Glaucoma suspect
[size=3]Glaucoma suspect (Ocular hypertension, suspicious nerves or fields)[/size]Glaucoma suspect is a term used to describe a person with one or more potential risk factors that may or may not lead to glaucoma, however this person does not show definite signs of glaucomatous damage to the optic nerve or any visual field defects.
Ocular Hypertension Treatment Study
Chat Highlights
October 30, 2002
Norma Devine, Editor
On Wednesday, October 30, 2002, Dr. George Spaeth, a glaucoma specialist at Wills, and the glaucoma chat group discussed "Ocular Hypertension Treatment Study."
Moderator: Welcome back, Dr. Spaeth. Tonight our topic is the Ocular Hypertension Treatment Study (OHTS).
P: What is ocular hypertension?
Dr. George Spaeth: Ocular hypertension is IOP (intraocular pressure) over 21 mm Hg. But the term "ocular hypertension" has come to mean IOP over 21 mm Hg in addition to visual field defect or optic disc damage. The problem is that field defects cannot be found in early glaucoma, and early disc damage cannot be identified. Therefore, you can never say a person does not have damage. All you can say is that you cannot find damage.
P: Is ocular hypertension a result of glaucoma or a cause?
Dr. George Spaeth: Glaucoma is damage to ocular tissues related to IOP. In most cases, it seems that the initial problem is the IOP, but there are other factors. Normal, that is average, IOP can cause damage.
Moderator: Did you participate in the Ocular Hypertension Treatment Study?
Dr. George Spaeth: I was involved in its design; we were not a participating center. Fascinating study. Depending on whether you are a glass-is-half-empty or half-full kind of person, your interpretation of the results differs.
P: Are the flaws in the study that have been reported significant flaws?
Dr. George Spaeth: The study was beautifully designed and implemented. I wish I had been a participant. The problem really only comes with the interpretation of the results.
Moderator: In an earlier chat you said: "Ninety percent of those with elevated IOP never get damage. Fifty percent of those with damage never have elevated IOP!" Have the results of the OHTS changed your thinking about that?
Dr. George Spaeth: No. The study showed that the overwhelming majority (over 90%) of patients with elevated IOP do not get worse.
Moderator: Were the treated patients better off or worse off than the untreated patients?
Dr. George Spaeth: The treated patients all had inconvenience and some side effects from the treatment. Were they any better off than the untreated patients? No, because an early field defect doesn't hurt anybody. Side effects do. At age 28, you may need treatment immediately, even surgery. The point is, it is not the IOP that determines the need for treatment. It is the nature of the optic disc and other factors.
P: Five percent got worse because of the treatment?
Dr. George Spaeth: No, they got worse because they were not treated adequately or because they really did not get worse. Determining that someone is a little bit worse is very tough. For example, in this study, 88% of the patients who were thought to have gotten worse on the basis of a change in visual field were found not to have gotten worse when the field was repeated! What this study shows that is hugely important is that patients with thinner corneas are more likely to get worse.
P: As a result of the OHTS, will all new glaucoma patients now have their central corneal thickness measured?
Dr. George Spaeth: Probably not. But my hunch is that in about five years the answer will be yes. And not just new patients. Measuring corneal thickness may give a clue to whether a person will get worse. That is what we really need to know.
P: Did the patients with elevated IOP and no damage complain of symptoms such as eye pain?
Dr. George Spaeth: Ocular symptoms are extremely rare in patients with ocular hypertension.
P: If approximately only 10% of the subjects sustained damage without medication, and 5% sustained damage with medication, doesn't that mean the medication utterly failed to prevent glaucoma half the time? Does the OHTS give any clues to why that is? Is it better to treat some patients differently from the outset, with trabeculectomies, perhaps?
Dr. George Spaeth: Good question. But did they get worse? As mentioned earlier, some probably really didn't get worse. Some probably were worse because they already had started to have a serious type of glaucoma that may need very vigorous treatment to prevent it from worsening.
P: This study only looked at IOPs up to about 30 mm Hg (24.9 mm Hg, on average). Above 30 mm Hg, there are other risks besides glaucoma, so isn't the "gray area" for treating ocular hypertension really only between 21 and 31 mm Hg?
Dr. George Spaeth: When IOP gets above 30 mm Hg, it is believed that the eye is predisposed to getting a blood-flow problem, specifically a blockage of the vein that drains the eye. That causes immediate visual loss. For that reason, there is a risk in having an IOP over 30 mm Hg.
P: Are you are saying that glaucoma patients do not benefit from medication?
Dr. George Spaeth: No. Glaucoma patients can definitely benefit from medications. Medications can prevent people with glaucoma from going blind, and that is a huge benefit.
P: As a person with ocular hypertension, normal optic nerves, and normal visual fields, I have some problems with the OHTS. On one hand, the study supports the idea that we can possibly prevent or delay the onset of glaucoma, which is what we need to hear, since we have options. On the other hand, we have to continue to wait for damage to start, which seems to defeat the purpose of the study in some ways.
Dr. George Spaeth: The question the OHTS did not answer (yet) is whether the development of early field damage is of any importance. That is, does early damage facilitate development of further damage? Some say yes; some say no.
Moderator: In "Answers From the Ocular Hypertension Treatment Study," Dr. Paul Palmberg says that "up to 20% to 50% of the optic nerve fibers may be lost focally before damage is recognized by conventional perimetry." That information frightens glaucoma patients. Yet Dr. Palmberg cites only two references for that statement, one of which is a study involving 10 rhesus monkeys. The other is a study by H. Quigley, J. Katz, and others involving 647 persons with "bilateral IOP higher than 21 mm Hg and initially normal visual field test results with the Goldmann perimeter." Do you know of any other studies supporting that or similar statements?
Dr. George Spaeth: Yes. In 1974 I published an article showing that disc damage preceded visual field loss. In fact, a major part of the nerve must be damaged before visual field loss develops. But that should not be frightening; rather it is reassuring. What that says is that we were made with many more fibers than we need. If we lose a lot, it doesn't matter. Or better, it doesn't matter at that time. The person doesn't really care how many nerve fibers he or she has but rather, does he or she have a problem? Is there any symptom? Is there any limitation to function?
P: That is quite amazing information. I have been on glaucoma medications for 25 years, always an increasing number of them. I have not had a trabeculectomy, but I do have substantial damage. I always say to the doctor: "I can see. Let's go slowly." Maybe I have been lucky.
P: You say that 88% of those who initially seemed to get worse did not, in fact, get worse. Does that mean that instead of 10% of untreated ocular hypertensives converting to glaucoma patients, only 1 or 2% converted?
Dr. George Spaeth: No, because they tightened up the definition of "getting worse" and required confirmatory visual field exams before saying a person was worse. Also, most people got worse because their optic nerve showed deterioration, even though their visual field remained stable.
P: Why did the study use the average IOP (and other eye-specific variables) of both eyes of each patient to calculate risks, and not the parameters of individual eyes?
Dr. George Spaeth: I don't think the two eyes were averaged.
P: According to the results in "Archives of Ophthalmology," they were. I can't figure out why.
Dr. George Spaeth: I will recheck. Something sounds strange (it may be me).
Moderator: Isn't the interpretation of the results of the study the most important thing? Shouldn't there be one clear result?
Dr. George Spaeth: No, there can't be one clear result in terms of interpretation. The goals of treatment vary, the goals of patients vary, the goals of researchers vary. The clear result was that few people with ocular hypertension get worse and that that number can be decreased by treatment. The real problem is, so what?
Moderator: Did the study change the way you treat patients?
Dr. George Spaeth: Not yet, but we will definitely get corneal thickness measurements. We will pay even more attention to the nature of the optic disc, because the nature of the optic disc, even when supposedly normal, was the second-best predictor of who would get worse.
P: Are you saying that even after visual field damage is sustained, further damage can be identified by examining the optic nerve even before the visual field gets any worse?
Dr. George Spaeth: No, even before field damage has occurred the disc can predict who will get field damage. But your comment is also correct in that even after field damage, the nature of the optic disc is the best predictor we have of who will get worse.
P: The number of us with ocular hypertension are few, but the consequences of developing glaucoma are a large concern for those of us who may progress to that point.
Dr. George Spaeth: The number of people with ocular hypertension is large. It is probably around two million or more in the U.S. But of those, about 5% will get actual glaucoma. For that 5%, it is terribly important.
Moderator: What about patients with narrow or closed angles and pressures in the mid 20's? Would you watch them closely or treat?
Dr. George Spaeth: They would get treated, but not because of their IOP. If their angles were narrow enough to occlude, they would need a laser iridotomy whether their pressure was 10, 20 or 50 mm Hg. If they had glaucoma, that is, damage to the tissues, they would probably need treatment whether they had wide or narrow angles and whether their IOP was 10, 20 or 50 mm Hg.
P: Do you know when the OHTS will be completed, the data analyzed, and the results published?
Dr. George Spaeth: I hope the OHTS will not be finished for 20 years. The interpretation of the OHTS study is a really important issue. Thank you all for being here.
Moderator: Thank you for helping us understand the results of OHTS.
Dr. George Spaeth: I would like to leave you all with a simple but important thought. Glaucoma is important only because it can decease the quality of people's lives. It does that by causing pain in some people or decreased vision. It also does that as a result of treatment. If the person is not going to develop a decrease in the quality of his or her life, treatment is not justified.
End of highlights for October 30, 2002.
CCT在OH中的重要性。如果CCT较厚，危险性大大降低，反之亦然。 [s:94] 青光眼病人的治疗有赖于准确的诊断。青光眼病人的诊断与其他病>疾病一样，根据病史、临床表现及检查结果进行综合分析。
对可疑患者，首先应测量眼压。眼压大于3.20kPa（24mmHg）为病理性高眼压，但一次眼压偏高不能诊断青光眼，而一次眼压正常也不能排除青光眼。因为眼压在一日内呈周期性波动。日眼压波动大于1.07kPa（8mmHg）为病理性眼压。正常人双眼眼压接近，如双眼压差大于0.67kPa（5mmHg）也为病理性眼压。其次应检查眼底，观察视盘改变，青光眼的视盘改变具有一定的特殊性，有重要的临床价值。常表现为病理性陷凹，目前普遍采用陷凹与视盘直径的比值（C/D）表示陷凹大小。C/D大于0.6或双眼C/D差大于0.2为异常；视盘沿变薄，常伴有视盘沿的宽窄不均和切迹，表示视盘沿视神经纤维数量减少；视盘血管改变，表现为视盘边缘出血，血管架空，视盘血管鼻侧移位和视网膜中央动脉搏动。此外，眼底检查可观察视网膜神经纤维层缺损，由于它可出现在视野缺损前，被认为是青光眼早期诊断指征之一。
视野检查对青光眼的诊断有重要价值。因为它代表了视神经的损伤。临床常见视野缺损类型有：视阈值普遍降低、弓形缺损、鼻侧阶梯、垂直阶梯、颞侧扇形缺损、中心及颞侧岛状视野。
通过上述检查，我们可以诊断青光眼，但在开始治疗前还应确定青光眼的类型。首先检查前房角，房角开放者为开角型青光眼，反之则为闭角型青光眼。通过房角检查，青光眼分类诊断仍有困难时，可查房水流畅系数（C值）。C值小于0.1为病理性，压畅比（Po/C）大于150为病理性，主要见于开角型青光眼。但需注意，闭角型青光眼反复发作后C值及压畅比也可异常。另外我们对一些疑似青光眼可选一些激发试验，以辅助诊断。
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