prescriptions three years after diagnosis.16

Additionally, in the US popula-tion, those in lower socioeconomic classes are known to have lower utilization of eye care services.17

Education level and socioeconomic status are closely tied together, and lower eye care utilization rates are also seen in Americans with lower educational attainment.17

While not directly related to edu-cation level, health literacy (or the ability to understand health-related information) has been shown to play a role in glaucoma adher-ence. Glaucoma patients with poor health literacy are less likely to fill prescriptions and adhere to medica-tion dosage schedules, and more likely to miss scheduled appoint-ments.18

Simplified dosages schemes, improved doctor/patient commu-nication and better education have been shown to increase patient adherence in glaucoma treatment.19

Providing appropriate education and strategies to patients that are increasingly diverse will be an ongoing challenge for ODs.

The increasing diversity of the US population will present challenges in delivering care to patients with

glaucoma. The public health task is daunting. Current estimates are that 60% to 70% of glaucoma in the US population is undiagnosed.21 This may be even higher among the rap-idly growing Latino population.8

When taking into account the low levels of adherence to glaucoma medication regimens, as much as 80% of glaucoma in the US popu-lation may be untreated.20,21 This is despite the fact that more than double the number of patients estimated to have glaucoma in the US population report using drops for the disease or ocular hyperten-sion.20 This suggests that there is a nationwide issue of diagnostic accu-racy among both optometrists and ophthalmologists.

The Challenges AheadOptometrists need to be prepared

to see a larger and more diverse glaucoma population. To meet the coming demand, vastly greater numbers of the higher at-risk population will need to be screened. The absence of a simple screen-ing test for glaucoma means more comprehensive examinations with appropriate follow-up testing are going to be need to be provided by optometrists.

Larger societal issues, such as lower levels of health insurance coverage, higher levels of poverty and lower education level, will make reaching this population dif-ficult. Once glaucoma patients are diagnosed, optometrists as a group need to take a far greater role in treatment.

The use of culturally sensitive materials and approaches can help reach the ultimate goal of preven-tion of visual impairment in this rapidly changing segment of the patient population. ■

Dr. Swanson is an associate professor of optometry at the Uni-

versity of Alabama at Birmingham School of Optometry.

1. Swanson MW. The 97.5th and 99.5th Percentile of Vertical Cup Disc Ratio in the United States Optometry & Vision Sci-ence: January 2011, Vol. 88, Issue 1, pp. 86-92 doi:10.1097/OPX.0b013e3181fc36382. Vincent GK, Velkoff VA. The Next Four Decades, The Older Population in the United States: 2010 to 2050, Current Popula-tion Reports.2010, U.S. Census Bureau, Washington, DC P25-1138.3. Klein R, Klein BE. The prevalence of age-related eye diseases and visual impairment in aging: current estimates. Invest Ophthalmol Vis Sci. 2013 Dec 13;54(14): doi: 10.1167/iovs.13-12789.4. Arias E. United States Life Tables, 2009. National Vital Sta-tistics Reports, Vol. 62, No. 7, January 6, 2014 . 5. Vajaranant TS, Wu S, Torres M, Varma R. The changing face of primary open-angle glaucoma in the United States: demographic and geographic changes from 2011 to 2050. Am J Ophthalmol. 2012 Aug;154(2):303-314.e3. doi: 10.1016/j.ajo.2012.02.024. Epub 2012 Apr 27.6. Ennis SR, Ríos-Vargas M, Albert NG. The Hispanic Popula-tion: 2010 Census Briefs. Issued May 2011C2010BR-04 Available at www.cdc.gov/nchs/data/nvsr/nvsr62/nvsr62_07.pdf. Accessed 6/2/2014. 7. Stein JD. Differences in Rates of Glaucoma among Asian Americans and Other Racial Groups, and among Various Asian Ethnic Groups Ophthalmology; 2011:1031-7.8. Kim E, Varma R. 9. Arch Ophthalmol. Glaucoma in Latinos/Hispanics.Current Opinion in Ophthalmology 2010 ;21:100–105. doi:10.1001/archopht.123.4.527.9. Karmel M. Glaucoma in the African American and Latino Communities. EyeNet Available at www.aao.org/publications/eyenet/201006/glaucoma.cfm. Accessed July 1, 2014. 10. Aung T, Winifred P, Nolan WP, et al. Anterior Chamber Depth and the Risk of Primary Angle Closure in 2 East Asian Populations FREE Arch Ophthalmol. 2005;123(4):527-32. doi:10.1001/archopht.123.4.527.11. Siegfried CJ, Shui YB, Holekamp NM, et al. Racial Differ-ences in Ocular Oxidative Metabolism, Implications for Ocular Disease. Arch Ophthalmol. 2011;129(7):849-54. doi:10.1001/archophthalmol.2011.16912. Chandra A, Mitry D, Wright A, et al. Genome-wide association studies: applications and insights gained in Oph-thalmology.Eye advance online publication 27 June 2014; doi: 10.1038/eye.2014.14513. Vajaranant TS1, Nayak S, Wilensky JT, Joslin CE. Gender and glaucoma: what we know and what we need to know. Curr Opin Ophthalmol. 2010 Mar;21(2):91-9. doi: 10.1097/ICU.0b013e3283360b7e14. Buys YM, Jin YP; Canadian Glaucoma Risk Factor Study Group. Socioeconomic status as a risk factor for late pre-sentation of glaucoma in Canada. Can J Ophthalmol. 2013 Apr;48(2):83-7. doi: 10.1016/j.jcjo.2012.10.00315. Dreer LE, Girkin C, Mansberger SL. Determinants of medication adherence to topical glaucoma therapy. J Glaucoma. 2012 Apr-May;21(4):234-40. doi: 10.1097/IJG.0b013e31821dac8616.Nordstrom BL, Friedman DS, Mozaffari E, et al. Persistence and adherence with topical glaucoma therapy. Am J Ophthal-mol. 2005 Oct;140(4):598-606.17. Zhang X, Beckles GL, Chou CF, et al. Socioeconomic dis-parity in use of eye care services among US adults with age-related eye diseases: National Health Interview Survey, 2002 and 2008. JAMA Ophthalmol. 2013 Sep;131(9):1198-206. doi: 10.1001/jamaophthalmol.2013.469418. Muir KW, Christensen L, Bosworth HB. Health literacy and glaucoma. Curr Opin Ophthalmol. 2013 Mar;24(2):119-24. doi: 10.1097/ICU.0b013e32835c8b0e19. Okeke CO, Quigley HA, Jampel HD, et al. Interventions improve poor adherence with once daily glaucoma medications in electronically monitored patients. Ophthalmology. 2009 Dec;116(12):2286-93. doi: 10.1016/j.ophtha.2009.05.026. Epub 2009 Oct 7.20. Swanson MW. Undiagnosed and Over Diagnosed glau-coma in the United States. Invest Ophthalmol Vis Sci 2012;53: ARVO E-Abstract 6379/A1721. Varma R, Ying-Lai M, Francis BA, et al; Los Angeles Latino Eye Study Group. Prevalence of open-angle glaucoma and ocular hypertension in Latinos: the Los Angeles Latino Eye Study. Ophthalmology. 2004 Aug;111(8):1439-48.


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Glaucoma on Trial: Clinical Implications of the Landmark Glaucoma Studies

Release Date: July 2014Expiration Date: July 1, 2017Goal Statement: Major glaucoma studies have asked the perplexing diagnostic and treatment questions that clinicians face each day. This course reviews these landmark clinical trials and highlights the clinical implications and practical usage of each study for optom-etrists.Faculty/Editorial Board: David Lynne, OD, Maria Mandese, OD, and

Erika Walker, ODCredit Statement: COPE approval for 2 hours of CE credit is pending for this course. Check with your local state licensing board to see if this counts toward your CE requirement for relicensure.Joint-Sponsorship Statement: This continuing education course is joint-sponsored by the Pennsylvania College of Optometry.Disclosure Statement: Drs. Lynne, Mandese and Walker have no financial relationships to disclose.

A51-year-old white female presented for a routine eye examination. She had no visual or ocular complaints,

and her visual acuity was 20/20 in each eye. But her intraocular pres-sure measured 25mm Hg OD and 26mm Hg OS. Her angles were open to the ciliary body on goni-oscopy, and her corneal thickness measured 477µm OD and 473µm OS.

Dilated fundus exam revealed cup-to-disc ratios of 0.55 OD and 0.60 OS. Optical coherence tomog-raphy (OCT) found the nerve fiber layer in each eye to be within nor-mal limits.

The patient returned in a month for further glaucoma workup. IOP

on that visit was 26mm Hg OD and 24mm Hg OS. Visual field results showed no significant defects OD and early inferior arcuate defect OS.

The patient returned for repeat visual field testing on the left eye, which now showed reduced depres-sions with good reliability.

Now what do we do? Should this patient—with moderately high IOP and thin corneas but relatively nor-mal visual field results and OCT of the nerve fiber layer—be treated?

In order to answer these ques-tions, and to understand the behav-ior of glaucoma and the correct treatment for its various offenses, glaucoma has been put on trial—clinical trial, that is. While expen-sive and time consuming, these

clinical trials are the gold standard for evaluating glaucoma therapies and management strategies, and their results have the power to influ-ence clinical practice.1

These landmark glaucoma stud-ies have asked the difficult diag-nostic and treatment questions that clinicians face each day: How do you deal with ocular hyperten-sion or early glaucoma? What is the best initial treatment for glau-coma? What do you do to manage advanced glaucoma? How do you best treat normal-tension glaucoma? And, what is the role of laser in glaucoma treatment?

To reach a verdict, let’s look at the results of several landmark glau-coma studies.

Treatment without evidence is like taking a shot in the dark. These major studies provide proof to apprehend the ‘sneak thief of sight.’ By David Lynne, OD, Maria Mandese, OD, and Erica Walker, OD

EARN 2 CE CREDITS (COPE approval pending)


OPTOMETRIC STUDY CENTER


To Treat or Not to Treat? EMGT

The Early Manifest Glaucoma Trial (EMGT) was the first ran-domized, clinical glaucoma trial to address whether treating or not treating intraocular pressure in patients with newly diagnosed pri-mary open-angle glaucoma (POAG) could delay disease progression.2

Researchers in Sweden recruited 255 participants between ages 50 to 80 with early POAG, visual field defects and median IOP of 20mm Hg. Testing included full-threshold automated 30-2 visual fields and tonometry every three months as well as optic nerve head photos every six months. Progression was defined as greater than or equal to three consecutive points decreased from baseline visual field in three different consecutive tests. The treat-ment group received full 360° laser trabeculoplasty plus Betimol (betax-olol, Alcon) twice daily.

At the end of the study, EMGT showed that IOP reduction delayed disease progression in POAG. Spe-

cifically, treatment reduced IOP by 25% on average (from 20.6mm Hg at baseline to 15.5mm Hg at the three-month visit), which was maintained throughout six years of follow up.

“The magnitude of this depen-dence on IOP change was impres-sive: an estimated 10% decrease in risk of progression with each milli-meter of mercury of IOP reduction,” the authors wrote.2

The study also provided a long-term comparison for the progression rate between treated and untreated patients with POAG. Progression was less frequent in the treatment group (45%) and occurred later than in the controls (62%).2

However, the study had several limitations: a homogeneous popula-tion (only whites), inclusion of only early glaucoma patients, exclusion of those with high IOP and advanced glaucoma, and no long-term follow-up of patients who displayed glau-coma progression beyond the study period.

Conclusion: The EMGT showed

that IOP-lowering treatment offers beneficial effects by significantly delaying progression.

Clinical implications: • Even small reductions in IOP

can make a difference. “Every 1mm of IOP reduction was associated with a risk reduction of 10% to 13%, depending on the analysis,” says lead author Anders Heijl, MD, PhD.3

• But that doesn’t necessarily mean all patients must be treated. Because we can’t know which patients will progress, in some cases, we can observe closely and tailor management to the individual patient. In particular, “It’s beneficial to lower pressure in patients pro-gressing quickly, even if IOP levels have been in the range of 15 to 18mm Hg,” Dr. Heijl says.

OHTSBefore the Ocular Hypertension

Treatment Study (OHTS), we had no consensus on whether to treat or to observe patients who had elevat-ed IOP but no glaucomatous

A 51-year-old white female presented for a routine eye exam, but her intraocular pressure measured 25mm Hg OD and 26mm Hg OS. Her corneas were thin and her cup-to-disc ratios were 0.55 OD and 0.60 OS. Does this patient have glaucoma? And if so, should she be treated? The answers may be found in the landmark glaucoma studies, such as the Ocular Hypertension Treatment Study.



damage—otherwise known as ocular hypertensives or glaucoma suspects. Treatment might prevent nerve fiber loss in some patients, but then again we could be unnecessar-ily medicating many suspects who might never convert to glaucoma.

Enter OHTS. The study’s purpose was to evaluate the safety and effi-cacy of topical ocular hypotensive medication in delaying or preventing the onset of POAG in individuals with elevated IOP.

OHTS enrolled a total of 1,636 participants, ages 40 to 80, who had no evidence of glaucomatous dam-age but whose IOP was elevated—between 24mm to 32mm Hg in one eye and 21mm to 32mm Hg in the other eye. (Because glaucoma is the leading cause of blindness in blacks, investigators made sure that 25% of the patient sample was of African-American origin.) The overall treat-ment goals were to reduce IOP by 20% or more and reach an IOP of 24mm Hg or less.4

Progression was defined more

stringently than in similar studies. OHTS required three abnormal visual fields to confirm a defect as well as clinically significant changes to the optic disc neuroretinal rim.

During the five-year study period, an IOP reduction was achieved in 22.5% (+/-9.9%) of the medication group and 4% (+/-11.6%) of the observation group. At the end of the study, the probability of developing POAG was 4.4% in the medication group and 9.5% in the observation group.4

Conclusion: This study shows strong evidence that lowering IOP in ocular hypertensive patients delays or even prevents the onset of POAG.

The study also identified which factors are more predictive for the development of POAG: older age, larger vertical or horizontal cup-to-disc ratio, higher IOP, greater Hum-phrey visual field pattern standard deviation, and thinner corneal thick-ness measurement.5

Clinical implications: • Not all patients with high IOP

require hypotensive treatment. Con-sider all factors—such as the age and health of the patient, as well as the condition of the disc, visual field testing results, optical coherence tomography, family history, corneal hysteresis, clinical appearance and pachymetry—before starting ocular medications.

• Subjects with corneal thickness of 555µm or less had three times the risk of developing primary open-angle glaucoma compared with those who had corneal thickness of 588µm or more. Therefore, measure central corneal thickness of all new glaucoma suspects.5

• Investigators concluded it is possible to separate ocular hyper-tensive patients into categories of high, medium and low risk. “The ocular hypertensive patients at high risk may benefit from close follow-up and some from early treatment, whereas the low-risk patients can have less frequent follow-up and may not need early treatment,” said OHTS principal investigator Michael A. Kass, MD.3

CIGTSWhen treating patients with

open-angle glaucoma, an important decision concerns choosing an IOP-lowering treatment method. Have you ever wondered whether your patients would have better outcomes if you chose one treatment initially vs. another? Would immediate surgi-cal intervention ever be warranted?

The Collaborative Initial Glau-coma Treatment Study (CIGTS) attempted to determine whether patients with newly diagnosed open-angle glaucoma would be bet-ter managed using IOP-lowering medications or having an immediate trabeculectomy.6

The study involved 607 patients with an IOP of 20mm Hg or greater, as well as optic nerve damage and/or visual field (VF) loss in one or both

OCT scans in our patient found the nerve fiber layer in each eye to be within normal limits. Does this mean she won’t convert to glaucoma? Again, we must look to the studies for insight.


eyes. The patients were randomly assigned to either initial treatment with a stepped regimen of topical medications or trabeculectomy. The main outcome measure used was progression of VF loss. In addition, a secondary measure—a health-related quality of life question-naire—looked at how the treatment affected the patient’s lifestyle.7

After five years, the results showed that both treatment groups had a substantial reduction of IOP (48% in the surgical group, 35% in the topical medication group) and no significant difference in their rates of VF progression.6,8 As expected, the surgical group was much more likely to develop a cata-ract, which affected their VF results. Patients who were older, diabetic, non-white, required cataract surgery and had more advanced VF loss at baseline were more likely to have VF loss progression.6 Those with greater IOP fluctuations (more often if treat-ed with topical medication initially) also had more VF progression.9

Interestingly, after more than eight years of follow-up, those patients with mild VF loss at baseline also did equally well in either treatment group.9 However, the patients with more advanced loss at baseline (with the exception of non-whites and those with diabetes) had better results with initial trabeculectomy, and major surgical complications were few.9

Conclusion: “When aggressive treatment aimed at substantial reduction in IOP from baseline is used, loss of visual field can be seen to be minimal in general,” the researchers wrote.6,10

The results also revealed that either treatment had a remarkably similar effect on patients’ quality of life. Though not associated with a particular treatment group, the fear of blindness was common, affect-ing 34% at diagnosis.11 Patients

who reported a decrease in visual functioning were more likely to experience depression and mood changes.12

Clinical implications: • Both topical and surgical inter-

ventions are safe and effective in treating most OAG patients. While this may not signal a major shift in glaucoma treatment, consider surgi-cal intervention earlier for patients with more advanced disease at the time of diagnosis (excluding non-whites and those with diabetes).

• It is very important to educate patients on glaucoma. Reassure patients that with proper treatment and follow-up, the risk of blindness is low, especially if the diagnosis is made before the disease is advanced.

Normal-Tension Glaucoma: How Low Can You Go? CNTGS

Lowering IOP in patients with normal-tension glaucoma (NTG) can be challenging. Is it even worth trying to lower an already-low IOP?

The Collaborative Normal-Tension Glaucoma Study (CNTGS) provided some valuable insight. The study, published in 1998, set out to determine whether IOP plays a role in NTG, and if lowering IOP in NTG patients can slow disease progression.

Investigators randomized 145 glaucoma patients, who had a median IOP of 20mm Hg or less in 10 baseline readings, into a treat-ment group and a non-treatment group.13 Patients in the treatment group were given medications, laser trabeculoplasty, filtration surgery or any combination in order to reduce the IOP by 30%. The main out-come measure used was visual field progression from baseline. Progres-sion was confirmed on two of three visual fields within one month, and verified on two of three visual fields done three months later.

After five to seven years of follow-up, the results showed that by decreasing IOP 30%, glaucoma progression could be reduced by 50%. The 30% reduction of IOP was achieved about 50% of the time using medication (pilocarpine or systemic CAI) and laser trabecu-loplasty.14 Cataracts developed in 38% of treated patients, predomi-nately those undergoing filtering surgery, and in 14% of non-treated patients.13

The study further looked at the natural course of NTG and found that progression in untreated patients was quite variable. More than 50% showed no progression after five to seven years, while oth-ers progressed quickly, threatening blindness.13

So, how is an eye care pro-vider to know who will progress and who will remain stable? The study revealed some risk factors to help predict those who are at risk for faster progression: history of migraine, female gender and the presence of a disc hemorrhage at diagnosis.

Conclusion: While there is still much to learn about NTG, the CNTGS clearly demonstrated that IOP plays a role in NTG and that, in such patients, the disease (or at least visual field progression) can be slowed by lowering IOP at least 30%.

Clinical implications: • Because of the variable natural

course of NTG, it is important to distinguish between patients who have progressive vs. non-progressive disease. In cases of mild NTG, consider monitoring until progres-sion is confirmed. However, factors that weigh more heavily for treat-ment are female gender, history of migraine and disc hemorrhage at diagnosis.

• When you suspect progression, be sure to confirm that it is actual



progression and not testing variabil-ity. This may require multiple visual fields to prevent over-diagnosing progression.

• Once the decision is made to begin treatment, set a goal (at least 30% IOP reduction) and be diligent in attaining it. The large arsenal of IOP-lowering medications available today makes this goal much more achievable without surgery.

LoGTSHave you ever been faced with

a chronic open-angle glaucoma patient with visual field loss, optic nerve/retinal nerve fiber layer loss and “normal” intraocular pressure? Have you wondered which hypo-tensive drop would best preserve the patient’s visual field?

The Low-Pressure Glaucoma Treatment Study (LoGTS) attempted to answer this question.15 The study, published in 2011, compared twice-daily brimonidine 0.2% vs. twice-daily timolol 0.5% to determine if either was better at preserving visual function.

Results showed a similar IOP

reduction for each medication. Not surprisingly, 28 of the 99 patients in the brimonidine arm of the study dropped out due to drug-related adverse events, compared with only nine of the 79 timolol patients. What was surprising was that patients on brimonidine had less visual field loss (9.1%) compared with patients on timolol (39.2%) during an average of 30 months.

Why did this happen? Was it due to a beneficial effect of brimonidine or a negative effect of timolol? Glau-coma experts cannot seem to agree, and questions abound.

Supporters of brimonidine point to the laboratory data indicating that alpha-2 agonists may be neu-roprotective. However, patients tended to stop using brimonidine due to adverse reactions such as burning and irritation, leading to poor adherence.15

Detractors of brimonidine say that the results in this study may be due to unique properties found in this group of patients only. Data may have been skewed due to the high number of patients dropping

out of the brimonidine group. Also, the IOP-lowering effect of each medication was not to the level believed to be the standard of care. No therapeutic goal for either medication had been set. Patients simply had to have their IOP remain below 21mm Hg. Baseline untreated IOP was just over 15mm Hg and the mean treated IOP was around 14mm Hg. Additionally, timolol, used to treat glaucoma since 1978, has been shown to preserve vision compared to no treatment as long as the IOP is lowered sufficiently.16 Timolol was also shown to be effective in the Ocular Hyperten-sion Treatment Study and the Early Manifest Glaucoma Trial. Finally, diurnal IOP analysis was not done.

Conclusion: LoGTS found that low-pressure glaucoma patients treated with brimonidine are less likely to have field progression than patients treated with timolol. But, before jumping on the possible neuroprotective bandwagon of bri-monidine, or abandoning timolol as a treatment for normal-tension glaucoma patients, it may be best

Our patient’s visual field results showed a full inferior arcuate defect OD and an early inferior arcuate defect OS. Is it time to begin medication? Not just yet. Repeat visual field testing is in order first.


to wait and see if these results are repeatable in future studies.

Clinical implications: • For now, optometrists should

use the therapy that reduces IOP in normal-tension patients to signifi-cant levels (minimum 30%), and modify treatment if the optic nerve, retinal nerve fiber layer or visual field changes.

• Prostaglandins have superb efficacy and less effect than other agents in lowering heart rate. These should be used as a first-line treat-ment whenever possible.

• Remember to check blood pres-sure and heart rate before initiating treatment with a beta-blocker such as timolol. Also, check if the patient is already taking a systemic beta-blocker.

• Be sure that patients use timolol earlier in the evening rather than before bedtime to avoid the hypo-tensive effect that might compro-mise ocular blood flow and induce systemic hypotension.

Laser Treatment: First-line Therapy?GLT and SLT/Med Studies

The Glaucoma Laser Trial (GLT) and the GLT Follow-up Study compared newly-diagnosed POAG patients treated with medical thera-py vs. those treated with argon laser trabeculoplasty (ALT).17,18 Patients were followed 2.5 to 5.5 years.

Two-year results showed that patients treated initially with ALT had lower IOP (1.2mm Hg lower on average) compared to patients who were initially medicated. Eyes that had initial ALT had a better visual field and better ONH status during the 5.5 years than fellow eyes treated initially with topical medications.

Keep in mind that this was prior to the advent of prostaglandins, CAIs or alpha-agonists. So, upon completion of the study, 56% of the

laser patients and 70% of the medi-cation patients needed additional treatment (more medication, laser or surgery) to reduce the IOP.

The GLT Follow-up Study evaluated 203 of the original 271 patients of the GLT for six to nine years. Seven-year results showed that IOP, visual fields and ONH status were all similar between ALT-first and medication-first groups.

Critics of the GLT study have pointed out that timolol used in one eye of the study may have had a crossover effect on the contralateral eye that was treated with ALT, thus introducing bias for the ALT-treated eyes. Also, they note that the effects of ALT have been shown to wear off over time.18

Several years later, the SLT/Med Study compared 360° selective laser trabeculoplasty (SLT) to drug thera-py (prostaglandin analog) as initial treatment for open-angle glaucoma or ocular hypertension.19 Target intraocular pressure was set for each group according to the CIGTS formula. Fifty-four patients (29 SLT, 25 medical) reached the nine- to 12-month follow-up. Baseline IOPs as well as the IOP at the last follow-up were similar between the groups (24.5mm Hg reduced to 18.2mm Hg for SLT vs. 24.7mm Hg reduced to 17.7mm Hg for medicine). Addi-tional treatment was necessary in 11% of the SLT group vs. 27% in the medicated group. Unfortunately, the SLT/Med Study was only for a year, so long-term data is unknown.

Conclusion: These studies found that initial treatment with laser tra-beculoplasty is at least as efficacious as initial treatment with topical medication for patients with open-angle glaucoma.

Clinical implications: • When choosing an initial treat-

ment, offer your patient the option of starting with either medication or laser trabeculoplasty (now SLT).

• Be sure to discuss the pros and cons of each treatment. All of our topical medications have potential side effects; discuss the most com-mon for the medication you would prescribe. Likewise, laser trabecu-loplasty is not without risk, and patients should be made aware that they could have a spike in pressure after the procedure that may require medication or surgery to lower the pressure as well as possible inflam-mation leading to pain, redness and transient blurred vision.

• Should the patient choose medi-cation, the optometrist should begin treatment. If the patient chooses SLT, refer the patient to someone who has the experience and capabil-ity to perform the procedure. (If you practice in Oklahoma, Kentucky or Louisiana, this may be you.) Make sure the patient understands that the treatment may not work, may wear off, and that additional laser or drops may be necessary if progres-sion occurs.

Surgical Intervention: Don’t Let Glaucoma Rob You BlindAGIS

While there is no cure for glau-coma, our current therapies are all aimed toward a simple goal: to preserve visual function—that is, visual field and visual acuity. How-ever, determining the best path to reaching this seemingly simple goal can be frustratingly complex. Even when patients are compliant, medi-cal therapies can fail, and glaucoma can progress to advanced stages despite our best efforts.

The Advanced Glaucoma Inter-vention Study (AGIS) was designed to determine the best sequence of surgical interventions in patients when medical therapies had failed.20 Some 789 eyes were randomly assigned to one of two intervention sequences. One sequence began with argon laser trabeculoplasty (ALT)



and the other began with trabecu-lectomy. If ALT failed in the first sequence, trabeculectomy was per-formed as the second procedure in that sequence. In the other sequence that began with trabeculectomy, failure dictated that ALT would next be performed.

In both sequences, if needed, another trabeculectomy was done as the third intervention.21 Keep in mind, this study began recruitment in the late 1980s so SLT and tube-shunt procedures had not yet been introduced.

Conclusion: Although not origi-nally predicted, racial differences in treatment outcomes became appar-ent upon analysis of the AGIS data.22 The treatment sequence that began with trabeculectomy did show a greater decrease in IOP regardless of race. However, black patients in the treatment sequence who began with ALT had greater preservation of visual field and visual acuity

than those who began with tra-beculectomy. In contrast, white patients in the sequence who began with trabeculectomy had greater pres-ervation of visual field on long-term follow-up than those who began with ALT.21 Therefore, researchers con-cluded that visual function was best preserved when black patients began with ALT and when white patients began with trabeculec-tomy.21

Effects of IOP on visual field progression were also specifically evaluated from AGIS data, and it was found that patients with an average IOP of greater than 17.5mm Hg had greater worsening of their visual fields than those with an average IOP of less than 14mm Hg.23 AGIS was one of the first studies to show that lower mean IOP results in a decreased risk of visual field progression.

Clinical implications: • Each patient requires individu-

alized care. AGIS demonstrated that race is an important consideration for surgical intervention in advanced glaucoma. This is not to say, for instance, that a white patient with medically-uncontrolled glaucoma should only be offered the option of trabeculectomy. Potential operative complications associated with the more invasive surgery may sway the patient toward laser intervention as a first option. Conversely, a black patient presented with the option of

laser intervention should be warned of the likely future need for both additional medications and addi-tional glaucoma surgery after the laser procedure is completed.21

• There is no magic number for target IOP. Patients in the AGIS group who consistently maintained IOP less than 18mm Hg at every visit over six years, with mean IOP of 12.3mm Hg as a group, had good preservation of visual field—yet a number of patients in this group still showed progressive visual field loss.23

TVT StudyWhen medical and laser therapy

fail in glaucoma, we are left with several surgical options. Trabecu-lectomy and tube-shunt implanta-tion are the two most common glaucoma surgeries worldwide.24

When patients have already under-gone previous intraocular surgery, which procedure should glaucoma surgeons choose?

Until 1995, glaucoma surgeons generally preferred trabeculectomy to the newer tube-shunt procedure, primarily used at that time only for high-risk eyes. However, Medicare claims data between 1995 and 2004 showed a 184% increase in tube-shunt surgery, revealing a paradigm shift in the approach to glaucoma surgical intervention.25

The Tube Versus Trabeculectomy (TVT) study was introduced as an evidence-based approach to either support or invalidate this para-digm shift and to observe whether tube-shunt implantation offered advantages over trabeculectomy in patients who had undergone previ-ous ocular surgery (specifically cataract extraction and/or previous failed trabeculectomy).

In eyes randomized to the tube group, surgeons placed a Baerveldt glaucoma implant in the superotem-poral quadrant, while all eyes in the

When our patient returned for repeat field testing of the left eye, it now showed marked improvement. Still, given the patient’s relatively young age, her large cup-to-disc ratios, her thin cor-neas and elevated IOP readings, we decided to begin medication after discussing the options with her.


trabeculectomy group underwent trabeculectomy with adjunctive use of mitomycin C.26

Conclusion: While both pro-cedures generally produced a sig-nificant and sustained reduction in IOP and both procedures showed reduced postoperative dependence on glaucoma medications, the trabeculectomy group had a sig-nificantly higher failure rate after five years of follow-up.24 The most common reason for failure was inadequate IOP reduction (IOP >21mm Hg or not reduced by 20% below baseline). Significantly higher failure rates remained in the trab-eculectomy group even when more stringent IOP criteria were applied (upper IOP limit of 17mm or 14mm Hg). Additionally, glaucoma reop-eration was needed more frequently in the trabeculectomy group.25

While TVT answered its intended inquiry, the results have spurred follow-up questions. Are the advan-tages seen with tube-shunt place-ment maintained when the patient has not undergone any previous ocular surgery? In other words, should tube-shunt placement be considered as a primary surgery option for glaucoma? A new study, the Primary Tube Versus Trabecu-lectomy Study, hopes to answer these questions; results are expected in April 2016.27

Clinical implications: • The researchers maintain that

the TVT study does not dem-onstrate clear superiority of one glaucoma operation over the other, but that both surgeries are viable options.24

• Potential pitfalls exist with the use of tube shunts. Subsequent surgical options after failure of tube-shunt devices become lim-ited—surgeons are left with the choice of a second, inferiorly placed tube or cyclophotocoagulation.28 Also, some patients are not com-

fortable with the idea of a tube-shunt device “or what they perceive as hardware in their eye,” says Brian Francis, MD, a contributing investigator in the TVT study.28

• Trabeculectomy is not without its travails. It requires the surgeon to tailor the procedure to each patient (i.e., number of scleral flap sutures and dosage of an antifi-brotic agent) whereas tube-shunt surgery is a more “standardized procedure” according to TVT lead author Steven Gedde, MD.28 Also, trabeculectomies require more fre-quent and more vigilant postopera-tive care than tube shunts.

Glaucoma has taken the stand. We have heard its testimony. Now, it is time to render our verdict.

In our patient’s case, the decision to treat or not to treat was influ-enced by the OHTS findings. An argument could be made to monitor our patient because she is relatively young, had full visual fields and normal OCT findings. However, our patient also had large cup-to-disc ratios, elevated IOP readings and very thin pachymetry measure-ments. OHTS has shown us how significant corneal thickness is in the development of glaucoma.

Based on all of the findings and after discussion with our patient, we made the decision to begin med-ical treatment with a prostaglandin.

Now, six years later, her IOP remains well controlled and her optic nerves and visual fields are stable. Would she have been the same had we not treated her? Pos-sibly, but we can’t know. Ultimately, treatment decisions, while guided by information learned from the landmark glaucoma studies, must be based on each individual patient and their optometrist’s best clinical judgment. ■

Drs. Lynne, Mandese and Walker are on staff at the Orlando VA

Medical Center in Florida. Thanks to John Spalding, OD,

also at the Orlando VA Medical Center, for contributing to this article.

1. Chew EY. The value of randomized clinical trials in ophthalmology. Am J Ophthalmol. 2011 Apr;151(4):575-8.2. Heijl A, Leske MC, Bengtsson B, et al; Early Manifest Glaucoma Trial Group. Reduction of intraocular pressure and glaucoma progression: results from the Early Manifest Glaucoma Trial. Arch Ophthalmol. 2002 Oct;120(10):1268-79.3. Stuart A. Landmark glaucoma studies: Key findings and treatment lessons. EyeNet. 2012 Mar 22;16(3):49-55.4. Kass MA, Heuer DK, Higginbotham EJ, et al. The Ocular Hyperten-sion Treatment Study: A randomized trial determines that topical ocu-lar hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002 Jun;120(6):701-13.5. Gordon MO, Beiser JA, Brandt JD, et al. The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002 Jun;120(6):714-20; discussion 829-30.6. Lichter PR, Musch DC, Gillespie BW, et al. CIGTS Study Group. Interim clinical outcomes in the Collaborative Initial Glaucoma Treat-ment Study comparing initial treatment randomized to medications or surgery. Ophthalmology. 2001 Nov;108(11):1943-53.7. Janz NK, Wren PA, Lichter PR, et al; CIGTS Study Group. The Collaborative Initial Glaucoma Treatment Study: interim quality of life findings after initial medical or surgical treatment of glaucoma. Ophthalmology. 2001 Nov;108(11):1954-65.8. Musch DC, Gillespie BW, Lichter PR, et al.; CIGTS Study Group. Visual field progression in the Collaborative Initial Glaucoma Treatment Study the impact of treatment and other baseline factors. Ophthalmology. 2009 Feb;116(2):200-7.9. Musch DC, Gillespie BW, Niziol LM, et al.; CIGTS Study Group. Intraocular pressure control and long-term visual field loss in the Collaborative Initial Glaucoma Treatment Study. Ophthalmology. 2011 Sep;118(9):1766-73.10. Wishart PK. Interpretation of the glaucoma “landmark studies.” Br J Ophthalmol. 2009 May;93(5):561-2.11. Janz NK, Wren PA, Guire KE, et al.; CIGTS Study Group. Fear of blindness in the Collaborative Initial Glaucoma Treatment Study: patterns and correlates over time. Ophthalmology. 2007 Dec;114(12):2213-20.12. Jampel HD, Frick KD, Janz NK, et al.; CIGTS Study Group. Depression and mood indicators in newly diagnosed glaucoma patients. Am J Ophthalmol. 2007 Aug;144(2):238-244.13. Collaborative Normal-tension Glaucoma Study Group. Compari-son of glaucomatous progression between untreated patients with normal-tension glaucoma and patients with therapeutically reduced intraocular pressures. Am J Ophthalmol. 1998 Oct;126(4):487-97.14. Anderson DR; Normal Tension Glaucoma Study. Collaborative Normal-tension Glaucoma Study. Curr Opin Ophthalmol. 2003 Apr;14(2):86-90.15. Krupin T, Liebmann JM, Greenfield DS, et al; Low-Pressure Glau-coma Study Group. A randomized trial of brimonidine versus timolol in preserving visual function: results from the Low-Pressure Glau-coma Treatment Study. Am J Ophthalmol. 2011 Apr;151(4):671-81. 16. Epstein DL, Krug JH, Hertzmark E, et al. A long-term clinical trial of timolol therapy versus no treatment in the management of glau-coma suspects. Ophthalmology. 1989 Oct;96(10):1460-7.17. Glaucoma Laser Trial Research Group. The Glaucoma Laser Trial (GLT). 2. Results of argon laser trabeculoplasty versus topical medi-cines. Ophthalmology. 1990 Nov;97(11):1403-13.18. Glaucoma Laser Trial Research Group. The Glaucoma Laser Trial (GLT) and glaucoma laser trial follow-up study: 7. Results. Am J Ophthalmol. 1995 Dec;120(6):718-31.19. Katz LJ, Steinmann WC, Kabir A, et al.; SLT/Med Study Group. Selective laser trabeculoplasty versus medical therapy as initial treatment of glaucoma: a prospective, randomized trial. J Glaucoma. 2012 Sep;21(7):460-8.20. The AGIS Investigators. The Advanced Glaucoma Intervention Study (AGIS): 1. Study design and methods and baseline charac-teristics of study patients. Control Clin Trials. 1994 Aug; 15(4): 299-325.



Y ou can obtain transcript-quality continuing education credit through the Optometric Study Center. Com-

plete the test form (page 59), and return it with the $35 fee to: Optometric CE, P.O. Box 488, Canal Street Station, New York, NY 10013. To be eligible, please return the card within one year of publication.

You can also access the test form and submit your answers and payment via credit card at Review of Optometry online, www.revoptom.com.

You must achieve a score of 70 or higher to receive credit. Allow eight to 10 weeks for processing. For each Optomet ric Study Center course you pass, you earn 2 hours of transcript-quality credit from Pennsyl vania College of Optometry and double credit toward the AOA Optom et ric Recog nition Award—Cate gory 1.

Please check with your state licensing board to see if this approval counts toward your CE requirement for relicensure.

1. The Early Manifest Glaucoma Trial showed intraocular pressure reduction delayed disease progression in cases of POAG. Specifically, treatment reduced IOP by what percentage on average?a. 20%.b. 25%.c. 30%.d. 40%.

2. Which one of the following was NOT a limitation of the Early Manifest Glaucoma trial?a. Moderate glaucoma patients were excluded.b. It included a homogeneous population.c. Inclusion of patients with high IOP.d. Exclusion of patients with advanced visual field loss.

3. The treatment goal in the Ocular Hypertension Treatment Study was to reduce IOP by: a. 25% and less than 24mm Hg.b. 20% and less than 24mm Hg.c. 25% and less than 20mm Hg.d. 30% and less than 24mm Hg.

4. All of the following factors should be con-sidered as reasons to lower IOP in ocular hypertensives EXCEPT:a. Repeatable Humphrey visual field SITA standard 24-2 tests showing a superior

arcuate defect.b. Corneal thickness thinner than 555µm.c. A normal OCT. d. Significant nerve fiber layer damage of the neuroretinal rim of the optic nerve.

5. The Collaborative Initial Glaucoma Treatment Study (CIGTS) evaluated which glaucoma treatment method?a. Observation vs. topical medication.b. Topical medication vs. SLT/ALT.c. SLT/ALT vs. trabeculectomy.d. Trabeculectomy vs. topical medication.

6. The primary outcome measure for the CIGTS was:a. A 30% reduction in IOP.b. Progression of visual field loss.c. Progression of optic nerve head cupping.d. Treatment effect on patients’ quality of life.

7. Based on the outcomes of the CIGTS, which is NOT true?a. Both treatment groups had a significant reduction of IOP.b. There was no significant difference in the rate of visual field progression between treatment groups. c. There was no significant difference in the development of cataracts between treat-ment groups.d. Over one-third of patients had a fear of blindness at the diagnosis of glaucoma.

8. The Collaborative Normal Tension Glaucoma Study (CNTGS) showed that by decreasing IOP by 30%, glaucoma progres-sion could be reduced by:a. 30%.b. 40%.c. 50%.d. 60%.

9. Which treatment method was NOT used in the CNTGS?a. Topical pilocarpine.b. Oral carbonic anhydrase inhibitor.c. Laser trabeculoplasty.d. Trabeculectomy.

10. Based on CNTGS, which is NOT a risk factor for faster progression of normal ten-sion glaucoma?a. Presence of disc hemorrhage at diag-nosis.b. Female gender.

c. Central corneal thickness.d. History of migraine.

11. In the Low-Pressure Glaucoma Treatment Study (LoGTS), which topical treatment drops were compared to deter-mine which better preserves a normal ten-sion patient’s vision?a. Timolol and betaxolol.b. Timolol and brimonidine.c. Timolol and latanoprost.d. Timolol and dorzolamide.

12. What was the main limitation of the LoGTS, which may have skewed the study results?a. Timolol caused drug-related adverse events.b. Brimonidine caused drug-related adverse events.c. Both timolol and brimonidine caused drug-related adverse events.d. Neither timolol nor brimonidine caused drug-related adverse events.

13. Which is true regarding the long-term results of the Glaucoma Laser Trial and GLT Follow-up Study?a. Prostaglandins and alpha-agonists were used for treatment in the medication group.b. 56% in the medication group needed additional treatment to lower IOP.c. IOP, visual fields and optic nerve head status were all similar between the medica-tion and ALT groups.d. All patients had undergone glaucoma treatment prior to the start of the GLT Study.

14. What was the duration of the SLT/Med Study?a. Seven years.b. Five and a half years.c. Ten years.d. One year.

15. What must you discuss with your patient when considering laser trabeculo-plasty?a. There are no known complications with laser trabeculoplasty.b. The effects of laser trabeculoplasty may wear off over time.c. They will never need to use drops for glaucoma again.d. Medication is always the better option.

OSC QUIZ

21. The AGIS Investigators. The Advanced Glaucoma Intervention Study (AGIS): 13. Comparison of treatment outcomes within race: 10-year results. Ophthalmology. 2004 Apr; 111(4): 651-64.22. The AGIS Investigators. The Advanced Glaucoma Intervention Study (AGIS): 4. Comparison of treatment outcomes within race. Seven-year results. Ophthalmology. 1998 Jul; 105(7): 1146-64.23. The AGIS Investigators. The Advanced Glaucoma Intervention Study (AGIS): 7. The relationship between control of intraocular pressure and visual field deterioration. Am J Ophthalmol. 2000 Oct;

130(4): 429-40.24. Gedde SJ, Singh K, Schiffman JC, Feuer WJ; Tube Versus Tra-beculectomy Study Group. The Tube Versus Trabeculectomy Study: interpretation of results and application to clinical practice. Curr Opin Ophthalmol. 2012 Mar; 23(2): 118-26.25. Gedde SJ, Schiffman JC, Feuer WJ, et al; Tube versus Trab-eculectomy Study Group. Treatment outcomes in the Tube Versus Trabeculectomy (TVT) Study after five years of follow-up. Am J Ophthalmol. 2012 May; 153(5): 789-803.e2.

26. Gedde SJ, Schiffman JC, Feuer WJ, et al; Tube Versus Trab-eculectomy Study Group. The Tube Versus Trabeculectomy Study: design and baseline characteristics of study patients. Am J Ophthal-mol. 2005 Aug; 140(2): 275-87.27. ClinicalTrials.gov. Primary Tube Versus Trabeculectomy Study. Available at: http://clinicaltrials.gov/show/NCT00666237. Accessed May 15, 2014. 28. Scheck A. Consider tube shunts for glaucoma surgery. EyeNet. 2012 Sep;16(9):33-34.


16. Which treatment sequence inves-tigated by the Advanced Glaucoma Intervention Study was found to provide the best long-term preservation of visual function in black patients?a. Trabeculectomy-ALT-trabeculectomy.b. ALT-trabeculectomy-trabeculectomy.c. Trabeculectomy-trabeculectomy-ALT.d. ALT-ALT-trabeculectomy.

17. What is the target IOP at which a patient can be guaranteed no further glau-comatous visual field progression?a. 12.3mm Hg.b. 14mm Hg. c. 18mm Hg. d.

18. What are the two most common glaucoma surgeries being performed worldwide?a. Trabeculectomy and tube-shunt implan-tation.b. ExPress mini shunts and cyclophotoco-agulation.c. Trabeculectomy and cyclophotocoagula-tion.d. ALT and trabeculectomy.

19. Which result of the Tube Versus Trabeculectomy Study is true?a. Failure rates were significantly higher in the tube group compared to the trabecu-lectomy group.b. Glaucoma reoperation was needed more frequently in the trabeculectomy group.c. Tube shunts were found to be superior to trabeculectomy.d. None of the eyes in the study had undergone any previous ocular surgery.

20. Which may be a potential downside to trabeculectomy surgery compared to tube-shunt implantation?a. The patient does not want hardware placed in the eye.b. Subsequent surgical options are more limited after trabeculectomy failure as compared to options after tube-shunt failure.c. Tube shunts were found to be superior to trabeculectomy.d. The patient lives far away from the clinic.

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Glaucoma on Trial: Clinical Implications of the Landmark Glaucoma Studies

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Cornea+Contac t Lens Q+A


A patient of mine presented with a dense, unsightly leu-

coma. My local corneal specialist recently recommended a corneal tattooing procedure. How does one perform such a procedure in this scenario, and what are some poten-tial complications to prepare for?

Using pigment to mask unsightly corneal scars is

not a novel concept. In fact, it was first introduced by Galen, a Greek physician, in 160 AD; however, the technique was used infrequently for centuries thereaf-ter.1 The process was not readily adopted until the early 20th cen-tury, when Frederick H. Verhoeff reported the safe and effective use of India ink to darken corneal scars.2

The most frequent indication for corneal tattooing over the years has been cosmetic—patients who present with a corneal leu-coma or scar may have these aes-thetically unpleasing conditions masked by the procedure.

According to James Aquavella, MD, professor of ophthalmology at the University of Rochester Flaum Eye Institute, who has performed variations of corneal tattooing over the past 50 years, it has also “occasionally been ben-eficial in creating a pupillary effect in aniridia, surgical or traumatic iridectomies, or post-traumatic mydriasis.” This can reduce glare, diplopia and photophobia, he says, resulting in improved visual acuity.

While the availability of cos-metic soft contact lenses has reduced the use of corneal tattoo-ing in recent decades, there are still a number of cases in which insertion and removal of these lenses can be problematic. Addi-tionally, some patients are intol-erant to contact lenses, making them ideal candidates for corneal tattooing.

Early corneal tattooing proce-dures involved using a hypodermic needle, a sharp, pointed instru-ment or a suture needle held on a forceps.3 Procedures such as these were performed under topical anesthesia through the existing epithelium.

To create the masking effect, a metallic dye is applied to each lesion. Typically, titanium dioxide pigments were used; Dr. Aqua-vella says he often used Chinese or India ink (the same inks discussed in the literature by Verhoeff) in addition to gold pigments. Cor-neal tattooing procedures that use needles often require “hundreds of superficial microstromal punc-tures,” says Dr. Aquavella.

Another technique involves the creation of an interlamellar pocket with a keratome.4 This is then followed by the introduc-tion of filter paper that has been soaked in platinum chloride salts. “Subsequently, a syringe needle is introduced beneath the filter paper and a small amount of hydrazine hydrate is injected, which then causes precipitation of the dye,” says Dr. Aquavella.

A more recent technique involves the use of a femtosecond laser to create pockets and chan-nels, which are then followed by the introduction of a number of colored dermatological patterns.5

While corneal tattooing is rela-tively safe, some complications may occur, such as allergic reac-tion to the dyes used, secondary infection, delayed epithelialization, recurrent erosion, perforation and intrastromal hemorrhage if ves-sels are damaged. However, Dr. Aquavella says complications are “extremely rare in the hands of an experienced corneal surgeon.” ■

1. Dougan C, Hill G, Villaverde N, Hill J. Seeing better through someone else’s eyes. Brown University. Avail-able at: http://biomed.brown.edu/Courses/BI108/2006-108websites/group11corneal%20implants/. Accessed June 29th, 2014.2. Verhoeff FH. India ink infiltration: a simple and effective substitute for corneal tattooing. Journal of the American Medical Association. 1917 Oct 24;LXIX(17):1420-21.3. Pitz S, Jahn R, Frisch L, Duis A, Pfeiffer N. Corneal tat-tooing: an alternative treatment for disfiguring corneal scars. Br J Ophthalmol. 2002;86:397-99.4. Khan AO, Meyer D. Corneal tattooing for the treatment of debilitating glare in a child with traumatic iris loss. Am J Ophthalmol. 2005 May; 139(5):920-21.5. Kim JH, Lee D, Hahn TW, Choi SK. New surgical strategy for corneal tattooing using a femtosecond laser. Cornea. 2009 Jan; 28(1):80-4.

A

Q

Corneal tattooing can mask scars and leucoma while improving visual acuity. But how is this technique performed? Edited by Joseph P. Shovlin, OD

Fresh Ink

Corneal tattooing can mask unsightly corneal leucoma and, in some cases, improve visual acuity.

Photo: Barry Lee, MD, FACS

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Comanagement Q+A


I have a patient in my chair who I diagnosed with anterior

uveitis two weeks ago. At that time, I had prescribed a potent topical steroid. (He’s had uveitis before, but was never a steroid responder.) The inflammation is now much improved, but his IOP has risen from 18mm to 28mm Hg. How should I manage this patient?

“It depends,” says Anthony Litwak, OD, who specializes

in glaucoma at the Baltimore VA Medical Center. “Because each ste-roid responder is unique, it’s best to focus on the individual patient’s history and presentation, and not expect an ‘average’ patient.”

For instance, “a typical steroid response happens within two to three weeks. But if you pass that point, it doesn’t mean your patient is in the clear,” he says. “Actually, I think that the longer that you keep the patient on steroids, the more likely that he’ll develop that steroid response.”

And if that happens, then what do you do? Here are some vari-ables to consider.

Does the Patient Already Have Glaucoma Damage?

“If the patient does not have glaucoma damage and develops a steroid response, then a short period of elevated IOP can easily be tolerated, and IOP-lowering

medication may not be necessary as you taper the patient off ste-roids,” Dr. Litwak says.

However, “if the patient already has glaucoma damage and devel-ops a steroid response, then that elevated pressure is probably going to exacerbate the damage,” he says.

If so, you’ll probably need to put the patient on additional glaucoma treatment—depending on how high the pressure is and how long the course of the steroids is going to be.

How Bad is the Uveitis? Grade the anterior chamber.

“Patients who seek early evalua-

tion and get treated immediately and aggressively tend to require a shorter course of steroids, whereas a patient who’s been symptomatic for a week or longer and presents with significant inflammation will probably need several weeks of ste-roid therapy,” Dr. Litwak says.

Also bear in mind that some patients simply respond sooner, while others are more refractory to treatment. See these uveitis patients often. “I tend to see patients with uveitis at least on a weekly basis, or more often if they’re showing significant complications,” he says.

If the inflammation is improving but the IOP is still going up, then taper the steroid. “But don’t taper

This uveitis patient is also a steroid responder. Which problem do you tackle first? Edited by Paul C. Ajamian, OD

Steroid Adds to the Pressure

A

Q

A patient with severe anterior uveitis was prescribed a potent topical steroid. Now, two weeks later, the inflammation has improved but the patient’s IOP has risen to 28mm Hg. It’s too soon to stop the steroid, so is it time to Rx a glaucoma drop?

Have a comanagement question for Dr. Ajamian? Send it to John Murphy, execu-tive editor, at [email protected].

Photo: Michael Trottini, OD, and Candice Tolud, OD

too quickly, or you can get a rebound in the inflam-mation,” Dr. Litwak says.

On the other hand, if the pressure has gone up but the inflammation is not improving, “it could be that the inflammation itself—not the steroid—is causing the pressure to go up,” he says. “In that case, you actually increase the steroid to try to quell the inflammation, which should bring the pressure down.”

Pick a Potent SteroidSoft steroids don’t penetrate the anterior chamber

as well as more potent steroids. This means that they tend to cause a steroid response less often—but it also means that they are less effective for uveitis.

“For mild to moderate uveitis we typically use Pred Forte (prednisolone acetate 1%, Allergan),” Dr. Litwak says. Use the brand name if you can get it. “However, in the unlikely event that the patient has a history of a steroid response on Pred Forte, I sometimes use Vexol (rimexolone 1%, Alcon), which is a slightly weaker steroid but it does penetrate into the anterior chamber. And some clinical studies have shown it delays the onset of a steroid response.”1

For severe cases, consider the “big gun” steroid Durezol (difluprednate 0.05%, Alcon). But be aware that it carries an increased risk for a steroid response, so monitor these patients even more closely.

Add Hypotensive Drops“Always check the pressure on your follow-up

visits,” Dr. Litwak says. If the patient has glaucoma damage on top of uveitis, and also has a steroid response, he’ll require additional glaucoma medica-tion along with steroid therapy.

But, avoid prostaglandins to lower IOP because they can mediate inflammation in the eye, he says. Instead, use aqueous suppressants—beta blockers, carbonic anhydrase inhibitors or alpha agonists.

Last but not least, Dr. Litwak says, “for those uve-itic glaucoma patients who already have significant glaucomatous damage and aren’t responding well to glaucoma therapy, a steroid response on top of that can be disastrous. This triad of problems suggests that this patient needs to be referred out.” ■

1. Biswas J, Ganeshbabu TM, Raghavendran SR, et al. Efficacy and safety of 1% rimexolone versus 1% prednisolone acetate in the treatment of anterior uveitis? A randomized triple masked study. Int Ophthalmol. 2004 May;25(3):147-53.

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Review of Systems

Ideally, our circulatory sys-tem operates like a well-oiled machine, with all the vessels and arteries making seamless

deliveries of blood throughout the body. When the lines of this com-plex system get tangled and arter-ies connect directly to veins with no capillary bed to cushion them, however, it can cause arteriove-nous malformations—and if those AVMs occur in the brain or spine, the impact on general and ocular health can be considerable.

This defect of the circulatory system is thought to arise during embryonic or fetal development, or soon after birth. AVMs can occur in various parts of the body with little health risk or symptoms, but neurological AVMs of the brain or spinal cord can cause cerebral bleeding, seizures and optic disc edema secondary to intracranial hypertension.

The Facts on AVMsNeurological AVMs affect about

300,000 Americans. Although

AVM occurs in both sexes and all ethnicities equally, it is most com-monly seen in young adults, with morbidity occurring in 30% to 50% of patients and death rates of 10% to 15%.1 Cerebral bleeding and seizures are the most typical modes of presentation.

AVMs produce neurological dysfunction via three primary mechanisms. First, through hem-orrhage. This most commonly

occurs in the brain parenchyma, but can be found in the subarach-noid or intraventricular space. Hemorrhage from cerebral AVMs represents 2% of all hemorrhagic strokes.2 In the absence of hemor-rhage: seizures. About 15% to 40% of patients present with a seizure disorder.

The third manifestation of arte-riovenous malformations is a pro-gressive neurological deficit, which occurs in 6% to 12% of AVM patients over a span of months or years. This process, known as the “steal phenomenon,” siphons blood away from adjacent brain tissue.1,2

Notably, a growing number of asymptomatic AVMs have been encountered due to increased MRI use. The clinical course of these cases is mild in comparison to those that present with symptom-atic cerebral hemorrhage.1,2

Arteriovenous malformations can have widespread effects on the body,including the eye. By Carlo J. Pelino, OD, and Joseph J. Pizzimenti, OD

The Tangled Web We Weave

ARUBAThe Randomized trial of Unruptured Brain Arteriovenous malformations—better known as the ARUBA study—is a clinical trial sponsored by the National Institutes of Health. ARUBA was designed to discover best practices for caring for those with a neurological arteriove-nous malformation (AVM) that has never bled.

ARUBA found that medical management lowered the risk of death or stroke in patients with unruptured AVMs at more promising rates than medical management coupled with interventional therapy, such as neurosurgery, embolization and/or stereotactic radiothera-py. Although the trial is continuing its observational phase, the results were so favorable to exclusive medical management after 33 months that a data and safety monitoring board halted the randomization. The trial will continue observation for five years post follow-up.4

T2 Axial cut shows partially empty sella. Partially empty sella visible on T1sagittal view.


Diagnostic Work-up It’s critical to always perform

careful evaluations of personal and familial history in cases of sus-pected systemic disease, and arte-riovenous malformations are no exception. It’s important to note that AVMs may be associated with other inherited disorders, such as Sturge-Weber disease, neurofibro-matosis and von Hippel-Lindau syndrome, a rare genetic disorder whose clinical hallmarks include the development of retinal and central nervous system blood vessel tumors.1,2

AVMs have a tendency to lurk silently. It’s common for the condi-tion to remain undetected until the presenting event, which means the diagnosis is usually made at the time of the first seizure or hemor-rhage.

Although exact diagnostic symptoms are difficult to pin-point, a history of headaches has been found in as many as half of all patients with cerebral arterio-venous malformation. Risk fac-tors—be they genetic, demographic or environmental—have not been clearly identified, further compli-cating diagnostics.

It is especially important for the optometrist to note symptoms of transient visual obscurations and recurrent headaches, should they exist. Proper ophthalmic workup includes visual acuity testing, along with eye movement evaluation, pupils, confrontation and Amsler Grid testing.

A comprehensive ocular health evaluation, including dilated fun-dus evaluation, is essential. Ancil-lary testing, such as color vision, central threshold perimetry, optical coherence tomography, and ocular ultrasound are often useful in such cases.

NeuroimagingProper diagnosis of AVM rests

on the shoulders of high-quality radiologic imaging.

AVMs appear as irregular or globoid masses within the hemi-spheres or the brain stem. The mass might be surrounded by, or inclusive of, a low signal of extra-cellular hemosiderin, indicative of prior hemorrhage.

While CT imaging can only identify relatively large AVMs, it can easily pinpoint intracerebral hemorrhage, which should alert clinicians to potential AVM—par-ticularly among younger patients. MRI is essential for initial diagno-sis.

Cerebral angiography is required for hemodynamic assessment, which is essential to charting a course of treatment.

The treatment plan will depend on the morphology of the AVM, including features of the feeding arteries, arterial and venous aneu-rysms and venous drainage pat-terns.3

Treatment ApproachesThe appraoch to treatment

of arteriovenous malformation is dependent on several factors, most notably the risk of initial or subsequent hemorrhage. This risk is typically determined by the patient’s demographic, historical and angiographic features. Smaller AVM size, deep venous drainage and high arterial feeding pressures increase the likelihood of subse-quent hemorrhage.1

Invasive treatment—including endovascular embolization, surgi-cal resection and focal beam radia-tion—is recommended for younger patients with one or more high-risk features. These treatments can be used alone or in combination.1,2

For older individuals and low-risk patients, anticonvulsants and analgesia for headaches may be the only necessary treatment. Common medications include phenytoin, carbamazepine, valproic acid and lamotrigine.1 No specific activity restrictions are placed on patients with AVM.

Case Report • History. A 48-year-old, non-obese white female presented recently to the clinic with

symptoms of transient visual obscurations in each eye and recurrent headaches. Systemic history was positive for a resolved intracranial vascular malformation diagnosed eight years prior.

• Diagnostic data. Dilated fundus examination revealed asymmetric optic disc edema (OS > OD). B-scan ultrasonography characterized the resulting asymmetric ONH elevation. Central 24-2 visual field test results showed inferonasal defects OD and scattered edge defects OD and OS.

MRI with and without contrast confirmed the previous vascular abnormality in the left parietal lobe. A neuroradiologist reported radiologic features consistent with AVM.

Axial and sagittal MR showed a decrease in the signal encircling the AVM, due to hemo-siderin from leaked blood.

• Management. Lumbar puncture revealed an opening pressure of 320mm H20. This established a diagnosis of intracranial hypertension secondary to AVM. Diamox 500mg BID was prescribed. Due to intolerable adverse reactions, this medication was switched to Lasix 20mg BID with KCl 20mEq BID.

The patient is receiving ongoing care by a multispecialty team, with invasive treatment the likely next step.

Review of Systems

A multispecialty approach should be taken with AVM patients, with eye care providers playing an important role among the neuro team, which typically includes a neurologist, neuropsy-chologist, neurosurgeon, inter-ventional neuroradiologist and neuroanesthesiologist.

Patients frequently present to the optometric physician with symptoms of headache and tran-sient blur. Often, these symptoms prove to arise from non-urgent causes. However, it is crucial for the practitioner to rule out sight-threatening and sometimes life-threatening causes during the encounter. Interrogate and inves-tigate for telltale ocular symptoms and clinical signs, particularly

those that may relate to the pupil-lary and visual pathways, as well as cranial nerves. Bilateral disc edema may occur due to several conditions. It is important to rule out neoplastic disease, as well as intracranial hypertension due to a variety of causes, including cere-bral AVMs. ■

1. Novakovic RL, Lazzaro MA, Castonguay AC, Zaidat OO. The diagnosis and management of brain arteriovenous malforma-tions. Neurol Clin. 2013 Aug;31(3):749-63.2. Laakso A, Dashti R, Juvela S, et al. Natural history of arte-riovenous malformations: presentation, risk of hemorrhage and mortality. Acta Neurochir Suppl. 2010;107:65-9.3. Halim AX, Johnston SC, Singh V. Longitudinal risk of intracranial hemorrhage in patients with arteriovenous malfor-mation of the brain within a defined population. Stroke. 2004 Jul;35(7):1697-702. 4. Mohr JP, Parides MK, Stapf C, et al. Medical manage-ment with or without interventional therapy for unruptured brain arteriovenous malformations (ARUBA): a multi-centre, non-blinded, randomised trial. Lancet. 2014 Feb 15;383(9917):614-21.5. Perez MA, Glaser, JS Shatz NJ. Idiopathic intracranial hypertension caused by venous sinus thrombosis associated with contraceptive usage. Optometry. 2010 Jul;81(7):351-8.

Secondary Psuedotumor Syndromes5

• Venous sinus thrombosis

• Arteriovenous malformation

• Hypertension

• Congestive heart failure

• Guillian-Barre

• Medications (vitamin A, tetracycline,

minocycline, lithium, penicillin, oral

contraception)

• Tumors

• Obesity and weight gain

• Hypercoagulability

• Anemia

• Systemic Lupus

• Sleep apnea

• Head trauma

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Re t ina Quiz


A22-year-old black female presented for an eye exam to determine if she met the

visual requirements for obtain-ing a driver’s license in the state of Florida. She reported being very nearsighted, and that she had poor vision her entire life. The patient also said that she wore glasses for as long as she could remember, and had undergone multiple eye exami-nations since early childhood.

Her medical history was signifi-cant for relatively light skin pigmen-tation, compared to her immediate family members.

Her visual acuity measured 20/80 OU with a spectacle correction of -14.50 + 2.75D X 110 OD and -13.50 +1.50D X 080 OS. At near, she was 20/40 OU. Extraocular motility testing revealed horizontal nystagmus in all positions of gaze. She did not display a head turn, nor

did she have a noticeable null point. Her pupils were equally round and reactive, with no evidence of affer-ent defect OU.

Dilated fundus exam revealed pronounced changes (figure 1). We also obtained a spectral-domain optical coherence tomography (SD-OCT) scan (figures 2 and 3).

Take the Retina Quiz 1. Based on the data provided,

what changes would you expect to see in the anterior segment?

a. Keratoconus. b. Anterior uveitis. c. Iris transillumination defects. d. Posterior subcapsular cataract.

2. How would you characterize the SD-OCT finding in our patient?

a. Macular edema. b. Choroidal neovascularization. c. Poorly differentiated macula.

d. Improper scan alignment.

3. What is the likely diagnosis? a. Oculocutaneous albinism. b. Myopic degeneration. c. Congenital nystagmus. d. Choroideremia.

4. What is the cause of her poor vision?

a. Macular edema. b. Macular hypoplasia. c. Optic nerve hypoplasia. d. Choroidal neovascularization.

5. Does our patient meet the usual legal requirements for obtain-ing a driver’s license?

a. Yes. b. No. c. Yes––for daytime driving only. d. Yes––with low vision aids.

For answers, turn to page 90.

This patient presented with a lifelong history of poor visual acuity in both eyes and abnormally light skin pigmentation. By Mark T. Dunbar, OD

Pale in Comparison

1. Our patient’s fundus evaluation reveals significant changes in both eyes (OD left, OS right).


Re t ina Quiz

DiscussionFrom external appearance alone,

it was obvious that our patient had cutaneous albinism. And, given her history of poor vision and nystag-mus, it was readily apparent that the albinism also had affected her eyes.

On slit-lamp evaluation, she had iris transillumination defects, and on dilated fundus exam we noted a striking lack of pigmentation within the retinal pigment epithelium. All these findings are consistent with oculocutaneous albinism.

Albinism represents a hereditary group of disorders characterized by a congenital lack of melanin pig-ment.1 Although the condition may be isolated to the eye (ocular albi-nism), most cases also involve the skin and hair––as was the case in our patient. Often, these individu-als present with an obvious lack of skin pigmentation, their hair has a bleached white appearance, and their irides are light blue or almost

white in appear-ance.

There are four types of oculocu-taneous albinism:

• Type 1 is characterized by white hair, very pale skin and lightly colored irides.

• Type 2 is often less severe, and the individ-ual’s skin usually is a creamy white color. Also, the patient’s hair may be light yellow, blond or light brown.

• Type 3includes a variant called rufous ocu-

locutaneous albinism, which usually manifests in dark-skinned people. Affected individuals often have rud-dy-brown skin, ginger-tinted or red hair, and hazel or brown irides. This form is often associated with milder vision abnormalities than the other forms of oculocutaneous albinism.

• Type 4 exhibits signs and symp-toms similar to those associated with type 2.

Because most of these clinical fea-tures overlap (e.g., those produced by types 2 and 4), the four forms of oculocutaneous albinism are most accurately distinguished by their underlying genetic cause––although all types of the condition are auto-somal recessive.1,2

Despite clinical variations between the types of albinism, most patients have varying degrees of nystagmus and reduced visual acu-ity. This is due to the lack of pig-mentation within the fundus as well as macular hypoplasia––the most consistent feature of albinism.1

The macula and fovea become poorly differentiated, with more rods and fewer cones present in the fovea. Also, the foveal pit may be reduced or not even present. This is evident in our patient on the SD-OCT scan, where the normal foveal depression is absent. Interestingly, the junction of the inner and outer photoreceptor segments can still be seen on the scan. Perhaps that finding explains why our patient’s acuity is 20/80, while most macular hypoplasia patients often see 20/100 to 20/200.

Iris transillumination defects are another common feature of albi-nism, and can easily be seen with minimal light directed at the eye. These patients are often highly pho-tophobic.

Our patient didn’t know what type of oculocutaneous albinism she had. Based solely on external appearances, however, we were fairly certain that it was type 3.

Finally, to address the question as to whether her acuity sufficiently meets the legal requirements to obtain a driver’s license… The answer is no. In Florida, the law states that the driver’s best-corrected visual acuity must be at least 20/70 in each eye; or if one eye is worse than 20/200, the fellow eye must be 20/40 or better.3 Thus, 20/80 OU fails to meet that mandate.

We explained these findings to our patient. Afterward, we provided her with several forms to fill out, so she could obtain disability as well as any rights and privileges offered to legally blind individuals. ■

1. Russell-Eggitt IM. Albinism. Pediatric Ophthalmology and Strabismus, 4th ed. Edingburgh: Saunders Elsevier; 2014:393-9.2. US National Library of Medicine. Genetics Home Reference: Oculocutaneous Albinism. Available at: http://ghr.nlm.nih.gov/condition/oculocutaneous-albinism. Accessed June 12, 2014. 3. Florida Department of Highway Safety and Motor Vehicles. Report of Eye Exam. Available at: www.flhsmv.gov/hsmvdocs/vision.pdf. Accessed June 12, 2014.

2, 3. How do you explain her SD-OCT findings (OD top, OS bottom)?

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Therapeu t i c Review

A35-year-old white female was referred for evaluation of elevated intraocular pres-

sure. She had no visual complaints or family history of glaucoma. Her IOP measured 19mm Hg OD and 22mm Hg OS. Her central corneal thickness was 549µm OD and 558µm OS. Biomicroscopically, she exhibited a distinct Krukenberg spindle on the back surface of each cornea, as well as rare mid-peripher-al iris transillumination defects OU. Gonioscopically, there was a classic appearance of pigment dispersion syndrome with dense trabecular meshwork pigmentation and evidence of Sampaolesi’s line in both eyes. Notably, the iris had a concave configuration with signifi-cant backward bowing.

Her optic nerves appeared healthy, with robust, symmetrical neuroretinal rims. Optical coher-ence tomography showed a normal retinal nerve fiber layer in both eyes. Additionally, threshold perimetry was normal OU.

We diagnosed her with pigment dispersion syndrome (PDS) and low-risk ocular hypertension. After discussion and education, we decid-ed to monitor her on a periodic basis without medical therapy. But, because she had classic PDS without glaucoma, could we do anything to reduce the amount of pigment being liberated and possibly prevent glau-comatous development?

Laser peripheral iridotomy (LPI) has been advocated as a means of changing the iris approach and

reducing pigment liberation. In this month’s column, we discuss PDS and pigmentary glaucoma, as well as address the potential therapeutic benefits of LPI.

PDS and Pigmentary GlaucomaPatients with PDS and pigmen-

tary glaucoma experience iris pig-ment liberation within the anterior chamber. Often, this is seen as a diffuse accumulation or possibly a granular, brown vertical band locat-ed along the corneal endothelium, which is known as a Krukenberg spindle. Pigment accumulation also may be evident on the lens or iris surface, within the trabecular mesh-work and on Schwalbe’s line (where it is referred to as Sampaolesi’s line). Radial, spoke-like transillumination defects of the mid-peripheral iris are common.1,2

Many patients with PDS and pigmentary glaucoma demonstrate a concave iris approach as it inserts into the anterior chamber angle, yielding a “backward bowed” appearance on gonioscopy. This change places the posterior iris into apposition with the lens zonules. As

the iris responds to light, iridozonu-lar friction results in pigment libera-tion from the posterior iris, which follows the flow of the aqueous convection current into the anterior chamber angle.1,2

It has been theorized that in cases with a markedly concave iris inser-tion, the iris functions as a flap valve lying against the anterior lens surface. The iris is forced backwards when a pressure gradient develops that is greater in the anterior cham-ber, closing the valve and trapping the aqueous from moving into the anterior chamber. This increased anterior chamber pressure sub-sequently forces the iris into the aforementioned concave approach, which is termed “reverse pupillary block.”3-7

There are two possible con-sequences of excessive pigment accrual. First, pigment may reside benignly in the trabecular mesh-work where IOP is unaffected and the condition remains PDS. Alternately, the IOP rises due to a breakdown of normal phagocytic activity of the endothelial cells and subsequent loss of normal trabecu-lar architecture and function, and pigmentary glaucoma develops.8-10

LPI to the Rescue?Laser peripheral iridotomy often

is considered and recommended for PDS and pigmentary glaucoma patients who exhibit significant iris concavity. Clinical researchers have clearly demonstrated that the iris can convert from a concave to a

Is there a role for iridotomy when managing patients with pigmentary glaucoma?By Joseph W. Sowka, OD, and Alan G. Kabat, OD

A Hole-in-One?

Heavy trabecular meshwork pigment and concave iris in a young female with PDS.

Therapeu t i c Review


planar approach following LPI.11-13

For this reason, LPI has been rec-ommended as a method to reduce melanin release and pigment deposi-tion in the trabecular meshwork.14

The popularity of LPI for eyes with PDS and pigmentary glaucoma seems to be cyclical. The procedure was commonly performed for some time and then abandoned. Today, it appears that LPI is again being done in PDS and pigmentary glaucoma to some extent––but the benefit in overall IOP management, as well as the risk reduction for visual disabil-ity, is unclear.

In 2005, the results of a retro-spective analysis shed some light on the role of LPI in the manage-ment of patients with pigmentary glaucoma. Retrospective data was analyzed on patients with bilateral pigmentary glaucoma, who had received uniocular LPI. The main outcome measure was the post-laser intraocular pressure course of the treated eyes, compared with the fel-low, untreated eyes.

The study included 46 patients who had been observed for two or more years.15 Among the patients observed for less than two years, the mean intraocular pressure in the LPI-treated eyes increased slightly compared with the fellow, untreated eyes. Among the patients observed for two or more years, the mean intraocular pressure in the LPI-treated eyes decreased by approxi-mately 2mm Hg over that seen in the untreated fellow eyes; however, subsequent analysis showed that a higher mean baseline intraocular pressure in the treated eyes account-ed for the apparent treatment effect of LPI.

Clearly, there were many limitations to this study––most notably, a lack of controls and a standardization of methodology. The authors concluded that LPI

does not effectively provide long-term IOP control in eyes with pig-mentary glaucoma, but that a large, prospective trial was still warranted to determine whether LPI holds any potential therapeutic benefit for such patients.15

Then, in 2011, a prospective, controlled, randomized study looked 166 eyes with pigment dis-persion syndrome and elevated IOP, but no glaucomatous damage, and randomized eyes to either LPI or no LPI. The primary outcome was conversion to pigmentary glaucoma at three years. Secondary out-come measures were whether eyes required topical glaucoma medica-tions during the study period and the time to conversion or medica-tion intervention.

During the study, 15% of eyes in the LPI group converted to glau-coma, compared to 6% of eyes in the control group. The proportion of eyes started on medical treat-ment was similar between the two groups. The researchers also documented no difference in time to visual field progression or topical therapy initiation between the treat-ment and control groups.

The authors concluded that LPI did not help limit or prevent disease progression from PDS with associ-ated ocular hypertension to pigmen-tary glaucoma within three years of follow-up.16

While acknowledging a lack of clinical evidence that LPI has a long-term effect in preventing glaucoma in eyes with pigment dispersion syndrome, a more recent report suggested that the procedure should only be undertaken in patients younger than 40 years, if the mid-peripheral iris shows backward bowing, and if the intraocular pres-sure is normal or slightly increased with no progressive signs of optic nerve damage.17

So, in 2014, where does LPI stand with regard to the manage-ment of patients with PDS and/or pigmentary glaucoma? It’s still not clear. While the procedure can change the anatomic configura-tion of the iris and theoretically help reduce pigment liberation and accumulation within the trabecular meshwork, there is no compelling evidence to suggest that LPI is ben-eficial in reducing IOP or preventing pressure elevation in this disease. For this reason, we do not advocate LPI for those with pigment disper-sion syndrome or pigmentary glau-coma. ■

1. Sugar HS, Barbour FA. Pigmentary glaucoma: a rare clinical entity. Am J Ophthalmol. 1949 Jan;32(1):90-2.2. Campbell DG, Schertzer RM. Pathophysiology of pigment dispersion syndrome and pigmentary glaucoma. Curr Opin Oph-thalmol. 1995 Apr;6(2):96-101.3. Campbell DG. Pigmentary dispersion and glaucoma: a new theory. Arch Ophthalmol. 1979 Sep;97(9):1667-72.4. Potash SD, Tello C,. Ultrasound biomicroscopy in pigment dis-persion syndrome. Ophthalmology. 1994 Feb;101(2):332-9.5. Karickhoff JR. Pigmentary dispersion syndrome and pigmentary glaucoma: a new treatment, and a new technique. Ophthalmic Surg. 1992 Apr;23(4):269-77.6. Karickhoff JR. Reverse pupillary block in pigmentary glaucoma: follow-up and new developments. Ophthalmic Surg. 1993 Aug;24(8):562-3.7. Campbell DG. Iridotomy, blinking, and pigmentary glaucoma. Invest Ophthalmol Vis Sci. 1993;34(4 suppl):993.8. Richardson TM, Hutchinson BT, Grant WM. The outflow tract in pigmentary glaucoma: A light and electron microcroscopy study. Arch Ophthalmol. 1977 Jun;95(6):1015-25.9. Mastropasqua L, Ciancaglini M. Early stadiation of pigmentary dispersion syndrome and long-term analysis of progression to pig-mentary glaucoma. Arch Ophthalmol. 1977 Jun;95(6):1015-25.10. Siddiqui Y, Ten Hulzen RD, Cameron JD, et al. What is the risk of developing pigmentary glaucoma from pigment dispersion syndrome? Am J Ophthalmol. 2003 Jun;135(6):794-9.11. Klingenstein A, Kernt M, Seidensticker F, et al. Anterior-segment morphology and corneal biomechanical characteristics in pigmentary glaucoma. Clin Ophthalmol. 2014;8:119-26.12. Aptel F, Beccat S, Fortoul V, Denis P. Biometric analysis of pig-ment dispersion syndrome using anterior segment optical coher-ence tomography. Ophthalmology. 2011 Aug;118(8):1563-70. 13. Niyadurupola N, Broadway DC. Pigment dispersion syndrome and pigmentary glaucoma--a major review. Clin Experiment Oph-thalmol. 2008 Dec;36(9):868-82.14. Laemmer R, Mardin CY, Juenemann AG. Visualization of changes of the iris configuration after peripheral laser iridotomy in primary melanin dispersion syndrome using optical coherence tomography. J Glaucoma. 2008 Oct-Nov;17(7):569-70.15. Reistad CE; American Glaucoma Society Pigmentary Glaucoma Iridotomy Study Group. The influence of peripheral iridotomy on the intraocular pressure course in patients with pigmentary glau-coma. J Glaucoma. 2005 Aug;14(4):255-9.16. Scott A. YAG laser peripheral iridotomy for the prevention of pigment dispersion glaucoma a prospective, randomized, con-trolled trial. Ophthalmology. 2011 Mar;118(3):468-73.17. Rosentreter A, Schwenn O, Funk J, Dietlein T. Is prophylactic YAG iridotomy useful in pigment dispersion syndrome? Ophthal-mologe. 2013 Apr;110(4):306-9.

CE CONFERENCES

Approval pending

MEETINGS CO-CHAIRS: MURRAY FINGERET, OD ROBERT N. WEINREB, MD

For faculty & more information, go to

www.revoptom.com/Meetingscall 1-800-835-9877, or email [email protected]

12 CE Credits(COPE Approval Pending)

6th Annual

East Coast Optometric Glaucoma Symposium

5th Annual

West Coast Optometric Glaucoma SymposiumDecember 12-13, 2014HUNTINGTON BEACH, CAwww.revoptom.com/WCOGS2014

October 24-25, 2014PHILADELPHIA, PAwww.revoptom.com/ECOGS2014

SAVETHEDATE!

Speakers: Michael Chaglasian, OD • Ben Gaddie, OD Nils Loewen, MD, PhD • Jonathan Myers, MD,

Speakers:Howard Barnebey, MD • John Flanagan, OD, PhDJeffrey Goldberg, MD, PhD • Richard Madonna, OD

Partially supported by an educational grant from

Alcon

www.rickbayfoundation.org

The Rick Bay Foundationfor Excellence in Eyecare Education

Scholarships will be awarded to advance the education

of students in both Optometry and Ophthalmology,

and will be chosen by their school based on qualities that

embody Rick’s commitment to the profession, including

integrity, compassion, partnership and dedication to the

greater good.

Support the Education of Future Healthcare & Eyecare Professionals

About RickRick Bay served as the publisher of The Review Group since 1991.

To those who worked for him, he was a leader whose

essence was based in a fi erce and boundless loyalty.

To those in the industry and the professions he served, he will be remembered for his unique array of skills and for his dedication to exceeding the expectations of his customers, making many of them fast friends.

Interested in being a partner with us?Visit www.rickbayfoundation.org

(Contributions are tax-deductible in accordance with section 170 of the Internal Revenue Code.)

(The Rick Bay Foundation for Excellence in Eyecare Education is a nonprofi t, tax-exempt organization under section 501(c)(3) of the Internal Revenue Code.)


InstrumentsGive Yourself an Edge

Ease the burden on your in-office finishing lab with Essilor’s Neksia, which unites a high-performance edger and frame tracing system with a computer-assisted centering and blocking device—together, Nek-sia is designed to finish modern premium lenses and frames with precision and ease.

Essilor touts Neksia’s accuracy, speed and ease of use as primary benefits. The edging system features a user-friendly interface that allows the user to launch jobs using icon-based functions on two simple, colorful touchscreens. Up to 1,000 jobs are stored in Neksia’s database.

Visit www.essilorinstrumentsusa.com.

See the Bigger PictureLow-vision macular degeneration patients who need

greater magnification for home or office now have even more options with Tech Optics International’s portable electronic digital magnifiers.

These mini-magnifying computers come in four mod-els, from basic to multi-functional, and feature LCD screens, adjustable brightness levels and allowances for

enlarging, reducing or freezing images. Lightweight and portable, they pro-vide magnification as low as 3x and as high as 18x-plus. Users also have the option of selecting full color, positive/

negative, high contrast and color blue/white, black/yel-low, blue/yellow and black/green.

Visit www.TechOpticsInternational.com.

Ready for RefractionEnjoy freedom of movement and full control of the

phoropter head and projection chart with Visionix’s VX 55, a new type of refraction prod-uct that allows for connectivity among diagnostic devices and easy importa-tion of measurement findings into EMR systems.

With the VX 55, you can digitize your manual pho-ropter and control the entire refraction process from your tablet, increasing efficiency and performing refrac-tions more quickly and easily.

Visit www.visionix.com.

Contact LensesSystems are Go

The FDA has issued marketing clearance for Bausch + Lomb’s Biotrue OneDay for Presbyopia, the first daily disposable multifocal contact lens from the Biotrue OneDay line.

Featuring a next generation three-zone progressive design, along with bio-inspired HyperGel material, the new lens provides comfortable vision throughout the day and exceptional vision across near, intermediate and distance, according to the company.

Visit www.bausch.com.

Color Millennials HappySurveys show that Millennials consider expression

of color an impor-tant way to enhance their appearance and express their individuality. Alcon has answered this call with its latest launch, Air Optix Colors. These lenses allow consumers to enhance their eye color in a way that mimics the natural, subtle color blend of the iris.

The lenses are offered in nine hues, from subtle to vibrant, and are the first monthly-replacement, daily-wear color lenses available in the US on a silicone hydrogel platform. Colors include pure hazel, blue, green, gray, brown, brilliant blue, gemstone green, honey and sterling gray.

Visit www.alcon.com.

Expansion PackResearch shows that patients who have access to

larger contact lens inventory pack sizes tend to be more compliant in replacing their lenses biweekly as recom-mended by their doctor and had a significantly better wearing experience, Johnson & Johnson Vision Care says. Thus, the company has replaced all three-month Supply Packs of Acuvue Oasys with a new six-month pack.

Visit www.acuvueprofessional.com.

P r o d u c t R e v i e w


Produc t Review

EyewearRighteous Courage

For every purchase from its Not of This World line—which now includes Righ-teous sunglasses and Courage frames—Eyes of Faith donates eye care or eyewear to faith-based optical mis-

sions. Features of Righteous, a unisex design, include an aviator shape and spiritual accent identifying them as NOTW eyewear. Courage, also unisex, combines mature colors with youthful style and features silver-toned diamond rivets and a distinctive logo.

Visit www.eofoptical.com.

Google Goes GlamFive stylish frames are now part of the Google

Glass craze. Partnerships with Diane Von Furstenberg, Luxottica, Ray-Ban and Oakley have made the glamorous life possible for Google Glass.

The hardware in the frames—which will come at a price of about $1,500—is unchanged, except for the designer element. Visit www.google.com/glass.

DiagnosticsGenetic Detection

Patients aged 55 and older with early or intermediate dry AMD could be educated about their risk assess-ment for the development of wet AMD/CNV through Nicox’s RetnaGene AMD, a test that evaluates geno-type and other known risk factors.

RetnaGene AMD provides an assessment for devel-opment of wet AMD/CNV within two, five and 10 years. Nicox’s RetnaGene portfolio also includes RetnaGene LR, which assesses the lifetime risk of advanced AMD (wet or dry) in patients who have not been diagnosed with AMD, age 55 and older and/or with a family history of the condition.

Visit www.nicox.com.

Mobile AppFind & Wear

The process of finding and wearing the right contact lenses has gone digital with CooperVision’s newest

mobile app, which provides consumers with access to useful contact lens info and tools, including ways to find a nearby optometrist, identify potentially ideal lenses to discuss with a practitioner, and a customizable reminder that will sound an alert when it’s time for a lens replacement.

Visit www.coopervision.com.

Dry Eye TherapySoothing Protection

A compromised lipid layer of the tear film is the defi-ciency most associated with dry eye symptoms. Bausch + Lomb’s Soothe Xtra Protection eye drops with Resto-ryl, an emulsion system featuring a blend of mineral oils and interfacial molecules, targets the main source of symptoms by restoring lipid layer thickness.

The product has been relaunched after a hiatus and is now preserved with polyquaternium-1 with a borate buffer system, commonly used in ophthalmic formula-tions. Soothe XP is now available at Walmart and Tar-get, and will soon be available at additional retailers, such as Walgreens, Rite Aid and CVS.

Visit www.bausch.com.

Patient EducationSun Safety

It’s just as important to shield your eyes from harm-ful sun rays as it is to shield your skin. To make this message clear, Johnson & Johnson Vision Care has introduced a free education resource, “The Sun & Your Eyes: What You Need to Know.”

The resource can be viewed or downloaded from the education and resources section of the website. It includes important information on unexpected sources of UV radiation exposure, as well as straightforward, practical advice on reducing risks of exposure. It also offers tips on what to look for when buying sunglasses.

Visit www.acuvueprofessional.com.

Contact Lens CareFlip Out for Flip-Tops

Forget the white screw-top cap—Alcon has intro-duced a convenient flip-top for its Clear Care Cleaning and Disinfecting Solution.

They’ve made it red to remind customers about the potential dangers of misusing hydrogen peroxide eye care products. The size of the bottle has also been made shorter and wider. The product inside remains the same.

Visit www.alcon.com.

Left your Review of Optometry magazine at the offi ce? No problem!

Read Review on the go from any mobile device!

Just simply go to www.revoptom.com and click on the digimag link to get your current issue.


Meet ings + Conferences

July 2014■ 24-27. Florida Optometric Association’s Annual Convention.

Boca Raton Resort & Club, Boca Raton, Fla. Hosted by: Florida

Optometric Association. CE hours: 22. Email Blake Moore,

[email protected] or call (850) 877-4697. Visit www.florida-

eyes.org.

■ 25-27. Tahoe Summit. Hyatt Regency, Incline Village, Nev.

Hosted by: Sacramento Valley Optometric Society. CE hours:

12. Email Jerry Sue Hooper at [email protected] or call

(916) 446-2331.

■ 26-28. National Glaucoma Symposium. Ocean Edge

Resort, Brewster (Cape Cod), Mass. Hosted by: National

Glaucoma Society. CE hours: 18. Email Blake Moore at info@

NationalGlaucomaSociety.org or call (877) 825-2020. Visit www.

NationalGlaucomaSociety.org.

August 2014■ 1-3. South Seas Educational Retreat. South Seas Island

Resort, Captiva Island, Fla. Hosted by: Southwest Florida

Optometric Association. Featured speakers: Ben Gaddie, OD,

Carlo Pelino, OD, April Jasper, OD, Ron Foreman, OD. CE

hours: 18. Email [email protected] or call (239) 481-7799. Visit

www.swfoa.com.

■ 1-3. Smoky Mountain Summer. Grove Park Inn, Asheville,

NC. Hosted by: Nova Southeastern University. Featured speak-

ers: Diana Shechtman, OD, Bill Jones, OD. CE hours: 14. Email

[email protected] or call (954) 262-4224. Visit optometry.nova.

edu/ce/index.html.

■ 8-9. 19th Annual Island Educational Conference. Casa

Marina Resort, Key West, Fla. Hosted by: Foundation for Ocular

Health and Aran Eye Associates. CE hours: 10. Email Gloria

Ayan at [email protected] or call (786) 405-

9723.

September 2014■ 12-14. Fall Conference. Point Lookout, Northport, Maine.

Hosted by: Maine Optometric Association. Call (207) 789-2000.

Visit www.MaineEyeDoctors.org.

■ 12-14. Fall Conference. Jay Peak Resort, Jay Peak, Vt.

Hosted by: Vermont Optometric Association. CE hours: 17.

Email Suzanne Corbitt at [email protected].

■ 12-14. Review of Optometry New Technologies and

Treatments. Tysons Corner, Va. Hosted by: Review of

Optometry. Email Lois DiDomenico at ldidomenico@jobson.

com. Call (610) 492-1000. Visit www.revoptom.com.

■ 13-14. Diabetic Management Update and Annual Glaucoma

Meeting. Nova Southeastern University, Ft. Lauderdale, Fla. CE

hours: 12. Email [email protected] or call (954) 262-4224. Visit

optometry.nova.edu/ce/index.html.

■ 17-20. Envision Conference 2014. Hyatt Regency

Minneapolis, Minneapolis, Minn. Hosted by: Envision University.

CE hours: 23. Keynote: Rebecca Kammer, OD. Email michael.

[email protected] or call (316) 440-1515. Visit www.envi-

sionconference.org.

■ 17-20. Vision Expo West 2014. Sands Expo & Convention

Center, Las Vegas, Nev. CE hours: 350+. Hosted by:

International Vision Expo and Conference. Visit www.visionex-

powest.com.

■ 18. IOA Annual Conference. Crowne Plaza Hotel, Springfield,

Ill. Hosted by: Illinois Optometric Association. CE hours: 15.

Email Charlene Marsh at [email protected] or call (217) 525-

8012. Visit www.ioaweb.org.

■ 19-20. New Mexico Optometric Association Mid-Year

Convention. Inn of the Mountain Gods, Mescalero, NM. Hosted

by: New Mexico Optometric Association. CE hours: 8. Email

Richard Montoya at [email protected] or call

(575) 751-7542. Visit www.newmexicooptometry.org.

■ 19-21. KOA 2014 Fall Congress. Marriott River Center Hotel,

Covington, Ky. Hosted by: Kentucky Optometric Association.

CE hours: 20. Email Sarah Unger at [email protected] or call

(502) 875-3516. Visit www.kyeyes.org.

■ 21. CPOS Annual CE Forum. Hotel Hershey, Hershey, Pa.

Hosted by: Central Pennsylvania Optometric Society. CE hours:

6. Email Mary Good, OD, at [email protected].

■ 21-23. CE in Italy. Rome, Italy. Hosted by: James Fanelli,

OD. CE hours: 12. Key faculty: Leonard Messner, OD, Lorraine

Lombardi, PhD, James Fanelli, OD. Email James Fanelli, OD, at

[email protected]. Visit www.CEinItaly.com.

■ 25-27. CE in Italy. Florence, Italy. Hosted by: James Fanelli,

OD. CE hours: 12. Key faculty: Leonard Messner, OD, Lorraine

Lombardi, PhD, James Fanelli, OD, Carlo Pelino, OD. Email

James Fanelli, OD, at [email protected]. Visit www.

CEinItaly.com.

■ 26-28. NOA Fall Convention. Younes Conference Center,

Kearney, Neb. Hosted by: Nebraska Optometric Association.

CE hours: 10. Contact Alissa Johnson at [email protected].

Call (402) 474-7716. Visit nebraska.aoa.org/fallconvention.

■ 28-30. CE in Italy. Tuscany, Italy. Hosted by: James Fanelli,

OD. CE hours: 12. Key faculty: Leonard Messner, OD, James

Fanelli, OD, Carlo Pelino, OD. Email James Fanelli, OD, at

[email protected]. Visit www.CEinItaly.com.

October 2014■ 2-4. OAOP Fall Conference. Renaissance Tulsa Hotel

& Convention Center, Tulsa, Okla. Hosted by: Oklahoma

Association of Optometric Physicians. CE hours: 18. Email

Heatherlyn Burton at [email protected] or call (405) 524-

1075. Visit www.oaop.org.

■ 2-5. 2014 Missouri Optometric Association Annual

Conference. University Plaza Hotel, Springfield, Mo. Hosted

by: Missouri Optometric Association. CE hours: 14. Key faculty:

Ben Gaddie, OD, Kia Eldred, OD, Sally Bodenhamer, OD. Email


Sue Brown at [email protected] or call (573) 635-6151. Visit

www.moeyecare.org.

■ 9-12. GWCO Congress 2014. Oregon Convention Center,

Portland, Ore. Hosted by: Great Western Council of Optometry.

CE hours: 70. Key faculty: Charles Brownlow, OD, Ben

Gaddie, OD, Jimmy Jackson, OD, David Kading, OD, Robert

Prouty, OD, Eric Schmidt, OD, Diana Shechtman, OD, Nancy

Torgerson, OD. Email Tracy Oman at [email protected] or call

(503) 654-1062. Visit www.gwco.org.

■ 18-19. Orlando Super Weekend. Nova Southeastern

University, Orlando, Fla. Hosted by: Nova Southeastern

University. CE hours: 12. Key faculty: Michael Chaglasian, OD,

Joseph Sowka, OD. Email Vanessa McDonald at oceaa@nova.

edu or call (954) 262-4224. Visit optometry.nova.edu/ce/index.

html.

■ 21-25. COVD 44th Annual Meeting. Sheraton San

Diego Hotel and Marina, San Diego. Hosted by: College of

Optometrists in Vision Development. Email Jackie Cencer at

[email protected] or call (330) 995-0718. Visit www.covd.org.

November 2014■ 6-9. Monterey Symposium 2014. Monterey Marriott Hotel,

Monterey, Calif. Hosted by: California Optometric Association.

CE hours: 40+. Key faculty: Melissa Barnett, OD, Jay

Binkowitz, Michael Chaglasian, OD, Dickon Chan, A. Paul

Chous, MA, OD, George Comer, OD, MBA. Email Rachael Van

Cleave at [email protected] or call (916) 441-3990. Visit

www.coavision.org.

■ 10. AFOS/Academy 2014. Denver Marriott City Center

& Colorado Convention Center, Denver, Colo. Hosted by:

Armed Forces Optometric Society & American Academy of

Optometry. CE hours: 45. Email Gina Borgognoni at execdir@

afos2020.org or call (214) 533-0227. Visit www.afos2020.org.

■ 11. Fall 2014 Educational Symposium. Colorado Convention

Center, Denver, Colo. Hosted by: Ocular Nutrition Society. CE

hours: 6. Email Jeffrey Anshel at ocularnutritionsociety@gmail.

com or call (800) 383-1202. Visit www.ocularnutritionsociety.

org.

■ 12-15. Academy 2014 Denver. Colorado Convention

Center, Denver, Colo. Hosted by: American Academy of

Optometry. Email Helen Viksnins at [email protected] or

call (321) 710-3937. Visit www.aaopt.org.

To list your meeting, please send the details to:Erin Kelly, Senior Associate Editor

Email: [email protected]

Phone: (610) 492-1005

Alcon Laboratories ............................... 11, 17, 23, 31, 43, 89, 92Phone ...................................................................... (800) 451-3937Fax ........................................................................... (817) 551-4352

Allergan, Inc. .................................................................................5Phone ...................................................................... (800) 347-4500

CooperVision ..............................................................................91Phone ...................................................................... (800) 341-2020

Diopsys .........................................................................................9Phone ...................................................................... (973) 244-0622............................................................................ [email protected]............................................................................ www.diopsys.com

Haag-Streit ..................................................................................12Phone ...................................................................... (800) 627-6286Fax ........................................................................... (603) 742-7217

HOYA Vision Care, North America ...........................................19Phone ...................................................................... (972) 221-4141Fax ........................................................................... (972) 436-9766........................................................................www.hoyavision.com

Keeler Instruments .................................................................7, 71Phone ...................................................................... (800) 523-5620Fax ........................................................................... (610) 353-7814

NicOx, Inc. ............................................................................. 24-25Phone ...................................................................... (214) 346-2913................................................................................ www.nicox.com

S4OPTIK ......................................................................................21Phone ...................................................................... (888) 224-6012

Sauflon ........................................................................................15Phone ...................................................................... (800) 682-3240Fax ........................................................................... (800) 644-3622............................................................................. [email protected].............................................................................. SauflonUSA.com

Vistakon .....................................................................................2-3Phone ...................................................................... (800) 874-5278Fax ........................................................................... (904) 443-1252

This advertiser index is published as a convenience and not as part of the advertising contract. Every care will be taken to index correctly. No allowance will be made for errors due to spelling, incorrect page number, or failure to insert.

Adver t i se rs Index

For advertising opportunities contact:Michelle Barrett (610) 492-1014 or [email protected] Henne (610) 492-1017 or [email protected] Tobin (610) 492-1011 or [email protected]

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CE COURSE TOPICS:Ocular Manifestations of Systemic Disease

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Contact Lens AdvancesSurgical Comanagement Pearls

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Surg ica l Minute

Anterior stromal puncture (ASP), first described as a treatment for recurrent

corneal erosion in 1986, improves epithelial adherence by inducing scar tissue formation between the epithelium and the anterior stroma.1

Researchers initially suggested that ASP should indent the cornea by one-half of its total register; how-ever, a subsequent report indicated that an insertion depth of just 0.1mm was adequate.2

ASP may be performed between erosive episodes or during active erosion, without the need for debridement (although debridement can be performed prior). The opti-mal candidate for anterior stromal puncture presents with a persistent area of erosion associated with pre-vious trauma or minimal anterior basement membrane dystrophy.

A single ASP procedure is effec-tive approximately 80% of the time. Surgical failures generally occur when the treatment area is too small to address all active erosions.

Your RoleWhen discussing the procedure

with the patient, the term “epithelial reinforcement” may sound more appealing––and yield less anxiety––than “stromal puncture.” After informed consent is obtained, instill several drops of a topical antibiotic and an NSAID. A lid speculum can be inserted, depending on patient

cooperation, but typically is not necessary. Instill a few drops of topi-cal anesthetic and place the patient at the slit lamp, instructing them to use the forehead rest at all times. Additionally, an intraocular pressure measurement prior to the procedure will establish a baseline for compari-son, and will help you determine if perforation was unsuccessful.

The technique involves bending the tip of a 22- to 27-gauge needle 90°. The bend at the needle tip should just be long enough to pen-etrate Bowman’s membrane (i.e., 0.2mm), but not so long that it can enter the anterior chamber (figure 1). The needle should be held tan-gential to the corneal plane, while the bend should be perpendicular to the corneal surface (figure 2).

Once the needle is prepared, gen-

tly indent the affected epithelium. Be sure to create enough punctures to cover the desired area, as well as a 1mm-diameter perimeter around the treatment zone. Place sufficient pressure so that resistance can be felt against the stroma, at approximately 5% to 10% stromal depth. Place the punctures 0.5mm to 1.0mm apart from one another.

Performing the procedure with fluorescein stain under cobalt blue light will allow bubbles to be visual-ized. Subepithelial bubbles will be round, while triangular intrastromal air bubbles will indicate that the needle has sufficiently reached the desired stromal depth. Immediately following the procedure, instill a drop of topical antibiotic and a bandage lens. Then, discharge the patient with instructions to use a combination of topical antibiotics and steroids QID for one week.

Although uncommon, the poten-tial risks with ASP include corneal perforation, corneal scarring, changes in refractive power and topographic irregularities.2

ASP is simple, cost-effective pro-cedure that, aside from the needle, doesn’t require special equipment. No chemicals are used, and because the epithelium remains relatively intact, patients heal very quickly and experience little discomfort. ■

Dr. Colatrella is the owner and medical director of PineCone Vision Center of Sartell, Minn.

1. McLean EN, MacRae SM, Rich LE. Recurrent Erosion: treatment by anterior stromal puncture. Ophthalmology. 1986 Jun;93(6):784-8.2. Rubinfeld RS, Laibson PR, Cohen EJ, et al. Anterior stromal puncture for recurrent erosion: further experience and new instru-mentation. Ophthalmic Surg. 1990 May;21(5):318-26.

Even Cleopatra would favor this simple, needle-based procedure. By Nicholas Colatrella, OD

Edited by Derek N. Cunningham, OD, and Walter O. Whitley, OD, MBA

ASP: Take a Bite Out of RCE

Go to www.revoptom.com or scan the QR code at left to see a narrated video of anterior stromal puncture.

2. ASP is performed tangential to the corneal plane.

1. A properly bent needle.

BRIEF SUMMARY OF PRESCRIBING INFORMATION

INDICATIONS AND USAGE

TRAVATAN Z® (travoprost ophthalmic solution) 0.004% is indicated for the reduction of elevated intraocular pressure in patients with open-angle glaucoma or ocular hypertension.

DOSAGE AND ADMINISTRATION

The recommended dosage is one drop in the affected eye(s) once daily in the evening. TRAVATAN Z® (travoprost ophthalmic solution) should not be administered more than once daily since it has been shown that more frequent administration of prostaglandin analogs may decrease the intraocular pressure lowering effect.

Reduction of the intraocular pressure starts approximately 2 hours after the first administration with maximum effect reached after 12 hours.

TRAVATAN Z® Solution may be used concomitantly with other topical ophthalmic drug products to lower intraocular pressure. If more than one topical ophthalmic drug is being used, the drugs should be administered at least five (5) minutes apart.

CONTRAINDICATIONS

None

WARNINGS AND PRECAUTIONS

Pigmentation

Travoprost ophthalmic solution has been reported to cause changes to pigmented tissues. The most frequently reported changes have been increased pigmentation of the iris, periorbital tissue (eyelid) and eyelashes. Pigmentation is expected to increase as long as travoprost is administered. The pigmentation change is due to increased melanin content in the melanocytes rather than to an increase in the number of melanocytes. After discontinuation of travoprost, pigmentation of the iris is likely to be permanent, while pigmentation of the periorbital tissue and eyelash changes have been reported to be reversible in some patients. Patients who receive treatment should be informed of the possibility of increased pigmentation. The long term effects of increased pigmentation are not known.

Iris color change may not be noticeable for several months to years. Typically, the brown pigmentation around the pupil spreads concentrically towards the periphery of the iris and the entire iris or parts of the iris become more brownish. Neither nevi nor freckles of the iris appear to be affected by treatment. While treatment with TRAVATAN Z® (travoprost ophthalmic solution) 0.004% can be continued in patients who develop noticeably increased iris pigmentation, these patients should be examined regularly.

Eyelash Changes

TRAVATAN Z® Solution may gradually change eyelashes and vellus hair in the treated eye. These changes include increased length, thickness, and number of lashes. Eyelash changes are usually reversible upon discontinuation of treatment.

Intraocular Inflammation

TRAVATAN Z® Solution should be used with caution in patients with active intraocular inflammation (e.g., uveitis) because the inflammation may be exacerbated.

Macular Edema

Macular edema, including cystoid macular edema, has been reported during treatment with travoprost ophthalmic solution. TRAVATAN Z® Solution should be used with caution in aphakic patients, in pseudophakic patients with a torn posterior lens capsule, or in patients with known risk factors for macular edema.

Angle-closure, Inflammatory or Neovascular Glaucoma

TRAVATAN Z® Solution has not been evaluated for the treatment of angle-closure, inflammatory or neovascular glaucoma.

Bacterial Keratitis

There have been reports of bacterial keratitis associated with the use of multiple-dose containers of topical ophthalmic products. These containers had been inadvertently contaminated by patients who, in most cases, had a concurrent corneal disease or a disruption of the ocular epithelial surface.

Use with Contact Lenses

Contact lenses should be removed prior to instillation of TRAVATAN Z® Solution and may be reinserted 15 minutes following its administration.

ADVERSE REACTIONS

Clinical Studies Experience

Because clinical studies are conducted under widely varying conditions, adverse reaction rates observed in the clinical studies of a drug cannot be directly compared to rates in the clinical studies of another drug and may not reflect the rates observed in practice. The most common adverse reaction observed in controlled clinical studies with TRAVATAN® (travoprost ophthalmic solution) 0.004% and TRAVATAN Z® (travoprost ophthalmic solution) 0.004% was ocular hyperemia which was reported in 30 to 50% of patients. Up to 3% of patients discontinued therapy due to conjunctival hyperemia. Ocular adverse reactions reported at an incidence of 5 to 10% in these clinical studies included decreased visual acuity, eye discomfort, foreign body sensation, pain and pruritus. Ocular adverse reactions reported at an incidence of 1 to 4% in clinical studies with TRAVATAN® or TRAVATAN Z® Solutions included abnormal vision, blepharitis, blurred vision, cataract, conjunctivitis, corneal staining, dry eye, iris discoloration, keratitis, lid margin crusting, ocular inflammation, photophobia, subconjunctival hemorrhage and tearing.

Nonocular adverse reactions reported at an incidence of 1 to 5% in these clinical studies were allergy, angina pectoris, anxiety, arthritis, back pain, bradycardia, bronchitis, chest pain, cold/flu syndrome, depression, dyspepsia, gastrointestinal disorder, headache, hypercholesterolemia, hypertension, hypotension, infection, pain, prostate disorder, sinusitis, urinary incontinence and urinary tract infections.

In postmarketing use with prostaglandin analogs, periorbital and lid changes including deepening of the eyelid sulcus have been observed.

USE IN SPECIFIC POPULATIONS

Pregnancy Pregnancy Category CTeratogenic effects: Travoprost was teratogenic in rats, at an intravenous (IV) dose up to 10 mcg/kg/day (250 times the maximal recommended human ocular dose (MRHOD), evidenced by an increase in the incidence of skeletal malformations as well as external and visceral malformations, such as fused sternebrae, domed head and hydrocephaly. Travoprost was not teratogenic in rats at IV doses up to 3 mcg/kg/day (75 times the MRHOD), or in mice at subcutaneous doses up to 1 mcg/kg/day (25 times the MRHOD). Travoprost produced an increase in post-implantation losses and a decrease in fetal viability in rats at IV doses > 3 mcg/kg/day (75 times the MRHOD) and in mice at subcutaneous doses > 0.3 mcg/kg/day (7.5 times the MRHOD).

In the offspring of female rats that received travoprost subcutaneously from Day 7 of pregnancy to lactation Day 21 at doses of ≥ 0.12 mcg/kg/day (3 times the MRHOD), the incidence of postnatal mortality was increased, and neonatal body weight gain was decreased. Neonatal development was also affected, evidenced by delayed eye opening, pinna detachment and preputial separation, and by decreased motor activity.

There are no adequate and well-controlled studies of TRAVATAN Z® (travoprost ophthalmic solution) 0.004% administration in pregnant women. Because animal reproductive studies are not always predictive of human response, TRAVATAN Z® Solution should be administered during pregnancy only if the potential benefit justifies the potential risk to the fetus.

Nursing Mothers

A study in lactating rats demonstrated that radiolabeled travoprost and/or its metabolites were excreted in milk. It is not known whether this drug or its metabolites are excreted in human milk. Because many drugsare excreted in human milk, caution should be exercised when TRAVATAN Z® Solution is administered to a nursing woman.

Pediatric Use

Use in pediatric patients below the age of 16 years is not recommended because of potential safety concerns related to increased pigmentation following long-term chronic use.

Geriatric Use

No overall clinical differences in safety or effectiveness have been observed between elderly and other adult patients.

Hepatic and Renal Impairment

Travoprost ophthalmic solution 0.004% has been studied in patients with hepatic impairment and also in patients with renal impairment. No clinically relevant changes in hematology, blood chemistry, or urinalysis laboratory data were observed in these patients.

NONCLINICAL TOXICOLOGY

Carcinogenesis, Mutagenesis, Impairment of Fertility Two-year carcinogenicity studies in mice and rats at subcutaneous doses of 10, 30, or 100 mcg/kg/day did not show any evidence of carcinogenic potential. However, at 100 mcg/kg/day, male rats were only treated for 82 weeks, and the maximum tolerated dose (MTD) was not reached in the mouse study. The high dose (100 mcg/kg) corresponds to exposure levels over 400 times the human exposure at the maximum recommended human ocular dose (MRHOD) of 0.04 mcg/kg, based on plasma active drug levels. Travoprost was not mutagenic in the Ames test, mouse micronucleus test or rat chromosome aberration assay. A slight increase in the mutant frequency was observed in one of two mouse lymphoma assays in the presence of rat S-9 activation enzymes.

Travoprost did not affect mating or fertility indices in male or female rats at subcutaneous doses up to 10 mcg/kg/day [250 times the maximum recommended human ocular dose of 0.04 mcg/kg/day on a mcg/kg basis (MRHOD)]. At 10 mcg/kg/day, the mean number of corpora lutea was reduced, and the post-implantation losses were increased. These effects were not observed at 3 mcg/kg/day (75 times the MRHOD).

PATIENT COUNSELING INFORMATION

Potential for Pigmentation

Patients should be advised about the potential for increased brown pigmentation of the iris, which may be permanent. Patients should also be informed about the possibility of eyelid skin darkening, which may be reversible after discontinuation of TRAVATAN Z® (travoprost ophthalmic solution) 0.004%.

Potential for Eyelash Changes

Patients should also be informed of the possibility of eyelash and vellus hair changes in the treated eye during treatment with TRAVATAN Z® Solution. These changes may result in a disparity between eyes in length, thickness, pigmentation, number of eyelashes or vellus hairs, and/or direction of eyelash growth. Eyelash changes are usually reversible upon discontinuation of treatment.

Handling the Container

Patients should be instructed to avoid allowing the tip of the dispensing container to contact the eye, surrounding structures, fingers, or any other surface in order to avoid contamination of the solution by common bacteria known to cause ocular infections. Serious damage to the eye and subsequent loss of vision may result from using contaminated solutions.

When to Seek Physician Advice

Patients should also be advised that if they develop an intercurrent ocular condition (e.g., trauma or infection), have ocular surgery, or develop any ocular reactions, particularly conjunctivitis and eyelid reactions, they should immediately seek their physician’s advice concerning the continued use of TRAVATAN Z® Solution.

Use with Contact Lenses

Contact lenses should be removed prior to instillation of TRAVATAN Z® Solution and may be reinserted 15 minutes following its administration.

Use with Other Ophthalmic Drugs

If more than one topical ophthalmic drug is being used, the drugs should be administered at least five (5) minutes between applications.

Rx Only

U.S. Patent Nos. 5,631,287; 5,889,052, 6,011,062; 6,235,781; 6,503,497; and 6,849,253

ALCON LABORATORIES, INC.Fort Worth, Texas 76134 USA© 2006, 2010, 2011, 2012 Novartis4/13 TRV13021JAD5/14 TRV14045JAD


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Diagnos t i c Quiz

HistoryA 22-year-old white female

presented to the ophthalmology department following an emergency room visit with a chief complaint of worsening facial asymmetry.

Her systemic and ocular histories were noncontributory. The patient reported no known allergies of any kind.

Diagnostic DataHer best-uncorrected entering

visual acuity measured 20/20 OU at distance and near. There was no evidence of afferent pupillary defect or visual field involvement OU. The anterior segment findings were nor-mal in both eyes.

Intraocular pressure measured 14mm Hg OU. Dilated funduscopy was within normal limits in both eyes. The external examination findings are illustrated in the pho-tographs.

Your DiagnosisHow would you approach this

case? Does the patient require any additional tests? What is your diagnosis? How would you man-age this patient? What is the likely

prognosis?To find out, please visit www.

revoptom.com. Click on the cover icon for this month’s issue, and then click “Diagnostic Quiz” under the table of contents. ■

Next Month in the MagAugust features our 38th Annual Contact Lens Report. Topics include: • 10 Essential CL Marketing Do’s and Don’ts • The Case for Daily Disposables: Pricing and Presentation • Why Aren’t We Doing Better with Multifocals? • Inventory and Delivery: Keeping Up with the Retail Giants Also inside: • Case Report: Endogenous Endophthalmitis

• Optometric Study Center: Managing Neovascular Glaucoma Secondary to Diabetes (earn 2 CE credits)

FeedbackReview of Optometry welcomes questions and comments. E-mail Jack Persico, editor-in-chief, [email protected], with “Letter to the Editor” as the subject line. Or, write to Review of Optometry, 11 Campus Blvd., Suite 100, Newtown Square, PA 19073.

Retina Quiz Answers (from page 69): 1) c; 2) c; 3) a; 4) b; 5) b.

A 50-50 SplitBy Andrew S. Gurwood, OD

Gross external images of our 22-year-old patient revealed obvious facial asymmetry. What is the correct diagnosis, and how should she be managed?

The attraction is natural.

*Evaporative Tear Deficiency or Aqueous Tear Deficiency (non-Sjogren’s only). ©2014 CooperVision, Inc.

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Through the OPENINGSTM Patient Support Program , TRAVATAN Z® Solution patients have easy access to financial savings* along with disease state education, and reminders to refill their prescriptions. To learn more, visit professional.openingsprogram.com.

Always dispense the as written®

INDICATIONS AND USAGETRAVATAN Z® (travoprost ophthalmic solution) 0.004% is indicated for the reduction of elevated intraocular pressure (IOP) in patients with open-angle glaucoma or ocular hypertension.

Dosage and AdministrationThe recommended dosage is 1 drop in the affected eye(s) once daily in the evening. TRAVATAN Z® Solution should not be administered more than once daily since it has been shown that more frequent administration of prostaglandin analogs may decrease the IOP-lowering effect.

TRAVATAN Z® Solution may be used concomitantly with other topical ophthalmic drug products to lower IOP. If more than 1 topical ophthalmic drug is being used, the drugs should be administered at least 5 minutes apart.

IMPORTANT SAFETY INFORMATIONWarnings and PrecautionsPigmentation—Travoprost ophthalmic solution has been reported to increase the pigmentation of the iris, periorbital tissue (eyelid), and eyelashes. Pigmentation is expected to increase as long as travoprost is administered. After discontinuation of travoprost, pigmentation of the iris is likely to be permanent, while pigmentation of the periorbital tissue and eyelash changes have been reported to be reversible in some patients. The long-term effects of increased pigmentation are not known. While treatment with TRAVATAN Z® Solution can be continued in patients who develop noticeably increased iris pigmentation, these patients should be examined regularly.

Eyelash Changes—TRAVATAN Z® Solution may gradually change eyelashes and vellus hair in the treated eye. These changes include increased length,

thickness, and number of lashes. Eyelash changes are usually reversible upon discontinuation of treatment.

Use With Contact Lenses—Contact lenses should be removed prior to instillation of TRAVATAN Z® Solution and may be reinserted 15 minutes following its administration.

Adverse ReactionsThe most common adverse reaction observed in controlled clinical studies with TRAVATAN Z® Solution was ocular hyperemia, which was reported in 30 to 50% of patients. Up to 3% of patients discontinued therapy due to conjunctival hyperemia. Ocular adverse reactions reported at an incidence of 5 to 10% in these clinical studies included decreased visual acuity, eye discomfort, foreign body sensation, pain, and pruritus. In postmarketing use with prostaglandin analogs, periorbital and lid changes including deepening of the eyelid sulcus have been observed.

Use In Specifi c PopulationsUse in pediatric patients below the age of 16 years is not recommended because of potential safety concerns related to increased pigmentation following long-term chronic use.

For additional information about TRAVATAN Z® Solution, please see Brief Summary of full Prescribing Information on adjacent page. *Eligibility terms and conditions apply. See openingsprogram.com

Reference: 1. Drugs@FDA. FDA Approved Drug Products. Travatan Z page. US Food and Drug Administration Web site. http://www.accessdata.fda.gov/scripts/cder/drugsatfda/index.cfm?fuseaction=Search.DrugDetails. Accessed April 28, 2014.

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