Diagnosing glaucoma is rarely black or white. Often, the diagnosis comes in a shade of graythere is usually some degree of uncertainty. Likewise, treatment decisions come in a multitude of shades. Which one will best match the patient?
Here, I present two difficult cases assessed by a small panel of glaucoma specialists. Their answers demonstrate the possible range of options (and some steadfast certainties) of glaucoma treatment decisions.
Here, I present two difficult cases assessed by a small panel of glaucoma specialists. Their answers demonstrate the possible range of options (and some steadfast certainties) of glaucoma treatment decisions.
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Case #1: Patient Parameters |
Case #1: What Do You Do When First-Line Prostaglandins Are Not Effective?
Xalatan (latanoprost, Pfizer) is approved as first-line therapy. Many clinicians use the other prostaglandins, Travatan (travoprost, Alcon) and Lumigan (bimatoprost, Allergan) also as first-line therapies. These medications can achieve a 30% to 35% or greater reduction in intraocular pressure (IOP). But what do you do if IOP is reduced 15% to 20% and does not meet target?
Dr. Fanelli: Because the patient hasnt achieved target pressure, would you switch to another prostaglandin before adding a second medication, as some studies suggest that a lateral move such as this may offer increased pressure reduction? If so, which other prostaglandin would you prescribe and why?
Dr. Fingeret: The IOP reduction is less than 20%, which is just not enough. I agree with a target IOP of 14mm Hg to 16mm Hg, and the need to get there one way or another. Xalatan, while apparently well tolerated, is not dropping the IOP enough. Still, you may want to take one more IOP reading before you decide.
Dr. Wooldridge: The target pressure of 14mm Hg is very optimistic for one medication; thats a 39% pressure reduction. Its unlikely that any single medication would achieve this effect. Ill often switch to another prostaglandin when the initial prostaglandin does not generate the expected result of approximately 30% pressure reduction.
Dr. Chaglasian: While there is no clear evidence yet to support switching between prostaglandin analogs, it makes sense to try to attain the maximum effect from a product category. A few studies with a small number of subjects have found that among some patients, different prostaglandins can perform more effectively, while other studies have found no real difference in IOP reduction (though there was a difference in side effects).1-3
Dr. Wooldridge: In this case, I might first try switching from Xalatan to Travatan to determine if indeed we get a greater reduction. I would choose Travatan rather than Lumigan because I generally find that the efficacy of these two agents is equivalent, but the side effect profile of Lumigan is greater.
Dr. Fingeret: I too would discontinue the Xalatan and try another prostaglandin. Travatan or Lumigan would be fine. Still, its not clear if this switch will be useful, but its worth a shot.
Dr. Fanelli: What if the change in therapy still does not achieve adequate control? How would you then proceed?
Dr. Chaglasian: I would stop all meds for two to four weeks, get a new baseline IOP and then try a medication from a different class. I would consider performing a trial of Alphagan P (brimonidine, Allergan) b.i.d. in both eyes. I would also suggest that practitioners make sure they have not missed a secondary glaucoma.
If the Alphagan P is also not effective (20% to 25% reduction) then I will try combination therapy, probably using the same prostaglandin plus Alphagan P to see if the combo can attain target IOP.
Dr. Wooldridge: If I truly feel that this pressure needs to be reduced to 14mm Hg or less, I would offer the patient the options of a second medication in addition to the Travatan and/or selective laser trabeculoplasty (SLT). In these cases, I typically review the options, risks and benefits and come to a mutual decision. If I were to prescribe a second medication with the Xalatan or Travatan, I would probably add Azopt (brinzolamide, Alcon), though a beta-blocker or Alphagan P would also be options.
Dr. Fingeret: My next step would be to try a beta-blocker. If the beta-blocker reduces IOP 20% to 25% and I still need further reduction, I could swap out the beta-blocker for Cosopt (dorzolamide/timolol maleate, Merck).
Dr. Fanelli: Dr. Wooldridge, you mentioned the possibility of proceeding to laser therapy in lieu of adding a second medication. Why is that an option so soon?
Dr. Wooldridge: In our office, I routinely offer SLT as an alternative to an additional topical eye medication for treating glaucoma. We generally review the options, risks and benefits of drops, laser treatment and surgery. The benefit of SLT over drops is that the laser treatment is a simple, safe and effective procedure performed in office. We eliminate the concern of compliance, which is a significant one with glaucoma drops. In my mind, the greatest risk of SLT is that it sometimes does not work or does not achieve the desired effect. The effect of laser treatment may also not be permanent. However, it is generally long-term enough to justify its use in lieu of a second or third medication. Risks of inadequate efficacy exist with drops and surgery as well, so there are no guarantees with any modality.
Ill often place the patient on a secondary medication for a trial of one month and then ascertain the response with this regimen. If the patient can tolerate the medication, can comply with its dosing schedule and can achieve an adequate effect, we may elect to continue the second medication. If the patient does not tolerate the medication well, cannot comply with instructions, and/or the second medication does not achieve the desired effect, we will then move on to SLT.
Dr. Fanelli: For the patient in this case, I set a target pressure of 14mm Hg or lower. In general, do you set target pressures at the time of the diagnosis of glaucoma, or does your determination of target IOP evolve over the first three to six months of therapy?
Dr. Fingeret: Yes, I set target IOP at the time of diagnosis, as you did, but I recognize that it is fluid and the target IOP needs to drop if progression is noted.
Dr. Chaglasian: I set my goals and target IOP at the beginning. Naturally, this can change as new data are collected. However, if you dont know where youre going (with target IOP) then how do you know when you get there?
Dr. Wooldridge: I generally determine a target pressure range during the initial assessment of a glaucoma patient. I then initiate treatment in an effort to achieve this target pressure range. Should the patient show evidence of progressive damage despite being within the target pressure range, I then readjust the target pressure range to a lower level.
Dr. Fanelli: What are your top three determinants when you first set the target IOP?
Dr. Fingeret: Corneal thickness, initial IOP and extent of damage (based on optic nerves and visual fields).
Dr. Chaglasian: Severity of optic nerve and visual field damage, the patients age and initial IOP.
Dr. Wooldridge: Certainly, the pretreatment pressure level and degree of damage are important criteria to evaluate in determining a target pressure. Patients who have severe damage require lower target pressures. Patients who have damage at lower pressures require lower target pressures than those who have damage within a higher-pressure range prior to treatment.
However, we need to remember that we are treating a patient rather than a pressure or optic nerve. We need to carefully determine the risk of symptomatic loss of vision that will affect the quality of life of an individual within his or her life span. The next factor that needs to be considered in setting target pressure is simply the benefit-to-risk ratio of the treatment required to obtain such a target pressure.
Dr. Fanelli: Its obvious that in cases such as this in which therapy is needed, there are several ways to look at and critically evaluate the patient.
Now well move on to a more complex case, in which there are compelling arguments for beginning intervention, and also valid arguments for deferring intervention. These dicey cases cause me to grow gray hair. Lets take a look at the specifics of the case.
Xalatan (latanoprost, Pfizer) is approved as first-line therapy. Many clinicians use the other prostaglandins, Travatan (travoprost, Alcon) and Lumigan (bimatoprost, Allergan) also as first-line therapies. These medications can achieve a 30% to 35% or greater reduction in intraocular pressure (IOP). But what do you do if IOP is reduced 15% to 20% and does not meet target?
Dr. Fanelli: Because the patient hasnt achieved target pressure, would you switch to another prostaglandin before adding a second medication, as some studies suggest that a lateral move such as this may offer increased pressure reduction? If so, which other prostaglandin would you prescribe and why?
Dr. Fingeret: The IOP reduction is less than 20%, which is just not enough. I agree with a target IOP of 14mm Hg to 16mm Hg, and the need to get there one way or another. Xalatan, while apparently well tolerated, is not dropping the IOP enough. Still, you may want to take one more IOP reading before you decide.
Dr. Wooldridge: The target pressure of 14mm Hg is very optimistic for one medication; thats a 39% pressure reduction. Its unlikely that any single medication would achieve this effect. Ill often switch to another prostaglandin when the initial prostaglandin does not generate the expected result of approximately 30% pressure reduction.
Dr. Chaglasian: While there is no clear evidence yet to support switching between prostaglandin analogs, it makes sense to try to attain the maximum effect from a product category. A few studies with a small number of subjects have found that among some patients, different prostaglandins can perform more effectively, while other studies have found no real difference in IOP reduction (though there was a difference in side effects).1-3
Dr. Wooldridge: In this case, I might first try switching from Xalatan to Travatan to determine if indeed we get a greater reduction. I would choose Travatan rather than Lumigan because I generally find that the efficacy of these two agents is equivalent, but the side effect profile of Lumigan is greater.
Dr. Fingeret: I too would discontinue the Xalatan and try another prostaglandin. Travatan or Lumigan would be fine. Still, its not clear if this switch will be useful, but its worth a shot.
Dr. Fanelli: What if the change in therapy still does not achieve adequate control? How would you then proceed?
Dr. Chaglasian: I would stop all meds for two to four weeks, get a new baseline IOP and then try a medication from a different class. I would consider performing a trial of Alphagan P (brimonidine, Allergan) b.i.d. in both eyes. I would also suggest that practitioners make sure they have not missed a secondary glaucoma.
If the Alphagan P is also not effective (20% to 25% reduction) then I will try combination therapy, probably using the same prostaglandin plus Alphagan P to see if the combo can attain target IOP.
Dr. Wooldridge: If I truly feel that this pressure needs to be reduced to 14mm Hg or less, I would offer the patient the options of a second medication in addition to the Travatan and/or selective laser trabeculoplasty (SLT). In these cases, I typically review the options, risks and benefits and come to a mutual decision. If I were to prescribe a second medication with the Xalatan or Travatan, I would probably add Azopt (brinzolamide, Alcon), though a beta-blocker or Alphagan P would also be options.
Dr. Fingeret: My next step would be to try a beta-blocker. If the beta-blocker reduces IOP 20% to 25% and I still need further reduction, I could swap out the beta-blocker for Cosopt (dorzolamide/timolol maleate, Merck).
Dr. Fanelli: Dr. Wooldridge, you mentioned the possibility of proceeding to laser therapy in lieu of adding a second medication. Why is that an option so soon?
Dr. Wooldridge: In our office, I routinely offer SLT as an alternative to an additional topical eye medication for treating glaucoma. We generally review the options, risks and benefits of drops, laser treatment and surgery. The benefit of SLT over drops is that the laser treatment is a simple, safe and effective procedure performed in office. We eliminate the concern of compliance, which is a significant one with glaucoma drops. In my mind, the greatest risk of SLT is that it sometimes does not work or does not achieve the desired effect. The effect of laser treatment may also not be permanent. However, it is generally long-term enough to justify its use in lieu of a second or third medication. Risks of inadequate efficacy exist with drops and surgery as well, so there are no guarantees with any modality.
Ill often place the patient on a secondary medication for a trial of one month and then ascertain the response with this regimen. If the patient can tolerate the medication, can comply with its dosing schedule and can achieve an adequate effect, we may elect to continue the second medication. If the patient does not tolerate the medication well, cannot comply with instructions, and/or the second medication does not achieve the desired effect, we will then move on to SLT.
Dr. Fanelli: For the patient in this case, I set a target pressure of 14mm Hg or lower. In general, do you set target pressures at the time of the diagnosis of glaucoma, or does your determination of target IOP evolve over the first three to six months of therapy?
Dr. Fingeret: Yes, I set target IOP at the time of diagnosis, as you did, but I recognize that it is fluid and the target IOP needs to drop if progression is noted.
Dr. Chaglasian: I set my goals and target IOP at the beginning. Naturally, this can change as new data are collected. However, if you dont know where youre going (with target IOP) then how do you know when you get there?
Dr. Wooldridge: I generally determine a target pressure range during the initial assessment of a glaucoma patient. I then initiate treatment in an effort to achieve this target pressure range. Should the patient show evidence of progressive damage despite being within the target pressure range, I then readjust the target pressure range to a lower level.
Dr. Fanelli: What are your top three determinants when you first set the target IOP?
Dr. Fingeret: Corneal thickness, initial IOP and extent of damage (based on optic nerves and visual fields).
Dr. Chaglasian: Severity of optic nerve and visual field damage, the patients age and initial IOP.
Dr. Wooldridge: Certainly, the pretreatment pressure level and degree of damage are important criteria to evaluate in determining a target pressure. Patients who have severe damage require lower target pressures. Patients who have damage at lower pressures require lower target pressures than those who have damage within a higher-pressure range prior to treatment.
However, we need to remember that we are treating a patient rather than a pressure or optic nerve. We need to carefully determine the risk of symptomatic loss of vision that will affect the quality of life of an individual within his or her life span. The next factor that needs to be considered in setting target pressure is simply the benefit-to-risk ratio of the treatment required to obtain such a target pressure.
Dr. Fanelli: Its obvious that in cases such as this in which therapy is needed, there are several ways to look at and critically evaluate the patient.
Now well move on to a more complex case, in which there are compelling arguments for beginning intervention, and also valid arguments for deferring intervention. These dicey cases cause me to grow gray hair. Lets take a look at the specifics of the case.
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Case #2: Patient Parameters |
Case #2: How Much Do You Weigh CCT When Deciding
To Treat or Monitor?
Years agoat least a decade or twonormal-tension glaucoma was considered relatively rare, and the decision of when to treat an ocular hypertensive with, say, 0.60 x 0.60 cups and normal fields was based on our own IOP threshold. In my case, I used 30mm Hg as the cutoff: If IOP was below 30, I tended to monitor; if IOP was greater than 30, I tended to intervene. The entire decision-making process of whether to treat or intervene was not based on clear evidence, and tended to revolve around one piece of clinical information: IOP.
Since the publication of the Ocular Hypertension Treatment Study (OHTS), eye doctors have placed more emphasis on the role of CCT in determining the risk associated with an ocular hypertensives conversion to glaucoma. While the evidence is clear that thin corneas are associated with a higher risk of developing glaucoma (as manifested by progressive cupping and field loss), there seems to be a tendency in clinical practice to make the decision to treat based on CCT. Are we not falling into the same trap that we did years ago? Has the decision to treat or monitor once again come down to one piece of clinical information: central corneal thickness?
Dr. Fanelli: Would you initiate therapy in this case? Please describe what role, if any, CCT plays in determining your management.
Dr. Fingeret: It depends upon my optic nerve evaluation. It sounds as if these nerves are not normal because a 0.60 to 0.70 cup is large for a normal-sized optic disc. This sounds like early glaucoma. While a thicker-than-average cornea reduces the risk, still I see patients every day with thicker corneas who have glaucoma.
Now, if CCT was 480m, I would treat without question. This is a patient in whom either SWAP or FDT threshold testing may be useful.
Dr. Fanelli: Great point. You would use SWAP or FDT to see if you could pick up a field defect earlier than with standard white-on-white (WOW) threshold perimetry. But many clinicians only have one field instrument, which is probably a threshold WOW perimeter. So lets assume that we do not have SWAP or FDT availability.
Dr. Wooldridge: OHTS gives us guidelines based on relative risks of development of glaucomatous damage based upon three factors: IOP, CCT and vertical C/D ratio. This patients IOPs and CCTs are in a moderate risk level, and her C/D ratio is in a high-risk level. In such a patient, I would review the results of OHTS relative to her particular situation and present the options, risks and benefits of treatment vs. follow-up without treatment. I dont feel that there is a strong indication to treat this patient; its a judgment call.
Some patients are very concerned about the prospect of losing vision to glaucoma and are eager to begin treatment. Other patients may not like taking medications and choose to wait and begin treatment when and if damage starts. Either option in this case would be reasonable. If the patient presses me for my opinion, I probably would recommend treatment, given the relative safety and tremendous efficacy of the topical prostaglandin agents.
Dr. Fanelli: Dr. Wooldridge, you are making good points, but youre not helping me with my gray hair problem! Dr. Chaglasian, can you help me?
Dr. Chaglasian: I would not treat this patient. Although the CCTs are not quite at the 588m cutoff identified by OHTS as conferring a reduced risk for the development of glaucoma, there is also no other evidence of disease.
Dr. Fanelli: I chose this case because it really can go either way: treat or monitor. So far, Dr. Fingeret is leaning toward intervening, Dr. Wooldridge has left a little wiggle room for going either way, and Dr. Chaglasian has opted to monitor the patient. Certainly, a gray area case.
What if we have a very similar patientsame exact patient parametersexcept for one thing: CCTs of 491m O.D. and 490m O.S. Given these thinner pachs, with all other factors the same, would you manage this patient differently than the patient above?
Dr. Fingeret: I would begin therapy because the risk of this patient converting is extremely high. The nerves already are suspect, independent of CCT and IOP.
Dr. Wooldridge: CCTs in the range of 490m put this patient in a high-risk category, according to OHTS. In such a case, I would recommend treatment because of the high degree of risk of damage if untreated in a 50-year-old patient.
Dr. Chaglasian: This patient absolutely requires treatment. This patients risk for developing glaucoma over the next five years is approximately 40%, according to OHTS. I would initially target a 30% reduction in IOP.
Dr. Fanelli: I too would treat this patient, as many indicators suggest that there is either glaucomatous damage already present or, at a minimum, there is a very high risk of developing glaucoma. So we all agree. And therein lies my initial concern: The only difference between this case and the earlier case was a significant difference in CCT, and we have allowed the significant difference in CCT to clearly sway us in managing two very similar patients. Are we treating the glaucoma, or are we treating the risk of developing glaucoma?
Dr. Wooldridge: Again, we need to always keep in mind that we are treating a patient, not a pressure, a nerve or an eyeball. Hence, an 80-year-old patient with no apparent damage but who is in a high-risk category based upon IOP, C/D ratio and CCT may still not need to be treated. On the other hand, I would more likely treat a 40-year-old patient with similar findings given the increased long-term risk in such a relatively young patient. Lets keep in mind that OHTS was performed in part to give us guidelines upon which to base decisions on whether to treat or monitor. These are not hard-and-fast rules, and we need to always consider the art of medicine in addition to the science.
Dr. Fanelli: Aha! So OHTS is not a cookbook. Thats a very important point to remember in our management decisions.
Dr. Chaglasian: OHTS identified patients with thin CCT (less than 555m) as high-risk individuals who are more likely to develop glaucoma within the next five years. Overall, the risk of developing glaucoma (from ocular hypertension) is only 1% to 2% per year, so the decision to treat an ocular hypertensive should involve pachymetry.
My gray zone is between 10% to 20% risk (as suggested by OHTS). In this zone, frank discussion with the patient can help in deciding whether to treat. Its also important not to over-treat these patientsthey dont have any disease! Perform a trial of a safe, effective medication that is well tolerated. If it works, great. If not, back off and monitor. Dont let the treatment be worse than the disease (or risk of the disease).
I am often very comfortable following these patients (assuming we have a good understanding of risk and follow-up) and then initiating treatment upon the first definitive evidence of disease or progression. Pachymetry is one test that can help us sort out who needs aggressive vs. conservative management.
Dr. Fanelli: I think its incredibly important to look at OHTS as a vehicle for outlining certain risk factors in the development of glaucoma, and not as a simple cookbooktreat if CCT is this thin or monitor if CCT is this thick. Quite often, I hear practitioners in various circles say, because the patient has thin corneas, they need to be treated, without consideration of other factors, such as optic nerve rim characteristics, visual fields and the age of the patient.
| Panelists Michael Chaglasian, O.D., is chief of staff of the Illinois Eye Institute, and associate professor at Illinois College of Optometry. Murray Fingeret, O.D., is head of the optometry service at the Brooklyn/St. Albans Veterans Affairs Medical Center, and president of the Optometric Glaucoma Society. Robert Wooldridge, O.D., is the clinical director of The Eye Foundation of Utah, an optometric comanagement center in Salt Lake City, and is the education director for the Mountain West Council of Optometrists. |
Dr. Fanelli is in practice in Wilmington, N.C., and author of Review of Optometrys Glaucoma Grand Rounds column.
1. Kaback M, Geanon J, Katz G, et al. Ocular hypotensive efficacy of travoprost in patients unsuccessfully treated with latanoprost. Curr Med Res Opin 2004 Sep;20(9):1341-5.
2. Gandolfi SA, Cimino L. Effect of bimatoprost on patients with primary open-angle glaucoma or ocular hypertension who are nonresponders to latanoprost. Ophthalmology 2003 Mar;110(3):609-14.
3. Parrish RK, Palmberg P, Sheu WP; XLT Study Group. A comparison of latanoprost, bimatoprost, and travoprost in patients with elevated intraocular pressure: a 12-week, randomized, masked-evaluator multicenter study. Am J Ophthalmol 2003 May;135(5):688-703.
Vol. No: 142:7Issue:
7/15/2005
