Download Issue 1 - New England College of Optometry

A Continuing Education Review for Optometrists from the New England College of Optometry
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Issue 1
Who Has Glaucoma?
Definitions and Diagnosis
Steven L. Mansberger, MD, MPH
With many questions still remaining in the field of glaucoma—
who has it, who will progress, when to intervene—clear definitions
lay the groundwork for effectively navigating the many clinical
challenges.
Like cancer, glaucoma is not a
single disease; rather, the term refers
to a group of degenerative disorders
of the optic nerve characterized by a
particular constellation of structural
and functional changes; key among
them are excavation and enlargement
of the optic cup, loss of the nerve fiber
TARGET AUDIENCE This educational activity is intended for
optometrists.
LEARNING OBJECTIVES Upon completion of this activity,
participants will be able to:
1.Define glaucoma and common subtypes.
2.Discuss the role of IOP in glaucoma diagnosis.
3. Delineate the relationship between aqueous humor dynamics,
IOP, and glaucoma.
4.Identify individual IOP reduction needs in glaucoma patients.
EDITORIAL COMMITTEE
Baharak Asefzadeh, OD, MS, FAAO, is an adjunct assistant
professor of optometry at the New England College of Optometry
and director of the VA Boston Optometric Research Fellowship.
Tony Cavallerano, OD, FAAO, is an adjunct professor of optometry at the New England College of Optometry, where he is also
the director of professional relations and the executive director
of clinical training and patient care.
Mark T. Dunbar, OD, FAAO, is the director of optometric services
and optometry residency supervisor at Bascom Palmer Eye Institute, University of Miami Miller School of Medicine.
Key Issues in Glaucoma Management: A Review for Optometrists
is sponsored by the New England College of Optometry and
supported by an unrestricted educational grant from Bausch +
Lomb, Inc. This publication is administered by an independent
editorial committee.
© 2015 Candeo Clinical/Science Communications, LLC. All rights
reserved. Neither the New England College of Optometry nor
Candeo Clinical/Science Communications, LLC, assumes any
responsibility for injury or damage to persons or property arising
from the use of information or ideas contained in this publication.
COURSE DIRECTOR
Tony Cavallerano, OD, FAAO
New England College of Optometry
Boston, MA, USA
layer rim, and corresponding visual
field deficit.1
A concise medical definition or
standard dictionary definition of
glaucoma typically includes mention
of intraocular pressure (IOP).2 This is
understandable in light of the strong
clinical association between glaucoma
and IOP and the fact that, at present,
IOP represents the sole therapeutic target of medical antiglaucoma therapy.1
Glaucoma and IOP
That said, elevated IOP (one description of which is IOP greater
than the 97.5 percentile for a specific
population) is no longer necessary for
a definition of glaucoma, nor is it required for the diagnosis, since it is not
universally present among glaucoma
patients.1 (“Elevated IOP” can also be
defined as IOP over 21 mm Hg or as the
IOP at which the optic nerve sustains
damage.) In fact, depending on the
population studied, between 30% and
80% of eyes with glaucomatous optic
nerve damage have “normal” IOPs (ie,
IOPs of 21 mm Hg or less).3
The converse is also true: elevated
IOP may be present, and quite often
is present, without evidence of glaucomatous optic nerve damage. It is
also true that some degree of ocular
hypertension may be present without
evidence of optic nerve damage or vi-
FIGURE 1 Gonioscopy showing angle
closure.
sual symptoms. Glaucoma risk estimation and when to treat at-risk patients
is the subject of significant debate and
ongoing research.
Primary vs Secondary
Glaucomas
Optic nerve damage associated
with glaucoma can be thought of as
the common endpoint of a variety
of pathophysiologic processes. Glaucoma categorization starts with the
designation of primary or secondary.
Primary glaucoma describes patients
with optic nerve damage and visual
field loss with no discernable cause;
primary open-angle glaucoma (POAG)
is a principal subtype of glaucoma in
which the angle between the iris and
cornea is open.
Among the non-POAG categories
of glaucoma, elevated IOP is consistently present at least some times
in the course of the disease. Primary
angle-closure glaucoma is a subtype of
glaucoma in which the cause of irridocorneal angle narrowing is unknown
(Figure 1).1 Secondary glaucoma may
More INSIDE:
Aqueous Humor Dynamics: What
IOP Means for the Clinician
by John J. McSoley, OD
Key Issues
in Glaucoma
Supported by an unrestricted
educational
grant fromManagement Bausch + Lomb, Inc.1
result from a long list of underlying
causes, and may affect individuals of
any age, from newborns to the elderly.
Like primary forms, secondary openangle glaucoma is associated with an
open angle; and secondary angle-closure
glaucoma with iridotrabecular contact.
Any process that impedes drainage
of aqueous fluid via the trabecular
meshwork—including preceding ocular
trauma, diabetes, pigmentary dispersion syndrome, pseudoexfoliation,
and dozens of other causes—can cause
secondary glaucoma.1
Risk Factors
Multiple studies have attempted
to identify risk factors for the development of primary glaucoma.
Subanalyses of two large multicenter,
prospective, randomized trials—the
Ocular Hypertension Treatment Study
(OHTS) and the European Glaucoma
Prevention Study (EGPS)—looked
specifically at patient characteristics
and disease parameters associated with
conversion from ocular hypertension
to glaucoma.4,5 Pooled analysis of untreated patients with ocular hyperten-
Key Issues in Glaucoma Management — Issue 1
STATEMENT OF NEED
Glaucoma, a group of ocular diseases characterized by progressive damage to the optic nerve, is the second leading cause of
blindness worldwide. It affects a significant and growing portion
of the US population.1,2
As primary eyecare providers, medical optometrists are well
positioned to identify patients at risk and to diagnose, monitor,
and treat glaucoma. However, given that the expanded scope
of practice incorporating glaucoma treatment is relatively new,
many optometrists lack confidence in their ability to treat this
potentially blinding disease. In order to instill confidence and
help optometrists make sound clinical judgments about the care
of glaucoma patients, Key Issues in Glaucoma Management
will help optometrists better understand the various aspects
and nuances of the disease, including our current understanding of the role of intraocular pressure (IOP) in glaucomatous
optic nerve damage. Course content will also include current
rationale on glaucoma diagnosis and evidence-based strategies for reducing IOP.
Each installment of Key Issues in Glaucoma Management will
look at an important topic in glaucoma diagnosis or therapy.
Each issue will build from a basic level to instill understanding
and confidence in medical optometrists. Key Issues in Glaucoma
Management aims to support optometrists’ clinical reasoning and decision-making abilities and help them turn medical
management of glaucoma into a vital segment of their practices.
REFERENCES
1.Resnikoff S, Pascolini D, Etya’ale D, et al. Global data on visual
impairment in the year 2002. Bull World Health Organ. 2004
November;82(11):844-51.
2.Eye Diseases Prevalence Research Group. Prevalence of
open-angle glaucoma among adults in the United States. Arch
Ophthalmol. 2004;122:532-8.
OFF-LABEL USE STATEMENT
This work may discuss off-label uses of medications.
GENERAL INFORMATION
This CE activity is sponsored by the New England College of
Optometry and is supported by an unrestricted educational
grant from Bausch + Lomb, Inc.
Directions: Circle the best answer to each question in the exam
(questions 1–10) and in the evaluation (questions 11–16). The New
England College of Optometry designates this activity for a maximum of 1 hour of COPE-approved continuing education credit.
There is no fee to participate in this activity. In order to receive CE
credit, participants should read the report and then take the posttest. A score of 70% is required to qualify for CE credit. Estimated
time to complete the activity is 60 minutes. On completion, tear
out or photocopy the answer sheet and send it to:
New England College of Optometry
ATTN: Ms. Margery Warren
424 Beacon Street
Boston, MA 02115
DATE OF ORIGINAL RELEASE October 2015. Approved for a
period of 24 months.
2 Key Issues in Glaucoma management
ACCREDITATION STATEMENT
This activity has been planned and implemented through the
joint sponsorship of the New England College of Optometry
and Candeo Clinical/Science Communications, LLC. The New
England College of Optometry is accredited by The Council on
Optometric Practitioner Education® (COPE® ), created by the Association of Regulatory Boards of Optometry (ARBO) to accredit
continuing education on behalf of optometric licensing boards.
CREDIT DESIGNATION STATEMENT
The New England College of Optometry designates this activity
for a maximum of 1 hour of COPE-approved continuing education
credit. Clinicians should only claim credit commensurate with the
extent of their participation in the activity.
EDITORIAL COMMMITTEE DISCLOSURE STATEMENTS
Baharak Asefzadeh, OD, MS, FAAO, is an adjunct assistant
professor of optometry at the New England College of Optometry
and director of the VA Boston Optometric Research Fellowship.
She has no financial disclosures related to this activity.
Tony Cavallerano, OD, FAAO, is an adjunct professor of optometry at the New England College of Optometry, where he
is also the Director of Professional Relations and the Executive
Director of Clinical Training and Patient Care. He has no financial
disclosures related to this activity.
Mark T. Dunbar, OD, FAAO, is the director of optometric services
and optometry residency supervisor at Bascom Palmer Eye Institute, University of Miami Miller School of Medicine. He states that
in the last 12 months, he has been a consultant for Allergan and
has participated in advisory boards for Carl Zeiss, Regeneron
Pharmaceuticals, Inc., Bio-Tissue, ArcticDx, and B&L Nutrition.
AUTHOR DISCLOSURE STATEMENTS
Steven L. Mansberger, MD, MPH, is vice-chair and director of
glaucoma services and fellowship program at Legacy Devers
Eye Institute in Portland, OR. Dr. Mansberger has received grant/
research support from the National Eye Institute, Allergan, and
Envisia. He has also been a consultant for New World Medical,
Allergan, Envisia, Santen Pharmaceutical Co., ForSight Vision5,
and Welch Allyn.
John J. McSoley, OD, is associate director of optometric services
and member of the glaucoma service at Bascom Palmer Eye
Institute in Miami, FL. He has no financial disclosures related
to this activity.
DISCLAIMER
Participants have an implied responsibility to use the newly
acquired information to enhance patient outcomes and professional development. The information presented in this activity
is not meant to serve as a guideline for patient care. Any procedures, medications, or other courses of diagnosis or treatment
discussed or suggested in this activity should not be used by clinicians without evaluation of their patients’ conditions and possible
contraindications or dangers in use, applicable manufacturers’
product information, and comparison with recommendations
of other authorities.
COMMERCIAL SUPPORTERS
This activity is supported by an unrestricted educational grant
from Bausch + Lomb, Inc.
sion enrolled in the two studies and
followed for 5 years (N=1341) revealed
that poorer outcomes were predicted
by: older age, higher IOP, decreased
central corneal thickness, increased
vertical cup-to-disc ratio, and greater
visual field index pattern standard deviation (PSD).6 In addition, low perfusion pressure was also identified to be
a risk factor in the Barbados Eye Study.
Family history is also considered
a significant risk factor for the development of POAG. Although some
controversy exists, there seems to be a
propensity to glaucoma among certain
ethnic groups. In the US, individuals
of African and Hispanic descent are at
highest risk for POAG.7 Asian individuals have high rates of glaucoma, and
represent 87% of patients with primary
angle-closure glaucoma worldwide.8
Other proposed risk factors for POAG
include diabetes mellitus, high blood
pressure, and myopia.
Glaucoma Suspects
A patient or eye considered “glaucoma suspect” has some features
suggestive of glaucoma but does not
meet the full diagnostic criteria.1 Such
patients generally present in one of
four ways: 1) elevated IOP and normal
appearing optic nerve; 2) large cupto-disc ratio and normal optic nerve
fiber layer; 3) abnormal visual field
but normal optic nerve and disc; or
4) unusual appearing optic nerve with
normal visual field and IOP.
This begs the question: does the eye
that is suspicious for glaucoma indicate a pre-glaucomatous state? And,
if so, can early intervention prevent
the development of glaucoma? These
are some of the questions that OHTS
and EGPS were designed to evaluate;
however, while helpful, they have not
put the issue entirely to rest. In the
OHTS, development of glaucoma was
reduced by 60% with the use of topical
hypotensive medication. Patients with
ocular hypertension (baseline IOP
24 to 32 mm Hg) treated with IOPlowering medication developed POAG
at a rate of 4.4% over 5 years compared
to a rate of 9.5% among untreated
patients in the control group.7 EGPS,
a similarly designed trial, did not show
statistically significant prevention of
POAG with treatment.9
Unfortunately, we lack data regarding early intervention outcomes for the
other groups suspicious for glaucoma,
and it remains unclear whether treatment is warranted for those groups.
sHould Glaucoma
susPects Be treated?
It is important to remember that
most patients with identifiable risk factors do not develop glaucoma. This has
been shown in prospective studies. As
noted, in the OHTS 90% of untreated
glaucoma suspect patients with IOP
between 24 and 32 mm Hg remained
glaucoma-free over the 5 years of follow-up.4 It might seem prudent, then,
to limit preventive medical therapy and
spare patients the burden of lifelong
medication whenever possible.
But the stakes are too high to
simply leave it at that. For those who
do develop glaucoma, the burden of
therapy—inconvenience, side effects,
cost—likely pales in comparison to
the vision-saving benefits they might
derive. Clearly, the ability to predict
who is at risk for glaucoma and thus
who would benefit from intervention
holds enormous value. To that end,
based on data from large studies, tools
for calculating individual risk have
been developed to assist clinicians in
recommending or not recommending
pre-glaucoma therapy. It is generally
recommended that individuals identified as having high risk should be
considered for treatment, whereas individuals at low risk should be observed
without treatment.
rIsk calculators
Like other medical predictive models—such as those used to predict risk
for heart disease or osteoporosis—
glaucoma risk calculators attempt
to enhance objectivity in clinical
management by distilling multiple
variables down to an actionable metric.
A glaucoma risk calculator based upon
findings from OHTS uses patient age,
baseline IOP, central corneal thickness,
PSD, vertical cup-to-disc ratio, and the
presence of diabetes to generate an idea
of patients’ 5-year risk.6 The algorithm
developed at our institution is available
online at: https://www.deverseye.
org/grc/. Other calculators can be
found at http://ohts.wustl.edu/
risk/calculator.html and http://oil.
wilmer.jhu.edu/risk/.
A separate risk calculator for the
progression of visual field loss among
patients being treated for glaucoma
has also been developed and validated.
treatInG Glaucoma
For patients with a clear diagnosis of glaucoma, treatment is almost
always indicated, assuming that the
patient is otherwise capable of maintaining an acceptable quality of life.
Aggressiveness of the treatment relates
to a number of factors, including stage
of glaucoma, age and health status of
the patient, and the health and visual
acuity of the fellow eye. For example,
a young patient with early glaucoma
would almost always be treated aggressively since s/he will most likely have
to live with glaucoma for a long time.
A glaucoma patient with a shorter
life expectancy, eg, a patient in his/
her late 80s with mild glaucoma and
significant heart disease, after a thorough discussion, might elect to be
periodically monitored for progression
without treatment. And, as a further
example, a patient with very advanced
glaucoma in one eye and good vision
in their other eye might only elect to
receive palliative treatment in the affected eye to keep it comfortable rather
than aggressive IOP-lowering drugs.
dIaGnostIc ProGress
In many of its forms, glaucoma is
a sly, often silent disease—by the time
patients notice visual change, up to
90% of the optic nerve may be affected.
Because glaucoma is progressive and
irreversible, timely diagnosis is paramount to controlling it and preventing
vision loss. Late diagnosis increases risk
for vision loss and raises the overall
costs of the disease.10
New means for detecting glaucoma
help to prevent late diagnosis and its
consequences. In the past, clinicians
core concePts
● Glaucoma is an optic nerve
disease characterized by
structural and functional
changes including: increased
cupping, optic nerve fiber layer
degeneration, and visual field
loss.
● The relationship between
glaucoma and IOP is complex:
glaucoma is common among
patients with normal IOP; and a
majority of patients with elevated
IOP will not develop glaucoma—
but patients with elevated IOP
are at higher risk of glaucoma
than patients with normal IOP.
● Primary glaucoma is glaucoma
with no known cause.
● Risk factors for POAG include
elevated IOP, decreased corneal
thickness, high cup-to-disc ratio,
visual field PSD, and older age.
● Family history is probably
a significant risk factor for
glaucoma.
● Other possible risk factors
include African, Hispanic, Asian
ethnicity; high blood pressure;
myopia.
● Risk calculators can aid in
predicting conversion from
ocular hypertension to glaucoma.
● Risk calculators also exist for
predicting progression among
patients undergoing treatment
for glaucoma.
● Glaucoma remains underrecognized and undertreated.
● State-of-the-art diagnostic
equipment and vigilance for the
disease are important for early
detection.
could only examine the optic nerve
with a handheld ophthalmoscope
and test the visual fields manually.
Currently, laser-based devices allow
for glaucomatous optic disc detection without dilation of the pupils.
At my practice, we evaluate the optic
nerve with ophthalmoscopy at every
visit, and we perform stereoscopic
disc photography at the initial visit or
Key Issues In Glaucoma manaGement 3
when the optic disc has a hemorrhage
or we suspect a change. Finally, we
use objective structural testing (ocular
coherence tomography and Heidelberg
Retinal Topography) at least yearly to
assess the optic disc and nerve fiber
layer for progression. In addition to
structural assessment, we use standard
automated achromatic visual field testing to assess for visual field loss.
Primary care physicians should
advise patients to have regular ophthalmic examinations, including testing for
glaucoma, every 2 years for individuals
over 40 years old and yearly for those
over 60. Patients with glaucoma should
be reminded to inform family members
so that they can be vigilant for the disease and receive appropriate screening.
Conclusion
Glaucoma is a group of diseases
that share a common pathophysiologic
endpoint: optic nerve degeneration.
4 Key Issues in Glaucoma Management
Early identification and prevention are
key to managing glaucoma. Increased
physician awareness and more aggressive screening and monitoring with
state-of-the-art equipment can be
expected to improve outcomes. Overall, the objective is to treat high-risk
suspects, monitor low-risk suspects
and treat those with glaucoma.
Steven L. Mansberger, MD, MPH is vice-chair and
director of glaucoma services and fellowship program at Legacy Devers Eye Institute in Portland,
OR. Dr. Mansberger has received grant/research
support from the National Eye Institute, Allergan,
and Envisia. He has also been a consultant for New
World Medical, Allergan, Envisia, Santen Pharmaceutical Co., ForSight Vision5, and Welch Allyn.
This manuscript was prepared with the assistance
of medical writer Noelle Lake, MD.
REFERENCES
1. Casson RJ, Chidlow G, Wood JPM, et al. Definition
of glaucoma: clinical and experimental concepts.
Clin Experimental Ophthalmol. 2012;40:341-9.
2. Glaucoma definition. Available at: http://www.
merriam-webster.com/dictionary/glaucoma.
Accessed on April 22, 2015.
3. Anderson DR. Normal tension glaucoma. Ind J
Ophthalmol. 2011;59(Suppl 1):S97-101.
4. Gordon MO, Beiser JA, Brandt JD, et al. The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle
glaucoma. Arch Ophthalmol. 2002;120:714-20.
5. Miglior S, Pfeiffer N, Torri V, et al. for the European
Glaucoma Prevention Study (EGPS) Group. Predictive factors for open-angle glaucoma among patients
with ocular hypertension in the European Glaucoma
Prevention Study. Ophthalmology. 2007;114:3-9.
6. Medeiros FA, Weinreb RN. Predictive models to
estimate the risk of glaucoma development and
progression. Prog Brain Res. 2008;173:15-24.
7. Kass MA, Gordon MO, Gao F, et al. for the Ocular
Hypertension Treatment Study. Delaying treatment of ocular hypertension. Arch Ophthalmol.
2010;128:276-87.
8. Cook C, Foster P. Epidemiology of glaucoma:
what’s new? Can J Ophthalmol. 2012;47:223-6.
9. Miglior S, Zeyen T, Pfeiffer N, et al. for the European Glaucoma Prevention Study (EGPS) Group.
Results of the European Glaucoma Prevention
Study. Ophthalmology. 2005;112:366-75.
10. Traverso CE, Walt JG, Kelly SP, et al. Direct costs
of glaucoma and severity of the disease: a multinational long term study of resource utilisation in
Europe. Br J Ophthalmol. 2005 Oct;89(10):1245-9.
Aqueous Humor Dynamics: What IOP
Means for the Clinician
JOHn J. McSOLEy, OD
Intraocular pressure is a
causative risk factor for
glaucoma and, at present,
the only target of available
glaucoma treatments. Although
elevated IOP is no longer
recognized as necessary for a
diagnosis of glaucoma, it is a
key element in the evaluation
and management of the disease.
Normal intraocular pressure (IOP)
is essential to maintaining the structural integrity and visual function of
the eye: it ensures inflation of the globe
and maintains the eye’s optical components in position. Underlying normal
IOP is a delicate balance between aqueous humor inflow and resistance to its
outflow. Altered aqueous dynamics,
predominantly due to outflow impairment, is the cause of IOP elevation
in glaucoma. An understanding of
normal aqueous humor dynamics is
a cornerstone of understanding both
the pathogenesis and treatment of
glaucoma.
aQueous dynamIcs and
IoP
Precursor to aqueous humor passes
from the microvasculature of the
ciliary body stroma, through the pigmented and nonpigmented epithelia
of the ciliary processes, and then as
aqueous humor into the posterior
chamber. Aqueous humor forms at
a typical rate of approximately 2 to
2.5 microliters per minute. Secretion
of aqueous humor is a complicated
physiological process that is influenced
by many factors, including ionic and
osmotic forces, enzymatic reactions,
activation of various receptors, circadian rhythm, age, neuropeptides, and
hormones. Additional information on
this complicated process is available.1-5
After secretion from the ciliary
body into the posterior chamber,
aqueous humor circulates through
the pupillary space to fill the anterior
chamber. From there, aqueous humor
exits the eye via one of two routes
in the anterior chamber angle: the
conventional outflow pathway via the
trabecular meshwork (which accounts
for the bulk of aqueous drainage), or
the uveoscleral pathway. In the trabecular pathway, aqueous humor drains
through the trabecular meshwork into
Schlemm’s canal and then out through
collector channels to the blood vessels and lymphatics (Figure 1). In the
uveoscleral pathway, aqueous humor
exits the eye via the supraciliary and
suprachoroidal spaces.
WHat Is normal?
It is important to remember that
the IOP range we call “normal” (IOPs
in the 10 to 21 mm Hg range) are derived from measurement of pressures
in normal populations, which typically
have mean IOPs close to 16 mm Hg
(with 2 standard deviations extending
about 5 mm Hg).6 In reality, IOP is
dynamic, differing considerably from
individual to individual and, for any
given individual, rising and falling in
a diurnal cycle. A normal individual’s
IOP may vary by as much as 4 mm Hg
or more over the course of the day as
aqueous humor production and outflow fluctuate.7 In glaucoma patients,
the diurnal IOP variation may be even
greater, likely a reflection of the pathophysiologic mechanisms modulating
aqueous humor dynamics and possible
effects of treatment.
The variability of IOP is an important consideration when checking
patients’ pressure. Multiple measurements, ideally taken at different times
of day, may be necessary for detection
of elevated IOP in potential glaucoma
patients. Wide ranges of IOP variability
may be associated with the clinical
course of glaucoma or the result of
core concePts
● IOP is maintained by the balance
between aqueous inflow and
resistance to outflow.
● IOP is the primary risk factor for
the onset and progression of
glaucoma.
● Increased resistance to aqueous
drainage due to abnormalities of
the trabecular outflow pathway is
responsible for IOP elevation in
open-angle glaucoma.
● Factors other than elevated
IOP, such as a patient’s genetic
susceptibility, contribute to
glaucomatous damage. It is
erroneous to assume that
pressures within the normal
range do not cause harm.
● IOP is particularly variable in
glaucoma patients. In evaluating
glaucoma, it is important to
take multiple measurements at
different times of day.
● Current glaucoma medications
lower IOP by reducing aqueous
formation or increasing aqueous
outflow.
● Choice of medical treatment
should be based on safety,
efficacy, and patients’ ability
to comply with/tolerate the
regimen.
missed medication. It is prudent to
avoid treatment decisions based on a
single isolated pressure reading.
IoP: relatIon to
Glaucoma
IOP has been historically linked to
glaucoma, and values exceeding the
statistically normal range were viewed
as leading to glaucoma. Today, glaucoma is defined by the characteristic
structural changes in the optic nerve
and corresponding impairment of visual function. IOP is not included as a
defining feature of glaucoma. Patients
Key Issues In Glaucoma manaGement 5
whose IOP exceeds the normal range
but have no glaucomatous damage are
considered ocular hypertensives.
Glaucomatous damage can be
identified in patients whose IOP remains within the normal range. The
development of glaucoma is related to
an individual’s susceptibility to various
risk factors, including IOP. Indeed,
many patients with open-angle glaucoma have IOPs within the statistically
normal range (< 22 mm Hg at a single
measurement).8-13
Although no longer included in
the definition of glaucoma, IOP is a
key component of glaucoma clinical
management. First, IOP is a causative
risk factor for the development and
progression of glaucomatous damage.14-16 As the level of IOP increases,
the prevalence of open-angle glaucoma
increases.8,17 On the other hand, IOP
reduction in known glaucoma patients decreases the risk of visual field
loss.15-17
Most importantly, IOP remains
the only glaucoma risk factor that can
be effectively modified, even though
many other potential factors—such
as a patient’s genetic susceptibility
to optic nerve injury, compromise of
blood flow, alterations of the lamina
cribrosa, and other potential contributors, some of which may not yet
be identified—may also contribute to
glaucomatous damage. In most cases,
a target IOP provides a short term
benchmark to evaluate treatment efficacy, and IOP measurement allows us
to monitor response to treatment in an
easy and straightforward manner. That
said, the ultimate and most important
measure of success is preservation of
the patient’s vision.
Glaucoma Evaluation
When a patient is identified as
having ocular hypertension, further
assessment is warranted. Typically,
this involves measurement of central
corneal thickness, gonioscopy, visual
field testing, and examination of the
optic nerve head, usually with the help
of photography and imaging devices
that allow additional qualitative and
quantitative measures of the struc6 Key Issues in Glaucoma Management
later. Once a baseline and track record
ture of the optic nerve and the retinal
have been established, and it is clear
nerve fiber layer. These tests serve as
that the patient is not progressing, it
diagnostic aids, help in staging, and
is then reasonable to lengthen followprovide baseline information for future
up intervals. At the same time, it is
follow-up comparison. In cases where
important to educate the patient about
the patient shows no signs of glaucomatous damage,
the most important step is to
determine the
risk of progression to glaucoma. Risk assessment includes
how elevated the
baseline pressure
is and the presence or absence
of other factors
that add to the
risk of glaucoma
(eg, age, family
history, etc.)
Visualizing
the anterior
chamber angle,
Figure 1 The trabecular meshwork conventional outflow
pathway. Aqueous humor is produced by the ciliary body and it
where the traflows (dashed line shown with arrowheads) from the posterior
becular meshchamber through the pupil into the anterior chamber. From there
work is located,
it flows out through the trabecular meshwork into the Schlemm’s
is an important
canal and is subsequently absorbed into the episcleral
veins via the collector channels. (From Goel M, Picciani RG, Lee
aspect of t he
RK, et al. Aqueous Humor Dynamics: A Review. Open Ophthalmol J.
clinical exami2010;4:52-9.)
nation for glaucoma. The cause
why the tests are necessary and why
of impaired aqueous outflow leading
ongoing follow-up will be necessary,
to IOP elevation varies by the subtype
probably for life.
of glaucoma, and gonioscopy is an es
sential diagnostic tool for determining
whether the angle is open or closed and
Managing IOP
for identification of other pathologies
Current glaucoma therapies are
that may cause pressure elevation. The
aimed almost exclusively at lowering
findings can not only provide helpful
IOP, which can be done by reducing
diagnostic clues but also have imporaqueous humor production or enhanctant treatment implications.
ing aqueous outflow. Beta blockers,
Based on the risk for progression,
topical carbonic anhydrase inhibitors,
the patient should be monitored over
and the alpha agonists all lower IOP
time for any structural or functional
by reducing aqueous formation; while
impairment. If there is no evidence for
prostaglandin analogs, the most widely
glaucomatous damage and the pressure
used class of glaucoma management
is moderate, it may be prudent to just
agents, work by increasing aqueous
follow up with that patient in 3 or 4
outflow. When a second medication is
months. If at the next exam there are
added from a different class, the effects
no changes in IOP or in the condition
may be additive.
of the optic nerve, a more detailed
A critical aspect of glaucoma manexamination, including visual field
agement is selecting the most appropritesting, can be scheduled for 6 months
ate IOP-lowering agent. In selecting an
agent (or agents), the best strategy is
the one that is safest, most effective,
and creates the least burden—including
economic burden—to the patient. This
explains how prostaglandin analogs
became the most popular first-line
therapy for glaucoma: they provide very
effective IOP lowering, are generally
well tolerated, and are taken only once
each day. Contrast that with an older
agent like pilocarpine, which although
effective, requires frequent dosing and
has multiple side effects. Today pilocarpine is rarely used to treat glaucoma.
For patients who cannot tolerate
prostaglandins, the next option is typically a beta blocker. Topical beta blockers are well tolerated by most patients,
but there are some caveats. Topical beta
blockers can greatly aggravate some
ailments, such as asthma and certain
cardiovascular conditions, and should
be avoided in patients with a history of
those disorders. Additionally, a topical
beta blocker to reduce IOP may be less
effective than expected when administered to a patient who is already on
a systemic beta blocker.
The bottom line is that no single
medication is ideal in all circumstances. It is necessary to individualize
each patient’s treatment regimen, and
the therapeutic choice comes down to
the patient’s response and ability to
tolerate the treatment.
Treatment Goals
The goal in treating glaucoma is to
halt or slow disease progression and,
to the degree possible, preserve the
current level of vision. How much IOP
lowering is required depends on several
factors: the severity of disease, the rate
of progression, and the baseline IOP.
The extent of damage at diagnosis and
the rapidity of progression are good
indicators of a patient’s susceptibility
to IOP-caused damage and, thus, indicate how low the target IOP should be
set. In general, a patient with minimal
damage over an extended period of
time would be at less risk for further
vision loss than someone who has extensive damage or one whose damage
has evolved quickly.
An initial treatment goal of 25%
to 30% reduction in IOP makes a
reasonable target for initial therapy in
patients with mild damage. Prevention
of progression in patients with more
advanced damage usually requires a
more aggressive target—eg, up to 50%
of their baseline IOP or to the low–normal range of IOP. Even when patients
reach their short-term goals for IOP
reduction, they still require ongoing,
careful follow-up.
The term “maximally tolerated
medical therapy” well encapsulates
the notion that IOP-lowering therapies should be effective, safe, and well
tolerated. This may vary from patient
to patient or may change for an individual patient during the follow-up
period. Laser trabeculoplasty may be
a good option at any point during the
course of follow-up care. If despite
having optimized medical and laser
therapy, there is progression (or a
high likelihood of progression) more
aggressive measures should be sought.
We are fortunate to practice at a time
when there are several good surgical options available to our patients.
Referral to surgeons skilled in these
methods has an important role in
visual preservation.
John J. McSoley, OD, is associate director of optometric services and member of the glaucoma service
at Bascom Palmer Eye Institute in Miami, FL. He
has no financial disclosures related to this activity.
Medical writer Ying Guo, MBBS, PhD, assisted in
the preparation of this manuscript.
REFERENCES
1.Brubaker RF. Flow of aqueous humor in humans
[The Friedenwald Lecture]. Invest Ophthalmol Vis
Sci. 1991;32(13):3145-66.
2.Brubaker RF, Nagataki S, Townsend DJ, et al. The
effect of age on aqueous humor formation in man.
Ophthalmology. 1981;88(3):283-8.
3.Do CW, Civan MM. Basis of chloride transport in
ciliary epithelium. J Membr Biol. 2004;200(1):1-13.
4.Freddo TF. Ocular Anatomy and Physiology
Related to Aqueous Production. In: Fingeret M,
Lewis TL, Primary Care of the Glaucomas. 2nd
Edition. New York, McGraw-Hill;2001:17-41.
5.Gabelt BT, Kaufman PL, Aqueous Humor Hydrodynamics In: Kaufman PL, Alm A. Adler’s
Physiology of the Eye. 10th Edition. St. Louis,
Mosby;2003:237-89.
6. Colton T, Ederer F. The distribution of intraocular
pressures in the general population. Surv Ophthalmol. 1980;25(3):123-9.
7.David R, Zangwill L, Briscoe D, et al. Diurnal
intraocular pressure variations: an analysis of 690
diurnal curves. Br J Ophthalmol. 1992;76:280-3.
8. Sommer AE, Tielsch JM, Katz J, et al. Relationship
between intraocular pressure and primary open
angle glaucoma among white and black Americans. Arch Ophthalmol. 1991;109(8):1090-5.
9.Leske MC, Heijl A, Hyman L et al. Early manifest
glaucoma trial: design and baseline data. Ophthalmology. 1999:106:2144-53.
10. Quigley HA, West S, Rodriguez J, et al. Prevalence
of glaucoma in a population-based study of Hispanic subjects: Proyecto VER. Arch Ophthalmol.
2001;119:1819-26.
11. Varma R, Ying-Lai M, Francis BA, et al. Prevalence
of open angle glaucoma and ocular hypertension
in Latinos: The Los Angeles Latino eye study.
Ophthalmology. 2004;111:1439-48.
12.Le A, Mukesh BN, McCarty CA, et al. Risk factors associated with the incidence of open-angle
glaucoma: the visual impairment project. Invest
Ophthalmol Vis Sci. 2003;44:3783-9.
13. Leske MC,Wu S-Y, Hennis A, et al. Risk factors for
open-angle glaucoma: the Barbados eye studies.
Ophthalmology 2008;115:85-93.
14.Gordon MO, Beiser JA, Brandt JD, et al. The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle
glaucoma. Arch Ophthalmol. 2002;120(6):714-20;
discussion 829-30.
15.Heijl A, Leske MC, Bengtsson B, et al; Early
Manifest Glaucoma Trial Group. Reduction of
intraocular pressure and glaucoma progression:
results from the Early Manifest Glaucoma Trial.
Arch Ophthalmol. 2002;120(10):1268-79.
16.The AGIS Investigators. The Advanced Glaucoma
Intervention Study (AGIS): 7. The relationship
between control of intraocular pressure and
visual field deterioration. Am J Ophthalmol.
2000;130(4):429-40.
17.Francis B, Varma R, Chopra V, et al, Los Angeles
Latino Eye Study Group. Intraocular pressure,
central corneal thickness, and prevalence of openangle glaucoma: the Los Angeles Latino Eye Study.
Am J Ophthalmol. 2008;146(5):741-6.
Key Issues in Glaucoma Management 7
Examination Answer sheet — Key Issues in Glaucoma Management — Issue 1
This CE activity is sponsored by the New England College of Optometry and is supported by an unrestricted educational
grant from Bausch + Lomb, Inc. Directions: Circle the best answer to each question in the exam (questions 1–10) and in
the evaluation (questions 11–16). The New England College of Optometry designates this activity for a maximum of 1 hour
of COPE-approved continuing education credit. There is no fee to participate in this activity. In order to receive CE credit,
participants should read the report and then take the posttest. A score of 70% is required to qualify for CE credit. Estimated
time to complete the activity is 60 minutes.
1. Which of the following
is true of glaucoma risk
calculators?
A. Their difficulty makes
them of value only to
glaucoma specialists
B. None is currently
available for clinical use
C. They help apply results
from large studies to
individual patients
D. They are meaningful
to research study
participants only
2. Which of the following
classes of glaucoma agents
reduces IOP by increasing
aqueous outflow?
A. Beta blockers
B. Carbonic anhydrase
inhibitors
C. Alpha agonists
D. Prostaglandin analogs
3. Which of the following
is NOT a risk factor for the
development of glaucoma?
A. Ocular trauma
B. Family history of
glaucoma
C. Thick central corneal
pachymetry
D. Large vertical cup-todisc ratio
4. How much pressure
reduction is typically
recommended when
initiating therapy in
glaucoma patients with mild
damage?
A. 5% or more
B. 10% or more
C. 25% or more
D. 65% or more
5.Early detection of glaucoma
is important because:
A. Glaucoma is reversible
with treatment
B. Newly available
neuroprotective agents
can halt disease
progression
C. Both A and B are true
D. None of the above is
true
6.Primary open angle
glaucoma:
A. Is glaucoma with no
known cause
B. Remains asymptomatic
at every stage
C. Does not affect Asians
D. Is caused by angle
closure
7. Which of the following
is true about the relationship
between IOP and glaucoma?
A. A single measurement
can give a true and
complete picture of a
patient’s IOP status
B. Glaucomatous damage
can occur in patients
whose pressure is
consistently found in the
normal range
C. The prevalence of
open-angle glaucoma
decreases as IOP
increases
D. IOP lowering is one of
many therapeutic options
for glaucoma
8. Which of the following
is NOT integral to the
definition of glaucoma?
A. Enlarged optic cup
B. Increased IOP
C. Loss of the retinal
nerve fiber layer
D. Visual field deficit
9.Which of the following can
influence aqueous humor
production?
A. Age
B. Circadian rhythm
C. Hormones
D. All of the above
10.Which of the following
changes in aqueous flow is
primarily responsible for
increasing IOP in open-angle
glaucoma?
A. Excessive aqueous
production
B. Increased outflow
through the trabecular
meshwork
C. Decreased uveoscleral
outflow
D. Both A and C are
correct
Examination Answer sheet — Key Issues in Glaucoma Management — Issue 1
This CE activity is sponsored by the New England
College of Optometry and is supported by an unrestricted
educational grant from Bausch + Lomb, Inc. Directions:
Circle the best answer to each question in the exam
(questions 1–10) and in the evaluation (questions 11–16).
In order to receive CE credit, participants should read
the report and then take the posttest. A score of 70% is
required to qualify for CE credit. On completion, tear out
or photocopy the answer sheet and send it to:
New England College of Optometry, ATTN: Ms. Margery
Warren, 424 Beacon Street Boston, MA 02115
CE exam expires September 30, 2017.
ANSWERS:
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8 Key Issues in Glaucoma management
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the following information. Retain a copy­for your records.
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