Lecture: Diagnosis and Management of Low Tension Glaucoma

Good morning. I’m going to go ahead and share my slides. My name is Dr. Claire Wright. I’m an assistant professor of ophthalmologist here at the University of Tennessee in Memphis. I’m going to be lecturing to you all about the diagnosis and treatment of low-tension glaucoma. I have received a number of really great questions which I hope most will be answered by this lecture and I will definitely take questions at the end through the chat feature. I have no financial disclosures. Our objectives are to discuss the epidemiology and clinical features of low-tension glaucoma or LTG. Review the diagnostic work up and differential diagnosis for LTG. And detailed management strategies for LTG and differentiating how these may differ from primary open glaucoma management. I have a couple poll questions to start. These will be the same poll questions at the end for review. The first question, low-tension glaucoma is the most common form of open-angle glaucoma in which of the following ethnicities. North American, Southern Indian, South African or Japanese. Low-tension glaucoma is the most common form of open-angle glaucoma in which of the following ethnicities. North American, Southern Indian, South African, or Japanese. All right. Pretty good spread of responses. Hopefully, this question will be answered in this lecture. Next question. All of the following are considered risk factors for low-tension glaucoma or associations except: Anemia, hypertension, obstructive sleep apnea or Raynaud’s phenomenon. The question is all of the following are considered risk factors or associations and we’ll get into this, for low-tension glaucoma except anemia, hypertension, obstructive sleep apnea or Raynaud’s phenomenon. All right. Pretty good spread. Split between anemia and hypertension. Next question, all of the following are classic clinical features of low-tension glaucoma except. Disc hemorrhages, nasal step, focal disc notching or paracentral scotoma. The question is all of the following are classic clinical features of low-tension glaucoma except, disc hemorrhages, nasal step, focal disc notching, paracentral scotoma. Pretty good mix of responses. Fourth question, according to the collaborative normal tension glaucoma study, which of the following is the target IOP reduction from baseline for patients with low-tension glaucoma? 10 percent, 25 percent, 30 percent, 40 percent. Again, the question is according to the collaborative normal tension glaucoma study, which of the following is the target IOP reduction from baseline for patients are low-tension glaucoma? 10 percent, 25 percent, 30 percent, 40 percent. All right. Pretty good spread. This is exciting. Hopefully, we’ll see kind of more uniformity with our follow up questions. Last question, which of the following topical glaucoma medications should be avoided, if possible, in the management of low-tension glaucoma? Timolol, lantanoprost, brimonidine or dorzolamide. Okay. Pretty split responses: I like seeing this because it gives me an opportunity to hopefully educate the audience. We’re going to move onto the lecture portion. A little about the background of low-tension glaucoma. The historical perspective. This is known as normal-tension glaucoma. I will primarily use the term low-tension glaucoma but essentially, they’re the same. The older terminology for LTG in the literature included soft glaucoma, pseudo-glaucoma, and glaucoma without hypertension. In one of the first reports about low-tension glaucoma, written by Van Graefe in 1857, he reported cases of disc cupping and pallor at normal IOP pressures. The literature review of low-tension glaucoma, there was an increase in frequency of reporting after the invention of the Schiotz tonometer in 1905. In 1931, Dr. Pickard delineated several cases of normal tension or low-tension glaucoma and recognized it as separate entity from glaucoma with elevated IOP. How do we define low-tension glaucoma. This is known as normal-tension glaucoma. This is more or less defined as optic neuropathy with associated nerve fiber layer thinning and eventual visual field defects that occurs at statistically normal intraocular pressures. So, as we counsel all of our patients, normal pressure is 10 to 21 mm of mercury. Any glaucoma that is occurring within the normal range of pressure can be defined as normal tension or low-tension glaucoma. But you have to keep in mind factors that influence intraocular pressure like diurnal fluctuation and corneal factors. Make sure you’re not excluding primary open glaucoma given these factors. It’s also with this particular disease, it’s important to keep in mind that intraocular pressure is just one of a myriad of risk factors that you can modulate to prevent progression. And we will get into that in this lecture. Let’s talk about the epidemiology of low-tension glaucoma. This incidence varies by region. There is a particularly high prevalence in Asian populations. Looking in the literature, you get quite a wide range of spread depending on the ethnicity with quite a high prevalence in the Japanese population. Of all open angle glaucoma patients, low-tension glaucoma makes up, according to literature, 92.3 percent of open angle glaucoma patients in Japan. 82 percent of those patients in southern India. 57 percent in South Africa and more like 1/3 of patients in the United States. With regard to genetics, approximately 2 percent of cases are inherited. Typically, autosomal dominant. And there may be a link between LTG and dementia, particularly vascular dementia. So what’s the etiology of low-tension glaucoma? Well, it’s not fully understood. But there are many hypotheses. Some postulate that it’s due to vascular dysregulation. Others think there is a contribution due to reduction of ocular perfusion pressure. And I had to look this up. Ocular perfusion pressure is mean arterial pressure minus IOP. Others think there are contributions from blood dyscrasias, anemia, coagulability issues and other think perhaps an impaired CSF circulation and/or low retro bulbar CSF pressure contributing. You do have to think about in these patients, what are other factors that may be contributing to optic neuropathy in addition to IOP which could be lower. Specifically asking and inquiring about ischemia, vasospasm, autoimmune diseases and coagulopathies. So diving into more of these systemic risk factors or associations. There seems to be emphasis on whether or not there is presence of vascular disease, including history of diabetes, stroke, hypotension, obstructive sleep apnea. Vasospasm including migraine and Raynauds and primary vascular regulation some call Flammer syndrome. Results in impairment or decrease in ocular blood flow autoregulation and vascular dementia. These are across various studies found to be associations and potential risk factors you can modulate as a provider in patients with low-tension glaucoma. I wanted to actually draw particular attention to the hypotension as a risk factor. A huge study came out in 2017 called the sprint study which found that for patients with hypertension who underwent intense blood pressure control. So target systolic blood pressure under 120, those patients faired much better with regards to fatal and nonfatal major noncardiac events compared to patients with standard blood pressure control. This played into the definition of hypertension here in the United States from the American — cardiology and American Heart Association. Now elevated blood pressure is anything over 120 diastolic and 80 diastolic. When I was a medical student 10 years ago, it was 140/nn90. Now in one review article I read, the authors advised its reader, we better watch for iatrogenic hypertension with subsequent nocturnal hypotension which can result in low-tension glaucoma. I thought this was very interesting. Kind of change in development and change in definitions of a very commonly diagnosed condition, hypertension. So let’s talk about briefly the differential diagnosis of low-tension glaucoma. General pillars of differential diagnosis, glaucomatous optic neuropathy versus non-glaucomatous optic neuropathy. You can think primary open angle glaucoma and you’re not catching the high-pressure readings because you’re seeing them in the afternoon or they have thin corneas so you’re under estimating pressures. These patients, other potential diagnosis can include traumatic glaucoma or steroid-induced glaucoma. And diagnosis to think of, in these patients that are non-glaucomatous causes of optic neuropathy, can include infectious, compressive, nutritional and vascular etiologies. Namely an infectious would be syphilis, B12 deficiency is under nutritional cause. Compressive, think CNS lesion, pituitary adenoma, meningioma. And vascular reasons is non-arteritic ischemic optic neuropathy and giant cell arteritis. Always good in a new patient presentation to think what is my differential diagnosis so I don’t miss anything, even though I might think this is low-tension glaucoma. So what’s going to be in the patient history or what are some things we should inquire about to our patients who present with what is thought to be low-tension glaucoma. You should elicit a history based on your differential diagnosis. And so you ought to inquire about any potential history of the following. We’ve dills cussed this before. Vascular and/or vaso spastic diseases. As with all glaucoma patients, think about a history of ocular trauma, previous procedures including refractive surgery and steroid use and family history of glaucoma and blindness. General information, diet and history of STDs. Syphilis maybe is a potential diagnosis. And obtain a con size review of systems inquiring about neurological symptom ifs you’re concerned about a CNS lesion and giant cell arteritis symptoms. The clinical work up pertains to any glaucoma patient in my opinion. With tailored details for a low-tension glaucoma patient. You’re obtaining visual acuity, intraocular pressure, pupil exam, refraction. Anterior segment exam including gonioscopy. And a posterior segment exam with careful examination of the optic nerve. And low-tension glaucoma can be characterized or classically seen to have focal rim notching, disc hemorrhages and/or peripapillary atrophy. So what are some clinical tests that we can obtain in clinic that may help our work up of these patients. I obtain a pachymetry reading in all glaucoma patients so I know approximately how accurate the pressure readings are. It’s helpful to obtain automated perimetry. We get Humphrey visual fields. You can also get an octopus perimeter et cetera. You may need to follow up with a 10-2 visual field as fixation tends to be involved early in these patients. That is an important note. I recommend getting a formal assessment of the retinal nerve fiber layer. You can pay particular attention to the macular retinal nerve fiber layer in early or late disease. This nerve fiber layer thinning as with all glaucoma patients should correspond with visual field loss. You can obtain disc photos. Getting into automated perimetry. Low-tension glaucoma patients, their visual field loss is characterized by deep and focal loss closer to fixation earlier in the disease compared with primary open angle glaucoma patients. So specifically, they can have paracentral or central scotoma. Versus the nasal step that can progress to arcuate scotoma. And these low-tension glaucoma patients may require 24-2c which includes a couple extra foveal points or 10-2 to further characterize the fixation-involving visual field defects that may be seen just a little bit on the 24-2 or 30-2. So some images to illustrate. The paracentral scotoma that characterizes low-tension glaucoma opposed to the nasal step which can progress to an arcuate scotoma and primary open-angle glaucoma. What are additional workups that you may want to consider in low-tension glaucoma patients? These, this work up ought to be reserved for cases with a high index of suspicion for a non-glaucomatous process. So you can think about nutritional, metabolic, infectious. Many times, you have clues for these in the history and review of systems and exams. You would see a history of significant exposures and limited diet, neurologic. If you’re thinking of a CNS lesion or compressive cause of optic neuropathy, many times these patients can have some neurological symptoms. And you’re also going to be — a big red flag also is non-corresponding clinical testing. By that I mean, visual field loss and disc pallor out of proportion to disc cupping and nerve fiber thinning. Everything should match up, disc cupping with nerve fiber layer thinning but that corresponds to a visual field defect and it should all line up. If not, if there is mismatch, you should think about potential CNS lesion. Other red flags, significant asymmetry of the optic nerve appearance with regards to cupping pallor, color vision loss, or vertical visual field defects. So how do we manage low-tension glaucoma. As with all glaucoma, intraocular pressure remains the most modifiable risk factor in disease management. You can lower the pressure as with primary open angle glaucoma with drops, laser, and surgery. But in addition to pressure control, you really have to think about mitigation of other risk factors. Think about what are these other potential comorbidities that the patient may have that we can work with, say the primary care doctor on or other specialists on: That can include blood pressure control, correction of anemia, treatment of coagulopathies, et cetera. So I wanted to use this time now to talk about a big, very important study in normal tension and low-tension glaucoma management which is the collaborative normal tension glaucoma study. In this study, patients were randomized to observation or treatment of their diagnosed normal tension glaucoma. And treatment could consist of any combination of drops, laser, or surgery at the surgeon’s discretion. The target for IOP reduction in the treatment group was 30 percent from baseline. These patients and their treatment, they were avoided beta blockers and alpha adrenergic agonists were avoided. The observation arm could be treated if demonstrated by evidence of deterioration. The rate of progression was reduced with treatment over five years. The treatment group, 12 percent progressed at five years versus 35 percent in the observation group. What is interesting is 65 percent of patients in the observation group did not progress. Curious. So it makes you wonder if potentially those patients had some of those other comorbidities contributing in a more important way. And so this study established that the goal of 30 percent IOP reduction from baseline as target for patients with normal or low-tension glaucoma. So let’s get into more of the pharmacotherapy of low-tension glaucoma management. So you can, it’s similar to primary open angle glaucoma management but there are some important caveats. In various studies, brim non-dean has been found to have a neuroprotective effect in these patients. And beta blockers has been found to actually reduce optic nerve head perfusion and, therefore, tends to be avoided in the management of these patients. Some studies have found that the newer class of agents, Rho-kinase inhibitors may enhance optic nerve head perfusion through the nitric oxide pathway. And there was a study that showed enhanced para papillary vessel density seen on OCT angina I don’t go phi with the treatment of ripasudil. Getting into the more details about brimonidine and timolol, the low-pressure glaucoma study compared the two in the management of low-tension glaucoma. And the study found the two medications had similar pressure lowering effects but brimonidine resulted in less visual field progression than timolol. There is talk that potentially calcium channel blockers, systemic calcium channel blockers may enhance vascular tone in these patients, particularly those with an underlying history of vasospasm. But larger clinical trials are lacking. So let’s get into low-tension glaucoma management with laser. Similar to primary open angle glaucoma, you can offer these patients trabeculoplasty and micro pulse and cyclo destructive procedures. You can get a 15 reduction from baseline, modest but half of what is recommended according to the glaucoma study. But you can get a big reduction in the number of drops. A modest effect with SLT. Micro pulse laser in this study found a 20 percent reduction in baseline. Modest. Still not 30 percent which is recommended. As with primary open angle glaucoma, cyclo-destructive procedures i.e. cyclophoto coagulation, is usually reserved for refractory cases due to side effects, hypotony, severe inflammation, and vision loss, et cetera. Before we get into the surgical management, I thought it would be interesting to bring up some of our medical history and I found this report from Dr. Bloomfield in 1953. He reported the surgical results for low-tension glaucoma. Mostly unused procedures which included the Elliot trephination, iridencleisis and cyclodialysis and modified Lagrange operation. Surgery is not significantly helpful in preventing further deterioration of visual function in that condition. A lot has changed since 1953. We have many more sophisticated techniques available today and I’ll be talking about those now. Surgical options for low-tension glaucoma can include contact extraction with lens implantation. Tube shunts and bleb forming procedures, namely trabeculectomy, express mini glaucoma shunt and XEN gel stent. Looking at cataract extraction with MIGS. Every time you see these patients, they need a low pressure goal. They have come in, the baseline pressure is normal or low. Then you try to lower it 30 percent. So many of these patients need sub 12, sub 10 pressure goals. And so really it’s difficult to obtain these pressure goals below what we know to be episcleral venous pressure which is 8 to 10 mm of mercury. And vascular resistance to distal to collector channels. This is difficult to obtain with cataract surgery alone. There is a role for these procedures at lowering the pressure postop and reducing the drop burden. So I found this review article which was a meta analysis of MIGS used for normal tension glaucoma management. They found reports on the use of iStent, iStent Inject, Hydrus, Kahook, and trabectome. And this meta-analysis found that all of these procedures demonstrated significant pressure lowering and reduction in the use of anti-glaucoma medications across all time points up to 36 months postop. There can be a role but at lowering the pressure some. And reducing the number of drops. So it’s an available option. I do want to talk about the use of trabeculectomy and tube shunts for these patients. Tube shunts first, we know based on the five-year, many of these studies compared Ahmed versus Baerveldt. The main pressure is in the low to mid-teens with or without drops. Think about the patient coming in with low-tension glaucoma, average pressure mid-teens, you need to lower that 30 percent. So the pressure of 10, you’re probably not going to get there just with a tube shunt. So these are certainly appropriate options if you’ve already tried a bleb forming procedure and that failed. That’s an option. But as a primary procedure, you maybe ought to consider first bleb forming procedures. So by that I mean trabeculectomy with Mitomycin C or shunt. Moving onto trabeculectomy with mitomycin C. Looking back about that. 43 percent of the patients needed a filtering surgery to maintain the 30 percent reduction from baseline. However, with this trabeculectomy, there is a very narrow margin of error between what is therapeutic and hypotony. If you have a patient coming in with a pressure of 15, you need to lower that 30 percent. To 10. What’s that line between therapeutic pressure and clinically significant hypotony. It’s narrow. Between 5 to 10, 8 to 10. That’s a narrow window. What are alternatives to trabeculectomy that can be less risky for hypotony. You can consider the XEN gel stent or express mini glaucoma shunt. The pressure reduction for a XEN gel stent, it managed to reduce the IOP from approximately 16.6 to 11.6. So pretty good. So you don’t usually risk as much hypotony with the XEN gel stent opposed to trabeculectomy. So what are some other therapies that we can consider offering these patients with low-tension glaucoma? I’ll just basically say there is less data on the following recommendations. And really, as with primary open angle glaucoma, the pillar of treatment is pressure lowering. Other considerations you can make to mitigate glaucoma progression or to offer patients who seem to be progressing at physiologically, like, great target pressures would be to offer careful monitoring of blood pressure with special attention to avoid nocturnal hypotension. Nocturnal hypotension can reduce perfusion of the optic nerve head and run the risk of visual field progression. So what I, how this translates is I tell patients, hey, if you don’t already, keep a blood pressure log checking morning and evening blood pressures and try to avoid nighttime dosing of blood pressure medicines. If it’s once a day dosing, I usually get in touch with the PCP to say can we consider morning dosing instead of evening to mitigate the risk of nocturnal hypotension. And usually, they’re accommodating. Other soft recommendations can include aerobic exercise. With avoiding prolonged inversions like downward dog. There is some data on ginkgo biloba which in some studies show it can enhance blood flow velocity and reduce vascular resistance. But it also can show adverse effects of bleeding and seizures. You can have a bottle of this from one company and have it be a different can of worms than another bottle of ginkgo biloba. I’m hesitant with recommendations of supplements. There is an antioxidant called resveratrol found in the skin of red grapes and red wines. And another is vitamin B12 supplementation. Particularly those with suboptimal levels. And then mindfulness and meditation, there are large trials, primary open angle management trials that has been demonstrated to show that there is reduced visual field progression for those who have a regular meditation mindfulness practice opposed to those who don’t. I think where I practice in the mid south, I have many patients that are practicing religious Christians and I do bring this up and I think it’s very validating for them to see that there’s not just spiritual benefits of prayer and meditation but potentially physical benefits. I do want to take this time now, we’re moving towards the end of the lecture, I want to have this grid here to compare and contrast low-tension glaucoma with primary open angle glaucoma. The chief affected demographic we can see in low-tension glaucoma as we reviewed primarily Asian populations with particular high prevalence in the Japanese population. Contrast this with primary open angle glaucoma where it’s very high incidence in Afro Caribbean populations. Visual field findings in low-tension glaucoma, you can get early involvement of paracentral, central area. Contrast with the early nasal step that can progress to an arcuate wing scotoma. Pressure reduction goal in low-tension glaucoma, 30 percent reduction from baseline according to the collaborative study. Which may entail early bleb forming procedures. And other studies in primary open angle glaucoma varies but what I see commonly is 25 percent reduction from baseline. Clinical features of low-tension glaucoma, as we’ve discussed, classically you can see frequent disc hemorrhages, focal notching of the optic nerve. You can also many times you have to inquire about this known history of vascular and vaso spastic conditions. And primary open angle glaucoma as we know, disc appearance generalized versus vertical cupping. There is not as much focal regions classically. Okay. So I’m finished with the lecture portion. Now what I’m going to do is go back to the initial five polling questions to review and see if hopefully we’ve acquired new knowledge and had a good review. So we will go ahead and kick off these polling questions again. Question No. 1, low-tension glaucoma is the most common form of open angle glaucoma in which of the following ethnicities? North American, southern Indian, South African, or Japanese. Low-tension glaucoma is the most common form of open-angle glaucoma in which of the following ethnicities. North American, southern Indian, South African or Japanese? All right. 84 percent of you answered the correct — correctly and it’s Japanese. Good. Second question, all of the following are considered risk factors or associations for low-tension glaucoma except? Anemia, hypertension, obstructive sleep apnea or Raynaud’s? Again, the question is, all of the following are considered risk factors for low-tension glaucoma except. Anemia, hypertension, obstructive sleep apnea or Raynaud’s? Good. About 2/3 of you answered correctly. The answer is hypertension. So actually what is considered a risk factor or association is hypotension, low blood pressure. And that is thought to be due to hypoperfusion of the optic nerve head. Now kind of as a corollary, you should ask about hypertension in these patients and then specifically if their dosing of their blood pressure medicines. Because that nighttime dosing can cause nocturnal hypotension. But in this, the answer to this question is B, because it’s primarily hypotension, low blood pressure. That is considered a risk factor or association for patients with low pressure. All of the following are classic clinical features of low-tension glaucoma except. Disc hemorrhages, nasal step, focal disc notching or paracentral scotoma. All of the following are classic clinical features of low-tension glaucoma except. Disc hemorrhages, nasal step, focal disc notching or paracentral scotoma? All right. Good. 76 percent of you answered correctly. Nasal step is not the answer because that is classically the early visual field finding on primary open angle glaucoma that can progress to an arcuate scotoma as the disease progresses. The other features, disc hemorrhages, focal disc notching, early paracentral scotoma is classic for low-tension glaucoma. The fourth question now, according to the collaborative normal tension glaucoma study, which of the following is the target intraocular pressure reduction from baseline for patients with low-tension glaucoma? Again, according to the collaborative normal tension glaucoma study, which of the following is the target IOP reduction from baseline for patients with low-tension glaucoma? All right. Good. 89 percent of you nailed it. The answer is 30 percent. So you think about this actually makes sense. These patients are coming in with already normal to kind of low normal pressures. You want to get that lower. You’re going to need a lower pressure goal compared to what they’re coming in with at baseline. So 30 percent target IOP reduction from baseline is the correct answer. As delineated by the collaborative normal tension study. Last question. Which of the following topical glaucoma medications should be avoided, if possible, in the management of low-tension glaucoma. Timolol, latanoprost, brimonidine or dorzolamide? Great. So about three quarters of you answered correctly. The correct answer is timolol. Various studies of treatment of patients with low-tension glaucoma studies, timolol, low-tension glaucoma, timolol has been found to, especially when compared with brimonidine actually results in visual field progression despite adequate pressure lowering. That postulates to potentially due to contributions to blood pressure, reduction in ocular perfusion pressure. So my first line treatment for patients topically for patients with low-tension glaucoma tends to be brimonidine or latanoprost and I try to avoid timolol. Let’s review some lecture take aways. And I’m a broken record. But we reviewed all these things just to take away points. Low-tension glaucoma can be associated with an exacerbated by certain systemic conditions. Namely hypotension, anemia, obstructive sleep apnea, Raynaud’s or migraine. Inquire if a patient has these conditions and work with the primary care doctor on optimizing those as part of the management for low-tension glaucoma. Classically, low-tension glaucoma demonstrates disc hemorrhages, focal disc notching, and early paracentral scotomas. And this contrasts with the more, earlier nasal step that can progress to an arcuate scotoma in primary open-angle glaucoma. With regards to pressure reduction goal, aim for 30 percent IOP reduction from baseline in LTG. This is from the normal tension glaucoma study. Those patients are less likely to progress thanker at that target pressure. With regards to medication choice, brimonidine may impart neuro protective benefits and timolol is associated with visual field progression. I try to avoid topical beta blockers in these patients. Whereas in primary open-angle glaucoma management, many times bring mono-dean is a second or a third choice. In low tension, it moves up higher on the list because of the neuro protective features. There are numerous surgical options available in the management for low-tension glaucoma. You have to keep in mind that low pressure gold. So these patients may end up requiring bleb forming procedures like trabeculectomy. XEN gel stents or express mini glaucoma valve replacement. These are my sources. We are all done. It’s 7:43 my time. We have a fair amount of time for questions. I’m going to hit stop share. Thank you for your attention. I’m going to look at the Q&A. And hopefully get some of these answered. When we do diagnosis low tension diagnosis in those with thin central corneal thickness. Great question. With regards to obtaining pressure with thin cornea, you’re underestimating the pressure. There is no verified conversion factor. Some people proposed charts, like if it’s this thickness, pressure translates to this. If the corneal vault is thin, it’s this pressure. Good question. Keeping in mind there are thin corneas so you’re underestimating the pressures. If a patient still doesn’t have a pressure higher than mid to high teens, that could be low-tension glaucoma. It’s a little where is the line between low-tension glaucoma and POAG. It can be a gray area. If I’m not sure, I inquire as to the potential risk factors of low tension and normal tension glaucoma and shoot to lower the pressure 30 percent opposed to 25 percent. There is not a cut and dry answer here. There is a lot of gray area. Not sure what this next one, GCC, not sure what that stands for. Screening tests for normal tension glaucoma. It’s going to be pretty much have the patient come in, do an exam, check the pressure and then do the visual fields and RNFL screening. Ganglion cell complex. Thank you. Retinal nerve fiber layer assessment can be helpful in determining if there’s nerve fiber layer thinning. But that should correspond with visual field defect. You can use that as a diagnosis of low-tension glaucoma. I guess you can use that to screen as well. Yes, I would say so. Is there any possibility of unilateral low-tension glaucoma? I mean you can get asymmetric disease in many of these glaucomatous optic neuropathies. So yes, I’ve seen it before. Yes. I still ask about the history and potential comorbidities and still shoot for 30 percent reduction of pressure in the affected eye and we’ll continue to watch the eye closely. What lab tests do you order and why? If we order lab tests for these patients, it’s because you’re highly suspicious for non-glaucomatous optic neuropathies. Those tests that I order can include vitamin B12, RPR, FTA, ABS. And if there is any concerning features or review of systems positive for giant cell arteritis get ESRCRP (ph) or CBC or compressive optic neuropathy and ordering an MRI. Can normal tension glaucoma be related to corneal hysteresis. That is a marker of shock absorption of the optic nerve. So low corneal history is a pretty well documented risk factor for primary open-angle glaucoma. I don’t know that much about particularly its role in diagnosis and management of normal tension glaucoma. But since normal tension glaucoma is an offshoot of primary open-angle glaucoma, I would think that low corneal hysteresis is a risk factor. What if a patient has 17 mm of mercury pressure and central corneal thickness of 440, that’s a really thin cornea. Yes. If the central cornea thickness is 440, that’s very thin. The pressure is 17. I would probably consider that primary open-angle glaucoma. Why were alpha agonists avoided in collaborative normal tension glaucoma study. I think it was thought that would affect optic nerve head perfusion but there is a follow-up study comparing Rimantadine, an alpha agonist and timolol which was found as we discussed, Rimantadine preserved the visual field better than timolol at comparable pressures. What are side effects of Rapasidil in LTG. It’s a ROC inhibitor. In the United States, we have netarsudil or rhopressa. Side effects I’ve seen not related to low-tension glaucoma specifically but across the board, conjunctival hyperemia and subconjunctival hemorrhages, and a bolus corneal an epitheliopathy that can result in high pressure. I have seen those across the board with ROC inhibitors. The effect of lowering IOP in glaucoma in general. So you can is — you want low therapeutic pressures. You can run the risk of hypotony. And different eyes have different thresholds for what is clinically significant hypotony. One person’s 8 may be visually fine and another person’s 8 may be clinically hypotonus. The effect is you can get to the target pressure but you run the risk of hypotony. What’s the role of color vision tests in the diagnosis? If you have reduction of color vision plates, that may be concerning for a compressive etiology opposed to glaucoma optic neuropathy. I don’t routinely check color plates in new glaucoma patients but if I’m concerned there is optic nerve pallor out of proportion to disc cupping I would recommend checking the color plate. For thin corneas from refractive surgery, how do we determine the IOP target? It’s challenging when there is not correctable, tables, again, the central cornea is this thickness, therefore the pressure is this. I just get a gestalt, it’s a thin cornea and therefore the pressures are going to be underestimated. The way I determine pressure target, is the patient more likely to have primary open-angle glaucoma or normal tension glaucoma. If in doubt, I shoot for a 30 percent reduction from baseline. There is a lot of gray area. If in doubt I go more aggressive pressure lowering target. Do you believe that some beta blockers don’t have vaso constrictive effects they would have intrinsic sympathomimetic effect. I don’t know how to answer that question. I will write it down and look into it. Beta blockers vaso constrictive effect. I will look into that. I can’t promise I know all the answer to these questions: I have to review and brush up on my basic science knowledge would be helpful for management of these patients. I will make note of your name. I like being stumped. What is your opinion of smart watch blood pressure monitoring. I guess smart watch, like an apple watch, blood pressure monitoring, I think especially if say there is concern for progression at pretty low pressures, if I’m seeing patients progress in low-tension glaucoma pressures 10 to 12, maybe you want to avoid a bleb forming procedure or they already had one, then, okay, monitor the blood pressure. I think a smart watch or device like that can be extremely helpful in getting a range of blood pressures throughout the day: Particularly late nighttime blood pressures. Nocturnal hypotension, hypoperfusion risk. I think it would be useful. I would recommend it. Do you perform MRI as part of the diagnosis — sorry, back to that question, there was a follow up question, what blood pressure goal should I have my patient obtain. That’s a good treatment. I’m not treating high or low blood pressure. I’m working with a primary care doctor on that. According to the big study performed regarding hypertension management, many patients are shooting for pretty low blood pressures. So if in doubt, if I’m concerned that maybe they’re getting some nocturnal hypoperfusion of the nerve head, I have them keep a log. I get concerned about patients can systolic getting close to 90 or below and diastolic 50 or below. That is arbitrary. It’s just what puts my antenna up. If we’re getting those on their logs, I may be picking up the phone and calling the primary care doctor and saying I’m worried about that affecting the optic nerve health. As glaucoma management experts here, we’re really maybe some of us are data freaks. It’s interesting to get more data so we have more to work with. And a good blood pressure log can give me good information as to whether or not I need to pick up the phone and make adjustments. I don’t have a blood pressure target. It’s a patient-specific thing depending on comorbidities: I like a log because if I see those diastolic or systolic looking low, I may work with their primary care doctor and cardiologist on optimizing that. Long-winded answer. Do you perform an MRI as part of the diagnosis? Only if I’m concerned about compressive optic neuropathy. That is where there is a mismatch between optic nerve appearance and nerve fiber layer scan and especially if they have neurological symptoms. Dose for gingko biloba. I don’t recommend it. Patients sometimes find their information on their own and say, hey, what do you think about this? Well, there is some data that suggests XYZ. I don’t recommend it because in the United States we don’t have FDA regulation of supplements: You can get varying amounts of dosing depending on the company you’re buying the supplement from: That is something you want to look up and see what other glaucoma specialists recommend. But I don’t routinely recommend it. Okay. I see a question in Spanish and I have some amount of Spanish knowledge. Low-tension glaucoma is the way it’s defined is glaucomatous optic neuropathy occurring at statistically normal pressures. Normal pressure is 10 to 21 range. So glaucomatous neuropathy is occurring in that range. But you can have the low teens. Is there a role for SLT in low-tension glaucoma? Yes. You can’t get as impressive a response because you’re starting from baseline pressures in the normal range: But you can get a modest effect. One study said 15 percent from baseline. Do you believe that dorzolamide can induce local vasodilation in the ONH by increasing the PCO2? I don’t know enough about the biochemistry of topical carbonic anhydrase inhibitors with regards to its effect on PCO2. I have to skip that question and look it up. Thank you for stumping me. I’m getting a question about eye drops causing conjunctivitis after six months of use, red eye. I hate Brimonidine but I see this effect all the time where patients can get follicular conjunctivitis and allergies. If they’re developing a sensitivity like that, just discontinue that. Probably getting a preservative free drop can help, too. Based on your experience do you evaluate the normal tension glaucoma prognosis compared to open angle hypertension glaucoma. So yes, I think trying to understand what question you’re asking here. Normal tension glaucoma and low-tension glaucoma patients are trickier to mention than primary angle open glaucoma. They’re starting from normal patients. Sometimes these patients need surgery earlier. And many of these patients I’m looking at systemic issues as we’ve discussed, like blood pressure and the like. So they are more nuanced and require more history collection and share time than primary open-angle glaucoma. There may be closer follow up. It’s a little less straightforward than the management of primary open-angle glaucoma in my experience. We talked about corneal hysteresis in LTG. Is a pressure of 5 mm too low. That depends on the patient. I had pressure with 5 or below who do fine. There are no signs of hypotony. But I have other patients with signs of hypotony at statistically normal pressures, 10 to 12. So pressure goal and whether or not patients are tolerating hypotony is patient specific. Do you regularly look into medications for hypertension to rule out hypertension, nocturnal hypotension. Especially in patients with low-tension glaucoma, I’m inquiring, are you being treated for hypertension. If so, what time of day are you taking your blood pressure medicines: I ask that question of all my low-tension glaucoma patients. Yes, I do ask, especially if they’re on systemic beta blockers and carbonic calcium channel blockers. Diurnal variation part of the work up? I consider diurnal variation of IOP in all glaucoma patients especially if I’m seeing a new patient for the first time in the afternoon, pressure tends to peak early morning and go down throughout the day. I think about that in all of my patients. So if I’m seeing a normal tension glaucoma patient who I think has normal tension glaucoma in the afternoon, I have them come back at 8 o’clock the next appointment, maybe see in the pressure is in the high range. I think about diurnal variation in pressure in all of my glaucoma patients. How do we differentiate POAG from LTG in patients treated with systemic beta blockers. I have to look and see how much of an intraocular pressure lowering effect we get from systemic beta blockers. If you’re seeing a patient that you’re concerned has low-tension glaucoma in the low teens, pressure in the low teens and they’re on metoprolol or what have you, they have the classic features of disc hemorrhage, paracentral scotoma. I have to look at the whole clinical picture and say, classically, it’s showing signs of low-tension glaucoma opposed to open-angle glaucoma. It can be nuanced and it’s not a straightforward answer, you have to look at the whole clinical feature. Do they have classic vertical cupping or a notch, a nasal step, arcuate scotoma, you have to look at everything. What is your experience with Netarsudil in low-tension glaucoma? I can’t think of — I don’t know. I think generally the way I use netarsudil is before surgery, it’s cost prohibitive for most patients. In one of the studies I reviewed, it’s been shown to potentially enhance vascularity of the optic nerve head. Because of, at least because of the pricing here in the United States, it’s cost prohibitive. It’s refractory treatment usually topically. What clinical drop treatment do you recommend to reduce 30 percent? 30 percent pressure reduction goal is aggressive. Many times, you can’t get there with one drop alone. If I’m starting initial treatment, unless I’m really concerned, typically I start with one drop first or if I’m starting medications, I start with one: I have them come back six to eight weeks for a pressure check and watch testing closely. It’s hard to get that 30 percent IOP reduction with one drop alone. To answer the question, I’m not seeing Brimonidine have that reduction but maybe prostaglandin analogue. Sometimes a combination of the two can be helpful. So we talked about when to do imaging when you’re highly concerned about CNS process. Neurological symptoms. Mismatch of clinical appearance. Pallor out of proportion to cupping. Testing doesn’t match up to neurological symptoms, get an MRI. Have you seen low pressure glaucoma associated with IFIS? I haven’t. I have not. That’s interesting. I will think about that. I’m not aware of an association with Tamsulosin and low-tension glaucoma. What I like is when other people answer other people’s questions. One person ask can we define low-tension glaucoma in one sentence and the answer which one of you all put is glaucomatous optic neuropathy occurring within a statistically normal IOP. That’s great. What is your threshold to send a patient to the primary care doctor for a coagulopathy work up and if they’re found to have either, does this change your management? I’m not the one to diagnosis anemia. Usually, they come in reporting that or a known history of coagulopathy. So I’m not typically the one sending the patient to the primary care doctor requesting a work up. Typically the patient comes to me aware of these comorbidities already. But that said, if I’m know this patient has low-tension glaucoma, they have pretty good pressures. There is evidence of progression despite good pressure control, I’m going to think about blood pressure monitoring, maybe rule out anemia, coagulopathy, et cetera. So does it affect my management? We’re treating the pressure goal aggressively, so not really. Like the ophthalmology management: But maybe it affects my counseling, this is a team taking care of you not just the ophthalmologist. Okay. Is there any association of low-tension glaucoma with keratoconus in the advanced stage. I’m not aware of that. Love it when you answer each other’s questions. Classically you get disc hemorrhages. So what is your first line glaucoma medication in normal tension glaucoma. I think brimonidine is a great choice. If the patient was on it before or it failed or allergic, try latanoprost next. Is normal tension glaucoma a diagnosis of exclusion? No. Have your antenna go up if you see on exam or history any red flags and we talked about that before, limited diet, exposure history, STD history. Review of systems concerning with many neurological symptoms or some neurological symptoms. Giant cell arteritis review of systems positive. I have that in mind if there is a mismatch on what I’m seeing on testing. Minimal cupping but disc pallor. The testing isn’t lining up. I would actually, I’m not saying normal tension glaucoma is a diagnosis of exclusion but think about other potential causes of optic neuropathy if there is a mismatch in your exam and history. What can you do for hypotension if a patient is not on hypotensive medicine. Great question. That is beyond my pay grade. So yes, you can get more patients, I think this may be related to that Flommer syndrome, classically seen in like tall slender Caucasian women. Highly myopic, the blood pressure runs low. I believe there’s a few clinics in the United States that focus on these patients. But I’ve heard of, you know, patients, or some ophthalmologists recommending a salty snack before bed to mitigate the risk of nocturnal hypotension. Not a lot of evidence-based medicine on that that I’m aware of but it’s something you can offer. If a patient’s got hypotension, typically and if they’re not already seeing a primary care doctor or a cardiologist, I would probably link them up and just have good close communication with them. Treatment available for vasospasm, I’m not sure because I wouldn’t prescribe that. So I don’t want to speculate. What’s your opinion about water drinking tests in patients with low-tension glaucoma? I don’t routinely recommend the water drinking test in the diagnosis of glaucoma. I think that is a little outdated and a little crural. Many of my patients have significant comorbidities, congestive heart failure, et cetera, so I wouldn’t recommend that. Diurnal variation related only to open-angle glaucoma? No. I keep that in mind for all glaucoma patients. And in the context of normal tension glaucoma, I think about that if I’m evaluating a patient for the first time in the afternoon. I think maybe you come back in the morning next time to make sure I’m not missing an IOP spike that could align you with primary open-angle glaucoma diagnosis. We didn’t review ghost cell glaucoma so I’m not going to — we didn’t cover that. I don’t really know the answer to that question. All right. Would you consider lowering episcleral VP with Rho kinase inhibitors to reduce IOP? The way that I use Rho kinase inhibitors is as a last-ditch effort before surgery. Namely because of the cost. Also, some of those side effects are not insignificant, conjunctival hyperemia hemorrhages. I don’t really think about it as mechanism per se. I think about it as literally we’re throwing the kitchen sink at you. But maybe I should think about it as a mechanism. This is the last topical thing we can try before we think about surgical procedures. So I think about it in that way. So we made it through all the questions. I want to thank you all. It’s 8:10. Thank you for spending the morning or whatever time of day you are in the world with me. And I appreciate you taking the time to listen. Have a good day.