When is enough too much? One OD’s perspective on glaucoma therapy

May 22, 2013

One of my favorite glaucoma patients is a 66-year-old white female with unilateral open-angle glaucoma OS. She moved to Augusta from the Midwest, loves my Georgia accent, and swears she’s never shoveling snow again.

One of my favorite glaucoma patients is a 66-year-old white female with unilateral open-angle glaucoma OS. She moved to Augusta from the Midwest, loves my Georgia accent, and swears she’s never shoveling snow again.

When I first saw the patient, I could tell immediately that her Chicago ophthalmologist’s diagnosis was correct. OD was essentially unremarkable, with a healthy optic disc and low intraocular pressure (IOP). OS had undergone an argon laser trabeculoplasty (ALT), and she was taking Xalatan (latanoprost, Pfizer) qhs, Cosopt (dorzolamide and timolol, Merck) bid, and Alphagan P (brimonidine tartrate, Allergan) 0.15% tid in that eye. She really didn’t like the tid drop because she wore multifocal contact lenses to play bridge during the day and hated having to remove her left lens during lunch. Her IOP OS was 10 mm Hg mid-afternoon. Her left optic cup was about 0.6 x 0.8 with a notch at 5:00, and her right optic cup was about 0.3 x 0.3 with healthy rim tissue. I took baseline dilated fundus photos and invited her to return in a week or two for baseline glaucoma testing, this time in the early morning. 

At that visit, her IOP was 12 mm Hg OU, pachymetry values were average OU, and gonioscopy showed she was open to ciliary body with moderate pigment and a flat iris approach in all quadrants OU. Her OCT scans corresponded to her optic nerve appearance, with a dense inferior wedge defect OS and normal findings OD. Threshold visual fields matched these findings, with a dense superior arcuate scotoma OS and a full field OD.

I obtained her medical records and determined that the highest pre-treatment IOP measured was 28 mm Hg in the affected eye. I also found out that her three different drops were initiated at essentially the same time as her ALT-about 4 years prior to her visit with me. I instructed her to return in 2 months to recheck her IOP and visual field. I also asked her to move her second dose of Cosopt to late afternoon instead of bedtime. She complied and returned 2 months later with unchanged IOPs and a stable, repeatable visual field defect.

So I tried something different. I determined that she was getting an excellent IOP decrease (an almost 60% reduction from her pre-treatment IOP). I instructed her to discontinue Alphagan P and leave everything else the same. She returned in another 2 months with unchanged IOPs (around the same time of day). We plugged along for about a year like this, with her taking Xalatan qhs and Cosopt bid OS and me checking IOPs every few months at different points in the day. She loved me because she could wear her contact lenses uninterrupted during the day, and I never measured an IOP of more than 12 mm Hg.

A year later, her optic nerve appearance, visual field defect, and OCT scans were unchanged from my baseline. I decided maybe I could do her one better. I instructed her to drop down to qam on Cosopt, keeping her on Xalatan qhs. Just like before, her IOP didn’t increase, and, just like before, we just kept plugging along. A year later, when there was no detectable structural or functional progression, I decided to see how she did without Cosopt. I instructed her to keep taking the Xalatan qhs OS and no other drops.

We’ve been going like this for 2 years, and I’ve never measured IOPs over 12 mm Hg at any point in the day or detected any structural or functional progression. She loves me, and I’m only now realizing what a quality-of-life change it’s been for her to need only one drop at bedtime.

Several variables about this case warrant discussion. First and foremost is the fact that she very likely will not reap the benefits of her laser procedure forever. The time to 50% failure for ALT-and also selective laser trabeculoplasty (SLT)-tends to be around 2 years,1 and we’re almost a decade out on her. Is she currently gaining any IOP reduction from her ALT? Probably not much. 

Secondly, was her previous doctor a little trigger-happy when he decided to give her an ALT and a prescription for three different drops at the same time? There are several individual patient factors afoot in light of this question. Take her age, for instance. We want to do everything we need to do in order to preserve her vision for the next 2 or so decades that she’ll likely be alive. Do no harm, right? However, when I first saw her I detected obvious perimetric glaucoma, but I didn’t see an optic cup of 0.99 with central vision threatened. If I did, I would have kept her on all three drops and would have likely obtained a consult with a glaucoma surgeon just for good measure (maybe we could get her IOP to 9 mm Hg instead of 12 mm Hg?).2 I would argue that a stepwise approach to dealing with this patient’s IOP would be acceptable. Many times in cases of suspected normal-tension glaucoma (NTG), or sometimes in other forms of glaucoma, I may get a few visual fields and OCTs under my belt before deciding to treat. 

Determining efficacy of therapy is extremely important in glaucoma. However, determining who is going to progress and how quickly that progression is going to take place is paramount. It’s a matter of figuring out with whom we need to be more aggressive or less aggressive. The do no harm argument holds considerable merit, and the last thing we want is to withhold treatment that could preserve vision. The second-to-last thing we want to do is give someone more than she truly needs. For instance, if I identify a glaucoma patient, put him on a prostaglandin and a combination drop, and vision is preserved throughout his lifetime, then I’m the hero. However, if that patient needed only a prostaglandin, then I’ve just cost that person unnecessary amounts of time and money.

Extrapolating beyond the patient in this particular case, there are many factors to consider when dealing with how to treat a newly diagnosed-or newly inherited-glaucoma patient. For instance, was the patient ever on corticosteroids for a long time, then taken off because the condition improved? In other words, did steroids cause ocular hypertension leading to detectable glaucoma, and did cessation of the steroids bring the IOP back down to target? Also, was there ever trauma to the affected eye(s)? Or, am I missing subtle “burned out” angle-recession glaucoma?

Another good question to ask a glaucoma patient is: “Did you ever almost die?” Maybe not asked so morbidly blunt, but look into the patient’s past for evidence of things such as a hemodynamic crisis. See if something could have caused the ganglion cells of the optic disc to die at one time without causing progressive damage.

On the other hand, there will be patients who progress despite achieving a low IOP with multiple drops and even various procedures. There may often be other risk factors, such as various forms of vasospasm, playing a role in ganglion cell death.3 This is especially true in the presence of NTG, but there’s no reason that someone can’t have every vascular risk factor in the world and also just happen to have IOPs in the 30s. As one of my former attendings at SUNY once said, “Patients can have as many diseases as they pleases.”

Of course I recognize that glaucoma is progressive and needs treatment. I also believe that waiting for someone’s glaucoma to become perimetric is waiting too long. However, in most cases, you’ve got time on your side. You’ve got time to iron out various risk factors for progression, maybe even time to get a couple of OCTs and visual fields so you can come to an educated conclusion about how aggressive you need to be. Of course, there will always be those patients who present nearly cupped out who truly need the kitchen sink all at once. 

I will continue to see this patient, every few months at different points in the day, and I will continue to check carefully for structural and functional progression. If I can prove that her glaucoma is getting worse, we’ll start, in a stepwise fashion, additive therapy. However, all I can say for her is “so far, so good.”

The number of untreated people out there with glaucoma who are losing functional vision is truly epidemic. However, taking a step back, breathing, collecting structural and functional data, and going over it in a logical manner before initiating treatment will often help you to not only be highly sensitive, but also quite specific, in the care you give to your patients.ODT


Bovell A, Damji K, Hodge W, et al. Long term effects of lowering intraocular pressure: selective laser argon laser trabeculoplasty? Can J Ophthalmol. 2011 Oct;46(5):408-413.

The Advanced Glaucoma Intervention Study (AGIS). Am J Ophthalmol. 2000 Oct;130(4):429-440.

Anderson D. Normal-tension glaucoma (Low-tension glaucoma). Indian J Ophthalmol. 2011 Jan;59 Suppl:S97-101.