CONTINUOUS INTRAOCULAR PRESSURE MONITORING WITH A WIRELESS OCULAR TELEMETRY SENSOR: INITIAL CLINICAL EXPERIENCE IN PATIENTS WITH OPEN ANGLE GLAUCOMA

Mansouri K, Shaarawy T*
British Journal of Ophthalmology, January 2011

How Close Are We to Continuous 24-hour IOP Measurement?

Elevated IOP is a leading risk factor for the development and progression of glaucoma and the only treatable one.1 The current clinical gold standard for measuring IOP is Goldman applanation tonometry (GAT). GAT's major limitation is that it only provides a snapshot, usually taken during regular office hours, of the very dynamic parameter that is IOP. IOP varies throughout the night and day, is affected by body posture,2 and in many patients may be highest outside the usual office hours.3 Medications that reduce IOP also have a variable IOP-lowering effect throughout the 24-hour cycle.4-6 By measuring IOP only during office hours, the clinician may be left without valuable information when planning, prescribing, and adjusting glaucoma treatment. In the past several decades, many have searched for an implantable permanent device or a removable temporary one to monitor IOP continuously in humans.7

In this article, Mansouri and Shaarawy8 describe the first clinical experience with a novel technology for continuous IOP monitoring. In a small group of open-angle glaucoma patients, the investigators used the Sensimed Triggerfish (Sensimed AG, Lausanne, Switzerland), a soft contact lens with an embedded microelectromechanical system with wireless communication developed by Leonardi et al.9 The microfabricated strain gauge works by recording the change in curvature at the level of the corneoscleral junction. A change in curvature of about 3 μm corresponds to a change in IOP of about 1 mm Hg.9 This relationship is based on the assumption of a linear correlation but may differ depending on the level of pressure.

Fifteen patients who showed signs of glaucomatous progression despite controlled IOPs during their routine office visit underwent 24-hour monitoring with this device. Because the data obtained are provided in an arbitrary unit, GAT was performed before and after the sensor's installation to obtain approximations. In almost 70% of the cases, the highest values were detected during nighttime hours, in agreement with data obtained from prior traditional sleep laboratory studies.10 Individual patterns, fluctuations, and peaks that occurred in between time points of low IOPs were also detected. Based on these findings, the authors adjust treatment for some patients.

For the first time, IOP data collected continuously for 24 hours without possible artifacts associated with nocturnal arousal could be observed.1 Although the device provides IOP information in arbitrary units and may be affected by corneal thickness and rigidity, it may provide an opportunity to better understand IOP fluctuations under physiologic and therapeutic conditions.

*Financial disclosures: Dr. Mansouri is a consultant to Sensimed AG. Dr. Shaarawy holds no proprietary interests in the materials discussed herein.

COMBINING STRUCTURAL AND FUNCTIONAL MEASUREMENTS TO IMPROVE DETECTION OF GLAUCOMA PROGRESSION USING BAYESIAN HIERARCHICAL MODELS

Medeiros FA, Leite MT, Zangwill L, Weinreb RN* Investigative Ophthalmology and Visual Science, June 2011

A New Methodology for Combining Longitudinal Information From Structural and Functional Tests to Improve the Detection of Glaucomatous Progression and Estimate the Rate of Change

Clinicians routinely compare structural and functional information to subjectively determine if glaucomatous progression has taken place. Previous studies have focused on describing how structural findings relate to functional findings or vice versa,11 but relatively little has been done to use this information together to objectively determine glaucomatous progression in a formal way.

In this study, Medeiros and colleagues propose a new methodology for combining longitudinal information from structural and functional tests to improve the detection of glaucomatous progression and estimate rates of change. As explained by the authors, this approach is based on joint modeling of longitudinal changes using Bayesian hierarchical models. Joint modeling enables a better characterization of the true underlying relationship between structural and functional tests. Information derived from one test is allowed to influence the inferences obtained from the other test. In other words, a change in the visual field that would otherwise be declared not statistically significant by an analysis of visual field data alone might be declared significant after considering the structural changes occurring in the same eye.

This study included 257 participants who were observed for an average of 4.2 ±1.1 years. Included patients had glaucoma, were suspected of having glaucoma, or were healthy and annually with standard automated perimetry, optic disc stereophotographs, and scanning laser polarimetry with enhanced corneal compensation. The rates of change over time were measured using the visual field index (VFI) and average thickness of the retinal nerve fiber layer.

The current Humphrey visual field tests (Carl Zeiss Meditec, Inc., Dublin, CA) analyse the rate of VFI change over time using ordinary least squares (OLS) linear regression. In a comparison of the Bayesian method with the OLS method, the Bayesian method showed greater sensitivity and specificity. It also identified a significantly higher proportion of glaucoma and suspect eyes as having progressed compared to the OLS method (22.7% vs 13%; P < .001). In addition, the Bayesian method identified a significantly higher proportion of eyes with progression by optic disc stereophotographs compared to the OLS method (74% vs 37%; P =.001). Of the 29 healthy eyes, none as identified as progressing by Bayesian slopes of change for VFI or retinal nerve fiber layer thickness average, resulting in a specificity of 100% (95% confidence interval: 88%-100%) for the combined method.

The authors concluded that the Bayesian hierarchical modeling approach for combining functional and structural tests performed significantly better than the conventional OLS method for the detection of glaucomatous progression, and they therefore suggested that this approach may provide better estimates of rates of change.

YAG LASER PERIPHERAL IRIDOTOMY FOR THE PREVENTION OF PIGMENT DISPERSION GLAUCOMA: A PROSPECTIVE, RANDOMIZED, CONTROLLED TRIAL

Scott A, Kotecha A, Bunce C, et al*
Ophthalmology, March 2011

Does Nd:YAG Laser Peripheral Iridotomy Significantly Reduce the Incidence of Conversion From Pigment Dispersion Syndrome With Ocular Hypertension to Pigmentary Glaucoma?

To date, the natural history of pigment dispersion syndrome has been characterized poorly. There has been scarce and conflicting information on the prevalence of the condition and the rate of conversion from pigment dispersion syndrome with ocular hypertension to pigmentary glaucoma. 12 There is also conflicting evidence as to when to perform laser peripheral iridotomy (LPI) during the course of this condition and whether it is beneficial.13-17 To address the question of whether Nd:YAG LPI prevents progression from pigment dispersion syndrome with ocular hypertension to pigmentary glaucoma, Scott et al conducted this prospective, randomized, controlled 3-year trial of 116 patients with pigment dispersion syndrome and ocular hypertension. Of 116 patients, 57 were randomized to LPI and the remaining patients to observation. The primary outcome measure was the conversion to pigmentary glaucoma within 3 years, based on an analysis of full-threshold visual field using the Ocular Hypertension Treatment Study criteria. Surprising to some, of the 105 eyes that completed the study, eight eyes (15%) in the laser group and three eyes (6%) in the control group converted to glaucoma. The authors acknowledged that there were a few sources of potential imprecision or bias in their study. Determining the main outcome as conversion based on the analysis of full-threshold visual fields might lack precision. They also suggested that, although iris concavity was one of the inclusion criteria, it was estimated subjectively and not measured by ultrasound biomicroscopy. The strength of this prospective study would have been improved if the authors had taken their analysis a step further and expanded on imaging of the anterior segment. They could have evaluated the anatomical and dynamic iris factors that might predispose individuals with pigment dispersion syndrome to progress to pigmentary glaucoma in spite of a patent LPI eliminating reverse pupillary block. An example of this would have been to evaluate the location of the insertion of the iris, as posterior iris insertion predisposes to the phenotypic expression of pigment dispersion syndrome and progresses to pigmentary glaucoma.18 As the authors acknowledged, the hypothesis assumes iridozonular contact as an explanation for pigment dispersion.19 If there is no documented evidence of contact, it is possible that there may be more than one mechanism for pigment dispersion and, therefore, different degrees of response to LPI.

In summary, despite its limitations, the authors concluded that this study provided little evidence to support the use of Nd:YAG LPI in patients with pigment dispersion syndrome and established ocular hypertension during its 3-year period. The authors suggested that a possible explanation for their findings might be that the onset of ocular hypertension in pigment dispersion syndrome indicates a combination of pathologic changes that are irreversible20 and, hence, any intervention to decrease pigment release once ocular hypertension is established, such as an Nd:YAG LPI, might be ineffective. They acknowledged, however, that it is possible that the treatment might be effective in patients without irreversible trabecular meshwork damage or in those with a documented increase in iridozonular contact.

Financial Disclosures: The authors cited that they have no proprietary interest in the material discussed herein.

Section Editor James C. Tsai, MD, is the chairman and Robert R. Young professor of ophthalmology and visual science at Yale University School of Medicine in New Haven, Connecticut. He acknowledged no financial interest in the products or companies mentioned herein. Dr. Tsai may be reached at (203) 785-7233; james.tsai@yale.edu.

Tomas M. Grippo, MD, is an assistant professor in ophthalmology at Yale University Department of Ophthalmology and Visual Science in New Haven, Connecticut. He acknowledged no financial interest in the products or companies mentioned herein. Dr. Grippo may be reached at (203) 785-2020; tomas.grippo@yale.edu.

  1. Liu J, Weinreb R. Monitoring intraocular pressure for 24 h. Br J Ophthalmol. 2011;95:599-600.
  2. Prata TS, De Moraes CG, Kanadani FN, et al. Posture-induced intraocular pressure changes: considerations regarding body position in glaucoma patients. Surv Ophthalmol. 2010;55:445-453.
  3. Mosaed S, Liu JH, Weinreb RN. Correlation between office and peak nocturnal intraocular pressures in healthy subjects and glaucoma patients. Am J Ophthalmol. 2005;139:320-324.
  4. Bagga H, Liu JH, Weinreb RN. Intraocular pressure measurements throughout the 24 h. Curr Opin Ophthalmol. 2009;20:79-83.
  5. Liu JH, Medeiros FA, Slight JR, Weinreb RN. Comparing diurnal and nocturnal effects of brinzolamide and timolol on intraocular pressure in patients receiving latanoprost monotherapy. Ophthalmology. 2009;116:449-454.
  6. Liu JH, Medeiros FA, Slight JR, Weinreb RN. Diurnal and nocturnal effects of brimonidine monotherapy on intraocular pressure. Ophthalmology. 2010;117:2075-2079.
  7. Sit AJ. Continuous monitoring of intraocular pressure. Rationale and progress toward a clinical device. J Glaucoma. 2009;18:272-279.
  8. Mansouri K, Shaarawy T. Continuous intraocular pressure monitoring with a wireless ocular telemetry sensor: initial clinical experience in patients with open angle glaucoma. Br J Ophthalmol. 2011;95:627-629.
  9. Leonardi M, Leuenberger P, Bertrand D, et al. First steps toward noninvasive intraocular pressure monitoring with a sensing contact lens. Invest Ophthalmol Vis Sci. 2004;45:3113-3117.
  10. Liu JHK, Zhang X, Kripke DF, Weinreb RN. Twenty-four hour intraocular pressure pattern associated with early glaucomatous changes. Invest Ophthalmol Vis Sci. 2003;44:1586-1590.
  11. Hood DC, Anderson SC, Wall M, Kardon RH. Structure versus function in glaucoma: an application of a linear model. Invest Ophthalmol Vis Sci. 2007;48(8):3662-3668.
  12. Scott A, Kotecha A, Bunce C, et al. YAG laser peripheral iridotomy for the prevention of pigment dispersion glaucoma: a prospective, randomized, controlled trial. Ophthalmology. 2011;118(3):468- 473.
  13. Karickhoff JR. Pigmentary dispersion syndrome and pigmentary glaucoma: a new mechanism concept, a new treatment, a new technique. Ophthalmic Surg. 1992;23:269-277.
  14. Karickhoff JR. Reverse pupillary block in pigmentary glaucoma: follow up and new developments [letter]. Ophthalmic Surg. 1993;24:562-563.
  15. Campbell DG, Schertzer RM. Pathophysiology of pigment dispersion syndrome and pigmentary glaucoma. Curr Opin Ophthalmol. 1995;6:96-101.
  16. Gandolfi SA, Vechi M. Effect of a YAG laser iridotomy on intraocular pressure in pigment dispersion syndrome. Ophthalmology. 1996;103:1693-1695.
  17. Reistad CE, Shields MB, Campbell DG, et al. American Glaucoma Society Pigmentary Glaucoma Iridotomy Study Study Group. The influence of peripheral iridotomy on the intraocular pressure course in patients with pigmentary glaucoma. J Glaucoma. 2005;14:255-259.
  18. Kanadani FN, Dorairaj S, Langlieb AM, et al. Ultrasound biomicroscopy in asymmetric pigment dispersion syndrome and pigmentary glaucoma. Arch Ophthalmol. 2006;124(11):1573-1576.
  19. Campbell DG. Pigmentary dispersion and glaucoma: a new theory. Arch Ophthalmol. 1979;97:1667-1672.
  20. Alvarado JA, Murphy CG. Outflow obstruction in pigmentary and primary open angle glaucoma. Arch Ophthalmol. 1992;110:1769-1778.