The issue of risk assessment in glaucoma has received increasing attention in the past few years since the publication of results from the Ocular Hypertension Treatment Study. Predictive models have been developed in order to estimate the risk that patients with ocular hypertension will develop glaucoma if left untreated. The purpose of this article is to review issues on the development and validation of predictive models to estimate risk of glaucoma development. Current models are reviewed and details about their development and validation are provided.

Purpose of review

To review current status and future of ambulatory 24-h intraocular pressure monitoring. Despite important advances in the diagnosis and management of glaucoma during the last decade, the fundamental understanding of intraocular pressure, its only modifiable risk factor, remains elusive. The current practice of single intraocular pressure measurements during a clinic visit does not adequately reflect the variability of intraocular pressure throughout the 24-h day.

Recent findings

There has been considerable progress recently with the prototype and commercial introduction of continuous 24-h intraocular pressure monitoring devices. Implantable intraocular pressure sensors have the advantage to directly measure intraocular pressure over many months and years, whereas temporary (contact lens based) approaches provide a noninvasive alternative for repeated 24-h periods. This review provides an overview of implantable devices as well as a critical assessment of a 24-h contact lens sensor.

Summary

Recent advances in microelectromechanical systems and nanoelectromechanical systems have enabled the development of 24-h intraocular pressure monitoring devices. Once these technologies have shown their safety and efficacy, larger questions as to the data interpretation and handling will arise. It is likely that the use of 24-h intraocular pressure monitoring will herald fundamental changes in our understanding and management of glaucoma.

Glaucoma is undergoing a paradigm shift and transitioning from merely disease staging to evidence-based risk assessment of in the individual patient.Initially introduced for ocular hypertensive patients, risk assessment calculators are now being developed for patients with established glaucoma.

The lamina cribrosa (LC) is the presumed site of axonal injury in glaucoma. Its deformation has been suggested to contribute to optic neuropathy by impeding axoplasmic flow within the optic nerve fibers, leading to apoptosis of retinal ganglion cells. To visualize the LC in vivo, optical coherence tomography (OCT) has been applied. Spectral domain (SD)-OCT, used in conjunction with recently introduced enhanced depth imaging (EDI)-OCT, has improved visualization of deeper ocular layers, but in many individuals it is still limited by inadequate resolution, poor image contrast and insufficient depth penetrance. The posterior laminar surface especially is not viewed clearly using these methods. New generation high-penetration (HP)-OCTs, also known as swept-source (SS)-OCT, are capable to evaluate the choroid in vivo to a remarkable level of detail. SS-OCTs use a longer wavelength (1,050 nm instead of 840 nm) compared to the conventional techniques. We review current knowledge of the LC, findings from trials that use SD-OCT and EDI-OCT, and our experience with a prototype SS-OCT to visualize the LC in its entirety. Key Points What is known? •     The LC is the presumed site of axonal injury in glaucoma •     Compared to spectral domain-OCT, enhanced depth imaging-OCT improves imaging of the LC •     Even so, currently used SD-OCT techniques are restricted by poor wavelength penetrance of the deeper ocular layers What our findings add? •    SS-OCT may be a superior imaging modality for deep ocular structures •    Prior studies used SS-OCT to evaluate choroidal thickness in both healthy and 'normal tension glaucoma' eyes •    SS-OCT enables good evaluation of three-dimension (3D) lamina cribrosa morphology. How to cite this article: Nuyen B, Mansouri K, Weinreb RN. Imaging of the Lamina Cribrosa using Swept-Source Optical Coherence Tomography. J Current Glau Prac 2012;6(3): 113-119.

Background

The aim of this article was to study the circadian intraocular pressure (IOP)-related effects of ocular hypotensive medications using a contact lens sensor (CLS).

Design

This is a university-based prospective, randomized, crossover trial.

Participants

A total of 23 patients with primary open-angle glaucoma participated.

Methods

Patients underwent ambulatory recording of IOP-related patterns for 24 h in one eye during 3 monthly sessions using a CLS. Patients were untreated in session 1 (S1), were randomized to one of four classes of glaucoma drops for S2 and had a prostaglandin analogue add-on for S3.

Main outcome measures

Changes in IOP-related patterns were defined using (i) slopes from wake/sitting to sleep/supine; (ii) cosinor rhythmometry modelling; and (iii) area under receiver operating curve (AUC) of sleep period.

Results

Mean patient age was 63.8 ± 11.8 years. Positive linear slopes were seen from wake/sitting to sleep/supine at S1 (17.1 ± 14.2 mVeq/h) and S2 (5.5 ± 23.9 mVeq/h) and negative slopes at S3 (-1.9 ± 29.4 mVeq/h) (S1-S2, P = 0.01; S1-S3, P = 0.02). In the prostaglandin group, slopes changed significantly with introduction of drops (S1-S2, P < 0.024), whereas they did not in a mixed group combining the three other classes (S1-S2, P = 0.060). Overall, cosinor amplitudes were 98.4 ± 46.5 mVeq (S1), 113.0 ± 35.6 mVeq (S2) and 109.6 ± 58.3 mVeq (S3) (S1-S2, P = 0.23; S1-S3, P = 0.66; S2-S3, P = 0.93). AUC were 91.8 ± 63.0 mVeq (S1), 76.3 ± 102.7 mVeq (S2) and 19.9 ± 135.8 mVeq (S3). Differences between sessions were not statistically significant (S1-S2, P = 0.541; S1-S3, P = 0.083; S2-S3, P = 0.092).

Conclusions

Prostaglandin analogues, but not other medications, seem to flatten the IOP-related increase at transition of the wake/sitting to the sleep/supine period, but do not seem to have an effect on acrophase and amplitude.

The recent advent of continuous intraocular pressure (IOP) telemetry has led to an increased awareness of the importance of IOP fluctuations, and theories have emerged that IOP variations could play as much a role in glaucoma progression as the mean level of IOP. The aim of the present study was to evaluate the direct effect of common daily activities on IOP-related profiles. Primary open-angle glaucoma and glaucoma suspect patients were prospectively enrolled from specialist clinics at the University of California San Diego (UCSD), USA. Patients were fitted with a SENSIMED Triggerfish (TF) contact lens sensor (CLS) and were instructed to return to their usual daily activities for 24 h. They were asked to record each specific activity or event in a diary. The protocol was repeated twice. The following events were recorded: "walking/cycling", "resistance training", "yoga/meditation", and "emotional stress". CLS measurements recorded 60-to-30 min prior to each event were used as a baseline reference, and all IOP-related fluctuations for 120 min after the start of each event were reported in relation to this reference. Forty relevant events from 22 CLS recordings in 14 patients were retrieved from the diaries. Walking/cycling (n = 10) caused a small but statistically significant elevation of the IOP-related profile during the activity (p = 0.018). Resistance training (n = 11) caused a persistent elevation of the IOP-related profile from the onset of the activity (p = 0.005) through 120 min after the activity was stopped (p = 0.007). Yoga/meditation (n = 4) caused a sustained drop in the IOP-related profiles through to 120 min, although this was not statistically significant (p > 0.380). Emotional stress (n = 13) was associated with a gradual elevation of the IOP-related profile from the start of the stressful stimulus. Both early and late variations were statistically significant (p = 0.038 and p = 0.021, respectively). The present study suggests that emotional stress and resistance training may be associated with persistent IOP-related profile elevation.

Importance

Glaucoma is a worldwide leading cause of irreversible vision loss. Because it may be asymptomatic until a relatively late stage, diagnosis is frequently delayed. A general understanding of the disease pathophysiology, diagnosis, and treatment may assist primary care physicians in referring high-risk patients for comprehensive ophthalmologic examination and in more actively participating in the care of patients affected by this condition.

Objective

To describe current evidence regarding the pathophysiology and treatment of open-angle glaucoma and angle-closure glaucoma.

Evidence review

A literature search was conducted using MEDLINE, the Cochrane Library, and manuscript references for studies published in English between January 2000 and September 2013 on the topics open-angle glaucoma and angle-closure glaucoma. From the 4334 abstracts screened, 210 articles were selected that contained information on pathophysiology and treatment with relevance to primary care physicians.

Findings

The glaucomas are a group of progressive optic neuropathies characterized by degeneration of retinal ganglion cells and resulting changes in the optic nerve head. Loss of ganglion cells is related to the level of intraocular pressure, but other factors may also play a role. Reduction of intraocular pressure is the only proven method to treat the disease. Although treatment is usually initiated with ocular hypotensive drops, laser trabeculoplasty and surgery may also be used to slow disease progression.

Conclusions and relevance

Primary care physicians can play an important role in the diagnosis of glaucoma by referring patients with positive family history or with suspicious optic nerve head findings for complete ophthalmologic examination. They can improve treatment outcomes by reinforcing the importance of medication adherence and persistence and by recognizing adverse reactions from glaucoma medications and surgeries.

We report the results of repeated ambulatory continuous 24-hour intraocular pressure (IOP) monitoring with a contact lens sensor (CLS) in a glaucoma patient with ocular pain after ab interno trabeculotomy (Trabectome™) surgery. Our findings show that a combined prostaglandin-pilocarpine treatment reduced nighttime IOP peaks and relieved the patient's symptoms.

Precis

Hypotony keratopathy is a potential complication of hypotony following trabeculectomy and successful treatment depends on increasing intraocular pressure (IOP).

Purpose

To evaluate corneal decompensation in patients following trabeculectomy with adjuvant mitomycin C (MMC). We propose "hypotony keratopathy" as a descriptive term.

Methods

Patients with trabeculectomy and follow-up performed by the authors were included in this retrospective single-center study. Patients were included if they had evidence of corneal decompensation (Descemet membrane folds or corneal edema) the following trabeculectomy with MMC with concurrent hypotony. Outcome measures included best-corrected visual acuity, average IOP at time of diagnosis, and changes in central corneal thickness. Clinical outcomes for the treatment of hypotony keratopathy were noted when performed.

Results

A total of 14 eyes from 12 patients were included in the series. Hypotony developed an average of 5 years after trabeculectomy, and hypotony keratopathy was diagnosed 7.5 years after trabeculectomy. Hypotony keratopathy ranged from nonvisually significant Descemet membrane fold without increased corneal thickness to visually significant corneal edema. Best-corrected visual acuity decreased 0 to 6 Snellen lines after diagnosis of hypotony keratopathy. Lower IOP was associated with increased corneal thickness. Vision improved after trabeculectomy revision (6 eyes) and cataract extraction with an intraocular lens implant (1 eye) but did not improve after Descemet stripping automated endothelial keratoplasty (2 eyes).

Conclusions

Hypotony keratopathy is a poorly described but potentially treatable complication of trabeculectomy with MMC. Hypotony keratopathy may be related to endothelial dysfunction secondary to hypotony.