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^Trademarks are the property of their respective owners.
Important information for AIR OPTIX
COLORS (lotraflcon 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 fle, 2013. 2. Based on in vitro measurement of contact
angles of unworn lenses; signifcance demonstrated at 0.05 level. Alcon data on fle, 2013. 3. Eiden SB, Davis R, Bergenske P. Prospective
study of lotraflcon 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
Page 32
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
20
th
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/les/VCUVReport2013FINAL.pdf.
Accessed May 7, 2014. 2. Chandler H. Ultraviolet absorption by contact lenses and the signicance 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
O
mega-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 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
ndings not only show promising
therapeutic potential for resolution
of neovascular AMD, but also for
other conditions or diseases that
involve pathologic angiogenesis
and inammation.
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
efcacy 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 identied
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 identied 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-nd
limbal stem cells. The research, published
online in Nature, is also one of the rst
successes in constructing a tissue from an
adult-derived human stem cell.
This breakthrough developmenta
collaboration among the Massachusetts Eye
and Ear/Schepens Eye Research Institute, Boston Childrens Hospital, Brigham and Womens
Hospital and the VA Boston Healthcare Systemoffers 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
N
ew research shows that the
brainnot the eyecon-
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 Alzheimers.
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 eyewithout 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 glaucomaapop-
tosisis remarkably similar to the
apoptotic mechanism that oper-
ates in the brains of people with
Alzheimers 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
studys 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. Rened 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 benet 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 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
T
here will be enough optom-
etristsand perhaps an
oversupplyinto 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 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 lled with
additional patientsan 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 specic 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-
nicantly 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 Point
At a press conference held dur-
ing Junes AOA meeting in Phila-
delphia, AOA and ASCO ofcials
underscored that this study is
merely a starta working model
from which to begin to continu-
ously assess eye care supply and
demand as factors change.
What weve 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
schoolsor 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
optometrys 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 AOAs
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 theres 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
patients 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 led patents
on an initial prototype, which they admit is radical, as no one has ever put electronics
inside the lens of an eyeyet. The current prototype is too large to t in an articial lens,
but the team says its condent that they can downscale it to a workable size.
Varel , Shih Y, Otis BP, et al. A wireless intraocular pressure monitoring device with a solder-lled microchannel antenna.
J Micromech Microeng. Published online March 13, 2014.
Monitoring IOP with an IOL
I
m
a
g
e
:

U
n
i
v
e
r
s
i
t
y

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f

W
a
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BUSINESS OFFICES
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VICE PRESIDENT, CIRCULATION
EMELDA BAREA
News Review
C
osts 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
90all 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 ination,
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
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
$1,000
900
800
700
600
500
400
300
200
100
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
TM
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 professionals recommended lens
wear, care, and replacement schedule. Consult package insert for complete information, available without charge from Alcon at (800) 241-5999 or myalcon.com.
contact lenses
Because todays world doesnt give your patients eyes a break...
THIS IS WHY I CARE
Choose Alcon Vision Care products
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haag-streit-usa.com
2014 Haag-Streit USA. All Rights Reserved.
800-787-5426
Tradition & Innovation.
Powered by
Time to give up on Old Floppy.
Seriously, some doctors are still routing data with power sticks or
floppy disks. But Octopus has incorporated connectivity into its DNA
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And the same holds true for our reproducible data and incredibly
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Get an online demo of the Octopus 600. Call 800-787-5426, and turn
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REVIEW OF OPTOMETRY JULY 15, 2014 13
50
Why Dry Eye Trials
Often 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 of
Dry 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
Contents
Review 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
20
th
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:
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 Management
38
Our success in managing glaucoma hinges on our ability to
recognizeand make sense ofboth 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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EDITORIAL BOARD
CHIEF CLINICAL EDITOR PAUL M. KARPECKI, OD
ASSOCIATE CLINICAL EDITORS JOSEPH P. SHOVLIN, OD;
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COLUMNISTS
CHAIRSIDE MONTGOMERY VICKERS, OD
COMANAGEMENT Q+A PAUL C. AJAMIAN, OD
CORNEA & CONTACT LENS Q+A JOSEPH P. SHOVLIN, OD
DIAGNOSTIC QUIZ ANDREW S. GURWOOD, OD
GLAUCOMA GRAND ROUNDS JAMES L. FANELLI, OD
RESEARCH REVIEW PAUL M. KARPECKI, OD;
DIANA L. SHECHTMAN, OD
RETINA QUIZ MARK T. DUNBAR, OD
REVIEW OF SYSTEMS CARLO J. PELINO, OD;
JOSEPH J. PIZZIMENTI, OD
SURGICAL MINUTE DEREK N. CUNNINGHAM, OD;
WALTER O. WHITLEY, OD, MBA
THERAPEUTIC REVIEW JOSEPH W. SOWKA, OD;
ALAN G. KABAT, OD
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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
62
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CONTRIBUTING EDITORS
PAUL 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, NC
FRANK FONTANA, OD, ST. LOUIS
GARY S. GERBER, OD, HAWTHORNE, NJ
ANDREW 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, NY
CARLO 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 BOARD
JEFFREY 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, NJ
GLENN 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, NY
IAN 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, NJ
CHRISTOPHER 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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Understand. Manage. Grow.
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 patients 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 specic 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 specic product. The
majority of patients surveyed chose the
doctors 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 useboth prescription and
OTC products. It is critical to effec-
tively communicate a specic 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 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 inuences 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 doctors recommendation is the
key to inuencing patient behavior. If it
is true that there is a difference in lens
care productsand it is truethen 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
drbrimer@crystalvisionservices.com.
Free is Not Always Effective
How 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 denitive direction
from the doctor have a greater impact on patient purchases?
ADVERTORI AL
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By Crystal M. Brimer, OD
WHATS THE SOLUTION?
KEY POINTS
Patients look to their eye care provider
for expertise, knowledge, and specic
direction.
Patients in a recent survey
indicated they would forgo a free
sample in exchange for a specic
recommendation from their eye care
provider.
2

Giving patients clear advice about
what products to useand how to
use themmay 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
specic product
recommendation
and proper lens
care protocol to
the patient.
Outlook
E
ven 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
arent decliningtheyre 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 its 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, its 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
testsvisual fields, OCTs, optic
nerve examscan make patient
visits time consuming for the prac-
tice. The clinical decision-making
responsibilitiesthough 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 optometrys 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
wont improve until ODs take charge
of it. Nows your chance to shine.
ODs: Were Up to the Task
Fortunately, 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.
Theres 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 wont be easy. Relating to the
increasingly diverse population will
pose challenges too. But glaucoma
is a public health crisis in the mak-
ingand 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
Rise and Shine
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OF THE INDEPENDENT
Chai r Side
iPhone Refraction? iLove It!
An app that refracts is like having an OD in your pocketwhich begs the question:
Is that an OD in your pocket or are you just happy to see me? By Montgomery Vickers, OD
I
hear theres 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
wont 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 Im 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
cant 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 Ill 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? Thats right! 64!
(If you dig deep enough, there must
be at least one website that will
say hes not 58.) 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 ladys anterior seg-
ment. (Ill just leave the joke on the
table there.)
trace a rectangle for my grandkids.
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 wont
come to an end because opticians
wont 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 weve 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 wont
really need to see at all. Well just
dangle two smartphones in front
of our eyes from a designer frame.
Your car will drive itself so youll 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 cant wait!
Contact S4OPTIK for more information.
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Codi ng Abstract
O
ne 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 Im 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, its 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 theres 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 careand our medical
recordneed to be specific to the
individual patient. We dont per-
form services based on an ICD-9
or ICD-10 code, nor do we bundle
care just because we dont 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 Reasons
Keep in mind that medical care
today is based on medical neces-
sitymeaning 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
its 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, its 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 CodingAbstract@
gmail.com.
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, its 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
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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 todays 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
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Clinical Care
Scleritis:
When a Red Eye Raises a Red Flag
S
cleritis manifests as
a very painful red
eyebut it sometimes
suggests that some-
thing deeper than the eye is
involved. Its often, but not
always, associated with an
underlying autoimmune dis-
order. So, its 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 Wegeners
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
Wegeners 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 incidencejust 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 Scleritis
Laboratory Test Systemic Condition
ACE (angiotensin-converting enzyme)
Chest X-ray
Sarcoidosis
ANA (antinuclear antibody) Lupus
c-ANCA (cytoplasmic antineutrophil cytoplasmic
antibody)
Wegeners 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 patients 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-
phonatescommonly used for
treatment of osteoporosiscan
also be associated with scleritis.
11
In this patients case, coman-
agement with oncology was
critical. We kept in close contact
with the oncologist and, because
of the patients 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. Episcleritis
Scleritis 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 vesselsthe deeper, episcleral vessels wont 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 patients
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 patients 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.
Wegeners 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. Wegeners 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-inflammatories
In 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
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The water gradient structure of DAILIES TOTAL1

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DAILIES TOTAL1
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7,8

A NEW OPPORTUNITY
Wearers 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 discomfortwhich 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 discomfortand letting them know that we may be able
to address itworks well. When I introduce DAILIES TOTAL1

water gradient contact lenses, I explain that the lens surface is
moist, lubricious, and very smoothso smooth that they may
not feel the lens at all.
10
Patients appreciate learning about new
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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 Kofer Vision Group in
Lexington, KY.
REFERENCES
1. Craig JP, Willcox MDP, Argeso P, et al. The TFOS international workshop on
contact lens discomfort: report of the contact lens interactions with the tear lm
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. Coefcient 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 delelcon A
lenses. Contact Lens Anterior Eye. 2012;35(Supp 1):e14.
6. Alcon data on le, 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. Prez-gmez 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 le, 2011.
*In vitro measurement of unworn lenses.
When placed on the eye, a contact lens alters the structure
of the tear lm 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 lm stability and
friction during blink.
But the surface of most soft contact
lenses lacks the corneas ability to bind
mucus, which aids in the formation of the
normal tear lm. In lieu of the corneas
mucin glycocalyx, a moist and lubricious
contact lens surface can create an appropriate environment for
tear lm stability and for the eyelids to pass over smoothly.
LUBRICITY: THE CONCEPT
Lubricity is dened 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 coefcient of
friction (high lubricity) is a principal factor in predicting contact
lens comfort.
3
Further, lens wearers with dryness symptoms
are signicantly 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 CHALLENGE
Though 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 modication for enhanced surface hydrophilicity.
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Plotting the Path of
Progression
W
ith just one health sta-
tus variable that yields
to medical or surgical
intervention, glaucoma
management at its core is very fun-
damentallower 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 Readings
Glaucoma progression tests are
only relevant if we can do some-
thing about the findings; namely,
adjusting the patients 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 recognizeand make
sense ofboth 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 patients RNFL
OCT and GPA revealed no progression over
a seven-year period, thereby meeting the
overall management goal.
20th Annual GLAUCOMA Report
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IOP
Average 20.7mm Hg
Standard deviation 1.15mm Hg
IOP
Average 16.2mm Hg
Baseline reduction: -22%
IOP
Average 16.2mm Hg
IOP
Average 15.6mm Hg
IOP
Average 15.2mm Hg
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: 68m
RNFL time-domain OCT
FOLLOW-UP 1
average RNFL: +4m
RNFL spectral-domain OCT
BASELINE [JAN. 2010]
average RNFL: 57m
BASELINE [JAN. 2010]
average RNFL: 57m
FOLLOW-UP 2 [FEB. 2011]
average RNFL: 0m
FOLLOW-UP 3 [MAY 2012]
average RNFL: -3m
FOLLOW-UP 4 [SEPT. 2013]
average RNFL: -2m
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 fluctuationthought 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: 108m
Average RNFL: 109m +1m
Average RNFL: 92m -16m
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 OCTs 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: 99m
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 thinningfea-
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 1m to 5m
for average RNFL thickness. There-
fore, if the average RNFL OCT
indices are reduced by greater than
5m 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 OCTwhich include focal
loss volume and global loss volume
measurementsmay 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
2m to 5m, 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 Picture
It 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
P
seudoexfoliation 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
isnt 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
OAGintraocular 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.
Epidemiology
Extensive 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 Risk
As 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
individualsall 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 Schlemms 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
Studywhich monitored the
natural course of PXGfound 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 Associations
Unlike 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 Aspects
Physiologic ocular findings of
this aggressive disease may be
subtle. The ocular presentation
generally is bilateral, but not neces-
sarily symmetrical. Corneal findings
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, anddue to con-
vection currents of the aqueous in
the anterior chambermay evolve
over time.
The corneal endothelial cells
often are affected dramatically
patients. Most individuals exhibit
fewer total endothelial cells with
morphological alterations. Such
endothelial changes are also seen in
Fuchs dystrophyalthough 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 thats
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 Schwalbes
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
lossboth 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 bulls 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
dilationalthough 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
uniquewith 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 patients 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
patients 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 Intervention
The 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
ALTs 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 Schlemms 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 Schlemms canal.
38

Because the iStent facilitates bypass
of the trabecular meshwork, the
resultant IOP is based on the cir-
cumferential flow of Schlemms
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 bulls eye pattern of
fibrillar material on a dilated, lightly
pigmented patient. Looking closely,
theres also a peripupillary accumulation
of material.
P
h
o
t
o
:

S
t
e
p
h
e
n

A
.

O
b
s
t
b
a
u
m
,

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 PXGs signs can be
subtle, its impact can be visually
devastatingso 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, Schltzer-Schrehardt U, Kchle M. Pseudo-
exfoliation syndrome for the comprehensive ophthalmologist.
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2. Cashwell LF, Shields MB. Exfoliation syndrome. Preva-
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3. Mitchell P, Wang JJ, Hourihan F. The relationship between
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4. Hiller R, Sperduto RD. Pseudoexfoliation, intraocular pres-
sure, and senile lens changes in a population-based survey.
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5. Sein J, Galor A, Sheth A, et al. Exfoliation syndrome: new
genetic and pathophysiologic insights. Curr Opin Ophthal-
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6. Taylor HR. Pseudoexfoliation, an environmental disease?
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7. Ritch R. Exfoliation syndrome-the most common identifi-
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8. Jeng SM, Karger RA, Hodge DO, et al. The risk of glau-
coma in pseudoexfoliation syndrome. J Glaucoma. 2007
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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, Schltzer-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, Ekstrm 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
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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, Flgel-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, Yksel 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. Schltzer-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):1834-41
34. 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, ODonoghue 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.
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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-
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40. Jordan JF, Wecker T, van Oterendorp C, et al. Tra-
bectome surgery for primary and secondary open angle
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41. Lin SC. Endoscopic and transscleral cyclophotocoagula-
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42. Lima FE, Magacho L, Carvalho DM, et al. A prospective,
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wettability and lipid deposit resistance
compared to other silicone hydrogel
lenses.
4
CLINICAL RELEVANCE
The 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
depositsof both tear lm lipids and of
cosmetic productsmay 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 lm lipids in vitro to various silicone hydrogels over
time. Invest Ophthalmol Vis Sci. 2008;49:120-4.
The Makeup Factor: Expanding the Denition
of Deposit Resistance
Cosmetics on the surface of a soft contact lens can affect wettability, t, 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 (lotralcon 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 quantied
by mean pixel brightness using darkeld
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 (lotralcon 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 lm
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
modication.
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
Mascaraespecially
waterproofand 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
Sponsored by Alcon
Glaucoma
The Changing and Challenging
Epidemiology of
W
hen 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 Population
The 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 continuethe 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
0
2010 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 Asian American 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, its 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-
cansthose 85 and olderthere 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 Distinctions
The 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 Status
Poverty 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
52
58
56
55
67
62
61
2030 2050
65 years and over 65 to 74 years 75 to 84 years 85 years and over
S
o
u
r
c
e
:

U
S

C
e
n
s
u
s

B
u
r
e
a
u
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 Ahead
Optometrists 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.0b013e3181fc3638
2. 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, Ros-Vargas M, Albert NG. The Hispanic Popula-
tion: 2010 Census Briefs. Issued May 2011
C2010BR-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.2011.169
12. 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.2014.145
13. 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.0b013e3283360b7e
14. 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.2012.10.003
15. 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.0b013e31821dac86
16.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.2013.4694
18. Muir KW, Christensen L, Bosworth HB. Health literacy and
glaucoma. Curr Opin Ophthalmol. 2013 Mar;24(2):119-24.
doi: 10.1097/ICU.0b013e32835c8b0e
19. 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/A17
21. 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.
Optometric Physician delivers UP-TO-DATE news and
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Glaucoma on Trial:
Release Date: July 2014
Expiration Date: July 1, 2017
Goal 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, OD
Credit 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.
A
51-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 477m OD and 473m
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
patientwith moderately high IOP
and thin corneas but relatively nor-
mal visual field results and OCT of
the nerve fiber layerbe 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, lets 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)
OPTOMETRI C 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 doesnt necessarily
mean all patients must be treated.
Because we cant know which
patients will progress, in some
cases, we can observe closely and
tailor management to the individual
patient. In particular, Its 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.
OHTS
Before 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.
damageotherwise 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 studys 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
Not all patients with high IOP
require hypotensive treatment. Con-
sider all factorssuch 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
pachymetrybefore starting ocular
medications.
Subjects with corneal thickness
of 555m or less had three times the
risk of developing primary open-
angle glaucoma compared with
those who had corneal thickness of
588m 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
CIGTS
When 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 wont 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 measurea health-
related quality of life question-
nairelooked at how the treatment
affected the patients 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
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%.
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.
LoGTS
Have 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
patients 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 patients 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.
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.
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: Dont
Let Glaucoma Rob You Blind
AGIS
While there is no cure for glau-
coma, our current therapies are
all aimed toward a simple goal: to
preserve visual functionthat 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.
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
fieldyet a number of patients in
this group still showed progressive
visual field loss.
23
TVT Study
When 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 patients
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
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-
itedsurgeons 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 patients 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 cant know. Ultimately,
treatment decisions, while guided
by information learned from the
landmark glaucoma studies, must
be based on each individual patient
and their optometrists 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.
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Y
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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 555m.
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 patients 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 QUI Z
Study (AGIS): 13. Comparison of treatment outcomes within race:
10-year results. Ophthalmology. 2004 Apr; 111(4): 651-64.
Study (AGIS): 4. Comparison of treatment outcomes within race.
Seven-year results. Ophthalmology. 1998 Jul; 105(7): 1146-64.
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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OSC QUI Z
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Glaucoma on Trial: Clinical Implications of the Landmark Glaucoma Studies
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Lesson 110261 RO-OSC-0714
Cor nea+Cont act 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 cosmeticpatients
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 elses 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.
P
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Administered by
Partially supported by an educational grant from
12 CE
Credits
(COPE approval pending)
Save the Date
EAST COAST
OPTOMETRIC
GLAUCOMA
SYMPOSIUM
6
th
annual
Loews Hotel
PHILADELPHIA, PA
October 24-25, 2014
Discounted Room Rates: $219 single/ $229 double. Call 888-575-6397 and identify yourself
as a participant of the East Coast Optometric Glaucoma Symposium (ECOGS)
12 COPE Credits for only $225!
Speakers:
Michael Chaglasian, OD Ben Gaddie, OD
Nils Loewen, MD, PhD Jonathan Myers, MD
MEETING CO-CHAIRS:
MURRAY FINGERET, OD ROBERT N. WEINREB, MD
3 Ways to Register
Online: www.revoptom.com/ECOGS2014
Email: Reviewmeetings@jobson.com
Call Lois DiDomenico: 800-835-9877
Approval pending
Alcon
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. (Hes 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, its best
to focus on the individual patients
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 doesnt 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 hell 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, youll probably need to put
the patient on additional glaucoma
treatmentdepending 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 whos 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 theyre showing
significant complications, he says.
If the inflammation is improving
but the IOP is still going up, then
taper the steroid. But dont 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 patients IOP has risen to
28mm Hg. Its 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 jmurphy@jobson.com.
P
h
o
t
o
:

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c
h
a
e
l

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o
t
t
i
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i
,

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,

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d

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i
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e

T
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d
,

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D
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 itselfnot the steroidis
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 Steroid
Soft steroids dont penetrate the anterior chamber
as well as more potent steroids. This means that they
tend to cause a steroid response less oftenbut 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, hell 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 suppressantsbeta 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 arent 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
I
deally, 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 malformationsand 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 AVMs
Neurological 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
ARUBA
The Randomized trial of Unruptured Brain Arteriovenous malformationsbetter known as
the ARUBA studyis 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 T1
sagittal view.
Diagnostic Work-up
Its 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. Its 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. Its 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-
torsbe they genetic, demographic
or environmentalhave 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.
Neuroimaging
Proper 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 AVMpar-
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 Approaches
The 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
patients 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 treatmentincluding
endovascular embolization, surgi-
cal resection and focal beam radia-
tionis 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 H
2
0. 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
Syndromes
5
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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Ret i na Quiz
A
22-year-old black female
presented for an eye exam
to determine if she met the
visual requirements for obtain-
ing a drivers 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 drivers license?
a. Yes.
b. No.
c. Yesfor daytime driving only.
d. Yeswith 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 patients fundus evaluation reveals significant changes in both eyes (OD left, OS right).
Ret i na Quiz
Discussion
From 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 hairas 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-
uals skin usually
is a creamy white
color. Also, the
patients hair may
be light yellow,
blond or light
brown.
Type 3
includes 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 causealthough
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 hypoplasiathe 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 patients
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 didnt 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 drivers license The
answer is no. In Florida, the law
states that the drivers 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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Ther apeut i c Review
A
35-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 549m OD
and 558m 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 Sampaolesis 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
months column, we discuss PDS
and pigmentary glaucoma, as well
as address the potential therapeutic
benefits of LPI.
PDS and Pigmentary Glaucoma
Patients 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 Schwalbes line (where
it is referred to as Sampaolesis 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.
Ther apeut 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 extentbut 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 studymost
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? Its 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.
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edger and frame tracing system with a computer-
assisted centering and blocking devicetogether, Nek-
sia is designed to finish modern premium lenses and
frames with precision and ease.
Essilor touts Neksias 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 Neksias
database.
Visit www.essilorinstrumentsusa.com.
See the Bigger Picture
Low-vision macular degeneration patients who need
greater magnification for home or office now have even
more options with Tech Optics Internationals 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 Refraction
Enjoy freedom of movement and full control of the
phoropter head and projection chart with Visionixs
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 Lenses
Systems are Go
The FDA has issued marketing clearance for Bausch
+ Lombs 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 Happy
Surveys 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 Pack
Research 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
Pr oduct Review
Eyewear
Righteous Courage
For every purchase from
its Not of This World line
which now includes Righ-
teous sunglasses and Courage
framesEyes 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 Glam
Five 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 frameswhich will come at a price of about
$1,500is unchanged, except for the designer element.
Visit www.google.com/glass.
Diagnostics
Genetic 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
Nicoxs 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. Nicoxs 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 App
Find & Wear
The process of finding and wearing the right contact
lenses has gone digital with CooperVisions 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 its time for a
lens replacement.
Visit www.coopervision.com.
Dry Eye Therapy
Soothing Protection
A compromised lipid layer of the tear film is the defi-
ciency most associated with dry eye symptoms. Bausch
+ Lombs 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 Education
Sun Safety
Its 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 Care
Flip Out for Flip-Tops
Forget the white screw-top capAlcon has intro-
duced a convenient flip-top for its Clear Care Cleaning
and Disinfecting Solution.
Theyve 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 ofce? 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 i ngs + Conferences
July 2014
24-27. Florida Optometric Associations Annual Convention.
Boca Raton Resort & Club, Boca Raton, Fla. Hosted by: Florida
Optometric Association. CE hours: 22. Email Blake Moore,
blake@floridaeyes.org 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 jerrysue13@comcast.net 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 swfoa@att.net 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
oceaa@nova.edu 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 ocularhealthfoundation@gmail.com 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 vt.od.ce@gmail.com.
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 oceaa@nova.edu 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.
epp@envisionus.com 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 ioabb@ioaweb.org 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 newmexicooptometry@gmail.com 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 sarah@kyeyes.org 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 cposrsvp@gmail.org.
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
jamesfanelli@CEinItaly.com. 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 jamesfanelli@CEinItaly.com. 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 noa@assocoffice.net.
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
jamesfanelli@CEinItaly.com. 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 heatherlyn@oaop.org 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 sue@moeyecare.org 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 gwco@gwco.org 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
jcencer@covd.org 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 contact@coavision.org 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 HelenV@aaoptom.org or
call (321) 710-3937. Visit www.aaopt.org.
To list your meeting, please send the details to:
Erin Kelly, Senior Associate Editor
Email: ekelly@jobson.com
Phone: (610) 492-1005
Alcon Laboratories ............................... 11, 17, 23, 31, 43, 89, 92
Phone ...................................................................... (800) 451-3937
Fax ........................................................................... (817) 551-4352
Allergan, Inc. .................................................................................5
Phone ...................................................................... (800) 347-4500
CooperVision ..............................................................................91
Phone ...................................................................... (800) 341-2020
Diopsys .........................................................................................9
Phone ...................................................................... (973) 244-0622
............................................................................ info@diopsys.com
............................................................................ www.diopsys.com
Haag-Streit ..................................................................................12
Phone ...................................................................... (800) 627-6286
Fax ........................................................................... (603) 742-7217
HOYA Vision Care, North America ...........................................19
Phone ...................................................................... (972) 221-4141
Fax ........................................................................... (972) 436-9766
........................................................................www.hoyavision.com
Keeler Instruments .................................................................7, 71
Phone ...................................................................... (800) 523-5620
Fax ........................................................................... (610) 353-7814
NicOx, Inc. ............................................................................. 24-25
Phone ...................................................................... (214) 346-2913
................................................................................ www.nicox.com
S4OPTIK ......................................................................................21
Phone ...................................................................... (888) 224-6012
Sauflon ........................................................................................15
Phone ...................................................................... (800) 682-3240
Fax ........................................................................... (800) 644-3622
............................................................................. info@sauflon.com
.............................................................................. SauflonUSA.com
Vistakon .....................................................................................2-3
Phone ...................................................................... (800) 874-5278
Fax ........................................................................... (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 ser s Index
For advertising opportunities contact:
Michelle Barrett (610) 492-1014 or mbarrett@jobson.com
James Henne (610) 492-1017 or jhenne@jobson.com
Scott Tobin (610) 492-1011 or stobin@jobson.com
5 WAYS TO REGISTER:
ONLINE: www.revoptom.com/tysonscorner
EMAIL Lois DiDomenico: ReviewMeetings@Jobson.com
MAIL: Review Group Meetings c/o Jobson
11 Campus Blvd., Ste. 100
Newtown Square, PA 19073
PHONE: 866-658-1772
FAX: 610-492-1039
Faculty:
Paul Karpecki, OD
(Program Chair)
Derek Cunningham, OD
Mark Dunbar, OD
Al Kabat, OD
CE COURSE TOPICS:
Ocular Manifestations of Systemic Disease
Glaucoma Management
Ocular Surface Disease Update
New Technologies in Eye Care
Contact Lens Advances
Surgical Comanagement Pearls
Posterior Segment Grand Rounds
Anterior Segment Disease Diagnosis and Treatment Grand Rounds
The Sheraton Premiere
Thank You to Our Sponsors
Approval Pending
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Full Registration - $495 ($100 off if registered by August 1st) $495 x ________ = $________
(Includes 15 hours of CE, breakfasts, reception)
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No refund past August 16, 2014
For more information or to register,
contact Lois DiDomenico at 866-658-1772
or at ReviewMeetings@Jobson.com.
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For reservations, call: 888-687-8087
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SHERATON PREMIERE TYSONS CORNER
Photo by: Destination DC
Review Classieds
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New! Distometer Set
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Continuing Education
Medical Facility
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The American Board of Certification in
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tence in medical optometry. ABCMO certifies
specialized competence of a higher level than
that required for licensure and general practice.
Visit www.abcmo.org to learn why medical
facilities require board certification of specialists
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Questions? myers.kenj@gmail.com.
NOTICE: After August 1, 2003, all applicants
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Sur gi cal Minute
A
nterior 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 Role
When discussing the procedure
with the patient, the term epithelial
reinforcement may sound more
appealingand 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 Bowmans 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,
doesnt 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 rst 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 ve (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 Inammation
TRAVATAN Z
Solution should be used with caution in patients with active intraocular inammation
(e.g., uveitis) because the inammation 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, Inammatory or Neovascular Glaucoma
TRAVATAN Z
Solution has not been evaluated for the treatment of angle-closure, inammatory 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 reect 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 inammation, 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/u 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 C
Teratogenic 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

benet justies 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 drugs
are 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, ngers, 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 physicians 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 ve (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 Novartis
4/13 TRV13021JAD 5/14 TRV14045JAD
REVIEW OF OPTOMETRY (ISSN 0147-7633) IS PUBLISHED MONTHLY, 12 TIMES A YEAR BY JOBSON MEDICAL INFORMATION LLC, 100 AVENUE OF THE AMERICAS, NEW YORK,
NY 10013-1678. PERIODICALS POSTAGE PAID AT NEW YORK, NY AND ADDITIONAL MAILING OFFICES. POSTMASTER: SEND ADDRESS CHANGES TO REVIEW OF OPTOMETRY, PO
BOX 81, CONGERS, NY 10920-0081. SUBSCRIPTION PRICES: US: ONE YEAR $56; TWO YEARS $97, CANADA: ONE YEAR $88, TWO YEARS $160, INTL: ONE YEAR $209, TWO YEARS
$299. FOR SUBSCRIPTION INFORMATION CALL TOLL-FREE (877) 529-1746 (USA); OUTSIDE USA, CALL (845) 267-3065. OR EMAIL US AT REVOPTOMETRY@CAMBEYWEST.COM.
PUBLICATIONS MAIL AGREEMENT NO: 40612608. CANADA RETURNS TO BE SENT TO BLEUCHIP INTERNATIONAL, P.O. BOX 25542, LONDON, ON N6C 6B2.
Di agnost i c Quiz
History
A 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 Data
Her 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 Diagnosis
How 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 months issue, and
then click Diagnostic Quiz under
the table of contents.
Next Month in the Mag
August features our 38th Annual Contact Lens Report.
Topics include:
10 Essential CL Marketing Dos and Donts
The Case for Daily Disposables: Pricing and Presentation
Why Arent 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)
Feedback
Review of Optometry welcomes questions and comments. E-mail
Jack Persico, editor-in-chief, jpersico@jobson.com, 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 Split
By 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 Deciency or Aqueous Tear Deciency (non-Sjogrens only).
2014 CooperVision, Inc.
coopervision.com
naturally attract water for a fresh,
hydrated lens-wearing experience.
Proclear 1 day lenses use exclusive PC Technology to
recreate the phosphorylcholine found naturally in human
eyes. So, like eyes, they capture a protective lm of water.
No wonder theyre the only daily lenses with the FDA
indication, May provide improved comfort for contact
lens wearers who experience mild discomfort or
symptoms related to dryness during lens wear.*
Ask your CooperVision sales representative about
current programs and promotions.
Natural comfort by design
Proclear
1 day contact lenses

2014 Novartis 5/14 TRV14045JAD
Through the OPENINGS
TM
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 USAGE

TRAVATAN 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 Administration
The 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 INFORMATION
Warnings and Precautions
PigmentationTravoprost 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 ChangesTRAVATAN 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 LensesContact lenses should be removed prior to
instillation of TRAVATAN Z Solution and may be reinserted 15 minutes following
its administration.
Adverse Reactions
The 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 Specic Populations
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.
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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(travoprost ophthalmic solution) 0.004%

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