 All right, so it's eight o'clock, so we'll go ahead and get started. We have Dr. Harry with us today. He's one of our faculty members here at the Moran. We all know him best probably for his ultrasound expertise in helping us with a lot of complicated diagnoses. He also works in private practice at the Salt Lake Clinic. Is that right? So we're grateful to have him here to talk to us today. He's going to talk to us about that dreaded 5 p.m. patient on Friday and how to handle those. So Dr. Harry, just call the resident. Yeah, that's what they're there for, exactly. Well, Randy and I both remember well from Jules Stein days that I think we sort of had a tradition for probably 5 o'clock with a famous Cornelholzer. For some reason, community area, it was sort of a tradition to 5 o'clock Friday, you know, late for your golf game, so send them to Jules Stein and they'll take care of it for you. So we start sharing these over there. I'd like to talk a little bit about some patients I've seen at kind of the late hour, out on patients and the things I've learned from them and maybe pass on a few things to you folks. This is a patient's 31-year-old woman. She lived in the Amana colonies near Iowa City. And she presented the emergency room with severe pain in her eye, hurt to move her eye, look over to the right, little proptosis, chemosis, edema, some double vision, and went to the ER, and their initial thought was orbital cellulitis, let's put her in the hospital, high dose IV antibiotics, get this taken care of. But on the way there, they had her stopped by the eye clinic. I just started my fetalship there in ultrasound, so I saw her and she'd had a CT scan, kind of early generation CT scans in those days, so it wasn't really that helpful. This was a scan, kind of amorphous, what's going on up there? Is that diffuse orbital inflammation? Is it something else? So it wasn't really obvious. So they had me refer to the ultrasound and I put the probe on and I pointed towards the lateral rectus muscle. And it's pretty obvious right away that the muscle is thickened. This is the lateral rectus muscle. Here's the tendon exertion near the globe. Here's the muscle belly. The A scan shows this great, big, thick muscle, very low reflective. So I really hadn't seen this before, at least this kind of presentation, so I called Dr. Osano, who I was training with at the time, and described the findings to him. He says, oh yeah, it's myositis, which we see all the time. And really this was a diagnosis I really hadn't been very familiar with in my residency. That was the early days of scanning, really you didn't have the capacity to really define these entities in the orbit as well. So he started on high-dose steroids. Well that was a challenge, trying to talk the infectious disease folks into, you know, here's a patient presumed infection, or we'll say elitis. I'm talking high-dose prednisone. And so they finally agreed to compromise antibiotics by IV, but also high-dose steroids at the same time. Started at 80 milligrams that night. The next day she was dramatically better. Really had shrunk down and 90% improved. Pain was pretty well gone. Immortality was returning, so discharged in a couple of days and sent home on maintenance steroids for a couple of weeks. So I was sort of introduced to the concept of myositis, and really hadn't been familiar with it, as I said before. What is myositis? Basically it's inflamed muscle, and the age range is quite a range from three years old to up to the 80s. And it's more common in females for some reason. It's usually acute, unilateral, often just one muscle. But there may be chronic, recurrent cases. It can be bilateral. It involves multiple muscles in these kind of recurrent cases. It's the third most common orbital disorder, following grays and proliferative conditions. It's actually a subcategory of orbital pseudotumor. Again, we kind of learned that with modern imaging techniques. Now we can sort of characterize, you know, is it myositis, is it altichloritis, is it scleritis, dachyritonitis, so we're able now to subcategorize these different entities that we used to lump in orbital pseudotumor. Example here of a scleritis. So here's the scleral layer thickened. Here's the muscle inserting with the tendon insertion. So adjacent scleritis and myositis going together. So a lot of these so-called pseudotumor entities that we used to lump are now broken down into these specific entities. Pain is, most patients have pain in the orbit, around the orbit, but about 5% don't really have much pain. So these are atypical. And you'd expect pain with all of these, but there are some that don't. Usually, motility impairment with double vision. A key finding always is, does it hurt to look either to one side or the other? Now a lot of patients with eye pain, so it hurts to look around. I say, well, does it hurt to look in one specific direction? That sort of helps to localize if it really is. Myositis kind of picture, compared to some kind of diffuse orbital pain. Proptosis, usually not extreme, but mild proptosis. Eyelid edema, conjunctival hyperemia, and chemosis are also common. Difference of diagnosis. Graves disease is certainly towards the top. And a lot of patients, there's kind of a spectrum that I see. Graves is inflammatory by definition. And you can have acute grays presenting with almost a myositis type picture. So you can have generally grays kind of muscles, but you can have one or two muscles that are quite inflamed and low reflective, consistent with a myositis kind of picture. So this can be a lot of overlap with grays disease in these patients. Vascularitis, coidosis, what we'll say, ullitus, oral tumors, infectious entities such as herpes, Lyme, sister socosis, and also association with giant cell myocarditis, lupus and Crohn's disease. So that's kind of what you think about when you see myositis. But most of these patients, already in my experience, don't really have anything systemically going on. It's just isolated to the muscle. You can work them up to all kinds of tests, but really just a good history and physical utility kind of pins down the fact that it's isolated to the muscles in the orbit. As far as involvement of muscles, one series stated that the medial rectus is the most common, followed by superior, then lateral, superior oblique, inferior oblique, inferior rectus and inferior oblique. So that's kind of the order of muscle involvement, but it can involve any muscle, and again, several muscles sometimes, and sometimes bilaterally. So therapy, the best treatment, of course, is high dose prednisone with rapid tape or either IV steroids to start them off if they're really extreme or high dose oral steroids and usually rather dramatic response. Now, the question always is when to taper the steroids, when to stop them, if the flare's up again, what do you do? I've had pretty good luck with endomethacin as kind of a, not as a primary therapy necessarily, but when they're starting to taper their steroids to concurrently start endomethacin towards the end of the taper of steroids. So to try to avoid a flare up. To a lot of these patients, dramatic as they respond to the initial therapy and they get better fast, they can flare up again. That's not uncommon to have recurrent myositis. So I think in the methods and maybe have a role in that to helping prevent that kind of recurrence. Antitissue and necrosis factors are popular now for arthritis patients, infusions, and even subcutaneous injections now of these, and they've been reported to help in cases of myositis. In methotrexate, I had one patient that had recurrent myositis. I had those steroids every couple of months just kind of getting cushionoid kind of symptoms. So we decided to try them with methotrexate and just responded dramatically. He's had no recurrences over a couple of years now. So that's a good kind of backup drug. Again, not primary, I think still steroids are the primary treatment, but this can be a good backup therapy. So in large muscles, what do you think of? Again, Graves is number one. Most common cause of unilateral proptosis and also a lot of proptosis is Grave disease. Myositis we're talking about, infectious causes, vascular lesions that can, especially with fistulas, CC fistulas, can actually increase muscles size just by congestion of muscles, metastatic tumor. Sometimes you get into the muscles. Lymphomas, rabdomyosarcoma, acromegaly, amyloid and lithium have been reported to sometimes cause increased muscle thickness. So these are all things to think about when you have enlarged muscles. It's kind of a montage here of three kinds of disorders of the muscles, at least two kinds. This is a normal muscle by A-scan. So here's a normal patient with A-scan to the muscles. The tendon's up here, a little tiny blip down there. Here's the muscle starting to get thicker. Here's the maximal muscle thickness. As you go back, you scan the probe along the muscle towards the apex. So this is a normal looking muscle, normal thickness, normal internal reflectivity, sort of a high irregular reflectivity. This is a Graves patient. So Graves patients, again, the tendon looks about the same. It's really not thick and engraves these normally. As you go further back in the muscle here, you get maximal thickness, so it's quite thick compared to that muscle. And reflectivity is really important with these patients. Reflectivity and Graves patients tends to be heterogeneous. It's not homogeneous. It's more kind of a mixed bag. You get high and low spikes based on the pathology correlation. And this is a myositis patient. The tendon is quite thick compared to the normal muscle and the Graves muscle. So that's a key finding in myositis. You look for tendon thickening. As you go further back, you see the muscle thickness here is maximally thick. And it's quite low reflectivity. Here is really important. A-scan is very helpful for that because lots of things can look big on CTs and MRIs as far as muscle thickening, but I can actually characterize the muscle with the A-scan as far as the pathology. So that's very helpful to be able to do that. This demonstrates, again, the concept of the normal muscle based on normal muscle architecture. Scepta, muscle fibers, fat. So you get some interfaces for reflection of sounds. So you do get some reflectivity inside the muscle. It's kind of a medium reflectivity kind of in this range here based on normal muscle architecture. You go into a Graves muscle. You get kind of an inflammatory edema along with normal muscle fibers. So you get, again, interfaces reflect sound. You get kind of a mixed bag of interfaces. You get some high, some low. So you get more of this heterogeneous reflectivity inside the muscle, which is typical for Graves muscles compared to a normal muscle. And the myositis muscle, diffuse inflammation, kind of replaces the muscle with inflammatory cells. And the more homogeneous a structure is, the lower the reflectivity on A-scan. So, again, vitreous is quite low because it's homogeneous. There's not much in vitreous to reflect sound back. So in the muscle with a lot of inflammatory cells, you get low reflectivity based on the pattern based on the inflammatory cells. So those are different architectures of muscles. So basically, when you see a patient, you suspect myositis is very easy to put the ultrasound probe on. And I do two views. I do kind of a longitudinal view with the white mark on the probe facing towards the limbus. And you get kind of this long view of the muscle. Here's the tendon here. Here's the muscle belly, quite thick. You can do a cross-section of the muscle. You do a transversory where you put the probe parallel to the limbus. Go across the muscle here. And here's the muscle being cut across in cross-section. And here's the A-scan, showing, again, thick muscle, low reflectivity. So that picture is very characteristic of myositis. So when you end out, grab that probe and check those muscles out. Because it's really easy. Five minutes in the clinic, you know, you save a lot of work up, you know. MRI CT scans are, you know, helpful, but really quick diagnosis. Five o'clock Friday afternoon patient. You got a cinch. Start the steroids. Better than it took a couple of days. It really is a nice kind of a tight package to be able to help a patient and make the correct diagnosis. Okay, and present another case in illustrating something here. This gentleman presented, again, late in the day. I'm not sure if it's Friday or not, but it was a late patient, had-on patient. 47-year-old gentleman with decreased vision in the right eye, noticed a few weeks ago. Vision was 2060. Right eye, left eye was 2020. Normal intracur pressure, normal examination, except for the fundus finding. And he had a branch of vein occlusion on examination of the fundus. Okay, so I'm going to get to pick on residents. Dan, any thoughts at this point? Friday, five o'clock, you're sitting there. He walks in with an add-on, dropping vision. Do you see this picture in the fundus? What's your next step? Okay, photography's gone home. Five o'clock. Okay? There's my man. Okay, you know, five o'clock Friday, this is really not super-emergent. You can certainly wait until Monday, get an OCT or whatever, having to see a retina. But the blood pressure cuff, okay? They dusted it off. And he denied any history of medical history. He said, well, I'm healthy. I don't like to see doctors. I think I saw a doctor. Well, I think about 70 years ago, I think. So, well, let's check your blood pressure. 250 over 160. So, I called the emergency room. I said, which hero do you want to go to? And you want to go to West Valley. So I called ahead, which, again, is a trick that you'll learn that if you send them to the ER just without any notice ahead of time, they'll sit there for two hours to get checked in. They'll finally see the doctor. You know, like this whole thing. But by calling ahead and just alerting the ER doctor to what you're expecting. So this guy's got really high blood pressure and getting him right in, managing him. So he was admitted, he was to the ER and they started him on medication. I followed up a couple of days later and he was improving while responding. So blood pressure is easy to check. Something easy to do at that five o'clock hour. We can all do. So branch vein occlusion, good prognosis on younger patients, females or fewer nervous risk factors. They tend to do better than the older patients, the male patients, multiple risk factors, and poor initial visual acuity. These are all things that are going to make the prognosis worse for branch vein occlusions. About a third of patients end up with vision better than 2040. Two thirds have vision worse, macular edema, ischemia, macular hemorrhage, vitreous hemorrhage. These are all things that can make the prognosis worse for branch vein occlusions. Mild obstruction may show just scan. Hemorrhage is very subtle, especially after a certain time period. But it's complete obstruction. Looks very impressive. Extensive hemorrhage, retinal edema, caught in wool spots. It almost always occurs at AV crossings. That's the classic teaching about branch vein occlusion. And the further from the optic disc, the better the prognosis. These are all things that improve the prognosis. Systemic association. These are all things associated with it. As Dan mentioned, blood pressure is certainly got to think about. What are we doing? Atherosclerosis, diabetes, cholesterol. This group here is probably the vast majority. Most patients have vasculopathic risk factors. And they usually have a history of something like this in that context. There are less common things, homostastanemia, lupus, protein, CNS, antiphospholipid, Factor 5, Leiden, syphilis, Waldenstroms, polycythemia, multiple myeloma, leukemia, lymphoma, sarcoidosis, and TB. These are things to think about. But, again, they're rare birds. Most of the groupers in this group up here have the common risk factors. So, Paul, Bernstein, do you work up for branch vein? Do you do much when they walk in the clinic acutely? Do you bother with much work up? Certainly with blood pressure. I don't. Is there one more than another that you're seeing that with? Is it just generally across the board? So, they have to stop it whatever they're doing. At least that discussion with them. So, one source said extensive testing is not really indicated except in the usual presentations such as bilateral or younger patients as Paul referred to. Anyway, generally, again, they're in that general risk category in older patients. If that's the case, I don't do a lot of extra work up. So, think blood pressure. It's easy to do again. We have those available, most of us, and it's easy to get one to check there. So, you can really, in this patient, I think we probably saved a life, I think, with that kind of blood pressure we had under a 60 diastolic, we're talking stroke, myocardial infarction, in the near future. So, hopefully, that can make a difference in his prognosis. Another patient, 91-year-old, again, add on late. This actually was Friday, 6 o'clock Friday. Sudden loss of vision left eye. He had a history of prosthesis in his right eye. Trauma years ago, lost the eye. And so, he suddenly loses vision. Started about 4 p.m. He calls his daughter. He's on watching television. And he says, I can't see. So, he got to the office by 6 o'clock and he had hand motions in fairly as all I could pick up. And by history, he had a vision of 2050, at least in the past. So, sudden loss of vision. So, this isn't him, but this is a similar case. So, what do we see in there? Yeah, a cherry red spot. And what makes it a cherry red spot? What is causing that? So, it's a neurofiber-lagradymid, pretty much. And that doesn't really occur in the macula. You don't have any neurofiber or something. You're showing through exactly. And what's this phenomenon? Can you see it? The fluorescent shows it better. What's that called? Box carring. It's pretty dramatic when you see it. This is another case showing the box carring. Just kind of the blood cells just kind of lined up. Marching through the through the arterioles. So, at this point, Jim, since you're already responding, at this point, so, what are you going to do with this guy? 91 years old, one eye. This is his only eye. He's got obviously a central but an artery occlusion. What's your next step? So, digital massage. Anything else to reduce pressure that you might try? So, those are kind of classic things. Even more heroic is to do an AC tap. You know, paracentesis, try to reduce pressure by taking out some aqueous and you get a pretty dramatic reduction of pressure that way. So, those are things that, certainly, you're in the literature. So, at that point, let's say nothing's really happening. What's your next step? What do you worry about in a 90 year old with sudden arterial occlusion? Okay, GCA workup. So, what can you get right away? We have a lab. We have a CBC, looking for what's especially with CBC. Bladelet, right? And then, cedrate and CRP. The cedrate was 70. I got within an hour, I got a cedrate. We have a lab there. So, at this point, 70, cedrate. This patient with the presentation. So, high-dose steroids. That'd be an obvious thought. You're not going to be hurting him. You know, putting him in the hospital for that with that age. But that certainly isn't going to hurt him just beyond that for a couple of days. So, you kind of sort things out and consider a biopsy. But in this case, again, the trusty ultrasound. I put it on. And this is a drusen. So, this is a patient with drusen. This is how they look. This is not him. This is him. This is a a pacification back behind the lamina crevosa. So, it's actually not a druse. This is in the central blood and artery. So, it's an embolus stuck in the central artery. So, I picked it up and just, you know, met it with the ultrasound. So, right away, I've immediately narrowed the diagnosis down. This is not... No real history of headaches or scalp tendon or anything. The 70 is probably a red herring with that age anyway. So, it's embolic. So, does that change your thinking at this point? Embolus to the artery? Okay. And I called the ER. I talked to the doctor directly. You know, waiting a long time, getting checked in and things. He said, we got a patient with central artery occlusion. I treated him like a stroke patient, basically. Just, you know, a sudden occlusion, a one-eyed patient. So, I discussed that with him. And this was just later. This became a couple days later. He was in the hospital. This is carotid angiogram. And this is his left side. And that's a big calcific plaque sitting down there. Carotid artery reconstruction. So, definitely that was a source calcific plaque in the carotid artery with the emboli flipping off to the ophthalmic artery, the central red artery. And this was, I asked the radiologist, I went down and looked at it, and I said, can you see that embolus on the CT scan? He looked really carefully. He could not see it. So, I think it's small enough that ultrasound was able to pick it up. It was missed on CT. It just wasn't visible even though looking for it. So, ultrasound was very sensitive in this case to be able to pick that up. Okay. So, Dr. Hay rate Iowa study has found irreversible cell injury after about 100 minutes after occlusion of the artery. So, that's kind of been the dictum that if you can't help them within a couple of hours, you probably isn't worth it, but still other literature says it's up to 24 hours. So, again, you've got one-eyed patient. That's your only chance. So, I would be fairly aggressive. I think the things you mentioned, digital massage, things like that are worth trying. They're really iffy in the literature. There's not really good evidence that they really do a lot. Have you heard of carbogen, anybody? 5% CO2, 95% oxygen. Sometimes that is said to help by dilation of the central arteries in the CNS. So, what do you think, Judith? Anything that you've central artery occlusion? Is that something that's kind of a hopeless situation? Have you ever had any cases of anything, did anything for them? Well, they're recent. You're exactly right. So, even medical legally, even though it probably doesn't work and we probably know that it doesn't, I think at least make the effort. I think the usual. We got bad air though. It's probably equipment. Probably once in 10 years. Something like that. They often will come to the emergency room and then there's not a clear diagnosis and then there's sort of the I thought I didn't do it. I did digital massage. I gave him a couple of drops of lume again and sent him to the ER. I asked him to get carbogen, which they could never get. I guess that's something he just don't do. They just don't. Right. Yeah, the paper bag. Right, right. Well, I called the ER and I pled my case and I think I convinced him enough that they did actually give TPA and they got the stroke folks there and within two hours after he got there he got some intravenous. They didn't enter arterial. And history was he got to the ER and his vision was completely gone. He blacked out at the time he got to the ER and he's back down to about 2400. The last check. So, I don't know. That did something. Or what happened. But at least in that case it might have done something. Anyway, presentation about early 60s. Patients with visualized emboli with their route obstruction have a fit for six mortality rate over nine years compared to 20% for age matched population without emboli, 27%. Emboli seen about 20% of patients with central blood and artery occlusion. Emboli definitely makes a difference in mortality and ulima prognosis for these patients. So, in this case it wasn't visible. It wasn't in the arterial tree on the ophthalmoscope, but I did see one on the ultrasound. High pretension about two-thirds of these patients, orthosclerosis in about a half. Cardiac valvular disease in about a fourth. And think of that in younger patients, certainly older patients you think of carotid but anybody probably below 50 or 60 think of the valve and echocardiogram probably trancisophageal, echocardiogram. Tempolar doritis with visual loss. Most of these patients have AOM but about 40% will actually have a central blood and artery occlusion. So, somebody to always think about, you know, tempolar doritis, et cetera, CRP, platelet count, good history. So, embolism associated with poor visual acuity, higher morbidity, mortality. Cholesterol emboli are the most common followed by calcific bacterial tauke. Cardiac emboli are the most common cause in patients under 40. And coagulopathies from sickle cell or antipostal listed, most common under 30. So, these are again things to think about with the presence of emboli. Other causes, hypercoagulable, collagen basket disease, oral contraceptives as you just mentioned, polycythemia, besets, syphilis, migraine, low pressure in unconscious patients. One of these horror stories about having surgery for, you know, back surgery for hours on the head against the pressure and they woke up with blind in one eye or both. Inner tube valve, what does that mean? My first year as a resident at Jules-Stein, I was called emergency room and there was a young lady, they had been in the swimming party, she dived through a big inner tube, the valve caught her in the eye, came in with light perception vision. So, I called the staff, by the time we finally got to the OR, about three hours later, we did a canthotomy that really never got any vision back. So, I guess the current dictum is, Bufi was here, he would say, do it right there. Anybody done that? Done an emergency canthotomy? Yeah. Okay, a lot of hands going up. Okay, right, just right there. So, anyway, that should have been done in this case. We probably know more now than we knew then, but at least at this point, that was a dramatic case in my experience. That's the inner tube, that's not hers, but that's an example of one, with a big valve sticking out. So, don't dive into that. So, laboratory, what do you think about it? Again, we talked about working up for hospital temporal arthritis, ER, CRP, fibrinogen, antifossilifid, PT, PTT, protein electrophoresis, blood sugar, cholesterol, triglycerides, lipids, blood culture, endocrinitis, septic emboli, all these things to think about in this setting of artery blockage. So, treatment, we talked about a little bit, digital massage, lab, dimox, topical agents, carbogen, TPA, and hyperbaric oxygen. That's something that's kind of now coming into four. They do have that capacity. So, whether we should have done it with this, it wasn't given to him, but that's something to at least think about. Some reports of possible success with that. Some improvement in vision. So, most patients end up with counter finger to hand motion vision. If they have a psilorentinal artery, they can gain vision about 10 percent, will gain 25th year better just in that little island of central vision. Neobascarization of the iris within about four to five weeks and 20 percent in the disc two to three percent. So, it's not as much as with central vein occlusions where you get the neobascarization problems. So, think humblest. Certainly, here's a hull and horse plaque. So, if you see it, that's evidence immediately. But in a case like this, again the ultrasound was helpful. Just the B scan, just put it on there. Just takes a couple of minutes and look in the area right behind the disc and see if you can see any kind of a high reflective thing like a plaque. Okay, another case. Brian, pick on you for this one. This is a patient with long standing glaucoma. I've seen him for years. He had cataract surgery in both eyes doing a while. Just came in for a routine follow-up on his glaucoma and no real symptoms. He said, my vision is doing great. Since the cataract surgery I'm doing fine. Pressure was 15 or so. I did a fill, just kind of a follow-up fill. And the previous fill a year ago had been pretty well like this. And this was his left eye and this was his right eye and this visibid. But the previous year, his right eye had been kind of like that, a little peripheral depression. But now he has this kind of a defect going on. Any thoughts on this patient? Good? Good thoughts? So you're sitting there at five o'clock. So what are you going to do at this point with all those things you're mentioning? Right, dilating. Critical. Which I did. But again, long standing glaucoma I didn't dilate that well. Just overpatient. Pseudophagic. So it's kind of hard to see the periphery real well of the retina. And so did the ultrasound and shallow detachment corresponding to that area of the field defect. So always think about that. These can really fool you. And especially it's hard to see the fundus. They can be really tough. They're shallow and they're just really kind of subtle. So this is superior. So he's a risk for spreading in the macula. So got him to the retina. Specialist. But always be thinking of shallow detachment in these kind of atypical cases. So detachment in general, 6% of people have asymptomatic atropic holes which do not detach. A lot of this was from the work of Norm Byer who was at UCLA when we were there and did a lot of this stuff with able to watch these things and they don't progress over time. Most of current patients age 40 to 70. The lifetime risk in the U.S. is about 1,300 or anybody to get a detached retina. Not getting all the different risk factors. Increased risk in high myopes. More than 6 diopters. Family history. Cataract surgery with vitreous loss with detachment. Rate of 10% trauma. And 15% in the other eye develop detachment. So Randy, current cataract surgery, high state-of-the-art FACO. What's your thoughts on detached retina? It used to be taught. It was pretty high with we used to do it. Is that pretty well evened out now as far as you know? We've done a lot of good studies on that in relatively large ones. So it turns out that if you're over 60 years of that age and you're glow anterior it seems like the big risk still continues in some services still up there. It turns out that treating everything prophylactically ahead of time doesn't work. If you break capsule which would really clean up vitreous risk and it would appear it's hard to find a pair of that. If I am large break capsule and you have to do dispersive viscoelastic in the chamber stabilize that hold it, high speed cut or make sure there's no strands in place group still left. The same for yagcapsillotomy too with that group I can't tell you this. So again, yagcapsillotomy you know where people are using relatively low power. A big series on that about six, seven years ago. Majid, you deal with these high patients all the time, ICLs and refractive procedures. Do you worry about RD? Do you send them all to retina doctors first to clear the retina or how do you approach it? You're probably inducing problems sometimes too with some attraction. The evidence is that you are inducing other treatment. Exactly. Okay. Clinical findings, hypotiny compared to the other eye, tobacco dust pigment, Schaefer sign, 70 percent and shallow detachment. Difficult to detect as we talked about. Here's another patient. This is an airline, commercial airline pilot in his fifties. He had kind of a visual loss in one eye that really couldn't be figured out. He went to a neurologist, had a CT scan kind of this weird shape thing in his right eye. He had previous trauma. He was pseudophagic years ago but 20-20 vision. He's kind of these weird vague symptoms and again hard to see peripherally because of the dilation problems with the previous trauma and IOL. The sound shows a shallow detachment, just that really thin, just really tough. Even in the best case where you can see well, in a case like this where it's hard to see, it's tough. So I hope the sound can really be helpful. So treatment, 85 percent, treated within one operation, 15 percent required, two or more. Is that accurate, Paul, in your experience? Is that a fair figure? We call it 95 percent. As far as first attempt. Failure, all the breaks not seen, breaks, PVR, macular on 90 percent, 24 year better vision. An example here of a patient with a mild vitreous hemorrhage hard to see but ultrasound can be helpful to actually find the retinal tear and that really can help to kind of speed things up. If you see that then you want to move more rapidly on vitrectomy and try to reduce the traction forces. So beware of the shallows. They're dangerous. So be thinking that. Always be aware of the funny things. Patients can't really tell you, I've got to attach retina. I see a shape or something funny. You know, you really can't see a good funnest exam. Ultrasound is just so quick and easy to do just to pick these up. So always be thinking that. Just a final word here. This is a project we did in Mongolia just this last fall. This is a gentleman that he had one good eye, lost the other eye from trauma years ago and diabetic and he had a vitreous hemorrhage about a year ago and he been to different doctors in Mongolia and there's no retina doctors in Mongolia at that time. So he was 12, he can't help you, go to China, go to Russia, they can treat you there but he couldn't afford to do that. You know, he's a sheep herder from the back country. So just kind of lived with it, just kind of got by. And so our project was to actually train a retinal surgeon. We identified a young Mongolian ophthalmologist about a year and a half ago and sent him to LB Prasad in India for a 15 month fellowship. Really hands on and very good training, excellent training. And I went back with Jim Howard, local retina guy here in town and we took supplies he needed and kind of mentored him for a couple of weeks and did a lot of patients. He's done over 200 patients. I found out since we were there and he has an ongoing retina practice. It's made a big impact on the country and this just shows our first patient. This is a gentleman I showed the sheep herder who's undergoing a surgery. The vitreous hemorrhage is pretty simple with the tractor and a good case to start out with for this young surgeon. And so it did his case and here's the smiling Dr. Munkhaza that we helped sponsor to train. It just shows the impact we can have in third world countries. I know certainly Miranda's certainly premier in doing these kinds of things throughout the world but it's just very satisfying to be able to sort of and again have this ongoing even though we're not there. He's still there doing cases and we're still supporting him. That sort of thing is very gratifying. So I appreciate the opportunity to do that. So any questions, discussion? What kind of a potpourri? Just again, think of these things. Friday at 5 o'clock so kinds of things to do. Thank you.