Glaucoma Grand Rounds

Protection for Normal Tension

Although IOPs were normal, a family history spurs glaucoma treatment.

By JAMES L. FANELLI, O.D.

A 51-year-old black male came in for a primary care eye exam. His chief complaint centered on a gradual decrease in clarity to both his distance and near vision.
His last eye examination was about 2 1/2 years earlier, although I hadn’t seen him in 7 years. His medical history was positive for non-insulin-dependent diabetes mellitus (NIDDM), which he was controlling with diet; hypercholesterolemia, for which he was taking Pravachol (pravastatin); and esophageal reflux disease, which he was managing with Prilosec (omeprazole) as needed.

He has a rather strong family history of glaucoma. His sister, a patient in our practice, has advanced open angle glaucoma, and his mother apparently suffered limiting vision loss from glaucoma.

Exam Findings
Following moderate myopic refraction, his best-corrected visual acuity was 20/20 O.U. Pupils reacted briskly to light and accommodation; there was no afferent pupillary defect. Confrontation fields and extraocular muscles were both full. A slit lamp examination of the anterior segments was unremarkable except for some early evidence of limbal arcus. Applanation tensions at 3:18 p.m. were 18mm Hg O.D. and 17mm Hg O.S. Through dilated pupils, his crystalline lenses were clear O.U. The anterior vitreous was clear O.U., also. There was a posterior vitreous detachment in the right eye.

Stereoscopic disc evaluation demonstrated C/D of 0.65 x 0.65 in the right, and 0.7 x 0.7 in the left, with a healthy neuroretinal rim.
The retinal vasculature was characterized by an arteriovenous ratio of 1:3, due partly to mild arteriolarsclerotic retinopathy and partly to mild dilation of the retinal venules from his NIDDM. There was no neovascularization of the disk or neovascularization elsewhere in either eye. I estimated his optic disc size to be approximately 2000µ O.U.1 His posterior pole evaluation at his previous visit was identical to that of this visit.

The patient returned for further testing. Threshold visual fields performed on two separate occasions were unremarkable, as was SWAP perimetry.
We established diurnal curve O.U. Pressures in the right eye ranged from 16-20mm Hg from 8 a.m. through 6 p.m., with the peak IOP at 9:15 a.m. Pressures in the left ranged from 16-21mm Hg, with peak IOP at 8 a.m. Gonioscopy demonstrated 360° open angles O.U. to Von Herrick grade IV; he appeared to have a normal amount of trabecular pigmentation O.U. consistent with his African-American heritage.

Discussion

This case is a classic example where either of two different therapeutic options may be equally correct and efficacious. You can argue for close observation, done every 3-6 months and including tensions, fields, photos and occasional diurnal curves. Or, you can choose therapeutic intervention.

I chose the latter for this individual for several reasons. Foremost was his strong family history. I had the advantage of knowing the specifics of his sister’s glaucomatous condition. She was a few years older, had untreated IOPs in the low 30s, significant optic nerve cupping and damage, and clinically significant visual field loss in both eyes. Establishing IOP control in her case—and subsequent retardation of the progressive visual field loss—was difficult at best. And then there is the issue of his mother’s visual loss, probably due to glaucoma. Another obvious significant risk factor is his African-American heritage.

In looking for other risk factors, the only one that may play a role is the size of his optic nerves. In general, larger optic disc sizes correlate with larger optic cup sizes in non-glaucomatous populations, but larger optic disc sizes seem to correlate slightly with a higher incidence of glaucomatous damage, especially in blacks.2
Secondly, even though perimetry was normal and IOPs were near normal, I had to keep in mind that 20-40% of glaucomatous optic nerve damage occurs with IOPs in the normal range. (We should have a clearer understanding of this at the conclusion of the Ocular Hypertensive Treatment Study.)

In choosing initial therapy, the least amount of medication that does the job is probably best. With that in mind, I considered two options: a non-selective beta-blocker qd or Xalatan (latanoprost) qd.

Both these classes of medications are equally effective. Although latanoprost is not indicated as a first-line medication, studies find that it’s as effective as 0.5% timolol in lowering IOP in ocular hypertensives and glaucomatous patients.3 But I chose Xalatan qd because it could have two distinct advantages over a non-selective beta-blocker in this particular patient. First, he has a history of hypercholesterolemia, and non-selective beta-blockers have the potential to decrease HDL levels.4,5 More importantly, however, is that latanoprost once daily lowers IOP in normotensive patients approximately 20%, while it has a more potent effect in cases of elevated IOP.6,3

In cases such as these, especially since the OHTS study is not yet completed, we must carefully evaluate the individual and all available treatment options prior to setting a course of action. In this case, I suspect highly that the patient will go on to develop frank glaucoma. So intervention now with a medication that has the highest likelihood of pressure reduction in the normotensive population seems the most prudent choice, as long as we do not aggravate other pre-existing conditions in the process.

1. Lim CS, et al. A simple clinical method to measure the optic disc size in glaucoma. J Glaucoma 1996 Aug;5(4):241-5.
2. Balo KP, et al. Correlation between neuroretinal rim and optic disc areas in normal melanoderm and glaucoma patients. J Fr Ophtalmol 2000 Jan;23(1):37-41.
3. Camras CB. Comparison of latanoprost and timolol in patients with ocular hypertension and glaucoma: a six-month masked, multicenter trial in the United States. The United States Latanoprost Study Group. Ophthalmology 1996 Jan;103(1):138-47.
4. Mitchell P, et al. Long-term topical timolol and blood lipids: the Blue Mountains Eye Study. J Glaucoma 2000 Apr;9(2):174-8.
5. Bartlett JD, et al. Central nervous system and plasma lipid profiles associated with carteolol and timolol in postmenopausal black women. J Glaucoma. 1999 Dec;8(6):388-95.
6. Rulo AH, et al. Reduction of intraocular pressure with treatment of latanoprost once daily in patients with normal-pressure glaucoma. Ophthalmology. 1996 Aug;103(8):1276-82.

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