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Use newer technologies to detect glaucoma in challenging patients

The condition is easily missed after LASIK and when IOP is normal.

Issue: January 2017

ByElliot M. Kirstein, OD, FAAO

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Optometrists perform 85% of all eye examinations in the U.S. (Fernando) and are best suited and have the greatest responsibility for recognizing and managing glaucoma suspects and early glaucoma. Given that about half of the 3 million glaucoma patients in this country are undiagnosed (Glaucoma Research Foundation), we have our work cut out for us.

Two types of glaucoma patients in particular — those with normal tension glaucoma (NTG) and glaucomatous post-LASIK patients – are easily missed and too often suffer from the effects of late diagnosis. The challenge of timely diagnosis in these patients is exaggerated by our own human behaviors as well as our technical limitations.

Human factors

The nature of the onset of glaucoma presents management challenges. It is seldom acute and tends to smolder along, so diagnosis can be delayed for any number of reasons.

Consider a patient with borderline IOPs, mildly suspect nerves and possible family history. It is 5 p.m. on Friday, there are two more patients in the waiting room, and you have Lakers tickets. The discussion with that suspect patient can be arduous. After all, you are introducing the notion of a potentially blinding disease to an asymptomatic patient who might also have Lakers tickets.

One way or another, we have all been in situations such as this, and the temptation to jot a few things down and push the whole mess onto the next visit is ever present but harmful to those who deserve prompt attention.

Normal tension glaucoma

Once thought to be rare, NTG tends to be a disease found in older patients, as the mean reported age in clinical studies generally is in the 60s. However, up to 30% of NTG patients will be younger than 50 years, and myopic patients with this disease are significantly younger, with an average age of 42 years. In Japan, NTG accounts for most of those diagnosed with glaucoma (Shiose et al.).

Patients with NTG are likely to be asymptomatic, and in population-based surveys, an average of 30% to 40% of patients diagnosed with a glaucomatous visual field defect have normal IOPs (Klein et al., Dielemans et al.). They are often diagnosed late in the progression of their disease, already having extensive visual field loss.

In patients with NTG, the optic disc rim may be significantly thinner, especially inferiorly and inferotemporally. Visual field defects tend to be more focal, deeper and closer to fixation. It is not unusual for patients with NTG to present initially with dense paracentral scotomas encroaching on fixation. This seems to imply that the disease has probably been present for a long time and has been missed in routine examinations.

Diagnosing NTG

The challenge in diagnosing NTG is that early and even moderate nerve changes, such as nerve fiber layer thinning and increased cup-to-disc ratio, are subtle and, understandably, easy to overlook. Consider a new patient presenting for a routine examination with a 0.45 vertical cup-to-disc ratio. How could one know that 4 years earlier it was 0.25? In contrast to that challenging subtlety, a patient with 30 mm Hg IOPs would be expected to jump out like a red warning light on our dashboard, causing us to take a close second look. For this reason alone, it is understandable that NTG tends to be diagnosed late.

Tracking subtle nerve changes can be nearly impossible, in part because healthy patients tend to move with their insurance plans or retail promotions. We rarely can compare mildly suspicious nerves with data from previous exams with other eye doctors. Without knowing it, we may often examine patients with unusual corneas that may cause our Goldmann tonometers to read significantly low. Routine pachymetry might help, but it is not often used in a typical clinical setting.

The diagnosis of NTG is most often made late in the disease – and only after obvious nerve changes are present. Loss of neural rim and nerve fiber hemorrhage should be head-turners because they are classic signs of normal tension glaucoma yet, unfortunately, even those patients are sometimes overlooked. It is necessary for clinicians to maintain greater sensitivity for subtle nerve changes even if the IOP is normal.

LASIK and glaucoma

Another population that poses a diagnostic conundrum is post-LASIK patients. Research clearly shows LASIK surgery deceptively decreases applanation values (Kaufmann et al., Kirstein et al., Lindfield et al., Pepose et al.). Surgical dissection, thinning and alteration of the cornea in LASIK causes a softening that confuses conventional applanation tonometers, causing them to read unpredictably low.

As of 2011, more than 11 million LASIK procedures had been performed in the U.S. (Lindfield et al.), and those patients are no less prone to have glaucoma than anyone else. In addition, they are all human and too often succumb to the illusion that their eyes have been “fixed,” so they are lost to post-LASIK follow-up. Showing up 15 years later for help with managing their presbyopia, they often fail to mention their old “fix” to their examining doctor. The doctor measures 20 mm Hg with applanation, which may be 29 mm Hg, overlooks the well-healed LASIK scars and misses the opportunity to recognize glaucoma suspicion, thereby delaying the diagnosis. Just consider the possibility that 2.5% (275,000) of the 11 million post-LASIK patients in the U.S. have or probably will have glaucoma (Kaufmann et al., Kirstein et al., Lindfield et al., Pepose et al.).

It is important to be on the lookout for LASIK in our patient histories. It is equally important to be aware of the shortcomings of conventional IOP measurement with these patients. Ultimately, using instruments that are less likely to be inaccurate because of the effects of LASIK on applanation IOP measurement, fewer glaucoma suspects will be missed.

Newer ways to check IOP

Because IOP is a major risk factor and the only available treatment for glaucoma, it makes sense to measure it as accurately as possible. Although Goldmann has often been cited as our gold standard, a wealth of scientific data demonstrate how it may fall short of our expectations as a glaucoma screening device, especially for patients with LASIK and those with atypical corneal properties. Research shows that corneal thickness, corneal properties and keratorefractive surgery will impose significant influence on measured Goldmann values.

IOP is often measured low in both post-LASIK and NTG patients who, ultimately, slip through the cracks and suffer the effects of delayed diagnosis. For patients who have normal IOP readings and only semi-suspicious nerves, the clock keeps ticking, and progression goes undetected.

Two newer technologies can reasonably manage these issues. The Pascal Dynamic Contour Tonometer (DCT) by Ziemer and the Ocular Response Analyzer (ORA) by Reichert Technologies have been shown to be relatively unaffected by individual variations in corneal properties and, most importantly, by corneal changes from LASIK.

The DCT is a novel measuring technique that uses the principle of contour matching instead of applanation. It was designed to eliminate or significantly reduce the systematic errors inherent in all previous tonometers, such as the influence of corneal thickness, rigidity, curvature or elastic properties. DCT values have been shown to remain unchanged in individuals before and after LASIK surgery. The absence of change in measured IOP after LASIK is compelling and reproducible evidence that relative corneal properties seem to have no effect on its ability to measure IOP (Kaufmann et al.).

The ORA delivers a metered collimated air pulse to the cornea, which results in a deformation through the initial applanation and beyond into concavity. The cornea then rebounds through a second applanation event. The inward and outward applanation events are recorded by a sensitive, infrared electro-optical detection system. The ORA’s corneal compensated IOP (IOPcc) considers the differential effect of altered corneal biomechanics, and studies have shown almost no net change in IOPcc before and after LASIK (Kaufmann et al., Kirstein et al., Lindfield et al., Pepose et al.).

Nerve analysis with OCT

In the past 40 years, eye doctors have progressed from colored pencil nerve drawings to precise cross sectional images with 5 microns of resolution. While the past standard of care defined the optic nerve simply in terms of the cup-to-disc ratio, optical coherence tomography now brings us millions of data points to contend with. OCT allows us to measure and document the optic nerve and surrounding tissue so that we can track progression and better understand the pathogenesis of glaucoma.

Having an individual’s OCT history on hand at the time of examination may be our best bet for more timely diagnosis of NTG and glaucoma in LASIK patients. While it is usually difficult now, as access to our patients’ electronic health records improves systems that might retrospectively search for significant nerve structural changes could highlight those LASIK and NTG patients who are at risk.

OCT is here to stay, and our patients deserve the benefits of the higher standard and greater possibilities that it can bring to our clinical decision making process. At present, it is necessary to be vigilant about taking excellent presurgical baseline and follow-up OCT measurements on LASIK patients, which can be made reasonably available for long-term follow-up. Refractive surgery alters our ability to rely on applanation tonometry, and baseline pre-LASIK OCT data can give us a valuable tool to evaluate glaucoma risk in post-LASIK patients. The test takes only seconds to perform, involves minimal cost and helps us make better clinical decisions.

• References:
• Collaborative Normal Tension Glaucoma Study Group. Am J Ophthalmol. 1998;126(4):487-497.
• Dielemans I, et al. Ophthalmology. 1994;101:1851.
• Fernando A, et al. J Ophthalmol. 2015;doi:10.1155/2015/435606.
• Glaucoma Research Foundation. Glaucoma Facts and Stats. www.glaucoma.org/glaucoma/glaucoma-facts-and-stats.php. Updated Nov. 18, 2016. Accessed Dec. 20, 2016.
• Kaufmann C, et al. Invest Ophthalmol Vis Sci. 2003;44:3790-3794. doi:10.1167/iovs.02-0946.
• Kaufmann C, et al. Invest Ophthalmol Vis Sci. 2004;45:3118-3121;doi:10.1167/iovs.04-0018.
• Kirstein E, et al. Optometry. 2005;doi:10.1016/j.optm.2005.08.002.
• Kirstein EM, et al. Tonometry – Past, present and future. www.intechopen.com/books/glaucoma-current-clinical-and-researchaspects/tonometry-past-present-and-future. Published Nov. 9, 2011. Accessed Dec. 20, 2016.
• Klein BE, et al. Ophthalmology. 1992;99(10):1499-1504.
• Lindfield D, et al. Nd:YAG Treatment of Epithelial Ingrowth. Cataract and Refractive Surgery Today Europe. Posted February 2013. Accessed Dec. 20, 2016.
• Pepose JS, et al. Br J Ophthalmol. 1997;81:428-429;doi:10.1136/bjo.81.6.428.
• Pepose JS, et al. Am J Ophthalmol. 2007;doi:10.1016/j.ajo.2006.09.036
• Shiose Y, et al. Jpn J Ophthalmol. 1991;35:133.

• For more information:
• Elliot M. Kirstein OD, FAAO, is director of Harper’s Point Eye Associates in Cincinnati. He can be reached at drkirstein@drkirstein.com.

Disclosure: Kirstein reports he is on the speakers alliance for Alcon, Alliance, Haag-Streit, Optovue and Reichert.