Volume 1, Number 3
June 2006
 

 

Inside This Issue 

 
 
  OGS PRESIDENT'S MESSAGE
 
  EDITORIAL
 
  MEETING NEWS
 
  OPTIC NERVE REVIEW
 
  VISUAL FIELD REVIEW
 
  QUARTERLY CASE
 
  INTERNATIONAL COLUMN
 
  PHARMACY REVIEW
 
  QUESTIONS AND ANSWERS
 
  AIGS CONSENSUS MEETING
 
  POLL RESULTS FROM OGS E-JOURNAL VOLUME 1, NUMBER 2
 
  A PERSPECTIVE ON GONIOSCOPY
 
  NEWS
 

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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 world’s glaucoma societies, describing itself as an independent, impartial, ethical global organization for glaucoma science and care. All of the world’s 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 doesn’t appear particularly scientific or dynamic because it tends to avoid innovative technologies and doesn’t 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 we’re 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.'


Table of Contents


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 couldn’t 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


Table of Contents

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 1980’s. 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


Table of Contents


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, let’s 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.


Table of Contents


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 patient’s 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 patient’s primary care physician. Given the elevated IOP, the patient’s 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 patient’s 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



Table of Contents

 

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


Table of Contents

 

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 carteolol’s 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 carteolol’s 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. Betaxolol’s 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 betaxolol’s 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 IOP’s 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.


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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)

 

QUARTERLY POLL
Please check one response for each question. What type of ‘standard’ (white-on-white) perimetry do you currently perform?
SITA-standard threshold perimetry
SITA-fast threshold perimetry
‘Classical’ full-threshold perimetry
Fastpac threshold perimetry
Suprathreshold ‘screening’ type test
I no longer perform standard perimetry, and use another test type instead.




All poll results will be presented and discussed in the next issue! Identity of voters remains anonymous.

 

 

Approximately how frequently do you perform routine visual field tests on stable open-angle glaucoma patients? (please check one)
More than 3 times per year
Three times per year
Twice per year
Annually
Less than annually



 

 

Do you currently perform another type of perimetry in addition to white-on-white? (please check one)
No
Yes - frequency doubling technology perimetry (FDT or Humphrey Matrix)
Yes - blue-on-yellow perimetry
Yes - both FDT/Matrix AND blue-on-yellow



 

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 won’t 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 you’ll ever get to the maximal effect using the drug once weekly. Secondly, with all drugs there’s 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 you’d 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 Society’s 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.

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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 individual’s 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

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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.

Table of Contents


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 patient’s 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

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NEWS ITEM

Table of Contents





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

 

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