 Okay. All right. Let's get started. I'm Leah Owen. I'm one of the residents and I'll be presenting grain rounds this morning. And the first topic I have is a patient presentation, a woman who came in and was certain she had a brain tumor. And thankfully she did not, but she did have optic disc edema and pressure elevation. So she was a 55-year-old woman. She complained of acute onset, right-sided, strong headache. She had spots in her vision unilaterally on that right side as well. She felt like she was looking through a nylon veil. And this occurred approximately six days actually before she presented to us. She did not seek treatment during that time. This was associated with injection of the right eye. There was some photophobia and associated discomfort, but no pain specifically with eye movements. The spots in the veil somewhat cleared after the first couple of days, but she had a reappearance or what she felt to be a reappearance of this cloudy vision, but now in the upper visual field, again, in her right eye. And this was just a 24 to 48 hours prior to her presentation to us. So longer in the course. She denied any trauma preceding these symptoms. She denied any history of migraine headache recently or remotely, any flashing lights, floaters, additional history. She did not take any medications. She doesn't have any significant allergies. She doesn't have any ocular pathology in her family, nor a history of migraine headaches in the family. Her father did have some sort of a brain tumor, which I think prompted her concern. She was a healthy woman. She had low blood pressure, but didn't have things like sleep apnea, anemia, autoimmune conditions, and migraine headaches. She occasionally used alcohol, but really didn't have any other pertinent social history. She was myopic, mildly myopic, but no other significant ocular history with surgery trauma, no history of infection, her headache or otherwise. Her review of systems was largely negative. So she had no jaw claudication, scalp tenderness, fatigue, weight loss, no subjective neurologic changes or fluctuations in her weight. When we examined her at presentation, which again was six days after her initial onset of symptoms, her best corrected vision was 2025 and the affected right eye in 2020 and her left eye. She did have a 0.3 log APD in her right eye associated with some mild red desaturation in that eye. Her pressure was elevated in the right eye, 36 versus 18 in her unaffected eye. Her visual fields were grossly full by confrontation, as were her movements, and they were painless. She also had no neurologic deficits on examination by Dr. Katz. A split-lamp examination demonstrated normal findings of her lids and lashes. Her conjunctiva was really fairly normal. I didn't see a lot of injection at this point in her presentation, but her cornea did show some very mild edema and scant, stellate KP on the right side and a normal appearance on the left side. Her anterior chamber demonstrated mild inflammation with cell and flare on the right and a normal appearance on the left. Her iris was normal. She didn't have any signs of atrophy or transillumination defects. She did have some anterior subcapsular cataracts that were equal bilaterally. Her vitreous was quiet, and she did undergo gonioscopy, and that's what that is supposed to be spelling there, and it was open to scleral spurs. She didn't have any evidence of chronic inflammation, PAOS, or any other findings of angle closure. Her optic nerve on fundoscopic examination demonstrated a stage 1 discodema on the right side, and this was marked for inferior sectoral swelling. Her left nerve was normal in appearance, but the cup-to-disc ratio was very small at 0.1. Her macula and vessels were normal. She didn't have any evidence of vasculitis, periphery completely normal, and the vitreous again clear without any hazer or evidence of inflammation. At presentation, she underwent visual field testing, which demonstrated a normal visual field on the left eye, but as you can see in the right eye, she had a superior defect, most notably in the nasal quadrant there. You could hallucinate to think that that was an enlarged blind spot as well. She wasn't as reliable with her right eye, but it's clearly not a normal visual field. Our assessment of this patient, she's an otherwise healthy 55-year-old woman. She has unilateral elevated intracular pressure, mild enter inflammation, optic discodema, correlating with visual field changes, and a contralateral disc at risk with a small cup-to-disc ratio. She essentially has two phenomenon here. She has kind of enter inflammation and elevated pressure, but she also has some posterior findings with optic discodema. In thinking about the differential, I kind of separated it into those two pathologies. In thinking about the optic discodema and what can cause that, certainly increased ICP is what this patient is worried about, as she's concerned about a brain tumor. That can be the spectrum of a compressive optic neuropathy to kind of an IIH picture, though she, at the age of 55, is not really in that demographic. Certainly, you can have unilateral increased optic discodema in the setting of a mass, for example, with a foster Kennedy syndrome, but we didn't see a contralateral optic nerve pallor, as you might expect in that syndrome. Certainly, this could be a presentation of optic neuritis, but she didn't demonstrate the classic pain with extracula movements. Her vision is still fairly good, so it's not as likely. It could certainly be an ischemic optic nerve injury, either an arteritic or a non-arteritic. As I mentioned on her review of systems, she didn't have jaw claudication, fatigue, scalp tenderness, things that we associate with an arteritic presentation. Of course, it could be pseudoadema, drusen, or an anomalous optic nerve, for example. Then other things that can generally cause a unilateral optic discodema, but are not as likely in this patient, are toxic, traumatic, nutritional, insult, neuroretinitis, or diabetic papillodema. Then thinking about her other findings of anterior inflammation and increased intracranial pressure, some things that come to mind would be Postner-Schlassman syndrome, which is characterized by both of these findings. Certainly an anterior uveitis, either an infectious or non-infectious form, can present this way. Usually you would see a little bit more in the way of inflammation, but you can have a spectrum, and HSV can have some similar findings with scant, KP, mild inflammation, and increased intracranial pressure. Then finally, Fuchs heterochromic eridosoclitus can also present in a similar way, but usually you would see more prominent erosatrophy. Based then on this differential, what we postulated to be the case in this patient is that she has Postner-Schlassman syndrome accounting for elevated IOP and anterior inflammation, and that this then was the cause of an ischemic optic nerve injury. To convince you that this is a legitimate hypothesis, I'd like to reference some cases of this reported in the literature. There are two that are fairly good reports of this type of pathology, and one that could be consistent with that, but these patients were older patients with very high presenting intracular pressures and a diagnosis of Postner-Schlassman syndrome. These cases had documented optic nerve edema unilaterally followed by pallor, and then they had risk factors for ischemic optic nerve injury that we'll go into in a little bit more depth in a moment, but a disc at risk, as I mentioned this patient has with a small cup-to-disc ratio, and then blood flow factors, things that can impact blood flow to the optic nerve, hypertension, and hyperlipidemia. To highlight this a little bit more, as Dr. Katz did for me, he referenced this particular paper, which he I'm sure is quite familiar with, where he saw a patient with a similar presentation, this 41-year-old woman, very similar presentation to what we were seeing, probably a little bit more optic disc edema than grade one, which is the patient I'm presenting today, but this disc edema correlated with diffuse deficits here on her visual field, and then at six months resolution of disc edema with pallor, but remaining visual field deficits. So in thinking about then the diagnosis and treatment of this patient, I thought it would be helpful to consider both entities, the Postner Schlossmann syndrome and the ischemic optic neuropathy, as Dr. Warner here, which is a neuro-ophthalmologic condition. So anteroschemic optic neuropathy, as we're familiar with, is infarction of the optic nerve head just posterior to the lamina crubrosa, and it's due to inadequate profusion by the posterior ciliary arteries. This is pictured here. This is the lamina crubrosa with the posterior ciliary arteries, and it usually leads to a painless monocular vision loss that can develop over hours to days. And there are two forms of the disease. There's an arteritic form secondary to a vasculitis, and what we think of mostly is giant cell arteritis with the symptoms that I mentioned before, or a non-arteritic form of the ischemic injury secondary to inflammatory small vessel disease or poor perfusion for other reasons that we'll discuss, and this actually constitutes most of the AIO and is the most common cause overall for optic neuropathy in patients over 50. So we feel that our patient was most likely to have a non-arteritic presentation of ischemic optic neuropathy, and what are the risk factors for this condition. So as I mentioned, a disc at risk, a small cup to disc ratio, which is postulated to crowd the optic nerve fibers in which that an insult in perfusion causing swelling will then create additional injury because of the combined space. Anemia is postulated to just be a risk factor for poor oxygen delivery to tissues in general, importantly the optic nerve, poor perfusion pressure in the setting of coronary artery disease and diabetes, as well as hypertension, and fluctuations in systemic blood pressure that we can imagine happen during the night as people can become hypertensive at night either on their own or when they take their blood pressure medications at night or in the setting certainly of low systemic blood pressure chronically that could then even go lower at night. And then finally for fluctuations, we also think of people who take medications like sildenafil that can cause systemic blood pressure to lower acutely and then decrease perfusion to the optic nerve. And finally sleep apnea has been postulated to be associated with risk for ischemic optic nerve injury. And then thinking about the risk for these specific factors, the ischemic optic neuropathy decompression trial demonstrated that 60% of patients with a non-arteritic ischemic optic neuropathy had at least one basculopathic risk factor, 47% having hypertension, 24% having diabetes. And the same trial demonstrated that approximately 15% of these patients then would develop ischemic optic nerve injury in the fellow eye, the initially unaffected eye within five years, which is a big deal if you've already lost a vision in one eye. And this could be even a greater risk for younger patients in some other studies. And so it is important to think about the risk factors that each individual patient has and how these can be modulated. However, the ischemic injury doesn't seem to recur as often in the affected eye because it's felt that if it truly isn't kind of an anatomic phenomenon that once some of the nerve fibers are lost, there's more space. And so even if subsequent swelling does occur, there's less risk of compression from that swelling and additional injury. So the natural course of AION in general, it's felt that the vision worsens progressively initially and then remains stable. Some studies have shown recovery over time, even up to three lines. But in general, this isn't felt to be the case. A recent study out of Singapore showing these initial visual field deficits demonstrated that about 77% of the patients had no change at six months after their initial presentation in their visual field. 15% did show some small improvement and then actually 7.5% worsened. But overall, people generally remain stable and it's difficult to get that vision back. But what are the types of treatments that have been studied to try and do so? Well, there's a nice review by Adkin that came out in 2010 of chronicling a lot of these trials. And some of the early trials are listed here, so the 60s through the 90s. And they really focused a lot on anti-coagulation, thinking it's a blood flow issue. But these didn't show dramatic benefit. There were some early trials, case-controlled studies looking at steroids, thinking that the swelling component is contributing to some of the nerve loss given the type environment of the optic nerve. So that a seroid could reduce some of the swelling. And these early data were promising in that regard. And so some of the later studies looked at that question, but also some of the treatments that we think about more often now, like bramonidine. And so to highlight some of these, the optic nerve decompression trial that I mentioned earlier didn't show any benefit of optic nerve decompression in the setting of the edema. But some of the more recent steroid trials have shown some visual improvement in patients treated with oral, high-dose, oral steroids. Bramonidine, which we occasionally will put patients on for neuroprotection in this setting, did not really show any benefit, though these trials were difficult to enroll in because of the time frames for enrollment. But they did show either no benefit or possibly a worsening in visual outcomes. And this is really surprising given what we've seen in animals for bramonidine. And I was interested in this question because we do frequently suggest to patients that they go on bramonidine in the affected eye and sometimes even in the unaffected eye as a preventative measure. And in animals, just in the setting of experimental glaucoma and monkeys, administration of bramonidine has shown increased retinal ganglion cell survival. And then in the specific setting of ischemic injury to the optic nerve, bramonidine does demonstrate a reduction in the retinal ganglion cell loss in response to this injury. So you can see in A, this is an untreated segment with more cell loss here in the ganglion cells than in B or in C, which is the healthy control. And so I think that there are questions about their model for ischemic optic neuropathy. Locally inject rosebengal into the vasculature. And I don't know how certainly that would cause a vascular insult. But I think if anything, it might be more severe than what we sometimes see in humans. So there are questions going forward, but I think that the animal studies are certainly promising and there may be more to this if we can design a trial that isn't quite as problematic for enrollment and quantification of results for bramonidine. But nonetheless, moving on to an important question of secondary prevention now and what's actually been studied for this, because as I mentioned, 15 to 35% of patients might experience this ischemic injury in the second eye after they've already had some catastrophic vision loss in one eye. And of course we would want to prevent that. And what the major studies really have looked at aspirin and they've all been retrospective. One showed a statistically significant benefit to aspirin, but all of them did show some trend towards statistical significance and putting your patient on aspirin to prevent this injury in the second eye. But I think that you have to kind of consider what type of patient you're looking at. For example, if you're looking at someone who is having an ischemic injury from a low flow system, they have low blood pressure, they're on sedentifil, they're taking their blood pressure medications at night. Aspirin may not have as much of an effect as if they have coronary artery disease and they're not getting good perfusion because of that setting. So in that setting I would expect more benefit from aspirin. So I think you kind of have to understand the physics of the system with regard to your patient. So moving on now to the other entity that this patient was felt to have, Pashner-Slasman syndrome, the form of secondary open-angle glaucoma first described in 1948, generally occurring in people aged 20 to 50 years old. And this is from one of the seminal papers and I thought it was really interesting as some of these criteria have changed over the years. But in general the features of this condition, it's a unilateral condition characterized by recurrent episodes of a very mild non-granulometous anterior uveitis. The patient will experience mild discomfort, halo, slight blurring of vision, similar to what our patient described. The slit-lamp findings are characterized by corneal edema, elevated intracular pressure, which is usually out of proportion to the inflammation that you see. So very mild inflammation but very high intracular pressures. Open angles on gonoscopy, fine KP, minimal inflammation, and sometimes medriasis in the affected eye. Attacks can last for a few hours or they can last for a few weeks and you can't know from the initial presentation which it will be. And then this criteria is interesting that the patient will have normal visual fields and optic discs in this condition and by and large this is true but there's some more recent data that bring this into question. And then in between attacks, initially it was felt that the IOP was always going to be normal and that provocative tests, by which I think they need visual fields, would be normal. So this is kind of our starting point and then trying to differentiate this condition from other glaucomatous reasons for having high pressure. These are some of the things that really distinguish postioners loss men. As I mentioned the very mild anterior inflammation that's out of proportion with the high IOP so a true uveidic glaucoma either infectious or non-infectious usually has a little bit more inflammation though a herpetic infection can have similar appearing KP. And then this condition never develops posterior synesthesia so in the uveidic and herpetic glaucomas you usually see some posterior synesthesia development. And then this is an interesting phenomenon in that we're now seeing in postioners loss men patients that they do develop some form of iris atrophy which was always felt to be more indicative of the Fuchs heterochromic, aerocyclitis or even a herpetic sequelae but these patients can develop some types of atrophy which can make it a little bit more difficult to distinguish between these types of glaucoma but certainly in Fuchs we see these fine abnormal angle vessels on gonoscopy which is very characteristic for that condition so it could help to distinguish these two entities. So in thinking about the treatment for postioners loss men we treat the pressure and the inflammation so usually we use topical cortical steroids as well as a glaucoma agent and usually that's pred forte and then carbonic anhydrous inhibitors have been found to be very efficacious and usually because these people present with such high pressures initially they usually are placed on oral diamox and then possibly a topical carbonic anhydrous inhibitor or a beta blocker. The prostaglandins that they usually do lower pressure a little bit better in general however they have been associated with recurrence of herpetic uveitis and so if that's on your differential which usually it would be in these patients it would probably not be a good idea to put these patients on a prostaglandin and just in general uveitis treatment there is a question as to whether prostaglandins can just potentiate other forms of uveitis and so for that reason it's not generally, that class is not generally used as much. So in the absence of underlying glaucoma damage usually these patients are not treated for glaucoma in the intermediate time points between attacks and I'll go into that a little bit more in a moment so our role as clinicians is to surveil the patients periodically for any signs of damage or recurrence of attacks though usually they're fairly symptomatic when they do have an attack and in general it's a medically managed condition, surgery is rare however a recent series by Japanese colleagues found that 26% roughly of patients studied had glaucomatous optic nerve damage so whether that was as a result of the acute attacks or whether they were having ongoing glaucoma in that population is a little bit unclear but initially when this condition was described it was felt to be benign actually that's how it's listed in the literature benign secondary glaucoma condition so in addition there has been an association with primary open-angle glaucoma and up to 45% of patients have been described with some form of primary open-angle findings so that between attacks they're having evidence of glaucoma and the study by JAP that looked at patients with glaucomatous changes you can see they had stable visual field changes which again were not postulated to be part of the syndrome initially and that this required surgical intervention looking at the patients who developed glaucoma I thought this was interesting really the only parameter of the parameters that they looked at they only looked at four things the things that they looked at the most indicative risk factor was duration of disease so it just makes you wonder if duration in and of itself is a factor but the number of attacks is not the factor is it the length of attack is it that they're having IOP spikes in between attacks that are not being properly treated because of course surveillance etc so I think there's a lot we still need to understand how these process and the risk for our patients and how we should be treating them and part of this is due to the fact that we're not quite sure why this condition develops and there's been so many theories ranging from an autonomic defect to an allergic process to an autoimmune versus an infectious process one patient in 1986 had a trap done and they looked at this pathology and noticed mononuclear cells in the trabecular interspaces but the reason for those cells being there was unclear another group actually went so far to look at H. pylori not in the eye but they looked at it in the serum and they were able to show an association with H. pylori antibodies and Postner-Schlesman syndrome though they weren't further able to describe what the mechanism might be perhaps autoimmune mimicry somehow to the H. pylori antigens but that's somewhat unclear I think the most credible data really is on CMV and so this was first postulated in 1987 when a group looked at patients with Postner-Schlesman syndrome and found about 70% of them demonstrated local synthesis of CMV antibodies and then this prompted a larger study in a cohort of 105 of these patients with enterubitis and elevated intracular pressure 24 were positive for CMV DNA in their aqueous by PCR and of these 18 had Postner-Schlesman syndrome and then 11 of the 18 were positive by reverse transcriptase PCR so there was active viral replication so that's suggestive but the data that I liked the most was that they then took these patients who were positive for CMV in their aqueous and were felt to have a phenotype consistent with Postner-Schlesman syndrome and they treated them with antivirals and it's a fairly small study and they use a lot of different treatment modalities but essentially they showed that there was a decrease in the attack frequency the degree of inflammation and the degree of IOP spike so I thought that was fairly interesting and this was just, you know only on the antiviral treatment they didn't use any other forms of treatment that we normally would for Postner-Schlesman and this was kind of a chronic treatment as a preventative measure so but it didn't reduce it to zero so either their treatment just isn't completely efficacious or there's something else going on so for our patient the treatment and clinical course we chose to treat with oral high dose steroids in the setting of AION and the studies that have shown some benefit for AION and then because Postner-Schlesman is generally treated with some form of steroids though normally topical but we kind of killed two birds with one stone she wasn't placed on topical treatment she was just placed on an oral high dose taper the pressure was controlled with Alpha-Gan for two weeks this was then discontinued and remained normal her Humphrey visual fields at four months out then demonstrated some resolution of this superior nasal defect her best-corrected visual acuity was improved to 2020 bilaterally where it had been 2025 corrected in that right eye the optic nerve appearance did appear fairly normal with a small cup though she did have a stable APD which was 0.3 log initially and the patient has since remained asymptomatic and just undergone normal surveillance so I think in light of the data presented this patient had a fairly good outcome she had a fairly mild presentation of AION but are there other things we should have done or should be looking for going forward and because this patient has low blood pressure we postulated that that was really the risk factor that she had for developing this AION condition so she had a low flow system systemically and then a transiently high interocular pressure and then the combination decreased perfusion to her optic nerve so if that is correct she is at risk for this occurring again because she continues to have low systemic blood pressure and so she probably will need to be surveilled very carefully she's a very reliable patient I think she will report any symptoms and we can get her on treatment on her own at home right when she begins to have symptoms but then should we treat her prophylactically with an antiviral just to try and reduce IOP spikes thinking that any IOP spike could result in AION in her so I think that's a question going forward not just for this patient but I think of other applications of this where you essentially have a lower flow system with a transiently high interocular pressure and as I've discussed through the talk the physics really are that the perfusion of the optic disc is directly proportional to the mean arterial pressure and inversely proportional to the interocular pressure and that the small cup to disc in certain patients then will crowd the nerve fibers and make them susceptible to even more damage from subsequent swelling than just the initial ischemic insult so other scenarios where this has been described include after cataract extraction with transient IOP spike and in the setting of acute angle closure glaucoma so I think it's something just to consider in any patient you see with a small cup to disc to just quickly assess what their perfusion risk factors might be to their optic nerve and how those might be modulated Do you have any questions? They did So they used patients with Poshner Schlossman that weren't treated with any antivirals and so they compared they compared to the control group but I felt like the most helpful data though it wasn't the most scientific was to compare to the previous spikes of that same patient so they did both I was just hoping to be the silver standard really Yeah so that chart had the different field defects and then the fact that all of those patients then underwent a surgical management which usually isn't thought of in Poshner Schlossman because they were having permanent vision loss based on fields and then I just have something really quickly I just wanted to talk really quickly about an opportunity I had to go to the Navajo Reservation Jim and I went down and is it, what time is it? Oh we have a little bit of time so Jim and I had the opportunity to go down with the marine outreach team to the Navajo Reservation and the purpose of the trip was to do screenings to understand what the population really needed a lot of these patients are limited even to going to doctors locally let alone coming up here so when we see patients up here we see a very select subset of severe pathology but we don't know because they're so severe they have to be transferred up here but we don't know what this population needs we could be more active in this community if we had a better sense of what they needed so that was the purpose of this trip and it was sponsored by the Moran Eye Center and the David Kelby Johnson Hope Fund which is a very generous donor to the Moran Eye Center and our outreach program so we went to two locations down in the four corners we went to Montezuma Creek and Monument Valley and we worked with the local clinics there which were very helpful in getting the word out to all of the people in the communities that we would be coming but we had a very good turnout we saw almost 500 people in the two days that we were down there and so I'll just go through kind of how we organized the clinics what types of things we were seeing et cetera we did partner with the Hope Alliance and so this is their group here which is a volunteer group who is very helpful in kind of accomplishing the logistics of flow and things like that so in general we saw 432 patients 314 were adults, 118 were children and the number examined this is what Jim and I this is the actual indirect enter segment and poster segment exam but the rest were examined in terms of vision and I'll go into that vision and refraction and things and so the age range was 3 to 95 years so it was just all comers and you can see that we were in gymnasiums of many sorts and people were just waiting for quite a long time to have their eyes examined so there is quite a need we started off with stations to try and have people flow through we started with vision pupils movements and confrontational visual fields and then the Hope Alliance helped us move to the auto refraction where you can see they had these portable auto refractors that then patients could move to a station where we had donated glasses and they just had these suitcases of all these donated glasses and then based on the auto refraction values they would try out different pairs that matched and the patient could decide what they liked best and then I didn't have a picture of this actually being done then there was a pressure and dilation station before the patients would then come for the examination and so this is where patients would kind of break off if they didn't have time to wait we encouraged everyone to get an examination but some patients didn't have time to wait and so they would just leave after getting the glasses so after dilation we would do their examination and this was quite an undertaking there was a lot of translation there were a lot of children but it was very exciting and very fun and the people were just so welcoming and thankful that it was pretty humbling so the adult scene this is kind of a list of some of the most common things that we saw certainly cataracts and so the percentages are either of the total patients refracted or of the total patients examined depending on which is more appropriate so for cataracts obviously we needed to examine them so almost 60% of the patients we saw had cataracts and about 19% of those had a dance stage which by indirect examination Jim and I said was about 3 plus and on and what I found was really interesting is there were a lot of hyper-opic adults many more than I was used to seeing certainly some myopic adults but not actually as much and we did see some pathologic myopia mostly indicated by the actual degree of myopia I didn't see a lot of other signs of pathologic myopia but we saw a good amount of diabetic retinopathy not quite as much was severe and not quite as much I mean 31% of examined based on the patients that we see up here from the Four Corners region I expected at like 100% but that wasn't the case we did see a good amount of really interesting astigmatism greater than 2 diopters was 19% of the adult population the range was about 2 to 7 diopters and really interestingly even in the very old this was still with the rule so it was an interesting type of astigmatism we saw some macular degeneration small percentage of wet changes a lot of turigia some hypertensive changes some people did have access and had cataract surgery we did see a good amount of elevated cup to disk and some increased indirect pressure even up to the 60s and beyond and we saw more amblyopia than I would have expected or this is presumed amblyopia based on inisomatropia no history of trauma and a good amount of chronic retinal detachment I guess maybe I should have expected that but didn't expect quite as much of that and so for the hyperopia I just looked that up because I just thought maybe I just don't see that much hyperopia but in fact the NEI says that there's only about 5 to 10% of Americans that are hyperopics so to have 42% of hyperopic patients was really unusual and then in terms of the astigmatism I looked and there really isn't that much investigation of this in the ophthalmic literature but the optometric literature has described this mostly in the pediatric population and so so this is commonly seen this high with the rule regular astigmatism is seen very commonly in the pediatric population and the most that's been described in the adults is that it persists with advancing age so the etiology and whether it's a form of keratoconus or something else is not really understood so in terms of children there are 118 children that were seen and this means that their vision was tested and they underwent auto-refraction and what we saw in these children quite a bit of myopia as compared to hyperopia which is a little bit different than what we normally would see here we did see a fair amount of pathologic myopia some very high values there and then again this interesting astigmatism fairly few deviations we did see a little bit of esotropia and some ambliopia and anisometropia we even saw at Trogeum and this was a very interesting patient I think I have a picture coming up of this Optic Distrusin because Jim saw the patient and then he said Leah, will you look at this patient it doesn't look very good so I looked and I thought oh we need a B scan and then Julie Crano was like oh well we have a B scan so it was very no idea we had a B scan but it turned out to be very useful because then we were able to examine this child and determine that he had Optic Distrusin bilaterally and he did not need an urgent MRI so in terms of unique adult findings we saw some very interesting things in native lens dislocation which was related to trauma saw some traumatic cataracts optic nerve pallor the retinal detachment mostly were related to trauma but there was one that certainly had some NV and that was probably why they ended up detaching but hard to tell when you see it kind of end stage we saw this interesting anterior perforation that had kind of granulated over and with a you know the eye was no longer open so it was a healed scleral perforation that the patient had had since birth and Jim actually saw retinoschisis which was really interesting and then we saw what we felt to be an end ophthalmitis after cataract surgery so not very many of the patients had had cataract surgery but the ones that had had some interesting lens placement and iris configurations and and this particular patient we felt had some pretty severe findings and we referred this patient to a local optometrist who could then put them up with a prepper ophthalmologist in the area because this patient we felt like had something that looked like CIN then we saw some you know a fair amount of NLP vision traumatic injuries to the seventh nerve dyschemic myelinated nerve hyperlare so I think that all in all we saw some very interesting things there were some busy days afterwards we went back we all stayed in the same house and we had a great time seeing we occasionally on the drive to and from the locations we did catch some of the scenery which was beautiful and kind of rainy when we were there but it was a good opportunity and I think it showed that there's going to be good turnout there's a lot of good coordination with the local clinics and things to get people to come to these screenings but I think that the ideal would be to have more targeted screenings now that we see what people are presenting with and have certain groups go down there was a huge need for pediatrics there were more pediatric patients than we could see because we needed parental consent for dilation and things and so that we can have a coordinated effort in that regard as well as some of the other specialty certainly I think glaucoma and retina would be too that would be really well received down there and cataracts although not as medically urgent I think would really help benefit some of these patients quality of life and things so there's a great need the patients are really welcoming and good to work with there's a great infrastructure for getting the patients into our clinics when we go down there and set them up and so I think it would be a great opportunity going forward for resident involvement and things like that any questions about that trip