Preventing Blindness Due to Glaucoma
HIGHLIGHTS FROM THE 2008 NATIONAL GLAUCOMA SYMPOSIUM
Preventing Blindness Due to Glaucoma
A specialist offers advice for protecting your patients' vision.
By Peter Libre, MD, Norwalk, Conn.
AS A GLAUCOMA SPECIALIST, I'm continually surprised and frustrated by the number of people who could've been spared significant vision loss if they'd received better care earlier in the disease process. Part of my mission is to educate primary care practitioners on the front lines to avoid these outcomes.
Perhaps the biggest mistake is believing that IOP measurement and HRT/GDx/OCT are all that's needed to keep patients out of trouble. Gonioscopy and careful observation of the disc are essential. This article highlights these skills and other glaucoma examination elements that can prevent many patients from losing their vision.
When evaluating whether an angle is occludable, be sure to use a small, dim beam. A bright, tall, wide beam will constrict the pupil and change many narrow angles into temporarily wide angles. However, after an initial view with dim light, brighten the beam (and/or indentation) to open the angle.1 This will help to confirm whether the pigmented line is Sampaolesi's line (pigment on Schwalbe line, the termination of the corneal endothelium), posterior pigmented trabecular meshwork or ciliary body. And that white line: was it anterior trabecular meshwork or scleral spur? Widening the angle also will show synechiae to the scleral spur or meshwork.
Remember that patients whose angles remain narrow despite iridotomy usually have plateau configuration: the ciliary body is rotated anteriorly, so the iris root is pushed forward. Iridotomy, to relieve that portion of the narrowness due to relative pupillary block, will keep most plateau patients out of trouble. Angle closure in a patient who already has had an iridotomy can be treated with pilocarpine, but ultimately will require either lens extraction or iridoplasty, although I prefer lens extraction to avoid inflammation and recurrence of the problem.
|Dr. Libre is a board certified ophthalmologist in solo practice in Norwalk, Conn. You can reach him at email@example.com.|
Evaluate the Rim
Evaluating the rim is crucial to avoid overlooking glaucoma in patients whose IOP isn't high. If you have a 78D or 90D lens, you can view the disc of almost every patient without dilating the pupil. Look for signs of rim erosion. Judge the rim loss on a scale of 0 to 4 plus. This will make you more attentive to rim loss (as opposed to simply estimating cup-to-disc ratios). Check for rim hemorrhages at every visit of every glaucoma patient, even though disc hemorrhage is present less than 5% of the time. Hemorrhages often are the earliest indicator of progression and the need for more aggressive therapy.
Also, watch for peripapillary atrophy. This is can be normal in myopes, but often is seen around damaged portions of glaucomatous discs.
Evaluate the Disc
Determine if the disc is small, medium or large. When using optical coherence tomography (OCT), you can see how much of the circle is filled by the disc. When using ophthalmoscopy, I rely on a 78D lens, mindful that a 1.5-mm height split beam corresponds to an average optic nerve diameter.
For a patient with a large nerve, such as 1.8 mm or 2.0 mm, a cup-to-disc ratio of .6 or .7 can be normal. On the other hand, a ratio of .4 could represent significant disease in a small disc.
Compliance will always be a challenge, especially during the first half of the disease process. Patients with severe glaucoma typically are compliant because they appreciate the vision they have lost. However, many asymptomatic patients stop taking their medications for months or even years, making a case for the early use of selective laser trabeculoplasty (SLT).2
Noncompliance often is associated with chronic use of medications that aggravate the ocular surface. Reducing the dosing frequency may improve ocular surface comfort without compromising IOP. For example, I'm not aware of any studies demonstrating that twice daily dosing of beta-blockers is more effective than once daily dosing. Morning is preferable since evening dosing can lower blood pressure undesirably, and nocturnal IOP is minimally influenced by beta-blockade.
Furthermore, prostaglandins can be dosed (off-label) every other day in patients who don't require maximum IOP reduction. Travaprost probably is the longest acting medication: if given every other day, IOP usually runs about 1 point higher on the second day.
Watch for Comorbidities
High myopia3 and pseudoexfoliation4 are comorbidities that can lead to more severe glaucoma. Consider these factors:
■ High myopia. When the correction is greater than roughly 5D, the lamina cribosa often is stretched thin (which means cupping will be more shallow and difficult to discern). At the same time, the thinned lamina is more vulnerable to backward bowing with pressure. Moreover, the nerve may be obliquely inverted, making the shallow cupping even more difficult to visualize. I've seen several high myopes who are practically blind because their glaucomatous cupping (with normal IOPs) eluded detection. Consider administering visual fields for these patients every few years, even if you have no other reason to suspect glaucoma.
■ Pseudoexfoliation. Many patients with this condition suffer from severely damaged nerves later in life. The earliest sign is atrophy of the pupillary ruff of the iris. This sign often appears before the characteristic dandruff-like material on the lens or the edge of the pupil, and before the exfoliative pattern on the anterior capsule. Always examine the lenses of older patients very carefully.
■ Intraocular pressure. IOP can increase rapidly, sometimes rising significantly from 20 mmHg to 40 mmHg in 6 to 12 months. Also, IOP fluctuates more in pseudoexfoliation, so an IOP of 20 in the office may indicate upper 20s on other occasions. Monitor more frequently — especially if the patient is 75 years or older or if the patient's IOP already is near 20 — treat early and consider referral for SLT.
Measure Central Corneal Thickness
The average corneal thickness is roughly 550 microns in Caucasians, and about 530 microns in African-Americans. There is uncertainty about how much to adjust IOP for CCT. Some doctors advise simply considering corneas as thick, thin or normal. However, I associate a 100-micron deviation from average thickness with the equivalent of about 7 mmHg of IOP, give or take 2 mmHg. As a result, you can dramatically underestimate IOP when corneal thickness is 450 microns, or you can do the opposite when the thickness reaches 650 microns.
IOP may not be wrongly measured by 7 mm for every 100 micron deviation of CCT, but it seems that CCT also may reflect structural integrity of the lamina cribosa. So, with a 450 CCT, the IOP may not be 7 points higher than measured, but after accounting for increased IOP sensitivity of the disc, the glaucoma may behave as though IOP is 7 points higher than measured. Therefore, with a corneal thickness of 450 microns and an IOP of 21 mmHg, I would treat the patient as if he were in the mid to upper 20s.
Evaluate Family History
Family history is important.5 The prevalence of glaucoma among patients with parents or siblings who've had glaucoma was as high as 10.4% in the Rotterdam Eye Study.6 Remember to take a discriminating approach, however, focusing more on parents and siblings and less on extended-family relatives. Age of death or onset of disease in parents also is important. Number of siblings, their ages and incidence of glaucoma among them are also significant factors.
Always ask the right follow-up questions when a patient says one of his parents had glaucoma. Was it really cataract surgery? Find out if the parent was using glaucoma drops and, if so, how many types of drops. Ask if vision was damaged to distinguish between a close relative who went blind and one who simply used drops for a thick cornea. Remember that corneal thickness is heritable. Many patients with thick corneas have parents with thick corneas who were treated unnecessarily.
To summarize, the history of a parent who developed glaucoma at age 50, used three types of drops simultaneously, and lost vision at 75 is much more worrisome than a grandparent who began using one bottle of drops at age 75 with no vision loss at 85.
Consider Non-IOP Factors
You may encounter a patient with glaucomatous optic neuropathy with midteens IOP and average corneal thickness. Look for hemorrhages. Hypoperfusion of the optic nerve may be a factor, typically in the presence of low-tension glaucoma.7 Watch for the following signs or symptoms in these patients:
■ Low blood pressure
■ Vasospasm, such as the type associated with symptoms of Raynaud's phenomenon
An important consideration is perfusion pressure, which is the blood pressure minus the IOP. Lowering IOP or raising blood pressure increases blood flow to the nerve head.
Sometimes, it's clinically appropriate to raise blood pressure. For example, if a patient (usually a thin middle-aged woman) runs a BP of 90/55, and has progressive glaucoma with low IOP, I encourage increased consumption of salt. If BP remains less than 110/70, I advise the patient to take licorice extract (glycyrrhizin, a mineralocorticoid agonist). Another option is prescription oral fludrocortisone (consultation with an internist would be advisable).
Elderly patients undergoing treatment for high blood pressure may have optic nerve hypoperfusion when sleeping (BP usually drops while asleep). Consider the possibility that hypertension is being treated too aggressively if you see disc hemorrhages, despite low IOP. If these patients aren't at special risk for cardiac complications or stroke, ask their internists to manage their blood pressure less aggressively, allowing it to drift up to 130/80 mmHg.
Another non-IOP factor to keep in mind is the cerebral spinal fluid (CSF) pressure. The retrolaminar portion of the optic nerve is at CSF pressure (since it is surrounded by it). If it's low, it's easier for IOP to displace the lamina posteriorly. Research suggests that IOP is less important than the difference between IOP and CSF.8
Striving for the Best Possible Outcomes
There is no single solution to prevent blindness in glaucoma patients. But if you follow these guidelines, you'll go a long way toward meeting our most important of objectives — preserving vision. nOD
- Friedman DS, He M. Anterior chamber angle assessment techniques. Surv Ophthalmol. 2008;53:250-273.
- McIlraith I, Strasfeld M, Colev G, Hutnik CM. Selective laser trabeculoplasty as initial and adjunctive treatment for open-angle glaucoma. J Glaucoma. 2006;15:124-130.
- Mayama C, Suzuki Y, Araie M, Ishida K, Akira T, et al. Myopia and advanced-stage open-angle glaucoma. Ophthalmology. 2002;109:2072-2077.
- Aström S, Stenlund H, Lindén C. Incidence and prevalence of pseudoexfoliations and open-angle glaucoma in northern Sweden: II. Results after 21 years of follow-up. Acta Ophthalmol Scand. 2007;85:832-837.
- van Koolwijk LM, Despriet DD, van Duijn CM, Pardo Cortes LM, Vingerling JR, et al. Genetic contributions to glaucoma: heritability of intraocular pressure, retinal nerve fiber layer thickness, and optic disc morphology. Invest Ophthalmol Vis Sci. 2007;48:3669-3976.
- Wolfs RC, Klaver CC, Ramrattan RS, van Duijn CM, Hofman A, et al. Genetic risk of primary open-angle glaucoma. Population-based familial aggregation study. Arch Ophthalmol. 1998;116:1640-1645.
- Ishida K, Yamamoto T, Sugiyama K, Kitazawa Y. Disk hemorrhage is a significantly negative prognostic factor in normal-tension glaucoma. Am J Ophthalmol. 2000;129:707-714.
- Berdahl JP, Allingham RR, Johnson DH. Cerebrospinal fluid pressure is decreased in primary open-angle glaucoma. Ophthalmology. 2008;115:763-768.
Optometric Management, Issue: October 2008