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Moderators' panel discussion
MODERATORS’
Moderators’
CONCLUSIONS
AND PANEL DISCUSSION,
439
Panel Discussion
SCHWARTZ: I would the panel what type of use to identify an early they would treat such
like to ask each member of tests or criteria they would glaucoma patient and how an individual.
DRANCE: I would identify as an early glaucoma patient any person who had a family history of the disease, a pressure elevation, a suspicious optic nerve head, and some abnormality in one of the psychophysical functions. If I were confident that the changes that I measured were not due to the media, 1 would then think seriously that this individual was in the early stages of the disease, and I would intervene accordingly. I would not hesitate to carry out psychophysical tests. I would certainly look at the retinal nerve fiber layer, preferably photographically, rather than with the cobalt blue filter. Of course, the patient must also have a good perimetric examination.
KITAZAWA: 1 feel that the following factors are of particular importance in deciding whether or not to intervene: family history, ocular pressure, and the rim area of the optic nerve head. Since we have little experience with psychophysical testing, we do not take these results into consideration. The presence or the absence of retinal nerve fiber layer defects is not crucial because we have seen patients who had nerve fiber layer defects in spite of the fact that we could not demonstrate significant visual field changes. GREVE: 1 tend to think in terms of risk factors. Intraocular pressure is one risk factor and we all agree that if it is 50 mm Hg, then we probably have an early glaucoma. Family history is also important. From the morphological point of view, I fully agree with the other speakers. I would look at the disc and the retinal nerve fiber layer very carefully. We should remember, however, that disc abnormalities are not that easy to judge. I would also be inclined to be more worried if the vasculature of the eye did not look good. Circulation may be important in an early glaucoma. Of course, I would also look at the hemorrhages. A visual field test should, of course, be taken and repeated. We should also realize that we are routinely using 6” visual fields, and that is quite a distance. Dr. Drance and others have showed that you can miss a blindspot in up to 20% of patients. SCHWARTZ:
PARTS I-III
I do many of the things
that the other
panelists have mentioned. I pay particular attention to asymmetry between the eyes. If I find asymmetrical ocular pressures that are associated with asymmetrical amounts of cupping and pallor of the disc, and also asymmetrical nerve fiber layer defects, then I think that you have pressure that is affecting one eye and will affect the other eye eventually. We routinely take optic disc and nerve fiber layer photographs when the patient is first seen. But we know you have to learn how to read them; it is a matter of art and not science at the moment. Diffuse nerve fiber loss is very diflicult to discern, and one has to compare eyes and quadrants within eyes to pick up any differences. 1 would like to mention one other point about treatment. What concerns me very much about not treating patients with ocular hypertension is not their risk of developing visual field loss, but their risk of developing a retinal vein occlusion, especially when the macula becomes involved. In such instances, the patient’s visual acuity will certainly be diminished. So if patients have pressures over 30 mm Hg, show marked arteriovenous nicking, especially in the superior temporal quadrant, have a history of high blood pressure and diabetes mellitus, I am more inclined to initiate treatment. DRAN(:E: I think one of the first things that one should do with a simple ophthalmoscope is look into the eye and determine disc size. If there is a large disc on one side and a small disc on the other, there will be a large cup on one side and a small cup on the other. This asymmetry will not have been produced by an acquired disease process. Our discussion has assumed that elevated pressures are responsible for some or all of the early changes in glaucoma. We have barely established that some ofthe early disturbances are predictive of subsequent field defects which gradually affect our patient’s vision. We do know that progression is slow, sometimes episodic, and that it becomes more rapid in the later stages of the disease. It may, therefore, be quite reasonable to advocate surgery earlier for such patients. The prognosis of glaucoma in the early stage is very uncertain, especially when no progression has yet occurred. We hope that pressure reduction will slow down, halt, or even prevent damage from taking place. I use the word “hope” advisedly, for I do not know of any convincing evidence that pressure reduction will do any of these things at that stage of the disease process. 1 do not know whether the process is the same in all patients. The concept of a low critical pressure level is a good
440
Surv Ophthalmol
33 (Supplement)
April
1989
one, as an hypothesis. It is not new. Goldmann and I, among others, planned to address this issue many years ago, using acetazolamide before glycerol was available for pressure reduction. As far as I know, this approach has not yet been validated for determining a therapeutic target pressure. It has been suggested that pallor regresses with timolol pressure reduction, but this is not always the case. I also know of evidence that visual function is not favorably influenced by successful pressure reduction with timolol in ocular hypertensive individuals with a 6-year follow-up and 18 threshold profiles per regression. The decision to treat an individual has implications in terms of cost, lifestyle, and side effects, and
should not be lightly undertaken. There is certainly no cause for hurry in the glaucoma suspect to make this decision. On balance, we have to undertake therapy that is of benefit to the patient. We need more nonanecdotal information and a broad, wellstructured discussion of this topic before we allow impressions to become rampant again without the basis of underlying facts. I, for one, am too ignorant at this time about the true nature of the history of chronic open-angle glaucoma and of the effects of pressure-reducing therapy in the early stages of the disease to know whether the superficial impressions on therapy which were created in some parts of this symposium are justified. Time and further study will finally uncover the truth.
Moderators’
CONCLUSIONS
AND PANEL DISCUSSION,
439
Panel Discussion
SCHWARTZ: I would the panel what type of use to identify an early they would treat such
like to ask each member of tests or criteria they would glaucoma patient and how an individual.
DRANCE: I would identify as an early glaucoma patient any person who had a family history of the disease, a pressure elevation, a suspicious optic nerve head, and some abnormality in one of the psychophysical functions. If I were confident that the changes that I measured were not due to the media, 1 would then think seriously that this individual was in the early stages of the disease, and I would intervene accordingly. I would not hesitate to carry out psychophysical tests. I would certainly look at the retinal nerve fiber layer, preferably photographically, rather than with the cobalt blue filter. Of course, the patient must also have a good perimetric examination.
KITAZAWA: 1 feel that the following factors are of particular importance in deciding whether or not to intervene: family history, ocular pressure, and the rim area of the optic nerve head. Since we have little experience with psychophysical testing, we do not take these results into consideration. The presence or the absence of retinal nerve fiber layer defects is not crucial because we have seen patients who had nerve fiber layer defects in spite of the fact that we could not demonstrate significant visual field changes. GREVE: 1 tend to think in terms of risk factors. Intraocular pressure is one risk factor and we all agree that if it is 50 mm Hg, then we probably have an early glaucoma. Family history is also important. From the morphological point of view, I fully agree with the other speakers. I would look at the disc and the retinal nerve fiber layer very carefully. We should remember, however, that disc abnormalities are not that easy to judge. I would also be inclined to be more worried if the vasculature of the eye did not look good. Circulation may be important in an early glaucoma. Of course, I would also look at the hemorrhages. A visual field test should, of course, be taken and repeated. We should also realize that we are routinely using 6” visual fields, and that is quite a distance. Dr. Drance and others have showed that you can miss a blindspot in up to 20% of patients. SCHWARTZ:
PARTS I-III
I do many of the things
that the other
panelists have mentioned. I pay particular attention to asymmetry between the eyes. If I find asymmetrical ocular pressures that are associated with asymmetrical amounts of cupping and pallor of the disc, and also asymmetrical nerve fiber layer defects, then I think that you have pressure that is affecting one eye and will affect the other eye eventually. We routinely take optic disc and nerve fiber layer photographs when the patient is first seen. But we know you have to learn how to read them; it is a matter of art and not science at the moment. Diffuse nerve fiber loss is very diflicult to discern, and one has to compare eyes and quadrants within eyes to pick up any differences. 1 would like to mention one other point about treatment. What concerns me very much about not treating patients with ocular hypertension is not their risk of developing visual field loss, but their risk of developing a retinal vein occlusion, especially when the macula becomes involved. In such instances, the patient’s visual acuity will certainly be diminished. So if patients have pressures over 30 mm Hg, show marked arteriovenous nicking, especially in the superior temporal quadrant, have a history of high blood pressure and diabetes mellitus, I am more inclined to initiate treatment. DRAN(:E: I think one of the first things that one should do with a simple ophthalmoscope is look into the eye and determine disc size. If there is a large disc on one side and a small disc on the other, there will be a large cup on one side and a small cup on the other. This asymmetry will not have been produced by an acquired disease process. Our discussion has assumed that elevated pressures are responsible for some or all of the early changes in glaucoma. We have barely established that some ofthe early disturbances are predictive of subsequent field defects which gradually affect our patient’s vision. We do know that progression is slow, sometimes episodic, and that it becomes more rapid in the later stages of the disease. It may, therefore, be quite reasonable to advocate surgery earlier for such patients. The prognosis of glaucoma in the early stage is very uncertain, especially when no progression has yet occurred. We hope that pressure reduction will slow down, halt, or even prevent damage from taking place. I use the word “hope” advisedly, for I do not know of any convincing evidence that pressure reduction will do any of these things at that stage of the disease process. 1 do not know whether the process is the same in all patients. The concept of a low critical pressure level is a good
440
Surv Ophthalmol
33 (Supplement)
April
1989
one, as an hypothesis. It is not new. Goldmann and I, among others, planned to address this issue many years ago, using acetazolamide before glycerol was available for pressure reduction. As far as I know, this approach has not yet been validated for determining a therapeutic target pressure. It has been suggested that pallor regresses with timolol pressure reduction, but this is not always the case. I also know of evidence that visual function is not favorably influenced by successful pressure reduction with timolol in ocular hypertensive individuals with a 6-year follow-up and 18 threshold profiles per regression. The decision to treat an individual has implications in terms of cost, lifestyle, and side effects, and
should not be lightly undertaken. There is certainly no cause for hurry in the glaucoma suspect to make this decision. On balance, we have to undertake therapy that is of benefit to the patient. We need more nonanecdotal information and a broad, wellstructured discussion of this topic before we allow impressions to become rampant again without the basis of underlying facts. I, for one, am too ignorant at this time about the true nature of the history of chronic open-angle glaucoma and of the effects of pressure-reducing therapy in the early stages of the disease to know whether the superficial impressions on therapy which were created in some parts of this symposium are justified. Time and further study will finally uncover the truth.