Clinical Challenges
The Case that Shouldn't Have Happened
The late diagnosis of glaucoma.
By Eric Schmidt, O.D.

We speak of glaucoma as being slowly progressive. We tell our glaucoma patients that we can usually control their condition with drops or surgery and that it can, but shouldn't, be a blinding condition. But certain cases don't follow the rules. Sometimes glaucoma isn't diagnosed until late in the disease. Every time this occurs I ask myself, "How could this happen?"

THE CASE: At our first meeting, Winford was smiling, but something seemed amiss. Winford was a 45-year-old African-American who, with embarrassment, stated that this was his first visit to an eye doctor. He said he was having difficulty seeing up close but as I spoke with him, I sensed that he was more worried about his eyes than he was expressing.

After the standard questions, he blurted out that he was seeing a "shadow" over his eyes at times and that he was missing things that he knew he should be able to see. He denied any pain, redness or discharge and said that it seemed his eye problems had been slowly getting worse over the past few months.

On the trail

Winford denied any health problems, wasn't taking any medications and said that he didn't know of a family history of eye disease. His uncorrected visual acuity at distance was 20/20 in each eye. His pupils were 6 mm in size, round and reactive to light OU with no afferent pupillary defect.

Using the confrontation visual field method, I discerned that his visual fields (VFs) were extremely constricted OU. Though it's a gross way of assessing for VF defects, this method does pick up central defects with fair sensitivity. I estimated that he had only about a 10-degree field remaining superiorly and inferiorly.

My slit lamp examination looked normal. Before dilating, I checked the intraocular pressure (IOP). It measured 38 mm Hg OD, 37 mm Hg OS. I also performed gonioscopy, which revealed Grade 3 and 4 open angles throughout, OU. I saw no peripheral anterior synechiae or angle debris.

Extreme damage

Before I checked his IOP, I was concerned that Winford's gross VF constriction was neurologic in nature. But with his IOP in the upper 30s, it seemed more likely that his condition resulted from open-angle glaucoma. This was confirmed when I examined his optic nerves after dilation.

The optic nerve head (ONH) OD showed extreme cupping, which I estimated at .95/.95. The remaining neuroretinal rim was thin 360 degrees around, but pink. A moderate ring of peripapillary atrophy encircled the ONH. The ONH OS showed even more pronounced damage, as there was no neuroretinal rim left inferiorly from 4:00 to 7:00. The remaining rim tissue was thin, but pink and a ring of peripapillary atrophy also surrounded this ONH.

With a red-free filter I saw marked nerve fiber layer dropout superiorly and inferiorly OU. The remaining retinal grounds were normal, as was the caliber of the blood vessels.

Winford had severe open-angle glaucoma. The IOP had to have been elevated for a long time to cause the extreme nerve damage. My immediate concerns were to reduce Winford's IOP dramatically and to assess how much VF remained. I instilled one drop of timolol maleate (Timoptic XE 0.5%) into each of his eyes and explained that he could go blind unless we could lower his IOP substantially. He told me that he understood the severity of his condition.

I gave him a prescription for the timolol OU q.a.m. and told him to return in 1 week for a VF test and IOP check. Winford asked if the medicine was expensive because he was on a tight budget and had no drug coverage through his insurance plan. I gave him a sample bottle of the drop and told him that I would try to keep him adequately supplied, but that he must use the drops every morning.

A continuing challenge

A week later, Winford returned for his VF test. As expected, it showed extreme constriction in both eyes with small central islands remaining temporal to only about 5 degrees OU. IOP was 28 mm Hg OD, 27 mm Hg OS. The 10 mL timolol maleate still wasn't enough to achieve a safe IOP level. I added brimonidine tartrate (Alphagan 0.2%) OU b.i.d. to the timolol maleate and used the VF printout to show Winford how dire his condition was.

Two weeks later, his IOP was 21 mm Hg OD, 22 mm Hg OS on the two drops -- still not low enough. I prescribed dorzolamide HCl 2.0% and timolol maleate 0.5% (Cosopt) OU b.i.d. in place of the timolol and told him to continue the brimonidine OU b.i.d. That got his IOP to 18 mm Hg OD, 15 mm Hg OS.

Winford could lose his remaining field of vision quickly if we didn't achieve an adequate IOP level. But how low did I need to go?

The norm and the exception

Studies and conventional wisdom say that an initial drop of 30% from the peak IOP should be the target. However, in cases of severe VF loss such as this where central fixation is threatened or already involved, a target of at least a 50% reduction is needed. It may need to be even lower if the patient is younger.

Our goal is to keep the patient's level of vision useful for his lifetime. In Winford's case, because of the extreme damage and his relative youth, this would be difficult. We had achieved an IOP decrease of more than 50%, but I felt the IOP needed to be even lower.

I arranged for an argon laser trabeculoplasty (ALT) to be performed at the temporal 180 degrees of the trabecular meshwork OU. The IOP dropped to 14 mm Hg OD and OS 1 month post-laser on the two drops (dorzolamide/timolol and brimonidine), but Winford was despondent because the drops affected his sexual performance. Topical beta-blockers can cause impotence, so I discontinued the dorzolamide and timolol and began latanoprost 0.005% (Xalatan) OU q.h.s. along with brimonidine tartrate OU b.i.d.

Ultimate outcome

Winford's IOP never got below 20 mm Hg on lantanoprost and brimonidine. When I added brinzolamide 1% (Azopt) OU b.i.d., the IOP did lower to 16 mm Hg, but Winford's compliance with three drops was less than stellar. Cost was also a big issue.

Six weeks ago, Winford underwent a trabeculectomy OS. This was risky because of the fragile remaining optic nerve. Fortunately, he has responded well. His IOP at his last visit was 19 mm Hg OD, 9 mm Hg OS. He's taking bimatoprost ophthalmic solution 0.03% (Lumigan) OU q.d., brimonidine OU b.i.d. and brinzolamide OD b.i.d. without side effects and with good compliance. He's to undergo a trabeculectomy OD soon. Eventually I'll try to get him to one drop in each eye, but only after I'm sure his IOP is stable.

When glaucoma presents late, a quick 50% reduction in IOP is vital to preserve whatever VF remains. Use any means to reach the IOP target and be honest with the patient. This may help improve his compliance with therapy and his understanding of the disease. Both will encourage a better outcome.

Contributing Editor Eric Schmidt, O.D., is director of the Bladen Eye Center in Elizabethtown, N.C. E-mail him at KENZIEKATE@aol.com.