OGS E-Journal
  Volume 4, Number 2
January 2010


Inside This Issue 


Click Here if you are having problems viewing the E-Journal.

To subscribe to the OGS E-Journal, Click Here!



As we draw to the end of another year it is a time to take a few minutes to reflect. Iíve just returned from the annual meeting of the Optometric Glaucoma Society in Orlando and 2009 will be remembered for yet another exceptional meeting. Our speakers shared their experience and at times life-learnt philosophies. Those in attendance enjoyed lively discussion on normal tension cases and the origins and significance of disc hemorrhage with Dr. Louis Pasquale. In the President's Lecture we learnt about race and glaucoma in a session led by Dr. Chris Girkin who gave an excellent update of the African Descent and Glaucoma Evaluation Study (ADAGES). Dr. Girkin also shared his insights on the plethora of non-bleb (or sometimes not so non-bleb!) alternatives to trabeculectomy. Our 2009 Honoree, and now the latest member of our society Dr. George Speath, led us down the road of lifelong learning with talks on gonioscopy and evaluation of the optic nerve. The inaugural Research Excellence Award was presented by Dr. Peng Khaw from Moorfields Eye Hospital in London. His talk entitled "Repair to Regeneration-Translating Laboratory Discovery to Clinical Advance" was simply astonishing. Many people talk about translational research, Dr. Khaw "lives the life". He shared his journey of discovery that led to anti-metabolites being used routinely with trabeculectomy, and also described successful gene therapy and the therapeutic use of stem cells. For those of you not able to attend these talks, along with the other excellent member presentations, a synopsis will be available soon in the annual meeting supplement kindly distributed by Review of Optometry.

The OGS year had many other highlights for me including the World Glaucoma Congress in Boston, the Educators and Residents meetings in Fort Worth and the trend setting E-Journal. I thank the organizers of all these events, you know who you are. I also thank our sponsors, without whose support our own life-long learning would not be quite as easy to achieve.

Have a wonderful holiday season and I hope you are looking forward to another action packed year in 2010. In the words of the great Ray Davies and the Kinks "Thank you for the days, those endless days, those sacred days you gave me." (1969)

John Flanagan, PhD, MCOptom, FAAO
President, Optometric Glaucoma Society


Table of Contents


"Acronyms and Advocacy"—Raising Awareness for Funding Vision Research

Opening my post today I found the Fall report for the National Alliance for Eye and Vision Research (NAEVR). Those who are OGS members have also received this, and have been receiving monthly emails from their Executive Director, James Jorkasky. So what exactly does the organisation behind this acronym do, why is this information distributed, and do you need to know more about them? Well, AEVR, the Alliance for Eye and Vision Research is an education foundation whose goal is to educate Congress and the public about the value of eye and vision research. NAEVR, the National Alliance for Eye and Vision Research, was formed as an affiliate of AEVR with the aim of achieving best eye and vision care through advocacy and public education for eye and vision research sponsored by the National Institutes of Health (NIH), the National Eye Institute (NEI) and other federal research entities.

The Optometric Glaucoma Society is a member of the coalition of 55 professional, consumer and industry organizations involved in eye and vision research that officially support NAEVR activities. There is no doubt that delivering information to key policy makers on the importance of sustaining vision research funding is crucial. Without ongoing research activity, the potential for improved visual health care outcomes is limited. Research groups can provide new pieces of information that could translate to improvements in clinical practice if allowed to. Continued advocacy for sustained research funding becomes all the more important when constraints in public spending lead to greater competition for the dwindling contents of a limited funding pot.

Various aspects of current glaucoma patient care are based on information funded by NEI grants. As such, I urge you to take a look at the NAEVR and AEVR website, www.eyeresearch.org and to consider putting your name to a very worthy cause.

Paul GD Spry, PhD, BSc, MCOptom DipGlauc


Table of Contents


The Lamina Cribrosa

Figure 1. Acquired pit of the optic nerve. Note circular depression in the superior half of the optic cup.

Figure 2. Visual field of patient in Fig 1. Note dense inferior nasal step and paracentral scotoma which corresponds to location of superior APON in the optic nerve.

Figure 3. Congenital pit of the optic nerve. Note grayish circular pit along the temporal aspect of the optic cup. Congenital pits may also be associated with visual field loss and serous sensory detachment of the macula.

The lamina cribrosa (LC) spans the neural canal opening and supports the retinal ganglion cell axons as they exit the eye to become the optic nerve. The LC is comprised of interconnected connective tissue "beams" each containing a capillary and wrapped by astrocytic (glial) processes. Blood flowing through the LC capillaries is supplied primarily by the short posterior ciliary arteries (SPCA) via the circle of Zinn-Haler with some anastomotic flow from recurrent branches of the central retinal artery anteriorly and posteriorly. Viewed axially, the LC has a "cribriform" or sieve-like appearance, which is particularly striking when the neural and other soft tissues are removed by enzymatic or alkali digestion techniques (1-5). Similarly striking images of the LC structure are produced by the 3-D histomorphometric reconstruction techniques developed by Downs and colleagues (6-8). Understanding the complex anatomy of the LC is important because it is believed to be the primary site of injury in glaucoma (4,6-8). Detailed images of the LC may someday even be obtained clinically in living human patients through advances in imaging technology such as second harmonic microscopy (9) and adaptive optics combined with confocal scanning laser ophthalmoscopy (CSLO) (10) or ultrahigh-resolution optical coherence tomography (11). Indeed, the cribriform appearance of the LC is manifest even upon direct ophthalmoscopy of the optic disc, where the contrast between the reflectivity of lamina connective tissue and axon bundles creates an appearance of LC "pores" within the optic cup, which can become especially prominent and abnormally elongated in eyes with advanced glaucomatous damage (12-14).

It is therefore important to consider changes in the appearance of LC pores—along with any other signs of structural change such as neural rim thinning, excavation, loss of the retinal nerve fiber layer, appearance of disc hemorrhages, etc.—when examining serial stereo-photographs of glaucoma patients and suspects. These changes can represent neural loss and/or deformation of the connective tissue architecture within the optic nerve head, itself likely to be prognostic for future glaucomatous vision loss. Another sign of potential glaucomatous structural alterations in the LC that should serve as an alert are acquired pits of the optic nerve (APON).

Acquired pits of the optic nerve (APON) are a clinical observation within the lamina cribrosa that can be a sign of glaucoma damage. An APON is a localized depression and expansion of a laminar pore (see Figure 1). The location of the APON corresponds with visual field loss that tends to be progressive and closer to fixation (see Figure 2). APON are more commonly seen in normal tension glaucoma than high tension glaucoma. APONs of the optic nerve can be differentiated from a congenital optic disc pit, in that the later is a localized coloboma of the optic nerve that tends to have a grayish halo surrounding the pit and lacking laminar dots. Congenital pits are most commonly located on the nasal segment of the disc and can have associated maculopathy (see Figure 3). Serial photographic documentation of the optic nerve provides a capability to clinically observe changes in the size and number of laminar pores in glaucoma patients or suspects. Other optic nerve imaging devices, such as CSLO can also be utilized to detect changes in laminar pores, such as in their number, size, and shape. (13,14).

Tony Litwak, OD, FAAO and Brad Fortune, OD, PhD

1. Quigley HA, Hohman RM, Addicks EM, Massof RW, Green WR. Morphologic changes in the lamina cribrosa correlated with neural loss in open-angle glaucoma. Am J Ophthalmol. 1983 May;95(5):673-91.
2. Quigley HA, Brown AE, Morrison JD, Drance SM. The size and shape of the optic disc in normal human eyes. Arch Ophthalmol. 1990;108:51-57.
3. Quigley HA, Addicks EM. Regional differences in the structure of the lamina cribrosa and their relation to glaucomatous optic nerve damage. Arch Ophthalmol. 1981 Jan;99(1):137-43.
4. Quigley HA, Addicks EM, Green WR, Maumenee AE. Optic nerve damage in human glaucoma. II. The site of injury and susceptibility to damage. Arch Ophthalmol. 1981 Apr;99(4):635-49.
5. Oyama T, Abe H, Ushiki T. The connective tissue and glial framework in the optic nerve head of the normal human eye: light and scanning electron microscopic studies. Arch Histol Cytol. 2006;69:341-356.
6. Burgoyne CF, Downs JC, Bellezza AJ, Hart RT. Three-dimensional reconstruction of normal and early glaucoma monkey optic nerve head connective tissues. Invest Ophthalmol Vis Sci. 2004;45:4388-99.
7. Burgoyne CF, Downs JC, Bellezza AJ, Suh JK, Hart RT. The optic nerve head as a biomechanical structure: a new paradigm for understanding the role of IOP-related stress and strain in the pathophysiology of glaucomatous optic nerve head damage. Prog Retin Eye Res. 2005;24:39-73.
8. Roberts MD, Grau V, Grimm J, Reynaud J, Bellezza AJ, Burgoyne CF, Downs JC. Remodeling of the connective tissue microarchitecture of the lamina cribrosa in early experimental glaucoma. Invest Ophthalmol Vis Sci. 2009;50:681-90.
9. Brown DJ, Morishige N, Neekhra A, Minckler DS, Jester JV. Application of second harmonic imaging microscopy to assess structural changes in optic nerve head structure ex vivo. J Biomed Opt. 2007;12:024029.
10. Vilupuru AS, Rangaswamy NV, Frishman LJ, Smith EL 3rd, Harwerth RS, Roorda A. J Opt Soc Am A Opt Image Sci Vis. 2007;24:1417-25. Adaptive optics scanning laser ophthalmoscopy for in vivo imaging of lamina cribrosa.
11. Kagemann L, Ishikawa H, Wollstein G, Brennen PM, Townsend KA, Gabriele ML, Schuman JS. Ultrahigh-resolution spectral domain optical coherence tomography imaging of the lamina cribrosa. Ophthalmic Surg Lasers Imaging. 2008;39:S126-131.
12. Miller KM, Quigley HA. The clinical appearance of the lamina cribrosa as a function of the extent of glaucomatous optic nerve damage. Ophthalmology. 1988;95:135-138.
13. Fontana L, Bhandari A, Fitzke FW, Hitchings RA. In vivo morphometry of the lamina cribrosa and its relation to visual field loss in glaucoma. Curr Eye Res. 1998;17:363-9.
14. Maeda H, Nakamura M, Yamamoto M. Morphometric features of laminar pores in lamina cribrosa observed by scanning laser ophthalmoscopy. Jpn J Ophthalmol. 1999;43:415-21.

Table of Contents


Imaging Adds Value to the Diagnostic Picture

This 60 year old African American Male presented for a comprehensive eye examination. His screening FDT N30-5 visual fields were within normal limits in each eye. Both optic discs are larger than average, and the "ISNT" rule was not obeyed in either eye (Figure 1A, B, C, D). Both cups were vertically oval in shape, and a notch is present in each eye inferiorly. There is peripapillary atrophy (zone alpha and beta) temporally in each eye and retinal nerve fiber layer (RNFL) loss is seen in the OS at 5 o'clock. There are no disc hemorrhages present. Both optic nerve heads have several signs consistent with glaucoma though surprisingly, the 24-2 SITA Standard visual fields are mostly within normal limits in each eye (Figure 2A, B). There are several points flagged temporal to the blind spot in the OS but this finding is generally not indicative of glaucoma, especially when disc diameter is large and therefore having the potential to overlie test locations that are usually outside the blindspot in small or average sized discs.

The right (A,B) and left eyes (C,D) are seen for this individual with primary open angle glaucoma. The disc size is slightly larger than average, and the ISNT rule is not obeyed in either eye. The cup in each eye has a vertical shape with a notch present inferiorly. RNFL loss is seen at 5 o'clock in the left eye and peripapillary atrophy is seen temporally in each eye.

Figure 1A

Figure 1B

Figure 1C

Figure 1D

Figure 2A and B: The HFA SITA Standard 24-2 visual fields are seen. Two points are flagged at a low confidence level inferiorly that are not significant enough to be considered a glaucoma defect. Repeat testing, if similar points are flagged again would increase credibility that this is early loss. The points flagged in the OS are temporal to the blind spot and are not consistent with glaucoma.

Figure 2A

Figure 2B

The HRT 2 image (Figure 3) shows a disc slightly larger than average with much of the disc occupied by the cup (red area). The Moorfields Regression Analysis (MRA) shows several sectors flagged in each eye at the lowest probability of falling within the normal range (red x); consistent with rim tissue that is thinner than expected in each eye taking into account the disc size. The GDx printout (Figure 4) also shows that both eyes have thinner than expected RNFL, with a NFI of 51 OD and 47 OS showing a high probability of each eye being glaucomatous. The RNFL maps show loss superiorly and inferiorly in each eye. The Optovue OCT printout (Figure 5) also shows thinning of the RNFL in each eye, flagged as yellow on the outer rim diagram (middle level of probability). The ganglion cell complex (GCC) analysis also shows thinning in the macula region, which supports the RNFL analysis. For this analysis, thinned areas are visible at the highest probability values in both eyes (red areas on the GCC section of the printout).

Figure 3: The HRT printout showing a series of sectors flagged on the MRA consistent with glaucoma.

Figure 4: The GDx printout showing darkened areas on the RNFL map consistent with a thin RNFL and pixels also flagged on the deviation map. The TSNIT curves show a reduced RNFL both superiorly and inferiorly. These findings taken together are consistent with glaucomatous damage.

Figure 5: The printout from the Optovue OCT which show thinned RNFL superiorly and inferiorly OD and OS. The GCC printout (top left and lower right) reveal areas in the posterior pole in which the ganglion cell complex is thinned, which may be consistent with glaucomatous damage.

The Cirrus OCT (Figure 6A) printout shows mild RNFL thinning, similar to the Optovue printout. Greater thinning is seen in the OD, which is also similar to the other devices. The superior quadrant analysis OD is flagged at the lowest probability value. The TSNIT curve shows the RNFL to be just within the confidence limits of the normal range. Figures from the Cirrus (Figure 6B, C) show cross sectional scans of the optic disc. Currently, there is no optic disc statistical analysis (disc size, rim area, etc) but this should be available shortly. The final imaging printout is from the Topcon 3D OCT (Figure 7A, B). With this device, the OCT image is registered against a retinal view. The RNFL thickness may be mapped but probability limits are not available at this time but should be available shortly.

Figure 6A: The printout from the Cirrus OCT which analyzes the RNFL cube of data is seen. For the right eye, the superior quadrant is flagged while RNFL defects are seen in the RNFL thickness deviation map in both eyes. The TSNIT curves reveal the thickness to be in the lower levels of the normal range for each eye.

Figure 6B and C: These printouts visually depict the shape and depth of the optic disc. In this case, the cup is deep with the walls vertical in shape.

Figure 7A and B: The Topcon 3-D OCT printouts are seen. A large area of the posterior pole is analyzed, and RNFL thickness measurements are available along with color coded maps. Probability values are not yet available.

Figure 7A

Figure 7B

Murray Fingeret, OD, FAAO
Table of Contents


Progressive Normal Tension Glaucoma

In 1995, a 56 year-old African-American male attended with a complaint of difficulties with near vision. His medical, family and ocular histories were non-contributory.

Figure 1.

On examination, corrected visual acuity was 20/20 in each eye with mildly myopic refractive correction. A 2.25D add was prescribed to allow reading vision of 0.37M at approximately 16". IOP by Goldmann applanation tonometry was 16 mmHg in each eye and gonioscopy revealed open angles and appearances of all structures being within normal limits. Dilated stereoscopic fundus evaluation revealed suspicious appearing optic discs with inter-eye cup-to-disc ratio (CDR) asymmetry (CDR OD>OS) corresponding to an asymmetry in disc diameter. There was also probable erosion of the inferotemporal neuroretinal rim (NRR) in each eye that was more apparent OD, and these ONH signs were considered to be suspicious of glaucomatous optic neuropathy. Disc appearances were documented using Polaroid© film and are shown in Figure 1. Visual field testing was ordered (see Figure 2). The SITA strategy was not available when this patient presented so 30-2 FASTPAC visual field tests were performed. The visual field tests were reliably performed by the patient. There is a single location that is deeply depressed in the superior nasal field of the right eye (see pattern deviation probability plot) with shallow sensitivity reductions present predominantly at the peripheral test locations in left eye. A diagnosis of suspect glaucoma was made and the patient was asked to return in six months. Repeated visual field testing in 1996 (Figure 3), revealed the deep nasal defect in the right eye to be repeatable, although fewer test locations were found to have reduced sensitivity in the left eye compared with the previous test. On the basis of the nasal defect in the right visual field being repeatable and corresponding to the area of NRR thinning, the patient was considered to have both structural and functional damage and the diagnosis was therefore modified to open angle glaucoma. Treatment was offered in the form of topical drops and the patient was prescribed latanoprost 0.005% (Xalatan®, Pfizer) and asked to return in 3 weeks. At a pressure of 16mmHg, the patient is considered to have normal tension glaucoma. A target IOP of 9-11 mmHg was established. When these visits took place the results of the CNTGS had been published and the recommendation was to lower IOP by at least 30% (1).

Figure 2.

The patient failed to attend for any scheduled future monitoring visits but re-presented 13 years later, aged 70, in 2009. He had not sought any eye care in the intervening period. Fundus photos from that visit are shown in Figure 4 and a number of obvious changes in disc appearance can be seen, including further inferior temporal rim thinning, an associated RNFL defect and baring of a small circumlinear arteriole at the inferior pole of the right disc. A disc hemorrhage can also be seen in the same area. Visual fields performed on the same date are shown in Figure 5 with the previous single defective test location in the right eye having extended to become an arcuate defect that encompasses many test locations in the superior hemifield. The left visual field also shows a moderate retinal nerve fiber layer type defect. The diagnosis was re-confirmed as normal tension glaucoma. The patient was offered a treatment recommendation of the prostaglandin analog travoprost 0.004% (Travatan®, Alcon Laboratories) once daily in each eye. This switch in medication was consistent with the patientís medical pharmacy coverage.

Figure 3.

When making a diagnosis of normal tension glaucoma, it is important to consider the potential impact of central corneal thickness (CCT). CCT may represent a risk factor for primary open-angle glaucoma (POAG) as well as being a confounding influence on Goldmann applanation readings that may reclassify the case as POAG if the cornea is sufficiently thin. Results of the OHTS, which highlighted the significance of CCT as a risk factor for conversion from ocular hypertension to glaucoma, were published in the interval during which the patient was lost to follow up (2). Pachymetry was performed when the patient returned in 2009 and was found to be OD/OS: 434/442 micrometers. This has more than one implication. First, the measured IOP is likely to be an underestimate of the true IOP. Second, if the IOP had previously been measured any higher (it was 20 mmHg at one point), then this patient's classification as NTG might have been incorrect, and in fact, the correct diagnosis may be POAG (3).

Figure 4.

Complicating this case further is the initial appearance of the optic nerves. The left ONH, especially could be interpreted to be an inferiorly tilted disc with RPE thinning. This would be expected to result in a relative superior visual field depression. Such a defect was present initially (1995) and had deepened by the examination in 2009 demonstrating visual field progression. So, on the basis of structural and functional progression there is ample evidence to refine the diagnosis and offer treatment to lower the IOP.

Figure 5.

The patient's IOP responded to travoprost by decreasing to 13mmHg OD and 14 mmHg OS. While this is above the initial target IOP, this was considered sufficient in view of the slow rate of progression whilst untreated over the preceding 13 years, as well as the patient's increased age and lack of deep paracentral loss that might otherwise threaten fixation in either eye. He will continue to be monitored for further progression with both subjective and objective measures, with education and encouragement regarding both compliance and attendance (4,5).

Leo P. Semes, OD

1. Schulzer M. Intraocular pressure reduction in normal-tension glaucoma patients. The Normal Tension Glaucoma Study Group. Ophthalmology. 1992; 99: 1468-70.
2. Gordon MO, Beiser JA, Brandt JD, et al. The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002; 120: 714-20.
3. Shah S, Chatterjee A, Mathai M, et al. Relationship between corneal thickness and measured intraocular pressure in a general ophthalmology clinic. Ophthalmology. 1999; 106: 2154-60.
4. Tsai JC. A comprehensive perspective on patient adherence to topical glaucoma therapy. Ophthalmology 2009; 116: S30-S36.
5. Budenz DL. A clinicianís guide to the assessment and management of nonadherence in glaucoma. Ophthalmology 2009; 116: S43-S47.

Table of Contents



How Best to Detect Progressive Field Defects: Wait and See?
Detection of progressive visual field loss is an essential element of glaucoma patient care. There are many different methods that can help us determine whether a series of visual fields exhibits either progressive or stable defects. These range from simple 'eyeballing' of successive test results, through to use of ordinal grading schemes as employed in large multinational trials (e.g. AGIS, CIGTS, EMGTS) or to other complex statistically-based methods such as those that look for change 'events' (e.g. GCP, GPA) or those that look for trends (e.g. linear regression of global indices such as MD (e.g. STATPAC overview analysis) or for individual test points (e.g. Progressor). Each of these has advantages and disadvantages which generally manifest an important clinical relevance as a trade-off or compromise between relative sensitivity for change detection versus specificity in unchanging eyes.

In a previous issue of the EJ, we reviewed a paper by Chauhan et al. [link to Vol 3, issue2, Visual Field Review] that introduced the concept that performing a greater number of repeated visual field tests over the first two years of a patients' follow-up permits one to establish a good baseline and assist in identification of those who are exhibiting more rapid progression. In the "New Ideas in glaucoma" paper session at the last ARVO meeting, Crabb and Garway-Heath of London suggest a variation of this theory by examining the hypothesis that estimates of glaucomatous visual field progression improve if more tests are performed at both the beginning and end of a defined FU period, compared with the conventional approach of regular periodic tests. They called their approach, "Wait and See."


Do you routinely check blood pressure in your glaucoma patients?

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



How often do you consider systemic blood pressure in your glaucoma patients?
Only in normal tension glaucoma cases
Only in patients with evidence of progression who have apparently controlled intraocular pressure
All of the time
Approximately half of the time
Almost never



How often do you consider systemic medications and the potential impact on pathophysiology of glaucoma in your glaucoma patients?
Only in normal tension glaucoma cases
Only in patients with evidence of progression who have apparently controlled intraocular pressure
All of the time
Approximately half of the time
Almost never

Using simulated VF data with a known progressive localised defect, the wait and see approach, using 3 fields performed at baseline and again at the end of a 2 yr period, was compared with the more conventional strategies of both 2 and 3 regular field tests per year.

They found that wait and see achieved;
1. Closer estimates to the true rate of progression than conventional examination strategies (the spread of estimated rate of loss reduced by 25%);

2. Detection or a higher proportion of truly progressive test locations, correctly identifying approximately 95% of progressive locations compared with approximately 60% and approximately 80% detection for conventional 2/yr and 3/yr strategies respectively;

3. Lower false positive rates of <1% compared with 2.5 and 6% for 2/yr and 3/yr respectively.
Overall, these gains meant that when compared with the conventional strategy of using 3 tests/year, their wait and see approach reduced the number of visual field tests required to identify progression, saving 1 test over a 2 year period.

At face value, these data suggest that wait and see may be a promising alternative to regular testing, providing the results can be validated empirically. However, although this strategy appears both efficient and able to discriminate well between stable and progressive field series, leaving periods of 2 or more years between field tests means that there is potential for delay in detection of those individuals with rapid progression to be missed. As such, wait and see is likely to be best suited to specific scenarios, such as clinical trials of a defined length, rather than routine clinical follow-up.

Paul GD Spry, PhD, BSc, MCOptom DipGlauc

1. D.P. Crabb, D.F. Garway-Heath. Wait and See: Varying the Interval Between Visits to Get Better Estimates of the Rate of Visual Field Progression in Glaucoma. Invest Ophthalmol Vis Sci. 2009;50:E-Abstract 1669.

Optic Disc Hemorrhages: Glaucomaís pregame or halftime show?
Where do optic disc hemorrhages fit in the glaucomatous disease process?

There has been a sense for some time among glaucoma practitioners and researchers that optic disc hemorrhages (DH) are harbingers or precursors of frank glaucomatous damage and that they probably precede loss of neuroretinal rim tissue and nerve fiber layer by a short time and precede damage in corresponding areas of the visual field by a longer time. A series of presentations (1, 2) at this yearís ARVO meeting have cast DH in a new light. Taken together, they suggest that DH appear as an integral part of the glaucomatous pathophysiological process, occurring in concert with visual field change, rather than as a precursor.

In the first presentation (1), the authors evaluated the rate and location of visual field deterioration before and after detection of DH in patients with glaucoma. Pointwise linear regression (Progressor) was used to calculate global and localized rates of visual field change both before and after DH was detected. 168 DHs were observed in 120 patients. DH occurred most often in the inferotemporal (62%), temporal (14%), and superotemporal (11%) sectors. Mean (±standard deviation) global visual field deterioration rates before and after DH were -0.80 ± 1.2 and -1.07 ± 1.4 dB/yr respectively, however these rates were not significantly different (p = 0.30). The mean rates of deterioration for visual field locations corresponding to the DH were -1.17 ± 1.5 dB/yr before and -1.90 ± 2.4 dB/yr after DH (also not significantly different; p = 0.06). Rates of visual field worsening, both before and after DH, were significantly more rapid than in eyes without DH (p < 0.05). DH appeared in a disc sector corresponding to the visual field region that displayed the fastest rate of worsening very often (80% of the time). After the occurrence of DH, the corresponding visual field regions continued to undergo the fastest rates of visual field deterioration in almost all eyes (92%).

Eyes with nasal DHs generally showed slower rates of visual field deterioration and less agreement between DH location and the location of past or future visual field change. This is not surprising given the scant attention the temporal visual field, corresponding to the nasal optic nerve head (ONH), is given in the 24-2 test pattern.

The authors concluded that the visual field showed its most rapid worsening in regions that corresponded to where DHs would later appear and that these visual field regions continued to worsen most rapidly after DH, although perhaps at a slightly faster rate. They also suggested that local neuroretinal rim structural collapse, with corresponding localized visual field worsening, might predispose a particular region of the ONH to DH. Visual field worsening continues because of the ongoing structural damage Ė with corresponding loss of, or damage to, RGC axons. The authors closed by stating that "...DH should be viewed not only as a risk factor for future progression but also as evidence of past localized progression" within the structure of the ONH and the corresponding regions of the visual field. Clinically, this suggests that whenever a DH is detected, it is likely that visual field change has already occurred in the corresponding region. This is not the same as saying that the visual field will be outside normal limits in the corresponding location, as sensitivity may have been in the high end of normal prior to disease development. If previous visual fields exist for a patient in whom a DH is observed it would be worth performing a change analysis if possible rather than looking at fields 'side by side' as both visual fields may still be within normal limits yet change may have occurred since the initial test was performed. One question that this study does not answer is whether the DHs detected were ever the 'first' DH in each eye—something that in reality is impossible to know. Could it be that there is something truly foreboding about the very first DH in an eye that is developing glaucoma and that the first DH almost always occur before the visual field has changed appreciably?

In a second presentation (2) from the same group, the authors examined whether recurrent DH is associated with a faster rate of functional decline when compared with eyes in which only a single DH was detected during follow up. It is important to recognize at the outset that clinicians probably only detect a small minority of all DHs that occur in the eyes of their patients, largely because many DHs occur and resolve between patient visits. However, it is safe to assume that patients in whom numerous DHs are detected are likely to be having more of them (assuming, perhaps incorrectly, that a greater number of DHs is not a reason for more frequent follow up). Disc photographs of glaucoma patients with ≥ 5 SITA-Standard 24-2 fields were examined for the presence of DH. Eyes with one DH were compared to eyes that had >1 DH during follow up. Pointwise linear regression analysis (Progressor) was used to calculate rates of visual field change after DH. Fifty-six patients were identified with DH, 40 with one and 16 with > 1. Patients with recurrent DH had significantly less visual field damage at baseline (MD = -2.75 ± 4.0 vs. -5.6 ± 5.0 dB, p < 0.01). However, the rate of visual field deterioration was not significantly different (-0.86 ± 0.8 vs. -0.67 ± 1.0 dB/Yr, p = 0.38). Interestingly, recurrent DH occurred within 2 clock hours of the initial DH in 88% of cases, and in the hemifield with less visual field damage in 75% of eyes with multiple DHs. In conclusion the authors suggest that recurrent DH is not necessarily associated with a faster rate of visual field decline. A potential clinical message that can be drawn from this study when combined with the previous one is that detection of a DH might cause one to become more vigilant or aggressive in a patient with suspected or actual glaucoma, but the appearance of DH at subsequent visits might not be reason to escalate further.

Shaban Demirel, BScOptom, PhD

1. De Moraes CV, Prata TS, Liebmann CA, Ritch R, Tello C, Liebmann JM. Localized visual field loss predicts the location of future disc hemorrhage and subsequent visual field progression. Invest Ophthalmol Vis Sci. 2009;50:E-Abstract 6197.
2. Beck HC, De Moraes CGV, Prata TS, Folgar FA, Ahrlich K, Teng CC, Ritch R, Tello C, Liebmann JM. Recurrent disc hemorrhage does not increase the rate of visual field progression. Invest Ophthalmol Vis Sci. 2009;50:E-Abstract 5835.
All ARVO abstracts from 2009 can be searched from the 'Meetings and abstracts' section of the ARVO website at www.ARVO.org

Table of Contents




New Glaucoma Care Guideline Launched for England and Wales from the National Institute of Health and Clinical Excellence.
The National Institute for Health and Clinical Excellence (NICE) is an independent organisation, originally established by United Kingdom (UK) government, responsible for providing national guidance on the promotion of good health and the prevention and treatment of ill health. NICE has a wide healthcare remit and is responsible for producing guidance on public health issues, approval of technologies and treatments for use in the UK's National Health Service (NHS) but also production of clinical management guidelines for the treatment and care of people with specific diseases and conditions. These clinical guidelines are effectively commissioned by Government for diseases according to need, such as where uncertainty and variation exist in clinical practice across the country. It is important to understand that guidelines are produced specifically for implementation in the publicly-funded NHS in England and Wales.

In April of last year, NICE published a recommendation on the diagnosis and management of chronic open angle glaucoma (COAG) and ocular hypertension (OHT). Full and abbreviated versions of the guideline are available for free download from www.NICE.org.uk.

The guideline consists of a series of statements ('recommendations') grouped into the following categories; (1) diagnosis; (2) monitoring; (3) treatment for people with OHT and those suspected of COAG; (4) treatment for people with COAG (5) organisation of care; (6) provision of information. The guideline was developed by a competitively appointed multidisciplinary group, including ophthalmologists, optometrists, orthoptists, nurses and patient representatives. This group was responsible for formulating relevant clinical questions and then reviewing the evidence-base to answer them, with assistance from methodologists who graded and assimilated the evidence performed cost effectiveness analyses and drafted the guideline. Recommendations took into account the findings and quality of clinical and economic evidence, patients views, benefit versus harms and equality. Where no evidence was available, recommendations were made by consensus opinion of the guideline development group.

In addition to making recommendations on treatment algorithms, diagnostic and monitoring strategies, the guideline is an especially valuable tool for UK optometrists because of recommendations on organisation of care. Although in recent years some UK optometrists have become increasingly involved in glaucoma care, the role of the majority of UK optometrists in glaucoma remains one of opportunistic screening for disease such that patients presenting for routine eye examination considered by their optometrist to have sufficient suspicion of glaucoma are referred to NHS ophthalmologists for all ongoing care. However, the NICE guideline extends this role to specified aspects of management and monitoring for those optometrists who are able to show that they have developed their skills and gained relevant experience.

Although some recommendations have prompted considerable debate within the UK optometric press, such as the requirement for demonstration of relevant qualifications (UK Optometric Training Institutions do not currently provide education in therapeutics for glaucoma or how to monitor patients with disease), strategies for treatment of defined OHT sub-groups and the requirement for diagnosis of glaucoma to be made by a consultant ophthalmologist, the majority confirm existing good clinical practice.

Paul GD Spry, PhD, BSc, MCOptom DipGlauc

Table of Contents




If you would like us to answer a clinical question, please send it to paul.spry@uhbristol.nhs.uk with "OGS question" as the subject. The questions can concern anything related to glaucoma, for example, analysis of an optic nerve image, optic disc, a challenging case or side effect of a medication. We welcome your questions and we will try to address as many as possible in each issue.

Q: I am aware of the possible pathogenic causes of Glaucoma being the Ischemic, Mechanical and the Glutamine theory. All have bearing to a pressure problem within the eye as we know. Could long haul flights in a pressurized aircraft impact on glaucoma patients? I realise that the impact may only be for the 15 to 20 hours in the case of a passenger, but what if the person is a pilot at risk?

Douglas Anderson, MD replies: The events that occur when the pressure goes up in the eyes are complex. Certainly the tissues of the optic nerve are subjected to a force that distorts the anatomy of the optic nerve. In addition, it challenges the blood flow, and if the vascular bed cannot respond with a proper regulatory response (most can), then ischemia may develop. From there these two fundamental effects of pressure, a cascade of many events follow, depending on the severity and duration of the anatomical distortion or ischemia. For example, pressing on the eye with a finger (rubbing the eyelids) will cause marked pressure elevation, but if it is relieved promptly, no harmful consequences are initiated. If ischemia lasts for perhaps half an hour or an hour, and is not severe (middle of the night, transient pressure from pillow or lowering of blood pressure), there may be no direct harm, but an element of "reperfusion injury" is known to occur in central nervous system tissues. Among the events in the cascade may be activation of free radicals in the optic nerve head, interruption of rapid orthograde and retrograde axonal transport, failure of the retinal ganglion cells to receive trophic factors, apoptotic death of the ganglion cell, release of glutamate, and according to a past hypothesis not presently believed, excitotoxic damage to nearby cells. The initial work on the latter theory has been discredited, although some feel it should be examined again. Others find the clinical appearance (failure of field defects to cross the nasal vertical meridian, for example) to place doubt on this concept.

Atmospheric pressure changes every day, not just when you get on an airplane, and one of the things about ambient air pressure is that it has no effect of fluid filled tissues and compartments of the body. So, for example, for escape of nutrient fluid from the vascular system to the tissues, it is the difference in pressure inside and outside that determines the flow. If both are high because you are on a deep ocean dive, or if both are low because you are in an airplane or at a mountaintop, the difference remains the same and has no effect. The one exception is a gas bubble, which changes size with pressure (whereas fluid does not—well, only a very tiny bit). So in eyes with a gas bubble after vitreous surgery, the bubble will expand at low ambient pressure. However, passengers and pilots, who don't have gas bubbles in their eyes, are otherwise not placed at risk of glaucoma damage.

Q: Deep vein thrombosis (DVT) has an impact regarding the haemodynamics in the legs due to poor circulation, but could this be extrapolated to the eye?

Douglas Anderson, MD replies: With regard to DVT, it occurs due to inactivity of the muscles because you are sitting still, perhaps with your knees bent in an uncomfortable position that compresses the veins at the bent knees, so there is no blood flowing through them. When there is no blood flow, the blood tends to clot. So jiggling your feet or walking around a bit once in a while is recommended. The problem is not for the legs, but that the blood clot may later come loose and be carried up the vein to the lungs, where it can cause a major disaster. These clots are large and can't get through the capillaries of the lung to reach the general circulation and the eye. When flying you move your eyes around as always, and in any event do not have them in a cramped position, so clots are not likely to be produced in the eye.

Table of Contents




In our last issue, we asked you what you thought about risk factors for glaucoma development. The question of central corneal thickness (CCT) being an independent risk factor for glaucoma development remains to be conclusively determined. Poll 1 shows that the complex nature of this question is reflected by a little more than twice as many respondents believing a cornea thinner than the expected average is associated with the development of glaucoma (58% vs 25%). Evidence for this, particularly outside ocular hypertensives, is not strong but ongoing study of ocular biomechanics including cornea, lamina cribrosa and peripapillary sclera may reveal a relationship in the future.

Eighty percent of respondents usually or always inquired about their glaucoma suspects' cardiovascular health status (see Poll 2).

With regard to the most important risk factors, Poll 3 shows that each of the four choices were considered by some to be the most important for the development of primary open angle glaucoma. Family history, specifically a sibling with glaucoma, was rated the most important risk factor by 42% of respondents, while an additional 26% selected age.

The prevalence of glaucoma is higher with increased age and higher intraocular pressure (IOP). There is strong support for the recognition of the role of family history. The prevalence of glaucoma being higher among those patients with a parent, and especially a sibling, with glaucoma is suggested by a number of epidemiological investigations, such as the Rotterdam Study (1)

A family history of glaucoma may reasonably contribute as a risk factor in a particular patient. It may also contribute to the level of patient anxiety with respect to their condition. The value of family history information (especially when self-reported and not confirmed) may be limited by the questions used and an incomplete or inaccurate understanding of the family member's condition by the patient or the clinician. Additionally, patients with a known family history of a potentially inherited condition are more likely to seek evaluation. Characteristics that prompt the diagnosis or suspicion of glaucoma (e.g. large cup-to-disc ratio) can be familial traits. In this circumstance, follow up questions regarding vision loss from glaucoma may be a useful filter to further clarify those with true glaucomatous damage.

Family history remains an important consideration to be investigated by the clinician who is caring for patients diagnosed with or suspicious for glaucoma.

Special thanks to all our respondents. Please continue to participate in future polls.

John McSoley, OD

1. Dielemans I, Vingerling JR, Wolfs RCW et al. (1994). The prevalence of primary open-angle glaucoma in a Population-based study in the Netherlands. Ophthalmology; 101 (11): 1851-1855.

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
G. Richard Bennett, MS, 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


Art/Production Director
Joe Morris


To subscribe to the OGS Journal, CLICK HERE!

The e-newsletter is offered free to clinicians and scientists and is supported by

Pfizer Ophthalmics Logo


This paid, promotional message was sent to you by Jobson Medical Information LLC. The content does not necessarily reflect the views, or imply endorsement, of the Group's editors or publisher. If you do not want to receive this type of information in the future, click here. Jobson Medical Information LLC never releases its e-mail list.
Jobson Medical Information LLC, 11 Campus Blvd., Newtown Square, PA 19073