| |
Volume
1, Number 3 |
June
2006
|
|
|
Inside
This Issue
|
|
|
|
Click
Here if you are having problems
viewing the E-Journal.
To subscribe to the OGS E-Journal, Click
Here!
|
OGS
PRESIDENT'S MESSAGE
When
the Optometric Glaucoma Society (OGS) was being formed several years
ago, one of our goals was to become a member of the Association of International
Glaucoma Societies (AIGS). The AIGS is the umbrella organization for
the worlds glaucoma societies, describing itself as an independent,
impartial, ethical global organization for glaucoma science and care.
All of the worlds major glaucoma societies are members and we
would be in elite company if we would be admitted. There were a series
of steps that were required, but these were well worth the effort when
we were admitted to this prestigious group. Since then, the OGS attends
and contributes to AIGS meetings and publications. The AIGS has been
instrumental in developing consensus statements for different glaucoma
conditions and topics. The first consensus meeting was on Structure-Function,
the second on Surgical Management and the most recent, Angle Closure
Glaucoma. By gathering experts from around the world to discuss and
describe different conditions, consensus meetings allow conditions to
become globally understood and described. One of the highlights of participating
in the different AIGS meetings is getting to know glaucoma specialists
from around the world. Due to a host of reasons, glaucoma as we know
and manage it in the United States is not how many clinicians in other
regions understand the condition.
In July 2005, the first World Glaucoma Congress was held in Vienna,
Austria. Eight OGS members participated in this meeting and everyone
came away with a new perspective of glaucoma as well as the AIGS. We
were surprised that several US optometrists and one from England learned
of the meeting and attended. The next World Glaucoma Congress will be
held in Singapore from July 18-21, 2007. I hope more optometrists will
be able to attend. Everyone is invited and information on the meeting
is available at www.globalaigs.org.
The meeting will have two tracks, one geared at the general clinician
and the other at the glaucoma specialist. Registrants can decide which
track best meets their needs. In addition, there are symposia and receptions
that are highly enjoyable. As optometrists become more sophisticated
regarding the care of patients with glaucoma, meetings such as the World
Glaucoma Congress will offer a level of expertise that will be difficult
to obtain at other meetings. The e-journal will provide updates on the
meeting through 2007 and then describe the highlights soon after the
meeting.
Murray Fingeret, OD
President, Optometric Glaucoma Society
murrayf@optonline.net
EDITORIAL
 |
Incident
Glaucoma Studies
This issue of the OGS E-journal concentrates on the annual meeting of
the Association for Research in Vision and Ophthalmology, known to most
as ARVO, held recently in Fort Lauderdale, Florida. This enormous and
vibrant meeting is aimed at everyone who has an interest in visual science
and eye care. If you have never attended, it is truly difficult to appreciate
its scale. This year there were over 10,000 delegates attending 5920 presentations.
Nearly 1000 presentations were within the glaucoma section alone!
This year one session that I attended was glaucoma epidemiology.* Now,
it is easy to think of epidemiology as a dry science. It can appear lacklustre
because initial impressions are that it only tells us how many people
have disease, which is only great for healthcare planners and not particularly
helpful to the patient sitting in your consulting room chair. Worse still,
it doesnt appear particularly scientific or dynamic because it tends
to avoid innovative technologies and doesnt involve new laboratory-based
techniques. However, these impressions are easily dispelled and I strongly
believe that current epidemiologic glaucoma research is more informative
and clinically relevant than at any previous time. Why do I think this?
Well, the primary reason is that results of powerful glaucoma incidence
studies are now being reported, providing information on the number of
glaucoma cases occurring per unit time in large, randomly selected populations.
Unlike the prevalence studies that were all familiar with, incidence
studies are robust and influential because they quantify exposures
or risk factors associated with subsequent disease development, which
prevalence studies cannot. Prevalence is estimated by a cross-sectional
survey at a single time point and provides information about
current population levels of disease, while incidence studies are prospective
longitudinal investigations that quantify the number of people who develop
disease per unit time. This information on significant relationships between
exposures (risk factors) and outcomes (glaucoma)
provides an essential and quantitative link between hypothesised causal
factors and the real thing -- patient populations.
So, provided the methodology of incidence studies is appropriate, their
findings can be generalised to our patients thereby directly influencing
everyday clinical care.
Of course, there is one other thing that is easy to forget about epidemiology.
Whilst prevalence figures tell us about the number of people at the time
of data collection, constantly changing population demographics mean that
prevalence data rapidly become outdated. Without knowledge of incidence
it is impossible to plan for the glaucoma care requirements of the future.
Only accurate knowledge of incidence will help the glaucoma community
plan for changing population sizes, age and racial distributions and glaucoma
care requirements that will affect us all in the future.
Paul GD Spry, PhD, MCOptom, DiplGlauc, Editor-in-Chief
paul.spry@ubht.swest.nhs.uk
*Abstracts of the 2006 ARVO annual meeting can be searched via the ‘program
planner' at www.arvo.org.
The session referred to in this editorial was 'Paper Session 316. Glaucoma
Epidemiology.'
MEETING
NEWS
Focus on ARVO, Fort
Lauderdale, Florida, USA, April 30th - May 4th 2006.
In this section we will review a number of studies presented at this
years ARVO annual meeting. These are our highlights, which we hope will
be of interest to you, but we couldnt include all the good stuff!
If you want to read the abstracts of our highlights, or search other
presentations, the entire program is available online using the '2006
program planner' in the 'meetings and abstracts' section of www.arvo.org.
To direct you towards the studies that we have reviewed, the session
numbers are provided -- sessions can be identified by number using the
advanced search facility.
Do you know what your mitochondria are doing?
Several sessions and presentations were particularly interesting to
me at the recent ARVO meeting. Surprisingly for a "dyed in the
wool" visual psychophysicist, many of these presentations were
concerned with retinal and optic nerve imaging. Imagine a system that
could detect metabolic processes taking place within structures like
photoreceptors and retinal ganglion cells. Such a device was described
in the "New Ideas in Glaucoma" session (paper session 340
for those who wish to view the abstract online). The Metabolic Mapper,
being developed by Biometric Imaging Inc., appears to allow visualization
of a crucial step in mitochondrial metabolic pathways using a non-invasive
optical procedure. If early results pan out, clinicians may look forward
to observing parts of the retina that are entering a period of metabolic
stress before cell death occurs. Searching for a period of dysfunction
in several retinal diseases is becoming a bit of a hot topic and this
type of device adds evidence for the contention that retinal cells may
feel the pinch before we can see any anatomical changes
in the retina. As was suggested by Dr. Douglas Anderson in the first
issue of the OGS
e-journal "When one axon is lost, there is some function
lost as well, assuming the axon was serving some purpose." However,
the converse may not necessarily be true. An axon that looks normal
anatomically may be having functional difficulties. Recently, the zeitgeist
within glaucoma circles has been that structural abnormalities (disc
or retinal nerve fiber layer (RNFL)) can be detected before functional
damage (perimetry). In the evolving search for early damage
in glaucoma, might function be poised to leap frog ahead of structure?
Time will tell.
Shaban Demirel, BScOptom, PhD
ARVO Highlights Roundup
Optic Nerve Experimental and Immunology (Session #219)
Harwerth et al: Data were presented that supported the conclusions,
"Standard automated perimetry (SAP) measures of visual field defects
and optical coherence tomography (OCT) measures of RNFL defects are
correlated measures of glaucomatous neuropathy. An analysis of normal
inter-subject variability and the dynamic ranges of the measurements
suggest that RNFL thickness may be a more sensitive measurement for
early stages of glaucoma and perimetry a better measure for moderate
to advanced stages of glaucoma." One caveat is that the estimate
of axon density in the RNFL used to convert OCT based thickness to axonal
number needs further histological validation.
Optic Nerve and RNFL Imaging III (Session #462)
Coops et al: These authors looked at Heidelberg Retinal Tomograph (HRT)
analyses and found that the newer Glaucoma Probability Score (GPS) had
similar diagnostic performance to the more established Moorfields Regression
Analysis. As always, disc size matters!
Artes et al: Disc Progression by Topographical Change Analysis using
HRT.
This study attempted to sort out which criteria (cluster size based
on number of superpixels and range of height changes) best separate
glaucoma and healthy controls over time (Kaplan-Meier analysis). The
investigators followed 60 eyes of 60 control subjects and 172 eyes of
91 glaucoma patients for 8 years. The best separation was achieved using
relatively small clusters (1-2% of the optic disc area) and moderate
height change criteria (20 to 50 microns).
Garway-Heath et al: Used a new technique known as "Statistic Image
Mapping (SIM)" to detect change over a series of HRT images. These
were compared with results of change criteria recommended by the HRT
operation manual for various stereometric parameters obtained from the
regular output of the instrument. SIM detected change earlier and more
reliably than monitoring the HRT stereometric parameters over time.
Will this become available for clinical use in the future?
Sanai et al: A comparison of Caucasian populations in Europe with persons
of African descent in Alabama, Southeastern US, with a population from
Hyderabad, India revealed that ethnic differences exist in stereometric
parameters obtained from HRT scans. This suggests that ethnicity-specific
normative data is important for diagnostic classification when using
these parameters (including analyses like the Moorfields Regression
Analysis). Interestingly, their data also suggests this might be more
important than age-specific normative data.
New Ideas (Session #340)
Chen et al: Ultra-high speed, ultra-high resolution spectral domain
OCT in vivo in human eyes with open angle glaucoma achieved resolution
of 6 microns 73 times faster than commercially available OCT machines.
Three dimensional analysis capabilities and high-resolution promise
better structural evaluation of glaucomatous optic nerve head and retinal
layers in vivo.
Optic Nerve and RNFL Imaging I (Session #382)
Huang et al: Presented further evidence to suggest that intra-axonal
microtubules are a major source of birefringence in the RNFL, but account
for only about half of the RNFL reflectance.
Knighton et al: Compared fundus photos and 3-D OCT (spectral domain)
images, both acquired in vivo, the latter with about 8 micron axial
resolution, demonstrating the power of newer OCT imaging techniques
to approach the level of detail previously only available in histological
sections.
Inoue et al: Fourier domain OCT, another method capable of 3-D imaging
(3.5 seconds for a volume consisting of 256 x 256 A-scans, each with
about 6 micron depth resolution), used to show exquisite detail, including
laminar structure and pores nearly through the full thickness of the
lamina cribrosa in vivo!
Gregori et al: Using high-speed spectral-domain OCT (axial resolution
of 6-8 microns), demonstrated effectiveness of new boundary detection
algorithm to delineate retinal layers and obtain thickness maps for
RNFL and RGC+IPL layers. Relatively subtle anatomical features (e.g.
individual RNFL bundles) and glaucomatous abnormalities were visible,
the latter correlating with functional loss (standard perimetry data).
Mujat et al: Using high-speed spectral-domain OCT and a new delineation
algorithm created RNFL thickness maps with excellent reproducibility.
Chauhan et al: in a longitudinal study (86 patients for >8 years),
found that changes in peripapillary atrophy occurred frequently, but
were not associated with extent nor rate of disc changes, suggesting
that the mechanisms underlying these two structural changes might be
independent.
Mora et al: evaluated 126 black and 98 white subjects (mixture of glaucoma
and controls) against the new HRT3 normative database and found that
"A new, larger, race-specific HRT-III database increases sensitivity
while maintaining specificity for white persons and increases sensitivity
but decreases specificity for black persons." Based on the latter,
they warn that: "New software and databases based upon race require
careful scrutiny prior to use in clinical practice."
Brad Fortune, OD, PhD

OPTIC
NERVE REVIEW

Figure 1. Normal RNFL. Note bright striations in the superior
and inferior arcuate bundles and less bright striations in the
papillomacular and nasal bundles.
|

Figure 2. Note relatively large optic disc with large cupping.
However the inferior rim tissue shows a localized notch which
does not obey ISNT rule.
|

Figure 3. Red-free photo shows inferior wedge defect in the
RNFL which corresponds to location of the thinning inferior
rim tissue. Note much brighter striations in the superior arcuate
bundle.
|

Figure 4. Serial visual fields of the same eye featured in
figures 2 and 3. The second visual field shows some early superior
nasal loss on pattern deviation plot which correlates to inferior
optic nerve damage. Note that defect is much less detectable
on 1st and 3rd visual fields. As further damage occurs the defect
will become more repeatable.
|
The
Retinal Nerve Fiber Layer in Glaucoma
The
retinal nerve fiber layer (RNFL) evaluation has been used as a clinical
technique to diagnose glaucoma damage since the early 1980s. Learning
the technique can be arduous and most clinicians do not routinely perform
the procedure. New imaging instruments, such as the GDx and OCT, have
rekindled the interest in the RNFL examination. More doctors now are incorporating
the information obtained from the RNFL to make diagnostic and management
decisions in glaucoma. This will be a two part article: in this issue,
clinical examination techniques will be discussed and the second article
in the next E-Journal issue will highlight the new imaging devices to
examine the RNFL.
The number of ganglion cell axons in the human eye varies from 1-1.5 million.
These axons traverse superficially across the retina in an organized pattern,
make a 90 degree turn at the optic nerve and make up the bulk of the neuro-retinal
rim tissue. Axons originating in the temporal periphery arc above and
below the macula and insert into the superior and inferior poles of the
optic nerve. These axons are called the arcuate bundles and are the most
visibly prominent (brightest striations) of the RNFL bundles (see Figure
1) Macular axons insert into the temporal rim tissue and are called the
papillomacular fibers. Nasal axons insert into the nasal optic nerve.
Clinical evaluation of the RNFL can be achieved with a clear 78 diopter
fundus lens at the slit lamp. The light source of the slit lamp should
be turned up to the brightest setting and the red free filter should be
clicked in. The green light produced will be absorbed by the pigment in
the deeper retinal layers which creates a dark background to highlight
the reflections from the superficial RNFL. The normal RNFL is brightest
in the superior and inferior arcades and less bright in the papillomacular
and nasal bundles (bright-dimmer-bright pattern). A lack of fundus pigmentation
or an increase in media opacities (cataracts) will result in a less visible
RNFL.
Glaucoma is a disease of the ganglion cell axons and damage to the axons
typically occurs in specific patterns. Superior and inferior arcuate fibers
are more selectively damaged than papillomacular and nasal fibers. This
damage results in less bright striations of the arcuate bundles.
There are two patterns of RNFL loss: diffuse and focal. Diffuse loss of
the arcuate striations is one common pattern of RNFL loss in glaucoma.
In diffuse loss, the striations are less bright and underlying retinal
structures (smaller blood vessels, pigmentation of the RPE and choroid)
become more visible. Diffuse loss is best appreciated by comparing the
superior and inferior arcuate bundles within the same and fellow eye.
Also, surface retinal vessels normally contained within a healthy RNFL
often appear to stand out proud of the underlying retinal structures in
areas of RNFL loss. Focal defects (often called slit or wedge
defects, depending on site) represent RNFL loss in a more specific location
in the optic nerve. These defects are much easier to identify than diffuse
RNFL loss, and an example is shown in figures 2 and 3. To be clinically
significant, rather than representing physiological variation, focal defects
should be larger than adjacent arteriole widths and should extend back
to the optic nerve. A common artefactual physiological appearance is when
apparent focal defects are seen that do not extend to the optic nerve
head.
RNFL loss can be used to corroborate optic nerve damage and glaucomatous
visual field loss. Interpreting RNFL loss in the context of other glaucoma
features is especially important because although RNFL loss occurs in
glaucoma, it is not glaucoma-specific and can be the result of any optic
neuropathy. The main advantage of the RNFL examination is to uncover glaucoma
damage before visual field defects appear on standard perimetry. It is
estimated that some glaucoma patients may lose up to 20-50% of their
ganglion cell axons before reproducible loss occurs on standard perimetry.
Changes in the RNFL can be the first sign of glaucoma damage.
Anthony B Litwak, OD, FAAO
VISUAL
FIELD REVIEW
Is this a case of early glaucoma?
In
this issue I will discuss how to interpret visual field outcomes.
This 68 year old female has been noted with bilateral peripapillary atrophy
(PPA, zone-beta) and cup-to-disc ratios of RE 0.5 and LE 0.4 with pallor
and thinning of the left neural rim, especially in the macula bundle.
Her acuities were R 6/9 (20/30) L 6/12 (20/40) with IOPs of 19 mmHg in
both eyes. She has moderate bilateral cataracts and her visual fields
are as shown. Her primary complaint is for blurred vision on the left
side that looks like a shadow. Do you think she has glaucoma?
Well, lets go over how to identify an abnormal field. A visual field
can be called abnormal if ONE of the following is abnormal in the presence
of a reliable test:
Glaucoma Hemifield Test (GHT: borderline or abnormal)
Pattern Standard Deviation (PSD, p<5%)
a cluster of abnormal (1 edge only) points flagged in the Pattern Deviation
plot (PD lowest right panel)
In this case, the lady has abnormal GHT, MD, PSD and a cluster of abnormal
points in the pattern deviation plots of both eyes. This means that both
fields are abnormal. The RE is reliable (allowing 20% for fixation
loss and 33% for false responses) but the left eye exceeds the expected
fixation loss criterion. So let's review what these criteria mean.
Katz and Sommer(1) have shown that 30% of normal and 45% of glaucoma
patients exceed these reliability limits -- sound familiar? The majority
of failures being due to the presence of excessive fixation losses (41-67%).
These arise from inaccurate mapping of the blind-spot so that remapping
the blind-spot during testing reduces the number who fail to 14%.
I use the eye monitor to gauge whether the patient is fixating and record
that on the chart using a 0-4+ score. The authors propose that a conservative
criterion of reliability for all indices should be 33%, as this would
fail only 3% of all field exams. Applying this criterion would suggest
reliable outcomes in both eyes.
Given reliable tests, the GHT is outside normal limits in both eyes, the
PSD is likewise (P<5%) and points cluster on the PD plot. Clustering
can be assessed against the Hoddap-Anderson-Parrish criterion (2) which
requires abnormality at 3 neighboring points at p<5% (one edge
point) with one of these being p<1%.
Both eyes show such clusters and fail at the other two criteria (GHT,
PSD) indicating abnormal field outcomes. The question that now needs to
be asked is: does this patient have glaucoma?
If you concluded that she has normal tension glaucoma, so did the consulting
physician who started her on latanoprost, after which her IOPs were 10
and 11 mmHg some 3 months later.
Glaucoma is sometimes one of the hardest diseases to diagnose. In this
case, peripheral RPE changes were found following dilated fundus examination
some 2 years after the field tests. ERG evaluation exposed the true diagnosis
of retinitis pigmentosa.
This case demonstrates how to evaluate a visual field and the importance
of keeping an open mind on the diagnosis. It reinforces the need to perform
a full battery of tests in considering a differential diagnosis; which
should always include a peripheral retinal examination through a dilated
pupil.
Algis Vingrys, BScOptom, PhD
1. Katz J, Sommer A. Reliability indexes of automated
perimetric tests. Arch Ophthalmol 1988: 106: 1252-54.
2. Hodapp E, Parrish RK, Anderson DR. Clinical decisions in glaucoma.
St Louis MO, Mosby-Year Book, 1993: 52-61.
QUARTERLY
CASE
A 62 year-old African American male presented
with a complaint of blurred vision at near. His medical history included
chronic obstructive pulmonary disease (COPD), prostate cancer, hypertension,
hyperlipidemia, rheumatoid arthritis and coronary artery heart disease.
Medications include Combivent, Albuterol, Nifedipine, Lisinopril, Hydrochlorothiazide,
Simavastin, Sulfasalazine, and Etodolac. There was no known allergies
or pertinent ocular or family ocular history.
Uncorrected visual acuity at distance is 20/25 OD and 20/25 OS, corrected
to 20/20 with a small prescription. FDT N30 screening visual fields
(Figure 1) are full in each eye and pupils are equal, round, reactive
without signs of an afferent pupil defect. Intraocular pressure was
26 mm Hg in each eye at 8:30am, pachymetry 540 µm OD/ 535 µm
OS and gonioscopy revealed wide open angles OD and OS. A dilated optic
nerve evaluation showed the optic disc to be average in size, the ISNT
rule obeyed, without evidence of peripapillary atrophy, optic disc hemorrhage
or retinal nerve fiber layer (RNFL) loss present in either eye (Figure
2). The retinal examination did reveal significant vessel tortuosity
and dilation, compatible with an individual with severe coronary artery
disease and hypertension.
Our assessment was Ocular Hypertension with the patient instructed to
return in four weeks for a visual field test and to measure the IOP
again. We got in touch with the patient's internist to alert her of
the retinal signs associated with cardiovascular disease. It turns out
that the blood pressure has not been well controlled, varying between
140/90-150/100 with concerns regarding drug adherence.
Upon return in 1 month, the IOP using Goldmann tonometry was 24 mm Hg
in each eye at 10am. The HFA II 24-2 SITA Standard visual fields were
reliable and full in each eye (Figure 3). Risk assessment using the
parameters found in table 1 and the STAR risk calculator showed a moderate
risk of 11-15%. The patient was educated about Ocular Hypertension.
It was decided that given the moderate risk, the best course was to
follow closely with the patient returning in 6 months.
The patient returned in six months with the IOP measured at 36 mm Hg
in each eye. A change was made to the patients medical regimen
due to a worsening of COPD. Advair, which contains Fluticasone (steroid)
and Salmeterol and used as an oral inhaler was added in December 2005.
Given the use of a steroid inhaled orally, it is possible that the patient
may be a steroid responder. Imaging was performed using the Heidelberg
Retinal Tomograph (Figure 4A) and GDx VCC (Figure 4B). Both examinations
showed the optic nerve and RNFL to be healthy. SITA SWAP visual fields
(Figure 5) and FDT 24-2 threshold visual fields (Figure 6) were full
in each eye. We assessed the patient to be Ocular Hypertensive (possibly
a steroid responder) and given the elevated IOP, started the patient
on a prostaglandin agent once per day in each eye. Given the excellent
health of the optic nerves and visual fields, our target level is approximately
18-19 mm Hg. The patient is to return in three weeks. We also reported
our concern of steroid responsiveness to the patients primary
care physician. Given the elevated IOP, the patients internist
is going to discontinue Advair and reassess the COPD. We will also reassess
the IOP once the drug is washed out of the system, possibly being able
to discontinue the drug if the IOP lowers. We will keep each other informed
of the progress, recognizing that the oral steroid combination medication
may be needed to control the patients COPD, at which case we will
need to manage the elevated IOP.
Ocular hypertensive patients need to be closely followed because one
never knows until multiple measurements are available what the highest
reading is. In this case, after multiple measurements we found a spike
in readings necessitating therapy. The spike was probably due to the
addition of a steroid agent. We are expecting the patient to return
in 3 weeks to assess the IOP and the tolerance to the prostaglandin.
Murray Fingeret, OD
Figure 1

|
Figure 2

|
|
Figure 3

|
|
Figure 4A

|
Figure 4B

|
Figure 5

|
|
Figure 6

|
|
Table 1
|
INTERNATIONAL
COLUMN
Emerging Optometric Glaucoma Care in the United
Kingdom
Optometrists within the United Kingdom have privileges allowing them
to only use topical diagnostic agents. In regards to the treatment of
ocular disease including glaucoma that require therapeutic agents, the
role of UK Optometrists has traditionally been to refer each patient
in whom treatable eye disease was suspected for diagnosis and management
by ophthalmologists within the publicly funded National Health Service
(NHS). This role was defined by principles laid down in parliamentary
legislation, the Opticians Act (1989). Registered (licensed) UK optometrists
have therefore always been the case-finders for detecting
the majority of incident glaucoma cases although they have had no subsequent
part in patient care beyond initial detection. The Opticians Act provided
UK registered Optometrists with use-only access to specified pharmacologic
agents solely for investigative purposes (e.g. oxybuprocaine
hydrochloride, tropicamide) and a very small number of therapeutic exceptions
under strictly defined circumstances (e.g. chloramphenicol 0.5% drops,
for sale or supply in emergencies only). This framework therefore precluded
optometric glaucoma treatment.
However, the UK demographics of an ageing and expanding population demands
changes in glaucoma care provision, as it is anticipated that the number
of individuals aged over 65yrs will grow by 10% over the next 25
years, with the average life expectancy for each individual steadily
increasing(1). In spite of the changing demographics, the number of
UK NHS ophthalmologists currently providing all glaucoma care remains
relatively static. To cope with increasing service demand a number of
co-management schemes between ophthalmologists and optometrists have
been developed, based upon randomised trials of co-managed glaucoma
care(2). These changes are occurring primarily within NHS hospitals(3).
Although such changes increase capacity to manage more cases of glaucoma,
their scope remains limited due to the dependence on access to medically-trained
staff to authorise medication changes. However, legislative amendments
to the Opticians Act in late 2005(4) are about to change and improve
this situation substantially. These changes include initiation of a
new category of registration, supplementary prescriber.(5)
This aims to extend the supplementary prescribing optometrists
role, with better use of their knowledge and skills, including making
it easier for them to prescribe. Supplementary prescribing has been
defined as, "a voluntary relationship between an independent prescriber
and supplementary prescriber to implement an agreed patient specific
management plan." Practically, the management plan provides a set
of rules for patient care, such as how often the patient needs to be
seen, which medications could be prescribed if required, follow-up intervals
and actions required if medical treatments fail. Supplementary prescribing
is not limited to glaucoma, covering any eye disease and most UK licensed
medications. Furthermore, use is not limited to optometrists working
in NHS hospitals: provided the rules are followed it can be applied
in private optometric practice.
What supplementary prescribing does not provide is a guarantee that
those who obtain the qualification have practical experience in glaucoma
management. However, Optometrists can demonstrate this by obtaining
the postgraduate glaucoma diploma (suffix DipGlauc), available from
the College of Optometrists since 2004(6).
In summary, new changes in legislation and recently available higher
qualifications have provided UK Optometrists with the formal opportunity
to become involved in glaucoma care beyond referral for the first time,
and to demonstrate their specialist knowledge and experience in glaucoma
care provision. Although these initial limited steps in prescribing
anti-glaucoma medication do not permit autonomy they do represent the
first significant opportunity for optometric involvement in glaucoma
management and increased opportunity to work collaboratively with our
ophthalmological colleagues for the glaucoma patients benefit.
Paul GD Spry, PhD, MCOptom, DiplGlauc
1. Office of National statistics website. www.statistics.gov.uk
2. Gray SF, Spry PGD, Brookes ST, Peters TJ, Spencer IC, Baker IA, Sparrow
JM, Easty DL (2000). The Bristol Shared Care Glaucoma Study - outcome
at follow-up at 2 years. British Journal of Ophthalmology; 84 (5): 456-463.
3. Whitaker A, Spry PGD (2004). Optometric shared care of glaucoma:
a current perspective. CE Optometry; 7(1): 33-37.
4. Statutory Instruments 2005 No 766, 1507, 1520.
5. NHS National Prescribing Centre. www.npc.co.uk
6. College of Optometrists. www.college-optoemtrists.org
PHARMACY
REVIEW
Beta Blocking Agents
Short of the introduction of pilocarpine in 1898, nothing has revolutionized
the medical management of glaucoma as much as the introduction of the
beta adrenergic blocking agents in late 1978. Adrenergic antagonists
block adrenergic receptor stimulation by competing with the endogenous
sympathetic neurotransmitters norepinephrine and epinephrine for available
receptor sites. These agents can be categorized by the type of receptor
inhibited: alpha or beta antagonist. They can be classified as selective
by their preference for a particular receptor type or non-selective
in that they have affinity for both beta 1 and beta 2 receptors. Beta
1 receptors are found on the heart and in general produce an increase
in cardiac output and workload by increasing the heart rate. Cardiac
workload is also increased by the vasoconstrictive effect of adrenergic
agents. The vasoconstrictive effect of sympathetic amines and their
effect on cardiac output are the major cause of increased cardiac oxygen
demand and workload. Beta 2 receptors produce dilation of pulmonary
bronchi. From the description of the effect of sympathetic amines on
the beta receptors the side-effects of beta blockers can be extrapolated.
Non-selective drugs can be expected to reduce heart rate (bradycardia),
produce systemic hypotension and bronchiolar constriction. These and
other side-effects of this class will be covered in greater detail shortly.
An additional sub-type of the beta-blocking agents is those that demonstrate
intrinsic sympathomimetic activity (ISA). ISA compounds both block and
mildly stimulate (partial agonist effect) beta receptors. One additional
characteristic seen in some agents of this class is their membrane stabilizing
activity. The drug exhibits an anesthetic-like effect that limits the
topical ocular use of some of these agents. A more recent development
is that most non-selective beta blockers are available generically,
which had led to their reduced cost.
Mechanism of Action
Both systemic and topical beta-blocking agents reduce the intraocular
pressure (IOP) by decreasing the rate of aqueous production. The rate
of aqueous outflow is not affected. The proposed site of action is non-pigmented
ciliary epithelium and the vasculature of the ciliary body. In spite
of the many similarities of these compounds, there exist specific examples
of clinically significant differences. This article will touch upon
these differences and their importance to the clinician.
Timolol. Timolol maleate is the prototype of the group. It is
neither selective nor does it exhibit ISA. It also does not possess
significant membrane stabilizing activity. It is available in both 0.25%
and 0.5% concentrations. A thixotropic (gel forming) once daily
dosage form is also available in the 0.50% strength. In some countries,
0.1% gel is also available. Timolol demonstrates excellent efficacy.
By reducing the production of aqueous by up to 50%, the IOP can
be reduced, on average, up to 25%. Studies have shown that timolol
demonstrates a limited ability to reduce IOP during sleep. Therefore,
the drug is commonly prescribed once daily upon awakening. Patients
using the drug once daily attained an 81% success rate in reaching target
IOP. This rose to 88% when the drug was used twice daily. Because
side-effects are dose-dependent, increasing the frequency to BID and
the concentration to 0.5% may increase the risk of side-effects
without providing an equal improvement in efficacy.
Carteolol. Carteolol HCl, a nonselective beta-adrenergic blocking
agent, differs from timolol because of its intrinsic sympathomimetic
activity. Like timolol it does not possess any significant membrane-stabilizing
activity. Drugs that possess ISA theoretically produce fewer cardiovascular
side-effects. This would include a reduced risk of bradycardia and decrease
in blood pressure.
Given topically twice daily in controlled domestic clinical trials ranging
from 1.5 to 3 months, carteolol produced a median reduction of IOP of
22% to 25%. No significant effects were noted on corneal sensitivity,
tear secretion, or pupil size.
A 2001 study by Montanari et al demonstrated carteolols ability
to reduce the resistance in the short posterior ciliary arteries. This
suggests a potential benefit of improved perfusion in patients with
normal tension glaucoma that use this agent and may be a function of
carteolols ISA activity.
Levobunolol. This agent is similar to timolol. It is non-selective,
has no ISA and does not produce membrane stabilization. It does however
possess an active metabolite, dihydrolevobunolol, therefore levobunolol
has a longer half-life than timolol. This allows for successful treatment
of approximately 72% of patients with 0.25% levobunolol and
a slightly higher number with the 0.5% dosage form. Levobunolol
is the purified isomer and is 60 times more potent than the dextroisomer.
Betaxolol. Betaxolol is unique among the topical beta blockers
used to treat glaucoma. It is considered beta 1 selective because it
shows 200 times greater affinity for cardiac tissue receptors than pulmonary
receptors. Betaxolols ability to lower IOP is generally less than
the non-selective beta blocking agents. Patients switched to betaxolol
0.5% from timolol 0.5% demonstrated a 1.5 to 2.5mmHg rise in
IOP. The drug shows no ISA or membrane stabilizing properties. Of special
note is betaxolols greater efficacy in combination with epinephrine
and dipivifrin therapy. Epinephrine increases outflow via beta 2 receptor
stimulation. This is not blocked by beta 1 selective betaxolol.
Of great interest are the results of two studies. Both Messmer and Collingnon-Brach
demonstrated that patients using betaxolol had higher IOPs than
patients using timolol therapy. Nevertheless, the betaxolol patients
demonstrated improved visual field results. This illustrates the fact
that betaxolol may improve some ocular factors other than IOP reduction.
One postulated theory is improved optic nerve perfusion. Neuroprotective
properties are the "holy grail" of glaucoma therapy. There
is a belief that betaxolol may accomplish this in several ways. One
line of study is the calcium channel blocking properties of betaxolol.
According to the glutamate pathway theory in cell death, calcium influx
is the terminal step in axon death. The ability to block calcium influx
can theoretically produce a neuroprotective benefit. Another mechanism
is the nitric oxide stimulating effect of betaxolol. Nitric oxide receptors
are, in part, responsible for modulating blood flow to the optic nerve.
Beta Blocker Side-Effects
The cardiac and pulmonary side-effects of the beta blocking agents are
well documented. These include bradycardia, angina, reduction in systemic
blood pressure, heart block and exacerbation of asthma and chronic obstructive
pulmonary disease. Other side-effects attributed to these drugs are
more controversial. These include:
1. Depression
Beta-blockers with high lipid solubility, timolol and levobunolol, can
penetrate the blood-brain barrier. Carteolol and betaxolol have lower
lipid solubility. In general, patients with diagnosed endogenous or
exogenous depression should avoid these drugs. This would include those
with a history of use of selective serotonin re-uptake inhibitors, tricyclic
and other antidepressant medications.
2. Elevated serum lipids
Except for carteolol and betaxolol, the non-selective beta blocking
agents can induce an 8-12% increase in serum lipids and a similar
reduction in HDL levels. This can result in an increased risk of coronary
artery disease.
3. Diabetes
Diabetics that experience significant episodes of hypoglycemia should
avoid beta blocking agents. During an episode of hypoglycemia epinephrine
is released and, in part, produces symptoms which include sweating and
tachycardia which serve to warn the individual that they may be experiencing
a significant hypoglycemic event. Theoretically the beta blocking agents
can blunt the warning signs of hypoglycemia and should be avoided in
those with a significant risk of hypoglycemia.
4. Impotence
Agents with the highest lipid solubility have a greater tendency to
induce this form of CNS side-effect. It is appropriate to question normal
male patients regarding this potential adverse effect in the course
of their therapy. Those using systemic treatment for erectile dysfunction
should avoid topical beta blocking agents.
5. Anaphylaxis
Certain individuals exhibit extreme allergic sensitivities to bee/wasp
stings, foods and other normal substances. The normal treatment of anaphylactic
episodes includes the injection of the sympathetic amine epinephrine.
Patients undergoing allergic skin testing are also at risk for anaphylactic
episodes. Topical beta blockers should be avoided because they may reduce
the ability of epinephrine to reverse the anaphylactic episode.
6. Concomitant oral beta blockers
There is no absolute contraindication to utilizing topical beta blocking
agents with oral beta blocker therapy. However their combined use, due
to pre-existing blood levels, could result in reduced efficacy and increased
risk of side-effects.
Conclusion
Beta blocking agents have a long history of efficacy and safety in the
management of glaucomatous disease. Side-effects can be significant,
but predictable. Adequate patient counselling and monitoring is mandatory
when using this group of agents. Because of their high efficacy and
predictability of their side-effects they remain an important option
in our treatment of the glaucomas.
Bruce Onofrey, OD, RPh, FAAO
1. Arend O, Harris A, Arend S, Remky A, Martin BJ
(1998). The acute effect of topical beta-adrenoreceptor blocking agents
on retinal and optic nerve head circulation. Acta Ophthalmol Scand.;76(1):43-9.
2. Bartlett JD, Olivier M, Richardson T, Whitaker R Jr, Pensyl D, Wilson
MR (1999). Central nervous system and plasma lipid profiles associated
with carteolol and timolol in postmenopausal black women. J Glaucoma.;8(6):388-95.
3. Clin Pharmacol Ther.; 61(5):583-95.
4. Collignon-Brach J (1994). Longterm effect of topical beta-blockers
on intraocular pressure and visual field sensitivity in ocular hypertension
and chronic open-angle glaucoma. Surv Ophthalmol. 38 Suppl:S149-55.
5. Gross RL, Hensley SH, Gao F, Wu SM (1999). Retinal ganglion cell
dysfunction induced by hypoxia and glutamate: potential neuroprotective
effects of beta-blockers. Surv Ophthalmol.; 43 Suppl 1:S162-70.
6. Hiett JA Ocular adrenergic agents(1991). Cl Optom Pharm and Ther.
7. Hoffman BB (1987). Adrenoreceptor-blocking drugs. Basic and Clinical
Pharm.
8. Juzych MS (1997) Beta-blockers. Text of Oc. Pharm.
9. Lama PJ (2002). Systemic adverse effects of beta-adrenergic blockers:
an evidence-based assessment. Am J Ophthalmol.;134(5):749-60.
10. Long D, Zimmerman T, Spaeth G, Novack G, Burke PJ, Duzman E (1985).Minimum
concentration of levobunolol required to control intraocular pressure
in patients with primary open-angle glaucoma or ocular hypertension.
Am J Ophthalmol. 99(1):18-22.
11. Messmer C, Flammer J, Stumpfig D (1991). Influence of betaxolol
and timolol on the visual fields of patients with glaucoma. Am J Ophthalmol;
112(6): 678-81
12. Montanari P, Marangoni P, Oldani A, Ratiglia R, Raiteri M, Berardinelli
L (2001). Color Doppler imaging study in patients with primary open-angle
glaucoma treated with timolol 0.5% and carteolol 2%. Eur J Ophthalmol;11(3)
:240-4.
13. Schmetterer L, Strenn K, Findl O, Breiteneder H, Graselli U, Agneter
E, Eichler HG, Wolzt M (1997). Effects of antiglaucoma drugs on ocular
hemodynamics in healthy volunteers.
14. Stewart WC, Dubiner HB, Mundorf TK, Laibovitz RA, Sall KN, Katz
LJ, Singh K, Shulman DG, Siegel LI, Hudgins AC, Nussbaum L, Apostolaros
M (1999). Effects of carteolol and timolol on plasma lipid profiles
in older women with ocular hypertension or primary open-angle glaucoma.
Am J Ophthalmol.;127(2):142-7.
15. Topper JE, Brubaker RF (1985). Effects of timolol, epinephrine,
and acetazolamide on aqueous flow during sleep. Invest Ophthalmol Vis
Sci. 26(10):1315-9.
16. Wood JP, Schmidt KG, Melena J, Chidlow G, Allmeier H, Osborne NN
(2003). The beta-adrenoceptor antagonists metipranolol and timolol are
retinal neuroprotectants: comparison with betaxolol. Exp Eye Res.;76(4):505-16.
TABLE:
COMMON BETA BLOCKING AGENTS
Timolol
maleate/timolol hemihydrate: 0.25%/0.5%
Carteolol: 1%
Levobunolol: 0.25%/0.5%
Betaxolol: 0.5%
Betaxolol: 0.25%
(Betoptic S-Alcon)
|
QUESTIONS
& ANSWERS
This
section contains questions from readers of the journal with answers
and comments from editorial board members.
Question: "In low tension glaucoma, it has sometimes been
suggested to obtain an MRI to find a neuro or neuro-vascular etiology
(in the anterior visual pathway) of compromised appearing optic nerve
heads and to obtain a carotid duplex. Are those tests really indicated
in cases of LTG?"
Answer: Douglas Anderson, MD, writes, "To say that
all individuals in whom normal-tension glaucoma (NTG) is being considered
should have neuro-imaging and evaluation of major vessels is to say
that the diagnosis is one of exclusion. I believe one should first consider
whether the clinical features support the diagnosis of NTG. Typically
the discs have excavations that are associated with localized thinning
of the rim, nearly always at the inferior or superior temporal meridian.
Disc hemorrhages may be observed by ophthalmoscopy intermittently, so
disc examination may be done over several visits 2 to 4 weeks apart
before considering expensive diagnostic tests. The likelihood that NTG
is the diagnosis increases if the visual field defect is pre-chiasmal
with nerve-fiber bundle characteristics, especially if bilateral, and
even more so if the patient has vasospastic symptoms or a family history
of glaucoma. If a sufficient number of these characteristic traits of
NTG are present, I would not feel the neuro-diagnostic tests are needed,
at least at the time of initial presentation. The exceptions would be
that I would undertake the tests at the time of presentation if the
field defect is a unilateral prechiasmal defect with pallor of the rim
without localized expansion of the cup and without ophthalmoscopically
recognizable retinal disease, if the acuity is poor (central scotoma)
and not explained by macular disease, or if the field defect was suspiciously
hemianopic, and would undertake the test later if there is unexpected
progression despite substantial lowering of the IOP."
Question: "I heard in a lecture by a Glaucoma specialist
that Xalatan works just as well when taken once a week as daily. Is
there any truth in this?"
Answer: Thom Zimmerman, M.D., Ph.D., writes, "The
basis for the statement that Xalatan works just as well when taken once
a week as once daily is derived from the fact that there is a very,
very long wash out period for Xalatan and the other prostaglandins.
This is flawed though because the patients have been taking the prostaglandin
analogues chronically and then when you stop it, there is a long wash
out period. No one knows what will happen if you are using it once a
week. My best guess is that it wont be nearly as efficacious as
Xalatan used once daily. My reasoning for this comes from a couple of
different directions. Xalatan and the prostaglandin analogues are not
as effective initially as they are later in therapy. I feel that you
have to have a prostaglandin analogue aboard for at least four to six
weeks before you really know what its maximal effect will be. Based
on this I doubt if youll ever get to the maximal effect using
the drug once weekly. Secondly, with all drugs theres a "loading"
and/or an "equilibrium" level that must be achieved before
the drug reaches its maximal effect. Based on the previous statements,
I doubt if this can be achieved with once weekly dosing.
In your practice, if youd like to take a look at this topic, there
are a number of studies that you could design. You could start new patients
on Xalatan once weekly and follow them for awhile to see what the pressure
response is. Alternatively, you could take patients who have been on
chronic Xalatan and then, move those to once weekly and see what the
difference from the chronic Xalatan to the once weekly dose is concerning
the intraocular pressure. Should you choose to do either or both of
these studies, I think it would be well worth reporting."
Thom J. Zimmerman, MD, P.D
Emeritus Professor and Chair, Department of Ophthalmology and Visual
Sciences
Emeritus Professor, Department of Pharmacology and Toxicology
University of Louisville, School of Medicine
Question: "I have recently incorporated glaucoma management
to the practice and I am asking if you have any clinically informative
glaucoma flow sheets or glaucoma suspect examination sheets that you
can share with me?"
Answer: Although we are unaware of any standardised examination
forms that are widely available, there is a set of excellent flow sheets
available to help you with clinical glaucoma decision-making. These
cover everything from help with arriving at a diagnosis through to treatment
stepladders and are available in "Terminology and Guidelines for
Glaucoma, IInd edition" by the European Glaucoma Society. The entire
book is published by Dogma Publications in Italy (ISBN: 88-87434-13-1).
However, the introduction and all the flow charts are included in the
preview version which can be downloaded for free as a *.pdf file from
the Societys website. Click on the following link to get directly
to the webpage: www.eugs.org/ebook.asp
Question: "As to the glaucoma risk calculators: Is PSD a
factor obtained from certain visual field units in particular?? Other
than the Devers risk calculator, it was mentioned that there is a Mansberger
glaucoma risk calculator; where can this be found?"
Answer: Firstly, PSD (pattern standard deviation) is one of the
global visual field indices obtained from Statpac single field analysis
by the Humphrey Field Analyzer, and provides a single figure quantification
of irregularities of the field surface and is conceptually
similar (although not numerically equivalent) to loss variance
in Octopus instruments. It is sensitive to focal losses, being low in
normal individuals with a smooth field surface, and rising when focal
defects become apparent, and falling again in extinguished fields. PSD
compliments the fellow global index Mean Deviation (MD) which quantifies
the average reduction between the patients test results
and those of an age-matched normal, providing a good measure of generalised
loss but is insensitive to early, focal defects typical of glaucoma.
Risk calculators currently available are based upon the Ocular Hypertension
Treatment Study and use of the Humphrey Field Analyzer (HFA). Unfortunately
the Octopus, Oculus, FDT or any other perimeter creates different measurements
that cannot be used with the risk calculator. With regard to risk calculators,
the Devers Risk Calculator was developed by Dr SL Mansberger: they are
the same thing. This risk calculator is available for use or download
from the Devers Eye Institute website (www.discoveriesinsight.org/GlaucomaRisk.htm).
For further information about the calculator, have a look at the review
featured in the OGS
E-Journal issue 2.
AIGS
CONSENSUS MEETING ON ANGLE CLOSURE GLAUCOMA
The third consensus meeting of the Association
of International Glaucoma Societies was held on May 3, 2006 in Hollywood,
Florida. This particular meeting was on Angle Closure Glaucoma (ACG).
The faculty was made up of experts from around the world with the goal
of developing consensus statements related to ACG. Primary angle closure
glaucoma is one of the leading causes of blindness throughout Asia and
may be more common than previously thought in the western countries.
Overall, open angle glaucoma is more common than ACG but many more cases
of blindness are related to ACG because it is more severe when it occurs.
With the aging population, more individuals will be afflicted with ACG.
New technologies like ultrasound biomicroscopy and anterior segment
optical coherence tomography allow pathologic mechanisms to be better
understood. Still, therapies remain similar to what they were years
ago, starting with iridotomy and moving on from there.
In 2002, a classification system was put forward that is used in epidemiologic
research. The International Society of Geographic and Epidemiological
Ophthalmology (ISGEO) describes three stages for ACG;
a. Primary Angle Closure Suspect: occludable angle, but normal IOP,
disc and field without evidence of peripheral anterior synechiae (PAS);
b. Primary Angle Closure: occludable angle with either raised IOP and/or
primary PAS: disc and field normal;
c. Primary Angle Closure Glaucoma: occludable angle with either raised
IOP and/or primary PAS: disc and field abnormal.
A large part of the discussion for the meeting was what is considered
an "occludable" or narrow angle, which conveys that there
is an anatomical predisposition to angle-closure. Prior studies have
used the definition of a narrow angle to be that the posterior (usually
pigmented) trabecular meshwork is obstructed by the peripheral iris
for three or more quadrants of its circumference. This stringent definition
is not embraced by all, and there was discussion to take a more liberal
stance. Another issue was to differentiate appositional versus synechial
closure, because the management will differ between these situations.
The preliminary consensus statements included:
1. Primary angle closure is characterized by iridotrabecular contact
that may lead to peripheral anterior synechiae, ocular hypertension,
glaucomatous optic neuropathy, damage to ocular tissues including corneal
endothelium and lens, loss of visual function and in a large population
of untreated cases, blindness.
2. Gonioscopy is indispensable to the diagnosis and management of all
forms of glaucoma and is an integral part of the eye examination. Dynamic
gonioscopy is the only way to determine if iridotrabecular contact is
appositional or synechial and is an essential component of gonioscopy.
Access to a magnifying Goldmann-style lens enhances the ability to identify
important anatomical landmarks and signs of pathology. The ideal standard
is to use both types of lenses.
3. Anterior segment imaging devices may augment the evaluation of the
anterior chamber angle.
4. Identification of the underlying cause of angle-closure is essential
to accurate diagnosis and treatment.
5. Angle-closure can be caused by one or a combination of abnormalities
in the relative or absolute sizes or positions of anterior segment structures
or abnormal forces in the posterior segment that may alter the anatomy
of the anterior segment. Angle closure may be understood by regarding
it as resulting from blockage of the trabecular meshwork caused by forces
acting at four successive anatomic levels: the iris (pupillary block),
the ciliary body (plateau iris), the lens (phacomorphic glaucoma), and
vectors posterior to the lens (malignant glaucoma).
6. Although the amount of pupillary block may vary among eyes with angle-closure,
all eyes with angle-closure require treatment with iridotomy.
7. The ISGEO framework should be used as the standard framework for
classification of the natural history of angle closure, to determine
prognosis and describe an individuals need for treatment at different
stages of natural history of the disease.
8. Additional clinical sophistication can be gained by describing sequelae
of angle-closure affecting the cornea, trabecular meshwork, iris, lens,
optic disc and retina. Specifically, the extent of PAS, level of presenting
IOP (in asymptomatic cases) and presence of glaucomatous optic neuropathy.
9. In order to effectively target management at the cause of angle-closure,
the ISGEO scheme must be used in parallel with the 4-point classification
of mechanisms.
10. Further refinement of these systems should be made on the basis
of peer-reviewed evidence.
11. The term "anatomically narrow" should be substituted for
"occludable" angle, as a more intellectually honest description.
12. Gonioscopy should be promoted as a standard part of the comprehensive
eye examination. The choice of lens is a matter of personal preference.
13. It is desirable to record gonioscopic findings in clear text, avoid
"derivative" schemes. The ideal standard is to assess and
record all features identified in the Spaeth grading system.
Angle closure glaucoma is a common and serious condition. Gonioscopy
becomes a crucial procedure when confronted with the patient at risk
for or having angle closure glaucoma.
Murray Fingeret, OD
POLL
RESULTS FROM OGS E-JOURNAL VOLUME 1, ISSUE 2
Gonioscopy, while challenging to master, is a
rewarding examination technique that is integral to glaucoma diagnosis
and management. A majority of our respondents always perform gonioscopy
on newly diagnosed glaucoma patients, glaucoma suspects and ocular hypertensives.
Gonioscopy is indicated in these circumstances. Assessment of the anterior
chamber angle using the slit lamp and von Herrick technique is incomplete.
The distinction of open or closed angle glaucoma is made with the help
of gonioscopy. Some forms of secondary glaucoma are identified based
on gonioscopic findings. One cannot make the diagnosis of primary open
angle glaucoma without performing gonioscopy.
Gonioscopy may need to be repeated during the course of follow-up. Eighty-four
percent of our respondents will repeat gonioscopy less often than once
a year or only if new signs or symptoms develop.
Some potential confusion may be associated with question 3. Zeiss and
Posner lenses are examples of 4 mirror type lenses. A majority of our
respondents (55%) prefer a 4 mirror type goniolens which have a
smaller diameter and a flatter curve than the cornea. While initially
more difficult to master, these offer some advantages over 3 mirror
type lenses for example the ability to easily perform indentation gonioscopy.
The technique and interpretation of gonioscopy is an important part
of patient assessment in glaucoma care. Look for an expanded review
of this in a future issue.
A PERSPECTIVE ON GONIOSCOPY
The question is often asked: "How often
should gonioscopic assessment of the iridocorneal angle be performed?"
We have read many divergent answers, and so are happy to offer ours.
For perspective, in most cases of glaucoma, gonioscopy is the least
important tool in establishing the diagnosis or quantifying risk. However,
there are indeed many cases where knowledge of angle patency can be
clinically important. One of us (RKT) relates a classic encounter by
one of our good M.D. friends. He had a patient whose IOP was recalcitrant
to medical therapy, and was keen to perform argon laser trabeculoplasty.
Upon placement of the laser-goniolens, however, it became apparent that
the patients IOP was elevated because the angle was in near total
closure. So instead of trabeculoplasty, a peripheral photoiridotomy
was performed, which resulted in successful reduction in IOP. In retrospect,
perhaps proactive gonioscopic assessment would have been wise.
There appears to be uniform consensus that gonioscopic assessment should
be accomplished at the first or second evaluative visit. If the angle
is wide open and there is no nuclear sclerotic cataract, then we repeat
the procedure about every five years - every three years if there is
moderate nuclear sclerotic cataract. If the angle is moderately narrow
without nuclear sclerotic cataract, then we repeat the gonioscopic assessment
perhaps every two to three years. In the presence of concurrent cataract,
the gonioscopic evaluation is done annually. If the angle is narrow,
the examination is done annually regardless of cataract status. The
enlargement of nuclear sclerotic cataract can slowly press the iris
diaphragm forward, potentially causing progressive compromise to the
patency of the iridocorneal angle. This is why the presence or absence
of nuclear sclerosis can influence the frequency of repeat gonioscopy.
In Volume 7-3, 2006 of the International Glaucoma Review, Paul Foster
reports on page 360, "Limbal chamber depth assessment (LCD -- the
Van Herick test) was used as method of identifying subjects with anatomically
narrow angles. The authors cite the high sensitivity of LCD in identifying
people with very narrow angles. The omission of gonioscopy for all subjects
was an understandable, pragmatic decision." Yes, there is always
the "plateau iris" to confound what would otherwise be a rather
straightforward assessment. So, perhaps not "standard-of-care,"
it may well be that if the IOP is CCT-adjusted normal, and the Van Herick
grade is 3 or 4, gonioscopic assessment will bring precious little to
the diagnostic table. Certainly for grade II or less, gonioscopy should
be performed because there appears to be a substantial prevalence of
undiagnosed intermittent and/or asymptomatic angle closure-related ocular
hypertension/glaucoma.
We most always use either Zeiss or Posner 4-mirror goniolens when performing
gonioscopy. Certainly a Goldmann 3-mirror goniolens enables an excellent
view, but requires a high viscosity interface liquid which is more cumbersome
and unpleasant for the patient. If the 3-mirrow is used, we always take
an extra minute to irrigate away the gonio-gel.
R. Melton and R. Thomas

Editor
in Chief
Paul Spry PhD MCOptom
Associate Editors
Brad Fortune, OD,
PhD
Shaban Demirel, BScOptom,
PhD
Algis Vingrys BScOptom,
PhD
|
Editorial Board
Douglas Anderson MD
Paul Artes PhD MCOptom
Dick Bennett OD
Murray Fingeret, OD
Ron Harwerth, PhD
Chris Johnson, PhD
Tony Litwak, OD
John McSoley, OD
Ron Melton, OD
Bruce Onofrey, OD, RPh
Leo Semes, OD
Randall Thomas, OD
Thom Zimmerman, MD, PhD
Art/Production Director
Joe Morris
Project Coordinator
Janice Miller
|
To
subscribe to the OGS Journal, CLICK
HERE!
The e-newsletter is offered free to clinicians and scientists,
through an unrestricted educational grant from
|
| This
paid, promotional message was sent to you by Jobson Professional
Publications Group. The content does not necessarily reflect the
views, or imply endorsement, of the Group's editors or publisher.
If you do not want to receive this type of information in the future,
simply reply to this message with the words "Unsubscribe Mailings"
in the subject header. Jobson Professional Publications never releases
its e-mail list. |
|