OGS PRESIDENT'S MESSAGE

Much of this issue’s content relates to tonometry and intraocular pressure (IOP), a topic we once thought we understood. Yes, a test and its outcome we long took for granted is now being questioned. Thinking about Goldmann tonometry and its changing perception led me to reflect back on my Optometry school days. I went to the New England College of Optometry in Boston where the general clinic was located in a restored building in Kenmore Square. The building was long and narrow with examination rooms found at the ends of the building, connected by corridors. It may seem strange now but at the time, not all the slit lamps had Goldmann tonometers. Thus the student would have to move their patient during the examination to the corridor where a slit lamp with a Goldmann tonometer as well as a noncontact tonometer was available. The student could choose which test to perform but the Goldmann tonometer was almost always utilized. The noncontact tonometer’s measurements were perceived as estimates while the Goldmann tonometer was seen as a precise Swiss instrument. The sentiment was that if the mires were sized appropriately and the rings adjusted properly, IOP measured by Goldmann reflected the pressure within the eye.

I first became aware of concerns regarding the accuracy of Goldmann readings just after refractive surgery became commonplace. Reports surfaced that IOP reduction was being seen after the procedure, questioning some basic tenets around which the procedure was based. We now recognize that several corneal biomechanical factors such as thickness, rigidity, curvature and hydration may affect IOP measurements. In this issue several authors report on these topics and describe some of the newer tonometric instrumentation. After approximately 50 years with little improvement in the equipment used to measure IOP, we are now seeing major changes. The outcomes should lead to improvements in how we take care of patients with glaucoma, though it will take years before we become comfortable in using the new set of measurements.

Murray Fingeret, OD
President, Optometric Glaucoma Society
murrayf@optonline.net

GUEST EDITORIAL

The Changing Role of Intraocular Pressure in Glaucoma

It is with pleasure I write this editorial in Paul’s absence. Given this is the final issue of this journal for this year, let me begin by wishing you all a very festive holiday season from the editorial board.

There was a time when glaucoma was defined as an IOP >21 mmHg. So what is the role of IOP within the context of the modern glaucoma clinic?

First of all, can IOP be measured reliably given that corneal curvature and thickness can influence the forces required for applanation? It would appear that although these issues are being addressed by considerable research, which attempts to quantify the relationship between IOP, corneal curvature and thickness, a consensus on this relationship and the potential impact of other biomechanical factors, has yet to be reached. This begs the question: how important is IOP to glaucoma? More specifically, is there any evidence to support the dogma that glaucoma is a disease caused by an IOP imbalance which damages axons by some, as yet, unknown mechanism?

Right now we need to differentiate the role that IOP has as a diagnostic indicator from the benefit of lowering IOP in glaucoma management. Lowering IOP is well recognised as an effective treatment to slow loss of vision in glaucoma suspects (OHTS), cases of early glaucoma (EMGT) and cases of advanced disease (AGIS). The problem of "treating" IOP is that we can run into the danger of becoming transfixed by the number (target pressure) and not by its significance to the patient. It is the balance between IOP and blood pressure (ocular perfusion pressure) that is important in sustaining the optic nerve.

IOP can vary diurnally as does blood pressure. The unfortunate thing is that in some patients, as IOP peaks in the early morning, blood pressure reaches its trough, reducing ocular perfusion pressure. It is these variations that are often unseen by the clinician who measures IOP (and/or BP) during office hours. More importantly, do we know how blood pressure medications taken by the patient impact on this relationship, or the effect that short-term transient perfusion pressure troughs (IOP spikes and/or blood pressure dips) have in compromising the optic nerve? In this edition some of these issues will be canvassed to give a modern slant to the IOP story.

Algis J. Vingrys, BScOptom, PhD

Does an IOP spike affect retinal function?

Despite the well-known association between IOP and glaucoma little is known about how short duration changes in IOP ("spikes") affect retinal integrity. Recent research from our laboratory (1) has considered this problem in rats (n=6-7 per group) by cannulating the anterior chamber and elevating IOP to 50 or 70 mmHg for periods of 15-60 minutes. Retinal integrity was quantified by measuring the retinal response to full-field flashes of light (i.e. the electroretinogram, ERG) and quantified in terms of specific ERG components known to reflect function of outer retinal (photoreceptor, P3), middle retinal (ON-bipolar cell, P2) and ganglion cell (scotopic threshold response, STR) layers. We assessed both the loss of function and how quickly function recovered from a given IOP challenge.

We found that 50 mmHg spikes (35 mmHg above baseline for 42 minutes) particularly compromised ganglion cell responses (STR 80 +/- 7% reduction), leaving outer retinal responses largely unaffected (P2, 33 +/- 11% and P3, 6 +/- 6% reduction). Not only was ganglion cell function more compromised during the insult, but it also took longer to recover after IOP normalisation, requiring 22 minutes to return to 50% of the original amplitude (versus 2-5 minutes for P2 and P3).

Our work has shown that both duration and peak IOP influence the function of retinal neurons. IOP spikes having a common integral (pressure x duration) did not result in the same level of dysfunction. In fact higher pressures produced greater ganglion cell functional loss (70 mmHg 100 +/- 1% vs 50 mmHg 80 +/- 7% reduction) and slower recovery. Thus, for insults having the same IOP integral, the peak IOP is the principal determinant of functional loss and recovery. This suggests that IOP fluctuations should be minimised in patients.

We also found that as the duration of insult was prolonged for a given IOP (70 mmHg), ganglion cell function took progressively longer to recover. In fact this relationship was linear. Taken together, these results suggest that treatment aimed at retaining ganglion cell integrity should not only attempt to reduce the "mean" IOP level, but also to limit IOP fluctuation.

Bang V Bui, Zheng He and Algis J Vingrys,
Department of Optometry & Vision Sciences
University of Melbourne, Victoria, 3010, Australia

References
1. Zheng He, Bang V Bui, Algis J Vingrys (2006). The rate of functional recovery from acute IOP recovery. Invest Ophthalmol Vis Sci.;47:4872-4880.

How should we best measure and react to spikes: IOP and the number of papers written about CCT

As interest swells over the effect that central corneal thickness (CCT) may have on the relative risk of glaucoma progression, much related research activity appears to be focused on the specific influence that CCT may have on the apparent intraocular pressure (IOP) measured by one tonometer or another. The fundamental problem here is that the current "gold-standard" method of tonometry, namely Goldmann Applanation Tonometry (GAT), is based on an inherent assumption that CCT is 520 microns, yet there is a wide variation in CCT across the population, which introduces qualitatively predictable error in the relationship between the measured (GAT) and the true IOP (i.e. manometrically measured). This problem has driven efforts to develop alternative methods of tonometry, such as Dynamic Contour Tonometry discussed elsewhere in this issue. One such method, generally known as "rebound" or "impact" tonometry, has been further developed into a new commercially available device called the ICare "induction-based" impact tonometer (Tiolat Oy, Helsinki, Finland). In a recent study [1], Brusini and colleagues proposed "to compare the IOP readings taken with the new ICare tonometer and with the GAT and to evaluate the influence of central corneal thickness (CCT) on the IOP measurements." They concluded that "a CCT change of 10 mum resulted in an ICare reading deviation of 0.7 mm Hg" and further, that "[ICare] measurements seemed to be influenced by CCT variations, and thus pachymetry should always be taken into consideration." It is crucial to point out that the authors are referring to the "deviation" from what they assume to be the true IOP, the GAT value "corrected" by the measured CCT according to a published formula [2]. Notwithstanding the circular logic of using CCT to calculate this "deviation" and then attempting to "evaluate the influence of central corneal thickness (CCT)", one of the most interesting findings from this study (which the reader will not see addressed in the Discussion section) is that the ICare tonometer appears to have an even larger error than GAT for corneas that are progressively thinner or thicker than average! For example, if one removes the CCT correction, and recalculates the "deviation" (of ICare IOP from measured GAT IOP), the linear function still has a positive slope of 0.2 mm Hg per 10 microns of CCT difference. Thus, if GAT underestimates IOP by 2 mm Hg in an eye with a relatively thin CCT of 495 microns [2], ICare further underestimates IOP by an additional 1.5 mm Hg! The essential conclusions of this paper are worthy of consideration, however, they are valid only if the true IOP can be estimated from GAT using a simple linear correction factor based on CCT. As we are learning, this is highly improbable.

Perhaps even more important than deriving an estimate for IOP "correction" is the need to develop better methods of 24-hour IOP monitoring. Firstly, glaucoma diagnosis should depend more on evaluation of optic disc structure, retinal nerve fiber layer integrity, and visual function anyway, rather than on IOP per se. Secondly, corneal biomechanical properties (and their effect on IOP estimates) are unlikely to change substantially throughout most patients’ lives, and we can use a consistent method of tonometry to assess the reduction of IOP over time brought about by therapy. The more important challenge may well be that significant IOP elevation commonly occurs outside of typical office hours, and we do not currently have any satisfactory way to monitor this. A recent study by Barkana et al [3] adds further evidence, and eloquent argument, to support this important point. They report on 32 patients that had been admitted to the hospital for 24-hour IOP monitoring. Four important findings were 1) the 24-hour peak IOP was 2 mm Hg higher, on average, than the "office IOP peak" (obtained between 7 am and 4:30 pm); 2) the difference between the 24-hour peak and the office IOP peak was at least 2 mm Hg in over 40% of eyes, and over 4 mm Hg in 19% of eyes; 3) the peak IOP was recorded outside of office hours in 69% of patients; 4) IOP fluctuation (peak minus trough) was 3 mm Hg larger over the 24-hour period than during office hours alone.

Unlikely to be stated more clearly in paraphrase, their concluding argument is quoted here in full: "...our data suggest that in glaucoma patients with advanced disease or with progression that is disproportionate to known IOP measurements, 24-hour IOP monitoring can reveal higher peaks and wider fluctuation of IOP than those found during typical office hours, measured either in multiple office visits or repeatedly during a single day. In these patients, 24-hour IOP monitoring may suggest a greater role for IOP-related risk for glaucoma progression than previously suspected and thus may justify a more aggressive IOP-lowering treatment strategy. Until accurate self-tonometry devices become widely available, or until a method is found to accurately predict the 24-hour peak and range of IOP in individual patients, we suggest that clinicians consider obtaining 24-hour IOP measurements for selected patients."

Brad Fortune, OD, PhD

References
1. Brusini P, Salvetat ML, Zeppieri M, Tosoni C, Parisi L. Comparison of ICare tonometer with Goldmann applanation tonometer in glaucoma patients. J Glaucoma. 2006;15:213-217.
2. Doughty MJ, Zaman ML. Human corneal thickness and its impact on intraocular pressure measures: a review and meta-analysis approach. Surv Ophthalmol. 2000;44:367-408.
3. Barkana Y, Anis S, Liebmann J, Tello C, Ritch R. Clinical utility of intraocular pressure monitoring outside of normal office hours in patients with glaucoma. Arch Ophthalmol. 2006 Jun;124(6):793-7.

INSTRUMENTATION UPDATE

In Vivo Cannulation Study (A. Weber, A.G. Boehm, E. Spoerl, L.E. Pillunat) The yellow curve is the manometric reference line (true IOP). The blue curve is the reported IOP from the PASCAL®. When the PASCAL is on the cornea, the two curves are almost identical.

At The University of Dresden, Germany, Andreas Boehm, MD performs PASCAL IOP measurement while a cannula is in the anterior chamber for pressure control and reference measurement.

Figure A

Figure B

Clinical studies have shown that CH can be used to identify conditions such as keratoconus and Fuchs’ dystrophy (1-3). Because CH measurements decrease significantly after refractive surgery, low CH is considered to be a contraindication for refractive surgery related to risk of developing post-LASIK ectasia (1). As such, clinical applications of the ORA in corneal and refractive disciplines are fairly obvious.

ORA and Glaucoma
Recent studies, including the Ocular Hypertension Treatment Study (OHTS), have suggested that low CCT is an independent risk factor for development of glaucoma. Some investigators have theorized that corneal properties may reflect overall ocular tissue characteristics, and thereby provide new information that will aid in diagnosis and management of glaucoma. Studies utilizing the Ocular Response Analyzer have supported this hypothesis. Compared to normals, glaucomatous subjects have a less than average CH and a much wider range. A recent study has suggested that CH may also be an indicator of glaucoma progression, independent of IOP, CCT, and other factors (4).

Measuring IOP
Goldmann applanation tonometry (GAT) was designed to provide accurate measurements in eyes with "average" corneas but corneas vary more than previously thought. It is clear however, that corneal influence on GAT cannot be accounted for solely by differences in CCT. In fact, "correcting" IOP based on CCT can lead not only to improper magnitude, but also to an incorrect direction sense of the adjustment. Corneal models indicate that biomechanical factors are of substantially greater significance than CCT (5).

ORA bi-directional applanation provides a basis for corneal-compensated intraocular pressure (IOPcc), that takes into consideration biomechanical properties. IOPcc appears significantly less affected by corneal properties than GAT and other methods of tonometry. IOPcc has insignificant correlation with CCT in normal eyes and stays relatively constant post-LASIK (6).

ORA’s unique ability to provide a Goldmann-correlated IOP measurement (IOPG) and IOPcc provides clinicians with an understanding of their difference. This understanding, coupled with CH, provides a powerful combination of tools to assist diagnosis and management of glaucoma.

David A. Luce, PhD
David A. Taylor,
Reichert Ophthalmic Instruments

References
1. Luce DA. Determining in vivo biomechanical properties of the cornea with an ocular response analyzer. J Cataract Refract Surg 2005;31:156 -162.
2. Change in Axial Length Following Surgical Decompression. A Surrogate for the Material Properties of the Eye Wall (2006). S.A. Tanimoto, L.A.S. Mello, Jr., J.D. Brandt. ARVO abstract No 4423.
3. IOP and Corneal Biomechanical Metrics in Eyes With Keratoconus and Fuchs' Dystrophy Compared to Pachymetry-Matched Controls (2006). J.P. Sanderson, M.A. Qazi, C.J. Roberts, J.S. Pepose. ARVO abstract no 2267.
4. Congdon NG, Broman AT, Bandeen-Roche K, Grover D, Quigley HA (2006). Central corneal thickness and corneal hysteresis are associated with glaucoma damage. Am J Ophthalmol; 141(5): 868-75.
5. Liu J, Roberts CJ. Influence of corneal biomechanical properties on intraocular pressure measurement: quantitative analysis. J Cataract Refract Surg. 2005;31:146-155.
6. Medeiros FA and Weinreb RN (2006). Evaluation of the Influence of Corneal Biomechanical Properties on Intraocular Pressure Measurements Using the Ocular Response Analyzer. J Glaucoma; 15: 364-370

QUARTERLY CASE

A 75 year old white man presented with a complaint of gradually worsening blurred vision in his left eye first noticed 6 to 7 weeks prior to the examination. He had not experienced ocular pain, haloes around lights or headache. He had no history of ocular disease or trauma and was not taking any ocular medications. He was on therapy for systemic hypertension, atrial fibrillation and raised cholesterol (warfarin, simvastatin, digoxin and lisinopril.) He did not report any known family history of glaucoma or blindness.

Visual acuities were OD 20/30 and OS 20/60, improving to 20/40 with pinhole. For his initial field tests a 24-2 SITA-Fast test was performed. This fast thresholding algorithm is less desirable than SITA Standard which has the more desirable characteristics of both higher threshold estimation validity and greater levels of reproducibility that are advantageous for detection of defect progression. We use SITA-fast as a ‘learning’ test and preliminary result although in this case both eyes’ results appeared reliable according to the indices. There was some evidence of loss of corneal reflex on gaze tracking of the right eye, evidenced by downward deflections of the plot, suggesting either drooping upper eyelid or backward head movement. Losses of central fixation, represented by upward deflections, were minimal. The right test (Figure 1a) shows evidence of mild diffuse loss, indicated by a significantly reduced mean deviation (MD) and widespread mild but significant reductions in threshold sensitivity on the total deviation and its corresponding probability plot. There was not definite focal loss, although a cluster of possible shallow depressed locations were present in the superior paracentral area, in addition to a likely temporal edge artefact. The result for the left eye (Figure 1b) showed marked, significant diffuse depression (MD -11.13dB). There was also significant focal losses present in the inferior arcuate and paracentral areas visible on the pattern deviation. PSD also highlighting irregularities of the field surface, consistent with glaucomatous losses. The superior hemifield showed a probable nasal step.

Examination of the anterior segment revealed normal corneas with deep quiet anterior chambers. Bluish-white translucent material was present around both pupil margins although the pigmentary collarettes and other areas of the irides appeared normal. There was no phacodonesis when the patient was asked to make small lateral eye movements.

Figure 1A

Figure 1B

Intraocular pressure (IOP) was elevated bilaterally at OD 32 and OS 45mmHg by Goldmann applanation tonometry. Central corneal thickness was OD 484 and OS 474µm. Gonioscopy revealed Shaffer grade 4 angles OU through 360degrees, although there was variable degrees of trabecular pigment present, greatest bilaterally in the inferior quadrants.

After pupil dilation, further bluish white material was visible on the anterior surface of the crystalline lens, in a target-type pattern of concentric circles (Figure 2). Crystalline lenses appeared centrally positioned and had nuclear sclerotic lens opacities, OD trace level and OS moderate.

Examination of the posterior segment demonstrated small vertical optic nerve head diameters of 1.6mm in height OU, measured at the slit-lamp beam. There was asymmetry in vertical cup-to-disc ratio OD 0.20 and OS 0.50. Excavation was shallow, with the cups exhibiting a saucer-shaped profile, making accurate identification of the cup edge difficult.

Figure 2. This figure shows pseudoexfoliative material on the anterior capsule surface, with arrows 1 and 2 showing the inner and outer boundaries respectively of the region where this material has been rubbed away by pupil movements.

The patient was diagnosed with secondary open angle glaucoma secondary to pseudoexfoliation syndrome and left visually significant cataract. The symptoms of substantial IOP elevations were explained and the patient was instructed to contact their clinician immediately should they experience these. This patient was commenced on topical treatment with travoprost once daily OU and left cataract extraction was arranged. After 2 months, IOP fell to 20 and 22 mmHg. In view of the low central corneal thickness, target IOPs for this patient should be in the low or mid teens. IOPs were therefore rechecked and found to be OD 18 and OS 17mmHg. An arrangement was made to closely monitor this patient to ensure IOPs remain at, or preferably below this level. Subsequent uncomplicated cataract extraction improved left visual acuity to 20/30.

Key Points
1. Signs of pseudoexfoliation can be subtle. Although some patients have iris atrophy, often most obvious at the pupil margin, many individuals, like this patient do not exhibit this. Pupil dilation therefore greatly aids diagnosis. Although variable degrees of angle pigmentation are common in this condition, pseudoexfoliative material is less easy to visualise gonioscopically.

2. Although PXF material may be visible unilaterally, it should be regarded as a bilateral but asymmetric condition.

3. Irregular angle pigmentation should alert the examiner to the possibility of pseudoexfoliation syndrome. Differential diagnoses include uveitis, Fuch’s heterochromic iridocyclitis, previous trauma, and pigment dispersion syndrome.

4. IOP level in pseudoexfoliative glaucoma can be exceptionally high for an open-angle state, and can be sufficient to cause corneal oedema with symptoms usually associated with sub-acute angle closure episodes. These variations are usually cyclic and so diurnal IOP measurement may be beneficial. These IOP spikes, or otherwise poor intraocular pressure control, can lead to progression at a rate much greater than that found in primary open angle glaucoma.

5. Pseudoexfoliation is associated with zonular weakening that can increase the chance of peroperative complications in cataract extraction. Care should be taken to ensure surgeons are fully aware of the diagnosis.

6. Pseudoexfoliation syndrome is likely to be a systemic condition, with involvement of other organs. Some reports describe associations with cerebrovascular and cardiovascular disease, although no evidence supports greater mortality rates amongst patients with pseudoexfoliative glaucoma.

Paul GD Spry, PhD, BSc, MCOptom, DipGlauc

To avoid the need to leaf through a large record of a patient with chronic glaucoma, it helps to have on the face sheet or problem list of the patient's chart a statement like: "Discovered in 1998 to have moderate cupping and field loss with IOP 25/22, confirmed 24/22 a week later before treatment". One may also then record a target pressure, remembering that it is tentative, or simply leave it implied by the statement of the pre-treatment pressure. As time goes on, the highest pressure ever recorded on or off treatment might also be recorded on the face sheet of the chart. Of course, the initially stated target is tentative, and after a few years, the course of events is a better guide to whether the IOP control is adequate or needs to be more aggressive. Remember that one doesn't always reach goals in life, and if something close to the initially stated target is achieved, and if to get more IOP lowering involves risk and side effects, one might accept a less ambitious goal, depending on the severity of the disc and field damage. Also, if progression occurs despite having reached the initial goal, one is permitted to change the target to a lower IOP.

So while I like the idea that the chart has recorded on its front page the pre-treatment pressure and the maximum pressure ever observed, it also seems a good idea to record as a reminder about what you may have expressed to the patient, that you are going to aim for a certain target pressure if you can get it easily enough, and if it proves difficult you will re-evaluate (and you can even write a range for target, "will try for 15 but accept 17". But putting the number down reminds you of what you told the patient, so you can say, "We have been aiming for 16 mm Hg, but with topical PG, beta-blocker, and CAI we have only achieved 17, and we have even tried laser. Before we contemplate filtration surgery, let's see what happens over the next 12 months, and if everything is stable we may put off being more aggressive". We can't fool ourselves into thinking that when we set an initial target pressure it is anything more than an educated guess, which for some people may be more IOP-lowering than needed and for others an insufficient goal.

I do not like the idea of NOT placing in the record something that helps me take care of the patient. Some people advocate not placing a target pressure in the record for the reason that there is risk of legal proceedings if the target is not met and there is visual loss. In fact, if it helps me care for my patients to have some number in mind and to write it down (I'm certainly not going to remember the target for every patient), then I take the stand that it compromises my first duty to my patients if I fail to write it down. I think it is a defensible position to say that the degree of IOP-lowering required is different for each individual, that you set an initial goal, but continually evaluate whether that goal is adequate and how necessary it is to reach that goal as you contemplate using more aggressive therapy when initial therapy failed to reach the tentative goal.

Douglas R. Anderson, MD

Is Diurnal IOP Fluctuation Associated with Glaucoma?

The major randomised clinical trials (RCTs) published on glaucoma over the past few years have provided strong and irrefutable evidence for treatment by reduction of IOP. These trials were reviewed in the OGS EJ volume 1 issue 2. Although each of these addresses a specific question, there is little doubt that their consensus indicates IOP lowering improves the glaucoma prognosis, in terms of both reducing the risk of initial development in ocular hypertension, (1) and of progression in those with an existing glaucoma diagnosis (2, 3, 4).

RCTs provide highest quality methodology for investigating the effects of an exposure, such as IOP lowering, on an outcome, such as glaucoma progression. The reasons for this are (a) they estimate the group effect of the exposure on the outcome and (b) they minimize the potentially devastating effects of bias and confounding effects that may inadvertently produce spurious results in other study designs. However, interpretation and generalisation of RCT results still requires caution. For example; standard operating procedures necessary in multicentre RCTs are unlikely to be representative of routine clinical practice; group effects may not apply to all individuals; and the way in which data were collected may not enable all aspects of a variable to be completely explored.

In the context of IOP, the well-known RCTs have not explored the impact of diurnal IOP variations on glaucoma. It is reasonable to hypothesise, given two individuals with the same mean IOP over a 24hour period, that the individual with greater diurnal IOP variation may be at greater risk of progressive glaucoma. Versions of this hypothesis have been explored by a number of investigators. One prospective cohort study recruited 64 glaucoma patients to perform baseline home-tonometry using self-administered applanation tonometry five times per day (waking, noon, mid-afternoon, evening and before bed) for 1 week. They then followed this group over a 5 year period. This study found that individuals with both greater diurnal IOP and larger IOP range over multiple days were at higher risk of progressive visual field loss (5). Conversely, a prospective study measuring IOP throughout office-hours amongst ocular hypertensive patients found no independent association between diurnal IOP variation and conversion to glaucoma (6). A recently published abstract of an observational study measuring IOP 5 times over 24hrs concluded that the apparent positive association between greater diurnal IOP amplitude and progressive glaucoma may be the result of the close relationship between diurnal range and mean IOP (7).

So, what is the true relationship between diurnal IOP variation and glaucoma? Can it be teased out from these conflicting pieces of evidence? Regrettably, at the present time, there appears to be no consensus. In the meantime, the pragmatic approach to understanding these data and assimilating them into clinical practice may be to remember that office IOP measurements do not provide a complete picture of IOP control, each measurement being a single sample, and to challenge the concept of good IOP control when the degree of glaucoma or progression seem disproportionate to the apparent IOP (8, 9).

It seems as if the ideal way to determine the relationship between diurnal IOP variation and glaucoma requires a RCT using diurnal IOP variation as an exposure variable.

Paul GD Spry, PhD, BSc, MCOptom, DipGlauc

References
1. Kass MA, Heuer DK, Higginbotham EJ, Johnson CA, Keltner JL, Miller JP, Parrish RK 2nd, Wilson MR, Gordon MO (2002). The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Arch Ophthalmol; 120(6):701-13.
2. Leske MC, Heijl A, Hussein M, Bengtsson B, Hyman L, Komaroff E (2003). Early Manifest Glaucoma Trial Group. Factors for glaucoma progression and the effect of treatment: the early manifest glaucoma trial. Arch Ophthalmol; 121(1):48-56.
3, Lichter PR, Musch DC, Gillespie BW, Guire KE, Janz NK, Wren PA, Mills RP (2001). CIGTS Study Group. Interim clinical outcomes in the Collaborative Initial Glaucoma Treatment Study comparing initial treatment randomized to medications or surgery. Ophthalmology; 108(11):1943-53
4. The AGIS Investigators (2000).The Advanced Glaucoma Intervention Study (AGIS): 7. The relationship between control of intraocular pressure and visual field deterioration. Am J Ophthalmol; 130(4):429-40.
5. Asrani S, Zeimer R, Wilensky J, Gieser D, Vitale S, Lindenmuth K (2000). Large diurnal fluctuations in intraocular pressure are an independent risk factor in patients with glaucoma. J Glaucoma; 9(2):134-42.
6. Bengtsson B, Heijl A (2005). Diurnal IOP fluctuation: not an independent risk factor for glaucomatous visual field loss in high-risk ocular hypertension. Graefes Arch Clin Exp Ophthalmol; 243(6):513-8.
7. Jonas JB, Budde WM, Stroux A, Oberacher-Velten IM, Junemann A (2006). Diurnal intraocular pressure profiles and progression of chronic open-angle glaucoma. Eye. Apr 7; [Epub ahead of print]
8. Hughes EH, Spry PGD, Diamond JP (2003). Phasing of intra-ocular pressure in glaucoma management: three case reports and a retrospective review. J Glaucoma; 12(3): 232-236.
9. Barkana Y, Anis S, Liebmann J, Tello C, Ritch R (2006). Clinical utility of intraocular pressure monitoring outside of normal office hours in patients with glaucoma. Arch Ophthalmol; 124(6):793-7.

NEWS

OGS member presentations at the forthcoming American Academy of Optometry Meeting in Denver.

December 7th
Joseph Sowka, OD. Topographical analysis of the optic nerve in migraine sufferers. Program no. 065065.

December 8th
Elliot M. Kirstein, OD. Paradoxical IOP in Post RK Patient with Pigmentary Glaucoma (Glaucoma grand round).

Leo P Semes, OD. Sleep apnea syndrome represents a risk for glaucoma in a veteran’s affairs population. Program no. 065217.

Michael Sullivan-Mee, OD. Comparison of diurnal intraocular pressure profiles between dynamic contour tonometry and Goldmann Applanation tonometry. Program no. 060052.

December 9th
David Sendrowski, OD. Acquired toxoplasmosis in an immunocompetent patient from a petting zoo. Program no. 065324.

POLLS RESULTS FROM OGS EJ VOLUME 1, ISSUE 4

Our respondents are divided on the value of monocular trials to assess effectiveness of initial therapy with anti-glaucoma medications. Fifty-seven percent incorporated monocular trials into their clinical practice prior to the debate featured in our last issue, however 12% indicated they will not continue to do this. Forty-two percent of respondents did not favor monocular trials and had not incorporated these into practice.

While many tonometers were represented in our survey, the vast majority (76%) reported normally using Goldmann-type applanation tonometers. Non-contact tonometers are used by 15%. Approximately 10% used other forms of tonometry, including the Tonopen, to assess their patients’ intraocular pressure.

The frequency of intraocular pressure measurement in stable glaucoma patients may be difficult to quantify. It is likely clinicians consider, among other things, the extent of damage and the amount of time the patient has been stable. These issues speak to the need to individualize management of our glaucoma patients. Our responses reflected this complexity with 49% indicating three times a year; 34% less frequently, 17% more frequently. Ninety-two percent agreed that checking the intraocular pressure at least two times a year in stable glaucoma patients was the practice they followed.

Thanks to all those who responded. We encourage all readers to participate.

NEWS ITEM

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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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