CLINICAL CHALLENGES

How Low To Go
An unusual glaucoma presentation may provide a template for diagnosis and treatment.
by Eric Schmidt, O.D.

A diminutive woman with a meek voice and a big smile was referred to my practice for a glaucoma evaluation. She told me that her "other doctor" told her she might have glaucoma, but she didn't think so. "My eyes don't hurt and I see very well!" she said. She was 75-year-old African-American with no family history of glaucoma.

Notice the pink color of the neuroretinal rims O.U., as well as the large cup-to-disc ratio.

The referring optometrist was concerned about the presence of normal tension glaucoma based on her optic nerve head appearance, which he estimated to be 0.5/0.5 O.D. and 0.6/0.6 O.S. The referring O.D. had seen her intraocular pressure (IOP) begin to rise over the past five years. In the early 1990's the patient's IOP measured between 12- and 14mmHg O.U. By the time of her referral in 2000, her IOP was consistently 15-16mmHg O.U. Visual fields had been performed twice, both of which showed normal results. The referring O.D. was also concerned that the neuroretinal rims looked paler than normal, thus his referral for another opinion.

She was on two types of medication for hypertension, though she didn't know which. She claimed her blood pressure was good, although it hadn't been checked for at least six months. She also took one aspirin every morning. Her eyeglasses were less than a year old and were +2.75 -0.50 x 90 O.D., + 3.00 -1.00 x 75 O.S. Her corrected visual acuity was 20/30 in each eye through those lenses. Her pupils were 4mm, round O.U. and briskly reactive to light. Slit lamp examination revealed 1+ nuclear sclerotic cataracts, but otherwise entirely healthy anterior segments. Her IOP that first visit was 16mmHg O.D. and O.S. Upon examination of her optic nerve heads (ONH), I noticed the neuroretinal rims were very pink. I was also struck by the relatively large cup-to-disk ratio (C/D) given her hyperopia. I estimated her C/D to be 0.6/0.5 O.D. and 0.6/0.5 O.S. (See the figures, below). (I did not routinely measure pachymetry on glaucoma suspects in 2000).

 I agreed with the referring O.D. with the exception of the nerve pallor. Her C/D was uncommonly large for a normal hyperope and the most significant indicator for glaucoma. However, given her normal visual fields and IOP, I suggested she follow up with her doctor in three months and asked her to return to my office in six months. The patient saw her other optometrist six months later, with IOP at 16mmHg O.U. Visual fields were still normal and IOP was 16mmHg at 3:30 PM in my office. I had my technician perform a GDx nerve fiber layer analysis, which reveal-ed mild to moderate nerve fiber layer attenuation O.D. and mild nerve fiber layer attenuation O.S.

This patient developed a visual field defect three years after initiating IOP therapy.

The Sentinel Sign

My suspicions for NTG were heightened by the GDx results, but they were confirmed when I looked at her ONH again. The C/D appeared to be unchanged O.U. and the neuroretinal rims had not developed any focal notches or pits, but there was a nerve fiber layer hemorrhage present at 11:00 O.D. In spite of normal VF and IOP, the patient did indeed have NTG based on the presence of the nerve fiber hemorrhage. The diagnosis was confirmed by the GDx results.

A treatment challenge

Diagnosing NTG is clinically challenging, possibly more so than primary open angle glaucoma. But, treating NTG can also be a daunting task. In POAG the goal is to lower the IOP into the normal range, but in NTG our chore is to decrease the IOP to the "subnormal" range. The question is how much to reduce IOP and what is the best way to achieve this?

The Collaborative Normal Tension Glaucoma Study (CNTGS) gives clinicians excellent clinical guidance for treating NTG. The CNTGS showed that lowering peak IOP by at least a 20% was beneficial at reducing progression. A 30% of reduction significantly reduced the progression of NTG. There was no difference in rate of progression in regards to treatment options, as long as IOP was reduced by around 30%. This suggests that surgery may be beneficial earlier in this disease process than previously thought. The CNTGS also showed that several VF were necessary before clinicians could identify progression.

Based on the CNTGS, we know that multiple IOP readings are necessary to identify peak IOP, and to make a diagnosis. Closely monitoring the patient's ONH and frequent VF testing are the keys to early identification of progression.

As for our patient, her peak untreated IOP was 16mmHg O.U., so I set a target IOP of 11mmHg, about 30% lower. I prescribed Betoptic S (betaxolol hemihydrate, Vistakon) O.U. bid, but this only lowered IOP to 13mmHg. I changed her medication to Xalatan (latanoprost, Pfizer) O.U. qhs and the IOP reached 11mmHg with great consistency. Despite this "good" IOP, the patient developed a VF defect three years later (See VF images at left). Rather than add another drop, which may have affected her compliance, I opted to try Lumigan (bimatoprost, Allergan) O.U. qhs, in place of Xalatan. This helped achieve a consistent IOP under 10mmHg.

Three years later, the patient's IOP measured 6mmHg O.D., 8mmHg O.S. Her VF and neuroretinal rims remain unchanged. I continue to monitor this patient closely every three months, with yearly VF tests and retinal imaging. Her optic nerves should be examined with a 78 or 60D lens at least twice. If her IOP goes over 10mmHg on a consistent basis, shows progression on VF or neuroretinal rim recession, I would consider adding a second drop, Alphagan p (brimonidine, Allergan) O.U. bid or a topical carbonic anhydrase inhibitor.

I eventually measured this patient's corneal thickness at 478 microns O.D., 470 microns O.S. Given her thin corneas, we can calculate actual initial peak IOP as 19-20mmHg in each eye.

Contributing Editor Dr. Schmidt is director of the Bladen Eye Center in Elizabethtown, N.C. E-mail him at schmidtyvision@bellsouth.net.