During this lecture, Dr. Alward discusses considerations when treating patients with glaucoma: who to treat, setting a target pressure, having realistic goals, and enhancing adherence.
Lecturer: Dr. Wallace Alward, Ophthalmologist, University of Iowa, USA
DR ALWARD: Well, hello. My name is Lee Alward. Wallace Alward. I’m at the University of Iowa. And welcome to our podcast today on general principles of glaucoma management. This is a fairly loose topic. Just: How do I approach somebody with glaucoma? When do I decide to start treatment? There’s a lot about target pressure, because I think a lot of you had questions about that. And I think it’s a really important part of management of people with glaucoma. I do have my chat window open. So if you have questions that are related to this topic, or things that I say that confuse you, please feel free to chime in. I may not be able to answer all of them, because there are quite a few people in this Zoom conference. So I have no commercial interests. I’m not gonna talk about anything that I have any financial benefit from. I am on a data and safety monitoring committee for a company. But I’m not talking about their implant today. And in the lecture — in the spreadsheet with some questions from the audience, there were a lot of questions that are not part of my talk today. A question on how to interpret visual fields. How to perform gonioscopy. Things like that. I am not gonna talk about any of that stuff. But I do have two websites that you may or may not have discovered. The Glaucoma Curriculum website, which you can find just by using your browser and saying Iowa Glaucoma Curriculum. It has 50 lectures. It basically covers — for my residents, but also for you, if you want — covers all of glaucoma. How to read a visual field. How to do gonioscopy, how to look at the optic nerve, and then all of the different glaucoma diseases and treatments. And then I have an older website, called gonioscopy.org. Which just teaches you how to do gonioscopy. So if I have questions — if you have questions that I’m not answering today, these are a resource. Plus Cybersight/Orbis has tremendous teaching resources. So I’ve been in practice for 34 years. I practice in a very large hospital, in a very small city. Which means that most of my patients don’t live in my town. They come from far away. And so they often have pretty severe glaucoma. And most of them have been managed elsewhere. Before coming to see me. And most of the people in my referring practice are excellent doctors. But there are some things that really bother me. I think when you see a patient sometimes, you just think… Well, what was he thinking? Or what was she thinking? Because the way that the practicing doctor took care of this patient wasn’t ideal. And so I’ve come up with some rules that I teach my residents and fellows. A lot of this is just my opinion. This is just — a lot of ophthalmology, a lot of glaucoma is something you develop opinions about over time. The first thing is: Make sure this person you’re gonna treat needs to be treated. Because if you start medications today, no one is gonna have the courage to stop those medications. So make sure the patient has active disease that really needs to be treated. And if you’re not sure, just follow them along. So if I saw this person in clinic, and they had a pressure of 22 millimeters of mercury, nothing really on the visual field that’s convincing, I wouldn’t treat them. I would see them back in 6 months and redo the visual field and make sure that they have active disease before treating them. Because in my practice, I’ve seen many people who I follow, they come in on medication, I follow them for years, and eventually I just stop their medicine, because it’s clear that nothing is happening. So I think the most important study that’s been done to help us manage our patients with glaucoma is the Ocular Hypertension Treatment Study. And Dr. Gordon and Dr. Kass looking at people who were not treated initially found that they really didn’t suffer. If you weren’t sure, in an ocular hypertensive patient, you weren’t sure, and you didn’t start the treatment for six months or a year or two or three years, that really didn’t adversely affect the patient. So their quote is that overall we can conclude that there’s a modest penalty for delaying treatment in ocular hypertension subjects. This penalty is minimal for low risk patients. So again, if you see somebody, you’re not sure: Should I treat this person or should I not treat this person? I would vote for not treating this person. A lot of you had questions about the normal tension glaucoma. And I think this is a particularly difficult category of patients to treat. Because I’m in a referral center. And because in my population, there’s a lot of normal tension glaucoma. We see a lot of these patients. And part of that is that nobody else wants to take care of them. So the Baltimore Eye Study — half of the patients with glaucoma didn’t have elevated pressure at initial exam. So this is something that comes up a lot. And there are a lot of things that are risk factors for developing normal tension glaucoma. Being older. Vasospastic disease, migraine, Raynaud, history of autoimmune disease, patients with hypotension or shock. Nocturnal hypotension. All are things you should be looking for in the history. And most of these patients, like our primary open-angle glaucoma patients, are asymptomatic until late in the disease. And this is a particular problem. Because many of your open-angle glaucoma patients are picked up because they had a high pressure, when they went in to get their eyeglasses tested. So normal tension glaucoma patients aren’t picked up this way. So they’re picked up — somebody notices their optic nerve, or because they have paracentral field loss, often, they may become symptomatic from their field loss. So when you see these people, somebody that has visual field loss, cupping of their optic nerve, you should probe their history for the fact that they might have had pressures that were elevated in the past. Were they on steroids orally at some point in time? Or in both eyes? History of inflammation. In our population, it’s not rare to see people who have burned-out pigmentary glaucoma. And so obviously my population is probably different than your population. Or do they have a history of severe systemic hypotension? This is a patient who had a normal visual field in 2011, and then we saw them two years later, but in between, they had had a heart attack. They spent two weeks in the intensive care unit. And a lot of their visual field changes were probably related to the systemic hypotension. Again, check for Raynaud, check for migraine in their history. Ask about medications that might lower the blood pressure, especially if taken at bedtime. So in our population, some elderly patients, they take their blood pressure medicines in the morning. And they get a little bit light headed, or their practicing internist might be concerned that they’ll fall and break their hip. So they say: Well, just take your medicine at bedtime. Because you’re already lying down. The risk of falling is low. But taking blood pressure-lowering medicines at bedtime is really bad for the optic nerve. So probe into that. If you discover that they have — that they’re taking their medicines at bedtime, then you need to have a conversation with their internist. I don’t personally adjust people’s blood pressure medicines, but I would write to their internist. I would send the papers that show that nocturnal hypotension is a risk factor for progressive glaucoma. And enter into a dialogue with their internist. Look for a history of autoimmune disease or some patients have normal pressure hydrocephalus. They have low cerebrospinal fluid pressure. So you should look for other things that can cause optic nerve damage at low intraocular pressures. And then do a full examination. Obviously I do gonioscopy, because that’s what I do. But this is not unusual in our population. To see somebody who comes in with normal tension glaucoma, they’re 75 years old, and you look at their slit lamp exam, and you see a Krukenberg’s spindle. And when you transilluminate them, you can see radial transillumination defects. And on gonioscopy, then, you see the pigmentation that you would expect to see in pigmentary. And another sign of burned out pigmentary is having pigment reversal. So in most of us, our inferior angle is the most pigmented. Superior angle is more lightly pigmented. But in these patients, they had a lot of pigment early in their life. It’s starting to clear away. And now they have more pigment above than below. And why does pigmentary go away? Because it’s reverse backbowing of the iris. And as we all get older, our pupils get smaller and our lens gets thicker. And that traps aqueous behind the iris, and moves the iris forward. And makes the active pigment dispersion stop, and so you’re seeing somebody in their 70s, who has cupping and field loss, and it’s from something that happened earlier in their life. So you need to look carefully at their optic nerves. Roll out congenital optic nerve disease, optic nerve drusen, et cetera. Like in this patient. We do diurnal curve testing if we’re concerned that somebody is progressing and all the pressures in the clinic are normal. We would bring them back for diurnal curve testing. Or now we can use — with the iCare Home, we can send them home to do home diurnal curve testing. And usually — not always, but usually — these patients have pretty characteristic-looking cupping. So they are much more likely to have notching in their optic nerves. Like in these pictures. And they’re more likely to have disc hemorrhages. And you should look really carefully for disc hemorrhages. They are poor prognostic signs. So if I’m trying to decide: Do I treat this patient who has a pressure of 14 millimeters of mercury and some field loss? If they have a hemorrhage, I’m much more likely to treat them, because my sense is that they have active disease. What I’m seeing is not something that’s old, from old pigmentary or old use of steroids. This is active disease. And sometimes these are subtle. Like these hemorrhages. Or sometimes they’re really subtle. Like this hemorrhage, which I could only see by comparing it to an earlier photograph. Because of this notching, their field loss is more frequently steeper and deeper, closer to fixation. And so if somebody showed you this nerve and field, I would be thinking: I wonder if this is normal tension glaucoma. So usually we would treat normal tension glaucoma similarly to primary open-angle glaucoma. In the Collaborative Normal Tension Glaucoma Study, they used 30% pressure lowering. And because of that, this has become the standard. When we see somebody with normal tension glaucoma, we try to lower their pressure by 30%. If the study had been done using 25% or 40% as the cutoff, then that’s what we would be using today. But 30% is what was done in the study. And I think that’s what most of us would do today. And remember — and I always tell my patients this — that lowering a pressure from a normal range is much harder than treating a high pressure. I always tell my patients: It’s like having a weight loss clinic for slender people. It’s very hard to take somebody who has a normal weight and make it subnormal. As opposed to taking somebody who’s already a little bit too big and having them lose some weight. Pressure is the same. If you came in with a pressure of 35, and my job was to get it to 18, that’s pretty easy. But if you come in with a pressure of 15, and my job is to get it to 12 or 11, that’s much more difficult. Remember that the episcleral venous pressure is around 8 to 12 millimeters of mercury. So anything that we try to do to open up the trabecular meshwork, to get the fluid to go more readily into the episcleral venous system, the normal trabecular outflow system, the bottom of that is 8 to 12 millimeters of mercury. So things like trabeculoplasty or drugs that open the trabecular meshwork aren’t that great at getting the pressure super low. So usually the usual medicines — the prostaglandin analogs, like latanoprost — have the advantage of having the fluid go through the uveoscleral system, bypassing the trabecular meshwork. Remember that beta blockers like timolol can lower the blood pressure. And they may not be the best choice. Especially we would be less likely to use these at night. If the pressure is 18, I think trying the trabeculoplasty — it makes sense. But not if the pressure is 13. And normal tension glaucoma patients in my practice are much more likely to need a trabeculectomy than patients who present with higher pressures. The target is just so hard to reach. So the Collaborative Normal Tension Glaucoma Study — I was fortunate that I was able to be an investigator in this study. And the question was: Does lowering the intraocular pressure slow the progression of normal tension glaucoma? Importantly, when this study was started, there was no randomized trial that showed that treating glaucoma was helpful at all. Even for high pressure glaucoma. I think we all knew it was helpful, but there was no documentation that was helpful. So this was a really important study. And the endpoint was: Glaucoma defined by progression of the field or by changes in the optic nerve photographs. There was no OCT back in those days. So 12% of treated eyes got worse. And 35% of untreated eyes got worse. So that clearly showed a benefit of treating normal tension glaucoma. But the thing… And so 12% of eyes progressed despite treatment. But the thing that, as an investigator, I took away from this study, was: A lot of patients don’t get worse. Right? And so it was frustrating for me as an investigator. Because we had people we wanted to randomize into the study, and we would follow them and follow them and follow them. And they just wouldn’t change. So that’s good for the patient. It was bad for my entering people into the study. But it gave me the sense that… I don’t need to treat everybody who comes in with normal tension glaucoma. If they have severe damage and visual fields or they have fixation splitting defects, then I’ll treat them. But if somebody has relatively minor field loss, and normal pressures, I would most times just follow them until I see a change. And in 65% of people, we won’t see a change. So that leads to my two rules for normal tension glaucoma that I pounded into the residents and fellows. Rule number one is: I’m slow to begin treatment. I need to either see severe field loss or I need to see a change. I need disc hemorrhage, I need field change, something that would make me believe that this is a progressive disease. And the other rule that I see broken all the time is: You need to be appropriately aggressive in treating people with normal tension glaucoma. Because I see patients who — their doctor feels that they need to be treated. They don’t write down a target pressure. They just start therapy. And then three years later, they’re happy, because the patient’s pressure is under 21. Forgetting that they started therapy when the patient’s pressure was 17. So once you pull the trigger and decide that you’re gonna treat this person, you need to be aggressive in treating them. So I really like these two rules. I think if you asked any of my residents, they could give you my two rules in a second. The other end of the spectrum… So be sure someone has active disease. Don’t treat somebody just because their pressure is 22. If they have normal tension glaucoma, be reluctant to treat them unless you’re sure it’s active. The other end of the spectrum is: Does the patient have enough vision to fight for? So if the right eye is healthy, 20/20 acuity, and the left eye has hand motion or light perception vision, on four drops… That patient might be wondering… Why am I taking all this medicine? I can’t see out of this eye anyway. And my patients are so polite that if I added another drop on or told them that we’re gonna do surgery, they would say yes. Because they have a lot of faith in their doctors. But sometimes the eye is just not worth the fight. Right? And so we have to have that conversation with the patient. And… Do you have enough vision in this eye that you want us to keep treating it? And they might say: You know, doc, I don’t really see anything out of this eye. It’s not useful to me. I always say: Well, if you lost your good eye, could you find the bathroom? Could you find your way out of the house if the house was on fire? And if the answer is no, then… Maybe we should stop treating so aggressively. And then I change my target. And we’re gonna talk about targets here in a second. But I would change my target to comfort. Keeping the eye comfortable. And so I might do what I call the patch test. Have the patient at home patch their good eye. Not while they’re driving or walking up stairs. And just see: Is this bad eye better than nothing? Can I find the bathroom? Can I find my way out of the house if the house is on fire? And if the answer is no, then together, you’ve made the decision that you’re not gonna be aggressive in treating this eye. Make sure they wear safety lenses to protect that other good eye. We always need to think about where this patient lies on the scale of birth to death and normal vision to blindness. And George Spaeth is the one, I think, who made us all think about this. And so this is just a graph of normal to blind. Birth to death. There are some major milestones here. Being able to drive. Being able to ambulate. And we need to remember that we’re all losing ganglion cells, as you’re listening to me here. All of us have some loss of ganglion cells that are age-related. And so if you see an elderly patient, in over 10 years, they’ve had that much visual field loss, they’re probably gonna do okay. They’re probably gonna be able to see okay for the rest of their lives. But if that same pace of visual field loss is in someone in their 20s or 30s, we need to be much more aggressive. And so I think about age a lot. We look at patients, if they come in and they’re clearly very sick, they’re on chemotherapy, or they’re on oxygen. You don’t want to play God, but you’re thinking: I don’t need to keep this person seeing for 30 years. But if you see a healthy 25-year-old, you cannot let them slowly get worse. And if you see somebody like this, you really need to intervene. Right? This person is not doing well. And remember too that if you see somebody with end stage field loss like this patient, regardless of what you do, they’re going to continue to lose some to just the normal loss of ganglion cells that we all have. So you really can’t prevent this person from getting slightly worse. So you don’t want to see your patients doing this, okay? This downward slope. So set a target pressure. I really believe strongly in target pressures. And there are some people who believe strongly against target pressures. So I’ll make my argument. Dr. Brubaker said: That’s the pressure at which the ganglion cell loss is no greater than age-related loss. And some people really don’t like this. My argument is: You do this every time you see a patient. Right? If you haven’t written down that the target is 17, when you look at that patient, you’re thinking… Well, how high was their pressure when they had damage? How severe is their nerve loss? Where do they need to be to be doing okay? And you process that every time you see a patient. My argument is: If you write it down, it just is a lot more time saving to have written it down. And the target is not just, quote, “normal”. Not just under 21 millimeters of mercury. The American Academy of Ophthalmology suggests lowering the pressure by 20%. As I said before in the Normal Tension Glaucoma Treatment Study, they used 30%. I think you’re gonna process this based on how severe the field loss is. How old the patient is. Where did the damage occur? So if somebody’s damage occurred at 48, and another person with similar loss, their damage occurred at 18, their targets are gonna be very different. Again, we’re thinking about longevity. How long does this person need to keep their vision? Corneal thickness, I think, has become very important in our processing of target pressure. And is there a family history of blindness or severe glaucoma? So two different 60-year-old patients. This one has normal visual field. No family history of glaucoma. Slightly thick corneas. Healthy nerve. They come in with ocular hypertension. Pressure of 38 millimeters of mercury. I’m probably not gonna leave them at 38. But I might be happy if the pressure is in the 20s. But this 60-year-old has a family history of glaucoma. Thin corneas at 480 microns. Nearly totally cupped out nerve. And this person’s pressure is 13 millimeters of mercury. And I’m thinking they need a pressure that’s very low, like 8. So I’m gonna be thinking this is somebody who’s rapidly heading towards a trabeculectomy. Recognize that the target can move. So you see a patient whose target is 18. And they present now at 18 with a new disc hemorrhage, a new field loss, then you set the target lower. And then in my record, I would make a note as to why the target is lower. One thing — as someone who just takes care of glaucoma, I would say that my records are incredibly accurate. And I write down everything that I’m thinking about. So in my electronic record, I would have the statement that in 2016, there was a new disc hemorrhage at a pressure of 18. Reset the target to 13 millimeters of mercury. Accurate record keeping, for anything, but for glaucoma, is really, really critical. And I think one of the things — in our country, people worry about being sued. They’ll set a target of 15, a pressure of 16, the patient might… They might get sued for that. I’ve never seen that happen. I think it’s kind of silly. It’s not something you have to react to. It’s just a goal. This is where I think this patient needs to be. So if I write down a target of 16, and I tend to write down a number — I don’t say “high teens” or “middle teens” or something. Because to me, that’s just too fuzzy. But if I wrote down the target pressure as 16, and they come in at 17, everything else is stable, I’m not obligated to react to that. And acting on a pressure above target is gonna depend on… How high is the next step, right? So if the next step is to change them from timolol to combination dorzolamide/timolol, that’s easy. I probably would do that. But if the next step is putting a second tube shunt, or doing cyclophotocoagulation, I might just follow them, just being slightly over their target pressure. I like this. When I retired from university, my daughter took over my practice. So she sent me this. I don’t think this is a thank you note. Wondering why I made this patient’s target pressure 6 millimeters of mercury. But sometimes, in our normal tension patients, targets are that low. Think about the patient’s lifestyle. You know, if they’re on all of these drops, they’re taking 9 drops a day, we’ll talk in a minute about eyelid closure. But then their eyes are closed for up to 45 minutes. So this is an argument, I think, for combination drugs. Particularly for people who are still working. It’s hard to fit all these things in their day. For busy people like all of you, taking a drop in the middle of the day is hard. Right? So going from twice a day drug to three times a day drug for someone who’s actively busy at work is kind of a big deal. And I’m not sure that it makes a lot of difference in pressure control. We should think about patients’ systemic health. Most of what we use are pretty safe. If somebody has asthma, I stay far away from beta blockers. Think about what medicines they’re on. In people on diuretics, if we’re using oral carbonic anhydrase inhibitors, which we don’t use very much anymore, it can cause very low potassium levels. Beta blockers in people who are on verapamil or quinidine can cause severe bradycardia. If someone is on an oral beta blocker and you give them a topical beta blocker, that may not do a lot. It might pull the pressure a little bit. But it’s not gonna be as effective as it would be in someone who wasn’t on a beta blocker. Think about the costs. Some of these medicines are very expensive. Is the cost-benefit ratio enough that it’s worth adding this medicine in? So maximum medical therapy to me right now might be a prostaglandin analog, a beta blocker, alpha adrenergic, and a topical carbonic anhydrase inhibitor. There’s rho kinase inhibitors. There’s lots of stuff you can add on there. But once you get past three medicines or so, the additional benefit of each medicine really is minimal. So this is of course United States. Every place is different. But in our country, generic medications are so much less expensive than name brand. So this is in US dollars. If I had my patient on these four classes of medicine, that’s $40/month. If they were on name brand medications, in the US, that’s 18 times more expensive. And if I swapped out their Trusopt — their Azopt and used brinzolamide instead of dorzolamide, that would be 25 times more expensive than if I had them on generic. So I’m a very big fan of generic medications. And that leads me to my position on samples. You know, 30 years ago, my partners and I decided that we would not have samples in my clinic. Because that makes you give the patient a name brand drug. They want to take that same name brand drug going forward, and in our population, in our country, and I recognize that things are very different everywhere in the world, particularly screwy here in terms of medication costs… That’s committing that patient to thousands and thousands of dollars worth of medicine over their lifetime. So I never use samples. And I used to think that the patients, when they came in, would be put off by that. Oh my other doctor gives me samples. Why don’t you? And I would just simply say that I don’t want the pharmaceutical companies deciding how to treat you. And they would always understand that. So I don’t believe in samples. In fact, I believe strongly against them. If there is one rule that you remember from my talk today, it’s: Be realistic. What are you doing to this patient? Is it gonna make a difference? Is the change that you’re instituting likely to bring the patient to his or her target pressure? So if you see someone with advanced glaucoma, their pressure is 30, they’re on three drugs, adding that fourth drug is not gonna bring them into the teens. And unfortunately, as I review records of patients referred to me, I see this all the time. We’re going from twice a day brimonidine to three times a day brimonidine. That’s not gonna make much of a difference. So you need to be realistic. And I think what happens in the reality of the patients we see in the clinic is: The doctor is busy. The patient needs a lower pressure. Let’s just do this and get them going. We’ll see them back in three months. But if you do that over and over and over and over again, the patient is gonna get worse and worse and worse. And so you have to think… Is this realistic? One thing that’s totally unrealistic is shuffling within a class. Changing from one beta blocker to another beta blocker. Or one prostaglandin analog to another prostaglandin analog. And let’s talk about this patient. This is a patient of mine. 50 years old. Has primary congenital glaucoma. He’s monocular. And his remaining right eye has had lots of surgeries. And his doctor at home has been managing him. And sent him in with this note. So his pressure was 24. It’s been up as high as 44. That’s not very good for someone who is monocular. But look at the medicines this man is on. So he’s on latanoprost. That makes sense. He’s on a beta blocker. So we’re doing okay so far. He’s on two cholinergic agonists. Right? Very high dose of pilocarpine, at 6%. And phospholine iodide, no longer made. But pilocarpine actually is an antidote to phospholine iodide. So phospholine iodide lowers the pressure more than a direct cholinergic. And in fact, a direct cholinergic counteracts the indirect cholinergic. So that’s really not a smart play. He’s on two different adrenergic drugs. He’s on both an oral and a topical carbonic anhydrase inhibitor. So each of these decisions was a non-realistic decision. The patient’s pressure is too high. Gotta do something. I’ll just add him on a topical carbonic anhydrase inhibitor, even though he’s on an oral carbonic anhydrase inhibitor. So none of this is realistic. So this doctor is letting this patient gradually get worse, while he flails around doing all kinds of things that are not based in reality. This man is on 18 drops a day. So if he does eyelid closure, his eyes are closed for an hour and a half every day. And there’s a cost involved with all of this. So I really want to emphasize: Be realistic. That’s if you only take one thing away. Take that away. What are you doing for this patient? Is it gonna help them? Or is it just gonna get them out of your office until the next visit? I think people need to learn nasolacrimal duct occlusion. That increases the amount of drug entering the eye. And it decreases the amount of drug entering the systemic circulation, by 2/3. So we always taught people to use their fingers to do this. But if you watch them later on, their fingers can be in all kinds of different places. I just tell people to close their eyes like they’re sleeping. Not squeeze their eyes. But close their eyes like they’re sleeping. Remember to leave proper spacing between drops. So they shouldn’t take one drop right on top of the other. And spread the drops out throughout the day. So if you tell someone to take a drop three times a day, they might not — they might take it at 8:00 am, 9:00 am, 10:00 am. So you need to be really crystal clear with what you mean by three times a day. I tell patients not to… If you say I want you to take this every 8 hours, but they’re used to sleeping 9 hours, I don’t want them to wake up just to take their glaucoma medication. And it’s really important to give patients written instructions. So we use an electronic medical record. And at the end — we have a lot of smart phrases that will help us fill out the drugs. So this part here I just copy out of my note and paste it into this aftervisit summary. So this is what the patient is given, when they’re given their next appointment. Tells them how to get ahold of us. Tells them what drops they’re supposed to be on. And what color the cap is. Because that’s helpful to them. My patients always talk about the drugs not by name, but by cap color. And then some general guidelines for them. You only need one drop. A lot of times, people take two. Talk about doing eyelid closure, about spacing the drops. We want the patients to bring their medicines for every visit. I want to actually see what the bottles are, and not to run out of their medicines. And then: What does twice a day mean? What does three times a day mean? It’s helpful if you print all that out for them. Plus if I print it out this way, they don’t have to deal with my handwriting. So if they bring their medicines, you might see something like this. This bottle has a yellow cap. You would think it’s a beta blocker. But it’s actually pilocarpine that looks like it’s been run over by a truck. This patient tells you that they’re on an orange cap. Which in our country is a topical carbonic anhydrase inhibitor. But the bottle says prednisolone. So that’s clearly not helping them. Watch your patients administer their drops. I don’t do this enough. Dr. Robin in Baltimore is really great at this. And he let me share these horrific videos of people who think they’re getting their drops in, but really are not. Or if they are, they’re risking corneal abrasions. That lady is clearly not hitting the eye. Nor is that lady. It’s helpful if you tell people what side effects they might experience. And there will be less concern if they’re not surprised that the dorzolamide is going to burn. Or if they’re on an oral carbonic anhydrase inhibitor, that their fingers are gonna tingle. Or they’ll have a funny taste in their mouth. Or they’ll have eyelash growth with their prostaglandin analogs. I think it’s important to learn and use generic names instead of brand names. It’s important that you know what’s in combination medicines. I’ve seen people, young children — you know not to give young people brimonidine. But if it’s in a combination drug, you might not think about that. And recognize that patients may not be adherent with their regimens. You know? Dr. Kass, back in the mid-’80s, did these brilliant studies, where they measured how often patients took their medicine. There was a little sensor in the cap. And this was back in 1986 and ’87, when computers were the size of refrigerators. But they were able to monitor how often patients actually took their drops. For twice a day timolol, only 83% of doses were taken, and almost half of patients missed a dose at least one day a month. And I always tell my residents: Well, the patient says he’s really compliant but he missed his drops today or yesterday. Remember the patient is most compliant on the day he sees you. This is from the Kass study. P-value very significant. And I always remind the residents: The one day you’re likely to floss your teeth is the day you see your dentist. And the one day you’re likely to take your pilocarpine or timolol is the day you see your ophthalmologist. So whatever you’re seeing on that day is probably as good as the patient gets. Simply telling the patient at each visit doesn’t help them. So if I see in outside records, quote, “stressed compliance” — you can have that discussion once with the patient. You can explain why they’re taking the medicine. Why it’s important that they don’t miss doses. But to say every visit: I stressed compliance with the patient… Every three or six months, as the patient is sliding downhill, is bad medicine. So you can do that once. You can have the conversation once, but then you basically have to take over. How do you make compliance better or adherence better? Tell them what the disease is like. Let them know why you’re doing what you’re doing. Make the medicine regimen as simple as possible. And people who have a strong doctor-patient relationship do better. If they trust you and believe in you, they’ll listen to you better. Don’t avoid surgery. So if somebody has a field like that, they’re heading to the operating room. And I think too often people become uncomfortable with surgery and just kick that can down the road and don’t do surgery soon enough. So what’s my algorithm? I think it’s gonna be different where you are, in your practice. I would say recently this was my algorithm. Start with a prostaglandin analog, latanoprost at bedtime, because it’s generic. And then a beta blocker. Then I would switch to a combination. And there are a lot of combinations out there that we don’t have in the US. So this is sort of my algorithm, but the LiGHT trial which came out in 2019, an excellent study where they randomized people with ocular hypertension or early glaucoma to either SLT or drops. And at 36 months, there was no difference in quality of life. I would have thought the drop patients would have lesser quality of life. But three quarters of the SLT patients were still drop-free. Patients were similarly at the target range. But if you look at this fourth line, that none of the SLT patients required surgery, versus 11 of the eye drop patients… And their system, in the United Kingdom’s system, there was a lower cost. And that’s obviously going to vary from country to country. But I think that this is pretty compelling, and makes me feel like if I was a patient with ocular hypertension, or early glaucoma, I might want to start off with an SLT. So this is probably my algorithm now. In my practice, I mostly see patients after they’re through all this. I don’t tend to start people on medicine for the first time. But I think it makes a lot of sense to move selective laser trabeculoplasty up to the top of the algorithm. What about brimonidine? I do use brimonidine. But it’s often the fourth drug, and the fourth drug doesn’t tend to do much and people tend to react to that. The rho kinase inhibitors for me, there’s no generic version, they tend to be very expensive, so I don’t use them a lot. And some of the minimally invasive glaucoma surgeries, I think, are really impressive for certain people. I think the GAAP procedure for juvenile glaucoma can be really helpful. I worry that we’re forgetting about trabeculectomy. Because for people with severe glaucoma, trabeculectomy is really a life saver. So why do I like trabeculectomy? This is a recent patient. I’ll show you his fields. He had glaucoma progressing at normal pressures, we did trabeculectomy with mitomycin C, and then he went back to his referral doctor, and I saw him back to do cataract surgery 11 years later. At this time, his pressure was 4. That’s lower than I’m usually hoping to get. But a lot of people do okay with pressures that low. But these are his visual fields. So this is 11 years later. And his fields — that’s his right eye. And his left eye — have not changed in 11 years. So key rules: Make sure the patient needs treatment. Do they have enough vision to fight for? Do they have active disease? If you’re not sure if they have active disease, then wait. You’re not hurting them. Obviously if their pressure is 40, you’re not gonna wait. But if their pressure is 16 and you’re not sure if they have active disease, I would wait. Think about the pace of the disease. And how long this patient is gonna be around. If they’re 30 years old, you have to be very aggressive. I think target pressures are really important. And I think it’s really important to be realistic. And I see this realistic rule broken constantly. Important to give written instructions and important to recognize that patients are not always adherent. These are the two big ones. If you remember two things from spending an hour with me today, please remember those two things. So a very similar version of this lecture is on my website. Chapter 34. Let me look at the questions that you folks sent in. And see if there’s… I can’t answer all of them. So one question is… Is blood pressure lowering effect of beta blocker significant to just any patients? I don’t think so. I think some patients are more susceptible to hypotension. Is it necessary to have a CT scan or magnetic resonance imaging to exclude other causes of cupping in normal tension? What a great question. I almost never do that. I think if you have someone who clearly has what looks like glaucoma and smells like glaucoma, then… I think doing an MRI scan is just a waste of money. But if they have something about their visual field that is suggestive that something else is going on, or their nerve doesn’t look like their field, absolutely think about neuroimaging, referring to a neuro-ophthalmologist. What about a patient who has poor compliance? Well, I think some people… You know, they’ll even admit that they have poor compliance. And… It’s sad. I mean, I would be compliant if my doctor told me to do something. But you think about things like trabeculoplasty. I might not do a trabeculectomy in someone who is poorly compliant. Because if they don’t take their glaucoma medicines, they may well not take their prednisolone after trabeculoplasty. So these are people — I might go directly to a tube shunt. Let’s see. Some of these questions are really long. Target pressure in normal tension glaucoma? I think we answered that. I would say 30%. How long do you have to wait for medication to surgery step? I think usually if I change the medicines… We used to do one eye trials. That’s been shown to not be very necessary. And so I stopped doing that. If I changed the patient’s medicine, I would see them back in three months. And if it didn’t do anything, I’m gonna stop that medicine and start something new. If it’s been effective but not effective enough, I’m gonna add something else, or change it to a new medication. What about devices to check the pressure at home? So there are iCare devices that check the pressure at home. They’re very expensive. So we actually have — Dr. Pao in our group has gotten some for our clinic that we can let the patients borrow. But for a patient to buy one at home is thousands of dollars. And I don’t think most people can do that. I have had people who have done that. I’ve had people buy Tono-Pens to check their pressure at home. Let’s see. Do you use mannitol? No. Basically mannitol is something you use in the clinic. Before you go to the operating room. But it’s not something we use in patients at home. And so there’s a question about pediatric patients, with a suspicious optic nerve, and the OCT has no normative data. That’s a problem. But certainly you can tell by looking at the heat maps and just looking at the shape of the OCT printout whether or not there’s damage. Even if there’s no normative data to compare it to. I don’t think that really prevents you from using the OCT in young people. If you have a patient who has been on latanoprost for three years and presents with a pressure of 16 and you have no idea what it was before, would you advise stopping medication? That’s an interesting question. I mean, if the patient had no cupping or minimal cupping and no field loss, I might stop the medicine and see how they do three months later. If you have no way of finding out from the old records, I think that would be a worthwhile thing to do. I really don’t like having patients on medicines for a life time who don’t have a need for a medication. It used to be in the old days one of the things people always did, when I was a resident and fellow, is they would stop medicines every couple of years to see if they were still working. That’s tachyphylaxis, where the medicine stops being really effective. But that doesn’t really happen with the medicines that we’re using now. So I don’t do that ever. But I think in the situation you’re describing, that makes sense. One question is: How do we define IOP as a key factor on glaucoma? There’s a lot of things that lead to glaucoma. Your age, your race, your family history, your intraocular pressure, your corneal thickness. But we can’t change your age, your race, your family, or your cornea. So we focus on your intraocular pressure. On the patient’s intraocular pressure. Because that’s the only thing we can do. And one of the questions that was sent at the beginning was: What about neuroprotective agents? I would love to have neuroprotective agents that worked. But we don’t right now. I mean, that’s not part of how we treat glaucoma in 2021. And so we have to manage what we can manage. And that is the intraocular pressure. So one thing is talking about corneal thickness. And I think the question is: What does corneal thickness affect? It certainly affects what you measure on pressure. Right? If someone has a 700 micron cornea and someone has a 400 micron cornea, you’re gonna measure the pressure differently. But I think the main reason that corneal thickness has become important is it tells you something about the structural rigidity of the eye. People who are born with thick corneas tend to have eyes that are tougher than people who are born with thin corneas. If you have thick cornea because you have corneal edema, or certainly in kids who have cataract surgery as babies, their corneas get thicker. But that’s not as protective for them as people who are just born with thick corneas. So it’s not just the error in the pressure measurement. But it’s the rigidity, the integrity of the eye, that the corneal thickness affects. What’s my opinion of treating someone with paracentesis to lower high pressure? Well, I would do that only if I had a plan. If I was starting them on oral carbonic anhydrase inhibitors and I was taking them to the operating room. But obviously that’s not a long-term plan. Question about Diamox or acetazolamide or methazolamide, oral carbonic anhydrase inhibitors. We used to use them a lot. Some people used them their whole lives. We don’t use them much anymore. It’s kind of a desperation thing for me to use oral carbonic anhydrase inhibitors. A lot of people just don’t tolerate them. We have topical versions now. To me, it’s something that I most commonly use if I’ve really exhausted everything. They’ve already got a tube shunt. The next step is a cyclophotocoagulation. I might use that. I really don’t like to use — in unilateral glaucoma, I hate to have somebody on oral medicine if I’m only worried about the pressure in one eye. What do you do in somebody who’s older and doesn’t cooperate with fields? You basically… Have to go with what information you have. And so go with the OCT if you have OCT. Go with the optic nerve if that’s all that you have. It’s a little bit like veterinary medicine, I think. Ocular supplements in glaucoma management… I think… We’re scientists. So you have to go with stuff that has evidence. If there’s no evidence-based medicine, ocular supplements — certainly evidence that it helps in macular degeneration, certain vitamin supplements. But there’s nothing for glaucoma. So I don’t ever tell people to use those. So that’s our hour. I didn’t get to all your questions. Sorry about that. But I got, I think, the ones that were most relevant to this talk. Again, if you have any… If you want to — if the have the ability and you want to watch this over again, you can go to the Iowa Glaucoma Curriculum. Thanks for sharing the day with me or sharing the hour with me. Take good care!
October 7, 2021
3 thoughts on “Lecture: General Principles of Glaucoma Management”
Thank you so much.
The lecture reflects what actually happens in clinics ,especially deciding if a patient need treatment or just close monitoring.
Dr. Alward, Excellent lecture and useful insights. Thank you so much!!!
Thanks a lot dr.Alward, it was very nice and teaching lecture. You experience is no doubt usefull for us.