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From drug therapy to lasers to surgery: Views on the current spectrum of care for glaucoma
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--- Alan L. Robin, MD
In spite of the advances made in glaucoma therapy and surgery in recent years, much remains unknown about the mechanisms behind the disease's development and control. Glaucoma treatment protocols vary widely from case to case and practitioner to practitioner. There is no simple answer to the question of how best to handle glaucoma. But that is not stopping researchers who are working to unravel glaucoma's mysteries. Alan L. Robin, MD, an associate professor at Johns Hopkins University, Baltimore, is involved in several research projects focusing on glaucoma. Robin is a graduate of Yale and the Tufts University School of Medicine. He completed a fellowship in glaucoma at the Wilmer Institute, Baltimore. He has published numerous articles.
Primary Care Optometry News: How do you approach treatment for glaucoma?
Alan L. Robin, MD: I take the medical therapy of glaucoma seriously. I do not randomly treat individuals who have statistically abnormal IOP. The risks of medications must be less than their potential benefits in order for me to consider their use. My experience with multiple pharmaceutical agents and multiple pharmaceutical studies has shown multiple risks inherent with medicine.
I look into the family history of glaucoma, blindness or a visual disability of glaucoma. If two or three members in a household have gone blind from glaucoma, the disease may be disabling in that genetic pool. It is important to consider the patient's potential life span. I'm much more aggressive with a patient with glaucoma damage who is 20 or 30 years old than I am with a patient who is 85 or 90.
In addition, a patient who has had high pressure without disease or other syndromes, such as pseudoexfoliation or pigmentary dispersion syndrome, is also at high risk.
Another risk factor concerns African-American patients. Most recent studies have shown that African-Americans are more likely to develop an aggressive form of glaucoma.
The other factor that might influence me to treat an individual would be a disc or a Drance hemorrhage, which is much more common in individuals likely to get progressive optic nerve damage.
I try to deal with patients who do not yet have field loss. I'm more likely to treat a patient with pressure higher than 30 mm Hg because we know that the relative risk of developing damage is much greater in those individuals. For people who have field loss, I consider the condition of the other eye. If one eye is affected with advanced glaucoma and the other eye has very early glaucoma, I will treat the eye with early glaucoma more aggressively. If the eye with early disease is not treated, chances are that eye will go blind, too.
PCON: How do you treat patients whose IOP must be lowered?
Robin: If a patient has normal perimetry, abnormal discs, abnormal nerve and an afferent pupillary defect—which can occur in individuals who have asymmetrical optic nerve damage or asymmetrical IOP—I will be more likely to treat that individual than the patient without an afferent pupillary defect.
For example, if I meet a patient with previously documented changes in the optic nerve (by stereoscopic photography), I would definitely treat.
When starting therapy, a one-eye therapeutic trial is very important in a patient with symmetric IOPs of 30 mm Hg. If I treat both eyes with medication X and the patient comes back in a couple of weeks and the pressure is 26 mm Hg in both eyes, I don't know if that is normal diurnal variation or if the medication has had any effect. Therefore, I will treat only one eye and use the other eye as a control. It is important to explain that to patients so they don't think they have disease in only one eye.
PCON: Which drug do you use first?
Robin: I start with a cardioselective beta-blocker. Although treatment will probably change in three or four years when the topical prostaglandins become available, at this time, the drug of choice is the beta-blocker.
I won't see the patient for a month because it takes that long for the effect to equilibrate. If that treatment is not enough, I will then go to a noncardioselective blocker. I usually start once-a-day dosing with the lowest concentration. Ours and other groups have shown that once-a-day therapy in most individuals is as effective as twice-a-day therapy.
PCON: What is your therapeutic goal in treating these patients?
Robin: I try to find a pressure that will complement my therapeutic goal, which would prevent the patient's vision from deteriorating. That goal in most individuals is either a 30% drop in pressure or an IOP under 16 mm Hg, depending on where they start. I reevaluate once I have reached that goal and then I follow them.
If after some years I have met a goal, if the pressures are still the same but I am beginning to see a change that I can substantiate on visual fields and the optic nerve, I determine that the goal has not been low enough and lower it further. The goal must be flexible, but you have to start out with a definite plan of attack.
PCON: What do you do if the beta-blocker treatment is not sufficient?
Robin: If I wanted to get a 30% decrease in IOP and I got a 25% decrease I will add another agent to the beta-blocker. My choices at this stage would be either pilocarpine or Iopidine (apraclonidine, Alcon).
I use pilocarpine primarily in people with pigmentary dispersion syndrome because it lowers the eye pressure and produces a relative pupillary block. Ocusert (Alza) is a delivery system of pilocarpine that is underutilized. It often works in those patients where pilocarpine drops don't. The pilocarpine is like a little wafer that you put under the eye lid and it could last for about six days. This treatment is better for people who would not be able to tolerate either the browache, the miosis or accommodative spasm. It works in about 60% or 70% of people.
PCON: How do you treat the majority of glaucoma patients requiring multiple medications?
Robin: When Iopidine is added to beta-blockers, IOP can be lowered an additional 20%. My experience has been that Iopidine is a very effective drug when added to either a selective or nonselective beta-blocker. It's not a primary drug in most individuals because there is a problem with two types of allergies. Thirty percent of patients after several months develop an allergy to this medication and are unable to continue with its use. These are patients who may have been responding very well and had good IOP lowering.
In those patients, I then go to pilocarpine. If the pilocarpine does not work, the next option would be either a carbonic anhydrase inhibitor (CAI) or argon laser trabeculoplasty (ALT).
I believe that many ophthalmologists procrastinate. Noncompliance [with drugs] can cause the pressure to increase. If I decide the patient has glaucoma damage and he or she is at risk for developing further damage, my job is to do everything I can to minimize progressive optic neuropathy. I have seen too many people go blind or lose visual function from glaucoma.
PCON: How do you use Trusopt (dorzolamide, Merck)?
Robin: I believe dorzolamide should be the last drug before ALT. Another use is for patients who have had filtering surgery in one eye. While you are waiting to filter the fellow eye, you can use dorzolamide in cases where you don't want to use a systemic CAI.
PCON: How do you make the decision between ALT or CAI?
Robin: I let the patient decide. I explain the procedure and its minimal downsides, and the fact that it may not work. I also warn patients about possible side effects of both therapies; including a huge pressure rise (one in a thousand), aplastic anemia, loss of appetite, anorexia or kidney problems.
I think letting the patient decide is better patient care because I do not want patients on a systemic medication. Many patients even have filtering surgery. A good place for systemic CAI is in patients who have had multiple failed filters. Research shows that ALT works in only a third of the patients for ten years. That is a very good perspective.
PCON: What do you do with the patients who fail?
Robin: I set my therapeutic goal considering the potential risks and the potential benefits. For example, in a patient who has elevated IOP, I have decided the patient is at high risk because his parents went blind from glaucoma. The pressure is 35 mm Hg and I want to get him down to 25 mm Hg.
If the patient doesn't reach the goal, the next step is a more aggressive therapy. You want to do the most good and the least harm at each stage. You want the earlier treatment to have the most chance of working, with the least amount of risk.
At the next stage, you are willing to accept more risks and you realize that the chance of success may be less. It used to be thought that medicine was best and surgery was worse. Studies now show that laser therapy isn't all that bad. It may not work for long term in many individuals, but it can buy time for more treatment.
PCON: Is there an ideal ALT procedure to achieve the best effect in any particular patient? Is further refinement of ALT possible?
Robin: Part of the problem of the optimization of ALT is that many ophthalmologists still are not experts in gonioscopy. This skill is critical for the proper performance of trabeculoplasty. There is also the question of the minimum amount of energy required to get the maximum, permanent effect out of ALT.
There are two camps: some surgeons treat half the angle and others treat the whole angle. I believe that in most patients the entire angle eventually needs therapy, so why not treat the whole angle the first time? The difference used to be that you might have a complication with an acute pressure spike after trabeculoplasty, which is why you would treat half an angle as opposed to the whole angle; but that problem has been obliterated with the advent of Iopidine 1%. The drug has changed the equation.
But if ALT doesn't work, is it worth repeating? No. But, if the procedure works and after three years the pressure again has risen from the target pressure, then it is worth repeating.
Lasers are the second order of therapy. If the medications don't work or you have tried a beta-blocker and pilocarpine and Iopidine, ALT is probably the next step.
PCON: Does that target pressure change at all when you begin considering ALT?
Robin: If the target pressure was 16 mm Hg and after a year the patient has developed increasing visual field loss, you can assume the target pressure has not been low enough.
You have two scenarios. If a patient has advanced glaucoma and the pressure is drifting up from 16 mm Hg to 20 mm Hg, and there is such bad optic nerve damage that you could easily detect a difference, I would become more aggressive and go to the next order of therapy.
If a patient has an IOP of 20 mm Hg and early damage and starts to drift up on medical therapy, I would do an ALT. Every time there is a change, it gives you a chance to reevaluate the patient. Assuming that you stick by your guns, then you would go into the next order of therapy: adding another medicine or doing ALT or surgery.
PCON: What if you do ALT and do not reach your target pressure?
Robin: One procedure may not be enough. It takes about four to six weeks to find out the true effect of an ALT. Stick with your target even though you don't see any optic nerve changes. It is often difficult to see the subtle changes. The goal in glaucoma is to prevent the development of any visible changes. If you see visible changes, the game is almost over.
PCON: What shape trabeculectomy flap do you use?
Robin: I use a triangle because it is technically easier for me. I use two releasable slip-knot sutures: one on each side. Then I titrate the effect after surgery.
PCON: How do you use mitomycin?
Robin: There have been no adequate placebo-controlled studies of mitomycin use in glaucoma surgery. However, I am a big proponent of mitomycin if used cautiously and judiciously at the time of surgery. The correct dosage, concentration and duration of treatment still has not been determined.
We are near the end of a study at this point; it seems to be very effective. There seems to be a small group of patients with IOPs that are too low and this creates a problem called hypotony maculopathy.
PCON: What is the ideal mechanism whereby surgery can be avoided to cure glaucoma?
Robin: I think the definition of glaucoma is an optic neuropathy or disease of the optic nerve that manifests itself by increased cupping and increased visual field loss. What is needed is some kind of medication—be it systemic, be it oral or be it topical—that would inhibit optic nerve damage. This medication might make an optic nerve stronger and more resistant to damage.
PCON: Are all potential cures linked to IOP?
Robin: There are medications out there that may work, may not work or could work. The problem is how to get it through the FDA. The FDA wants two geographically distinct studies each with statistical significance. Visual field loss and progression are the gold standards of diagnosing glaucoma. Our definitions of progression are, at best, arbitrary. One would need thousands of patients in each study followed for a decade to prove a medication's efficacy.
New technology exists. There are more sensitive and potentially specific ways of analyzing optic nerve head and nerve fiber layer morphology and thickness of the nerve fiber layer: the actual details of the optic nerve that could be compared over the years. Some instruments have the capacity to do that right now, but the software for the analysis really isn't there yet. The high cost of researching and engineering a marketable new product is reflected in the end price of that product. Many companies decided that it was not profitable, nor would such an expense be justifiable in many practices. Health care coverage has squashed new research.
PCON: Do you see a direct correlation between physical changes and vision loss?
Robin: We know that eye pressure is not a good screening tool for glaucoma. A laser ophthalmoscope or another noninvasive technology would be ideal. It would be easy to screen people. This would be much better than eye pressure screening.
We are looking at different ways of analyzing the optic nerve, and we are looking at different ways of looking at visual field. There are many questions that still need answering.
PCON: How would you sum up the field of glaucoma at this time?
Robin: Glaucoma is an exciting specialty now, with a lot of potential. There's the whole concept of better defining glaucoma and better detection of damage at various stages of the disease. There are also many new potential ways of attacking glaucoma and preventing optic nerve damage.
POAG Risk Factors
source: American Academy of Ophthalmology
- African-Americans
- Blindness = 3 to 4 times more common
- Age > 70 = 10% prevalence (2% for whites over 70)
- POAG occurs at earlier age
- POAG more advanced when discovered
- Elevated IOP
- High IOP correlates poorly with presence of optic nerve damage
- Height of IOP is related to POAG prevalence, regardless of race
- Other Risk Factors
- Positive family history for POAG
- Possibly:
- High myopia
- History of systemic hypertension or cardiovascular disease
- Diabetes