Treating glaucoma patients can be a work of art, not just science

Issue: October 25, 2010

ByRichard L. Lindstrom, MD

Richard L. Lindstrom

The diagnosis and treatment of glaucoma is an art. Despite dozens of textbooks, preferred practice patterns and multiple well-designed prospective clinical trials that help us understand how the average or typical patient behaves, we busy clinicians know that in glaucoma, art often dominates over science.

In the cataract patient, for a given IOL, I use the same size capsulorrhexis, the same personalized A-constant, the same viscoelastic, and outcomes are, in most patients, consistent in the absence of unexpected complications. In glaucoma, one patient gets a 40% drop in IOP with a single drop of a prostaglandin analogue and the next patient gets a less than 5% drop. One patient takes his drops reliably, while another uses them only on the day before his eye examination. Still, being aware of the knowledge gained in well-performed clinical trials and listening to those with years of clinical experience can be helpful. So, I will add a few personal thoughts.

One difficult challenge is deciding whether or not to initiate therapy in the patient with ocular hypertension. Here, the Ocular Hypertension Treatment Study is helpful to me. Using the data from this study, one can calculate the risk of developing glaucoma in the patient with ocular hypertension. Sharing this numerical risk with the patient can help the doctor and patient make a decision together to treat or follow.

IOP remains the No. 1 risk factor for the development of progressive glaucoma damage. If there is a typical glaucoma patient, several studies, in which patients with mild to moderate glaucoma are taken off medications, suggest that the average IOP off medications is about 25 mm Hg to 28 mm Hg in those with glaucoma. If one uses the guideline that a 1 mm Hg drop in IOP reduces the risk of progressive glaucoma damage 10%, then an ideal outcome for the typical patient would be maintenance of an IOP of 15 mm Hg or less.

While the management of glaucoma is much more than treating pressure alone, studies and clinical experience suggest that if we can maintain an IOP of 13 mm Hg to 15 mm Hg, the chances of progressive glaucoma damage are minimal. For me, it helps to know that the median IOP in a white American is about 15 mm Hg and that a standard deviation is 3 mm Hg. I therefore think in terms of targets that are consistent with this finding, such as 13 mm Hg to 15 mm Hg; 16 mm Hg to 18 mm Hg; 19 mm Hg to 21 mm Hg; and 22 mm Hg to 24 mm Hg. Another deviation in IOP is one that is 22 mm Hg or higher, and this occurs in only 2.5% of the normal population. So, an IOP of 22 mm Hg to 24 mm Hg is a red flag, similar to a corneal thickness of 450 µm to 480 µm in a preop LASIK patient. It is a red flag that makes me look very carefully for other corroborative findings. The typical washout IOP of the glaucoma patient of 25 mm Hg to 28 mm Hg occurs in far less than 1% of patients. I treat most patients with a repeated IOP in the 25 mm Hg to 28 mm Hg range, as the risk of glaucoma damage is quite high over time.

The next key issue I look at is corneal thickness. In a white American, the mean corneal thickness is about 540 µm and one standard deviation is 30 µm. So, 510 µm to 570 µm is the majority of people, and anything under 480 µm is similar to a pressure over 22 mm Hg. This is an important risk factor to consider. Others include family history, especially on the maternal side; race; and associated diabetes mellitus or hypertension. The examination, including optic nerve, perimetry and the often neglected gonioscopy, is well known. One additional finding that I personally find useful is that a subtle afferent pupillary defect is present in many patients with glaucoma damage, as the glaucoma is almost always worse in one eye than the other. Asymmetric pressures and optic nerves are also an important observation.

Finally, the therapeutic trial, treating only one eye initially, is critical in determining the efficacy of our drug regimens. In the typical glaucoma patient with an IOP of 25 mm Hg to 28 mm Hg, I expect using monotherapy with a prostaglandin analogue to generate a 6 mm Hg to 7 mm Hg pressure drop. I expect a 4 mm Hg to 5 mm Hg drop with a beta-blocker and a 2 mm Hg to 3 mm Hg drop with an alpha-agonist or a carbonic anhydrase inhibitor. Unless there is a contraindication, I always start with a prostaglandin analogue at bedtime, then add a beta-blocker in the morning, and then go to the combination drops twice daily while continuing the prostaglandin analogue at bedtime.

I find that the second medication usually adds only a 1 mm Hg to 3 mm Hg drop to the therapeutic benefit achieved with the first drop. I prefer the beta-blocker/alpha-agonist combination in patients with corneal endothelial disease. In pseudophakic eyes, I still find miotics useful in some cases. This is a forgotten medication, and in the patient with a posterior chamber lens in place, it can work well, improving, much to their delight, uncorrected distance, intermediate and even near vision in many patients. For me, the systemic carbonic anhydrase inhibitors are only used temporarily to reduce the risk of postop pressure spikes or help the patient on the way to glaucoma surgery.

All of the thoughts presented here are but the musings of a single clinician and are open to debate and discussion, proving again that the practice of medicine remains as much art as science. We can only hope that we retain, as physicians dedicated to the best outcome for each unique, individual patient, the right to customize our treatments to their best interest.

Reference:

Ocular Hypertension Treatment Study Group; European Glaucoma Prevention Study Group, Gordon MO, Torri V, Miglior S, et al. Validated prediction model for the development of primary open-angle glaucoma in individuals with ocular hypertension. Ophthalmology. 2007;114(1):10-19.