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Ocular hypertension (intraocular pressure greater than or equal to 21 mm Hg, normal visual fields, normal optic discs, open angles, and the absence of any contributing ocular disease) occurs in 4-10% of the population over age 40. The question of whether to treat ocular hypertensive patients remains controversial. The author recommends prophylactic treatment for selected ocular hypertensive individuals who are at high risk of developing primary open angle glaucoma. The primary risk factors are high intraocular pressure, optic disc abnormality, increasing age, a family history of glaucoma, and systemic vascular disease. In addition, certain features of the patient's personality or medical condition favor treatment; for instance, treatment would probably be indicated in (1) a young patient, (2) a one-eyed patient, (3) an unreliable patient, (4) a patient who cannot do reliable visual fields or in whom the optic disc cannot be visualized, (5) a patient who prefers to be treated, and (6) a patient who has suffered a retinal vascular occlusion.
Ocular hypertension is a statistical concept, but its presence should arouse suspicion of glaucoma. Glaucoma is an optic neuropathy. Screening for ocular hypertension may not be economically sound because of the high false positive detection rate. Glaucoma is without cost until it is treated or too late. If treatment prevents visual loss it is worthwhile. However, treatment may not prevent glaucoma-induced visual loss. It could be argued that it is more economical to ignore glaucoma than to either screen for ocular hypertension or treat glaucoma. Ophthalmologists will continue to disregard these points, partly because they don't believe them or are fearful of liability, but more likely because they are more concerned about an individual person than about statistical proof of benefit and their primary goal is to avoid risk to the patient even if this is not clearly cost-effective. That decision is correct until better techniques are developed for predicting visual field loss and more effective therapies are established to prevent visual field loss.
OBJECTIVE: To determine the frequency with which visual field abnormalities observed on follow-up visual fields for patients in the Ocular Hypertension Treatment Study were confirmed on retest. METHODS: Between April 1, 1994, and March 1, 1999, 21,603 visual fields were obtained from 1637 patients in the Ocular Hypertension Treatment Study. When follow-up visual fields are outside the normal limits on the Glaucoma Hemifield Test, the Corrected Pattern Standard Deviation (P<.05), or both, subsequent follow-up visual fields are monitored to confirm the abnormality. Abnormalities are confirmed if they are again abnormal on the Glaucoma Hemifield Test, the Corrected Pattern Standard Deviation, or both; if the defect is not artifactual; and if the same index and location are involved. Reliability criteria used by the study consisted of a limit of 33% for false positives, false negatives, and fixation losses. RESULTS: Of the 21,603 regular follow-up visual fields, 1006 were follow-up retests performed because of an abnormality (n = 748) or unreliability (n = 258). We found that 703 (94%) of the 748 visual fields were abnormal and reliable, and 45 (6%) were abnormal and unreliable. On retesting, abnormalities were not confirmed for 604 (85.9%) of the 703 originally abnormal and reliable visual fields. CONCLUSIONS: Most visual field abnormalities in patients in the Ocular Hypertension Treatment Study were not verified on retest. Confirmation of visual field abnormalities is essential for distinguishing reproducible visual field loss from long-term variability. Arch Ophthalmol. 2000;118:1187-1194
Ocular hypertension was found in 54 (5.4%) of 1000 consecutive patients of an optometrist. In a separate trial, 50 ocular hypertensive subjects were followed for a mean follow-up time of 6.9 years. Five of the ocular hypertensive subjects (10%) developed primary open angle glaucoma and 2 (4%) developed primary angle-closure glaucoma. No single test could have enabled diagnosis in all five cases that developed open-angle glaucoma. Guidelines are recommended for the optometric management of patients having ocular hypertension.
INTRODUCTION: A practical nomogram has been designed in order to present the results obtained from the Ocular Hypertension Study (Gordon et al. Arch Ophthalmol 2002; 120: 714-720), where the relation between intraocular pressure (IOP) and corneal thickness becomes apparent, involving the risk of evolution from ocular hypertension into glaucoma within a 6 year period. MATERIAL AND METHODS: We used a multiple logarithmic regression for the nine parameters shown in figure 1 of the above mentioned paper. RESULTS: A correlation coefficient of 0.91 (p<0.001) permits to establish the following equation: Probability of evolution (%) = 13539.5 x (1.1385IOP) x (0.9818(CORNEAL THICKNESS)). This implies that a variation of 10 microns on corneal thickness leads to an IOP's modification of 1.5 mmHg in the same sense. From these data, we designed the nomogram included in this paper. CONCLUSIONS: IOP and pachymetry together allow an estimation of the risk of evolution from ocular hypertension into glaucoma in a graphical practical way. From this indirect estimation, the influence of corneal thickness on IOP's measure seems to be much higher than previously estimated.
PURPOSE: The Ocular Hypertension Treatment Study (OHTS) demonstrated that medical treatment of people with intraocular pressure (IOP) of > or =24 mm Hg reduces the risk of the development of primary open-angle glaucoma (POAG) by 60%. There is no consensus on which people with ocular hypertension would benefit from treatment. DESIGN: Cost-utility analysis with the use of a Markov model. METHODS: We modeled a hypothetic cohort of people with IOP of > or =24 mm Hg. Four treatment thresholds were considered: (1) Treat no one; (2) treat people with a > or =5% annual risk of the development of POAG; (3) treat people with a > or =2% annual risk of the development of POAG, and (4) treat everyone. The incremental cost-effectiveness ratio was evaluated. RESULTS: The incremental cost-effectiveness ratios for treatment of people with ocular hypertension were 3670 US dollars per quality adjusted life-year (QALY) for the Treat > or =5% threshold and 42,430 US dollars/QALY for the Treat > or =2% threshold. "Treat everyone" cost more and was less effective than other options. Assuming a cost-effectiveness threshold of 50,000 to 100,000 US dollars/QALY, the Treat > or =2% threshold would result in the most net health benefit. The decision was sensitive to the incidence of POAG without treatment, treatment effectiveness, and the utility loss because of POAG. CONCLUSION: Although the treatment of individual patients is largely dependent on their attitude toward the risk of disease progression and blindness, the treatment of those patients with IOP of > or =24 mm Hg and a > or =2% annual risk of the development of glaucoma is likely to be cost-effective. Delay of treatment for all people with ocular hypertension until glaucoma-related symptoms are present appears to be unnecessarily conservative.
Sixty ocular hypertensive patients receiving no treatment with ocular pressures of 21 mm Hg or more were followed up for a median time of 42 months for changes in ocular pressure. Three significant patterns were observed--stability, downward trend, or an upward trend. The majority of patients showed relatively stable pressures over the course of time. Cyclic swings of pressure over one- or two-year periods were also observed. A group of 43 normal patients with ocular pressures less than 21 mm Hg showed no trends of pressure with time except for three who had a small increase. For some patients, ocular hypertension appears to be a specific entity that represents either stable pressures with time or an episode of increased pressure that eventually decreases. In patients whose pressures continue to increase, ocular hypertension may become true glaucoma. Evaluation of the course of ocular hypertension in relation to diagnosis and treatment is important, especially in terms of the efficacy of treatment.
PURPOSE OF REVIEW: The detection of optic disc and retinal nerve fiber layer damage and change is the cornerstone of glaucoma management. Assessment of the retinal nerve fiber layer for localized and diffuse damage has been traditionally based on clinical examination, with documentation of change primarily qualitative. With the latest improvements in optical imaging instruments, objective and quantitative measurements of the retinal nerve fiber layer are now possible. This review summarizes the results from recent cross-sectional studies evaluating the discriminating ability of automated retinal nerve fiber layer measurements to detect glaucoma, and from longitudinal studies assessing the ability to predict and monitor glaucomatous changes. RECENT FINDINGS: Numerous cross-sectional studies have documented good diagnostic accuracy of a scanning laser polarimeter (GDx VCC), the optical coherence tomograph (Stratus), and the Heidelberg Retina Tomograph retinal nerve fiber layer measurements for differentiating between healthy and glaucoma eyes. There are only limited data available on the ability of these retinal nerve fiber layer measurements to document change over time. SUMMARY: It is essential that the clinician understand the specific strengths and weaknesses of each technique so that only good quality retinal nerve fiber layer information will be used in conjunction with careful clinical examination and visual function testing for glaucoma management decisions. Longitudinal studies are needed to evaluate the ability of these instruments to document retinal nerve fiber layer change over time.
There is substantial evidence that prostaglandins (PG's) mediate acute elevations of intraocular pressure (IOP) due to laser irradiation of the iris. In the present study, we determined the optimal laser parameters needed to produce the maximal rise in IOP in anesthetized rabbits. Application of argon laser (0.75 watts, 0.5 sec. duration, and 8 spots of 500 micron size) to the iris of pigmented rabbits elicited an acute rise in IOP and miosis accompanied by an increase in aqueous protein concentration. This response was followed by a delayed ocular hypotension that lasted for more than 3 days and returned to baseline by day 5. The onset of ocular hypertension occurred within 15 min. and remained elevated for at least 90 min. The laser induced rise in IOP was related more to the number of laser spots applied to the iris than to the intensity of the total laser energy utilized. Pretreatment with either indomethacin or flurbiprofen produced a dose dependent inhibition of ocular hypertensive response and significantly reduced aqueous protein concentration. Indomethacin (0.01-30 mg/kg) was administered intraperitonially 1 hr. before laser treatment and flurbiprofen (0.03-0.3%) was administered topically 45 and 15 min. prior to laser application. The hypertensive response was reduced by more than 90% of control after both drugs, whereas the delayed hypotension was significantly antagonized only at the highest dose of indomethacin. Neither indomethacin nor flurbiprofen altered the maximum miotic response to laser irradiation of the iris. However, 0.3% flurbiprofen and 30 mg/kg indomethacin significantly increased the recovery rate of the miotic pupil. The results of this study support the contention that argon laser induced ocular hypertension may provide a quantitative assessment of inhibition of prostaglandin mediated responses.
The ocular hypotensive effect and the safety of levobunolol hydrochloride (0.5% and 1%) were compared with vehicle in this double-masked study of 42 patients with chronic open-angle glaucoma or ocular hypertension. After a washout of ocular hypotensive medication, patients received one of the three test treatments in both eyes twice daily for three months. Both concentrations of levobunolol produced significant reductions in intraocular pressure, while decreases in vehicle-treated patients were minimal. Over the three-month study period, average pressure reductions were approximately 9.0 mm Hg in patients receiving either concentration of levobunolol and 0.5 mm Hg in patients receiving vehicle. Fewer patients were terminated from the study for inadequately controlled intraocular pressure in the levobunolol groups than in the vehicle group. No patients were terminated for drug-related adverse experiences.
Ocular hypertensive patients were enrolled in a 6-week double-masked safety study of 2% MK-927 (27 patients), a topically active carbonic anhydrase inhibitor, administered bilaterally b.i.d.; 9 additional patients received 0.5% timolol as the control agent. Intraocular pressure (IOP) was measured weekly prior to a.m. drug administration; twelve hour diurnal curves were performed prestudy and at 3 and 6 weeks. The mean reduction of IOP prior to a.m. drug administration ranged from 1.2 +/- 4.4 mm Hg (SD) to 3.0 +/- 4.2 mm Hg with MK-927 and from 4.7 +/- 3.9 mm Hg to 8.8 +/- 0.6 mm Hg with timolol. Mean outflow facility measured tonographically prestudy and on days 33 to 42 four hours after a.m. drug administration was unchanged in both groups. Corneal sensitivity (Cochet-Bonnet), corneal thickness (ultrasound pachymetry), Schirmer tear testing, and extensive ophthalmologic and medical examinations, and hematologic studies were not substantially altered throughout the study. In this longest chronic administration study to date, MK-927 did not cause adverse ocular or systemic side effects.
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PURPOSE: To compare ocular blood flow in untreated primary open-angle glaucoma and ocular hypertension using scanning laser Doppler flowmetry and pulsatile ocular blood flow. METHOD: Fourteen ocular hypertensive subjects and 10 patients with primary open-angle glaucoma were matched for intraocular pressure, mean arterial blood pressure, and age. They had scanning laser Doppler flowmetry images taken centered on the optic disk. Pulsatile ocular blood flow readings were performed in sitting, standing, and supine positions. No subjects were receiving topical antiglaucoma treatment, systemic beta-blockers, calcium antagonists, or nitrates at the time of measurement. RESULTS: Laser Doppler flowmetry results showed a significant reduction in blood velocity, volume, and flow at the lamina cribrosa and the temporal neuroretinal rim in glaucoma compared to ocular hypertension (P < .05). No difference was found between the groups at the nasal neuroretinal rim or the nasal juxtapapillary retina. There was a significant increase in minimum velocity (P = .03) at the temporal juxtapapillary retina in glaucoma compared to ocular hypertension. The ocular pulse amplitude, pulse volume, and pulsatile ocular blood flow were significantly lower (P < .05) in the glaucoma group compared to ocular hypertension in sitting and standing positions. CONCLUSION: Having controlled for factors known to affect perfusion pressure, we found evidence of reduced ocular blood flow in primary open-angle glaucoma compared with ocular hypertension. Our findings indicate a reduction in choroidal and short posterior ciliary artery circulation in primary open-angle glaucoma. Whether these changes in blood flow are a cause or a consequence of glaucomatous optic atrophy is still unknown.
Ocular hypertension (OHT) is defined as intraocular pressure (IOP) elevated above normal levels which occurs without detectable damage to the papilla or visual field. It is considered to be the most important risk factor for developing primary open-angle glaucoma (POAG). The "Ocular hypertension treatment study" (OHTS) addresses the issue of whether lowering IOC before damage to the papilla or visual field occurs can hinder their development and whether OHT can be treated categorically. This randomized, prospective, nonmasked and non-placebo-controlled, multicenter study documents the protective effect of prophylactic lowering of IOC and identifies and explains the risk factors for developing POAG. These include advancing age, reduced corneal thickness, increased pattern standard deviations in white-on-white perimetry, and elevated vertical or horizontal cup to disc ratio. Due to the large individual differences in risk distribution and the very high costs of treating OHT, the question of whether OHT should be treated on principle remains open in the OHTS. This decision must be made on an individual basis after each patient's risk has been assessed.
Thirty patients with ocular hypertension were tested for contrast sensitivity loss. Seventeen were not on treatment, and thirteen were receiving some form of pressure reducing therapy. The contrast sensitivity results of 63% of ocular hypertensive eyes were abnormal (greater than 2 SDs from the age matched norm). Thus it appears that contrast sensitivity can detect early visual loss in patients who have normal visual fields and it is suggested that this test might be used as a criterion for therapy in ocular hypertension. There was no significant difference in the intraocular pressures between patients who gave abnormal contrast sensitivity results and those who did not in the untreated group (p greater than 0.05), suggesting that intraocular pressure level is a poor predictor of optic nerve fibre damage in patients with ocular hypertension.