 All right, well, hopefully a lot of you have had a chance to see our patient who is upstairs, but our patient is actually joining us here at Grand Rounds right now, so thank you very much for coming and taking time out of your busy schedule to be here with us and kind of be a part of this learning experience. So first presentation is by Dr. Barlow, persistent positive dysphotopsia after ICL surgery for high myopia. Good morning, everybody. So this case is, as you can see, after ICL surgery and persistent dysphotopsia. Dysphotopsia, of course, is not unique to the ICL. It's something that we're all familiar with, with a fake intraocular lenses for cataract surgery, but also see it in other optical systems, whether it be glasses, contact lenses, where optical systems are used to image, such as a telescope or microscope. This is an issue that we see with any form of lens, and so it's not unique to this specific lens. Just a brief clinical history for those who didn't get a chance to see the patient. He's a 28-year-old young man, very healthy. In the eye exam, he had stable high myopia at his initial refractive consultations. He has spherical equivalent of about minus eight. He had normal topography and pentacan, but thinner corneas, and thus, given his higher correction, laser vision correction, surgery is not felt to be the best option for him. You can see his pupils fairly normal in terms of a little larger pupil for young gentlemen. Other measurements that are specific to the ICL, good endothelial cell count and deep anterior chamber in both eyes. Now, surgically, everything went very smoothly. He had his peripheral iridotomies placed two weeks prior to the ICL implantation, times two, security. In his ICL surgery, you can see the powers and size of the lens there. He performed June 1st of last year. The size was determined using sulcus to sulcus measurements and nomograms that have been published with that. There were no complications with his surgery. His postoperative course, first postoperative visit, you can see uncorrected vision is very good at 2020 and 2015. Pressure is normal as ICL vault is about as ideal as you can get there, just under 500 microns. His one month visit is where the issues started to present themselves. His vision is good. Pressure and CELAMP exam, unremarkable. Minimal refractive error left over there. But he was starting to notice problems with night vision, with glaring halo effect, and unwanted visual symptoms, some of which sounded like they might be attributable to his PI, with specific point light sources at specific angles. He asked about the possibility of removal of the ICL enclosure of the PI if these symptoms do not improve. Of course, encouraged him to give it a little more time as we know many times patients do improve with what we call neural adaptation over time. At his three month post-op visit, no significant change in terms of the exam or symptoms. And most recently here earlier this month, a six month post-op visit, vision is still doing very well, so LAMP exam unchanged. I repeated his manifest refraction again, no significant refractive error. Still having the symptoms, noticing some subtle improvements with PRN use of AlphaGam, and maybe some softening to a modest degree. We discussed a trial of AlphaGam three times daily to see if we could improve his adaptation to these symptoms, hopefully reduce them at least temporarily and allow him to adapt. And then of course presentation at Grand Rounds to give him a chance to meet some of our other refractive surgeons, get further inputs on his case. I just wanted to do just a brief overview. There's not a lot in the scientific literature on this specific issue. This specific issue, of course, Glare and Halo with any type of intraocular lens. We know with time tends to improve thought due to neural adaptation, the brain's ability to soften the effects of unwanted visual phenomenon, focus on the information that's important to visual processing. What results in poor adaptation? These may be more rhetorical questions. If anybody knows the answer, please type up and let us know. And poor adaptation may be personality related based on some literature if we look at IOLs, but not a lot of great answers to that question. How can we redirect those that are not adapting well? Not a lot of great treatments, AlphaGam, of course, used for night vision symptoms. Others like negative dysphotoxy can be corrected with solid glasses with frames that cover that shadow effect that we see with AFAKIC IOLs. Looking at some of the literature specific to the ICL in Glare and Halo, not a lot specific to that, but several that do at least address it as a secondary outcome measure. This study was a quality of life study published in ophthalmology in 2010 as a prospective case series. They see 34 total patients. The main outcome was the QIRC score. And you see pre-op and post-op, and improvement that was statistically significant. So quality of life overall was improved. Most of the items on that questionnaire were significant improvements specific to the difficulty with driving in glare conditions. There was no significant difference. It wasn't worse or better after the procedure. There were seven patients that initially noted about 20% of patients initially noted Glare, Halo, or Starburst. The questionnaire was administered about three to four months post-op. All of them had noted some subjective improvement in those symptoms. So another paper here. This was actually an abstract from ARVO, Risk Factors Associated with Glare and Halo. This particular cohort had a higher percentage of Glare and Halo. I can see the 55 AIs of 30 patients. It's a 12 month post-op assessment chart review with questionnaire for those patients. The incidence of Glare, you can see 40%. Halo and Glare, although the severe incidence was a little bit lower, about 15%. Halo correlated with pupil size. You can see the correlation coefficient, 0.25. Not a strong correlation, but there is some positive correlation. Severity only correlated to the actual ICL power. And with multivariate analysis, the ICL size was the only factor using a cutoff of 12, essentially cutting off to the smallest size that affected that. Other symptoms, they were not able to find any statistically significant association with specific factors as a causative feature for Glare. This is a Canadian study, CJO, just very recently published in 2017 as your retrospective case series, looking at their outcomes in general, looking specifically at our interest at the adverse event, Glare and Halo was reported in 6 AIs, 7.9%. They did not categorize it in terms of severity or discuss treatments other than the expectation that over time these symptoms would improve. This is a study looking at different reasons for ex-plantation of an ICL percent at the King Khaled Eye Specialist Hospital in Saudi Arabia. It's a retrospective chart review. You can see they performed just under 800 ICL implants, only had to remove 30 of them, so about 3.8% removal. Most of them due to sizing issues, the cataract, high residual stigmatism, one retinal detachment, and only one patient that had the ICL removed for intolerable glare, so consistent with what we typically see clinically and what is felt to be an issue that tends to improve the glare, not typically being a strong cause or reason for ICL exploitation. Looking at the original FDA approval study, it actually has a little more detailed information. This was published in 2004. It was three-year safety and efficacy data. You can see a large cohort to 526 eyes, 294 patients. You see satisfaction rates overall very, very good. Specific to glare and halo, you can see that most patients did not notice significant changes pre and post-op, about 80% in that category. Improving by one or two categories and their questionnaire or worsening by one or two categories, you can see very small numbers in terms of improving or worsening. And then one category change, about 10% in each group there with glare and halo, about 5% to 8% there. So most patients, again, do not notice significant differences pre and post. So that's a review of the literature that I could find specific to this issue. In general, the overall points that are made in these studies with time, these symptoms tend to improve. And when we compare this to other refractive procedures, PRK and LASIK, the glare and halo numbers seem to corroborate or similar, and the experiences they tend to improve over time. For those patients with persistent dysphotoxy, sometimes it's going to be a little bit challenging in terms of treatment options. Does anybody have any experience that they could share or thoughts on this specific clinical case regarding his symptoms and treatments that you might suggest that could be helpful? Roger? Have you considered low-dose polycarpene? Have you got more people with it? I haven't considered that yet, but certainly that would be an option. Obviously, we're using alpha-gain with a similar sort of thought process behind it to try and blunt pupil dilation, particularly in mesopic circumstances, but I haven't thought about that just yet. Mark and Amy? We're fucked upstairs, but it seems like his symptoms are a little bit worse in the left eye. Okay. As many of us know, we do a lot of eye surgery where we can make de-eyes. It's really kind of a confusing geometry of what's actually happening, because in his case, on his right eye in particular, I mean, those de-eyes are tiny. They're covered by a removable mask. So there's light being reflected from the inside of the eye out for the de-eyes. Right. And so, and we talked about this upstairs, even the literature is kind of all over the place as to where the best place to put a de-eyes. I have an anecdotal experience of a patient who was being prepared for ICL at another center, a very reputable place, but I think a surgeon and a clean-in just completely freaked out after the de-eyes were performed and didn't actually go into the conservatory. So we know that de-eyes can cause issues. Having said that, I've had my own patients with well-placed de-eyes that have done really well with alpha-gad and just encouragement. I think knowing that it's okay and kind of explaining what's going on, generally, people can adapt to it. But I do think constricting people just because it lets the light in, I know he's going to make an interesting comment. I haven't actually done this, but I guess for you to know where that glare is coming from, is it coming from the P.I.'s themselves or something else is trying to cover up the P.I.'s? Not surgically, but you can take apparently like a permanent marker, like a sharpie, and color on the cornea over the P.I.'s and see if that cuts down on glare and halos. Okay. Yeah, we try to see. And then if it does, maybe you could consider like cosmetic contact lens as the next step. Okay. Thanks. Well, that's what I was going to say. It's maybe a plane of tinted contact lens just to see if that would walk the P.I.'s. To see if the P.I.'s more likely the source versus the lens itself. Mark said if it's coming, if it's reflecting off the inside of the P.I.'s, I could follow that. Walk the P.I.'s up. Thank you. Nick. The difficult thing with this flotops is in a faking IOL, as we still don't know the etiology. And I know that P.I.'s, certainly something's going to add to it, P.I.'s not something we have in pseudo-faking this flotops. So I think the mechanism in pseudo-faking this flotops is people have looked at many of the different etiologies, IOL, imperial, edge design, relationship to the capsule on the edge of the chamber. All those are always interesting is it's pseudo-faking. This flotops is constricted. People doesn't do anything. And, you know, you would think that it would because of the takeaway and the issues with the edge, but to be honest, it doesn't. Whereas in someone who is still faking and having this flotops is if it's not related to the P.I.'s itself, I have real difficulty coming up with an etiologic mechanism because the crystalline lens is still intact. You don't have the, you know, the interface of the lens and the capsule bag to worry about it. So if it's not coming from the P.I.'s, I still don't know exactly what the etiology will be in a faking this flotopsia. Yeah, it's difficult because it's in the sulcus, which is the position for a pseudo-faking that you would want to move the lens to. So you're not having interactions. You're not having the change in the depth of the chamber. So, you know, you've got to really look seriously at the P.I.'s. I saw another comment just in general for patients with nighttime vision symptoms, whether it's a refractive surgery, cataract patient, whatever, it's just making sure to separate out the component of untreated refractive. Yes. Even a little bit of a cynicism, if they have a bigger pupil, that's going to cause some quote-unlater or Gala or whatever. We know that young patients in particular may be a little more myopic later in the day etc. So, just be more separating that out. Yes, I agree. I agree. Thank you. Any other comments? Thank you.