 How's everybody doing? Is that Storm? Wake you guys up? No. No. It's just me. I'm Rachel DeCrube. I'm one of the retina attendants. So we're supposed to cover retinal vascular occlusions. And it's two parts. So today we're going to do kind of vascular occlusions. And then I come back in a few weeks and we'll talk about some less common entities. So hopefully, since it's a small enough group, you guys can just ask questions. Hopefully there's a fair amount of participation. I could talk about the images and kind of what we're thinking. But we'll just get started. So the first picture. Oh, wait. Oh, this one. That's right. Okay. So anybody? What do we have? This is pretty straightforward. Yeah. So there are some patches of white in the reds. Yeah. What part of the retina, which retinal layer is affected by a continental spot? Yeah. So it's a nerve fiber layer infarct. So nerve fiber layer infarcts. It's caused by a retinal arterial obstruction. Usually they'll fade over a couple of months. So back ahead on differential for a continental spot. Does anybody have anything else that they would keep in mind for continental spots? HIV retinopathy. Vasculitis, leukemia. This patient I actually saw a couple weeks ago, and this was radiation retinopathy. She'd had optic nerve meningioma that had been treated with radiation. So that's the big thing with continental spots. They're really never normal. You see a continental spot. You're not just going to say, oh, that's nice. You've got to really investigate a continental spot and figure out why they got a continental spot. But it's typically hypertension, diabetes. Keep in mind HIV retinopathy, anemia, radiation retinopathy, sickle cell disease, which we hardly ever see here, but it does exist. And leukemia, vasculitis. So investigate a continental spot if it shows up in your clinic. Okay. What about this picture? See, like retinal whitening along what looks to be like maybe retinal artery. It's like a branch retinal artery occlusion. Exactly. So that's the branch retinal artery occlusion. So it's a block of different retinal artery and you'll get this edematous pacification that can happen within hours. And then this is another example of a branch retinal artery occlusion. This was a 44-year-old woman I saw in my clinic a few weeks ago that had this branch retinal artery occlusion. And this... So what kind of embolus? Does anyone know what kind of embolus we call that? I think platelet fiber and embolus, yeah. So it's usually several disc diameters in weight that completely occlude the arterial. She came in complaining of this banana-shaped defect in her vision that had been there for a few days. And this was her OCT... Oh, sorry. I'm doing two computers, so... Does anybody see this OCT finding before? Rachel. It's like PAM. It's PAM, yeah. So it's paracentral acute middle maculopathy. And do you know which retinal layer it's? So it's the... the... internuclear, like, typically, but, yeah, it does look like it's affecting the outer plexiform layer. Sometimes it can be a little more patchy, but it's this diffuse hyperreflective band here in the internuclear layer. And it's been described mostly in vascular disease, but it's also videopathic. And you can see the arterial obstructions. Okay. Next one. See this on call? Ever? Okay, so... Yeah, so this is kind of our classic cherry red spot right there. And you have this edematous kind of whitening of the posterior pole. What kind of finding are we seeing in the blood vessels? Does anyone know what we call that? Box carving. Yeah, so you can see this kind of segmental opening of the blood vessels from the occlusion. And then this picture is interesting. I think... I just got a note from Dr. Tabin. I think I'm seeing this patient next week. Can you guys tell me what it looks like is happening here? It's kind of blurry. I just screen-grabbed that off-axis. I guess that's not the best way to do it, huh? She has the fellas. Anyway, so right here, what does that look like? A little plaque, an embolus there. Some plaques in the blood vessels here. You have edema and a pacification of the posterior pole with the cherry red spot. But what's happening here? Yeah, so there's that silio-retinal artery that's perfusing this little area. And the OCT is pretty cool, actually. Because you can see on the OCT, so kind of the typical findings of an OCT and a QR, arterial obstruction, is this kind of diffuse hyper-reflectivity. You lose the cellular details and the cellular layers. But in the area... Can you guys see the pointer? I can't really see it. It's so tiny, isn't it? Look at that little dot. But over where the area of the silio-retinal artery, you can see the normal cellular layers pretty nicely. So that is a CREO. Most of the retinal sparing. And then this patient actually had a ultrasound, too. And you can see the plaque in the central retinal artery. Oh, yeah, that's a really tiny dot. All right, so that's the B scan that Dr. Harry did. So for causes of arterial occlusions, what's the most likely cause? Were you looking? Embolic, yeah. And where's the most likely sources of embolic? Exactly, that's where you've got to look, is the carotids in the heart. That's about 90%. What's the less likely cause of arterial occlusion? I think it's... Yes, giant cell arteritis. So that's what you've got to keep in mind. Especially if you don't see an embolus, you really want to keep giant cell arteritis in mind and you've got to roll that out, especially in elderly patients. Less likely causes are going to be trauma, sargulophates, collagen vascular disease, bushets, leukemia. So those are the most likely sources, causes. Okay, this... So these are just pictures of different embolic sources. So usually we have cholesterol plaques, platelet-fibrin plaques, which we showed you a picture of calcific plaques, which are coming from the heart. And those are usually kind of this chalky white plaque. And that one's a calcific plaque. Yeah, this one looks like a calcific plaque and it's kind of chalky white. I think the biggest thing to emphasize is you see the plaque, it's not really a highly predictive value to determine if it's heart or cardiac. You've got to look at both. You can't just say, oh, yeah, that's chalky white. Yeah, that's the heart. Really, you've got to have a pretty aggressive workup and figure out where it's coming from. Less common causes of emboli are fat talc and you can also see corticosteroids that can travel through the arteries and cause emboli. So here's some more examples of different embolic photographs that really aren't showing up that well. Sorry about that. So for the hole-in-horse plaque, usually you'll see it kind of lodging at a bifurcation of an artery. And the hole-in-horse plaque, usually it doesn't occlude the flow. It doesn't really cause an arterial obstruction very well. Very often, usually kind of the blood will travel around it. But the calcific embolus, you'll see it often at the optic nerve head and it will occlude flow. And usually a calcific embolus doesn't fade away. That will be there forever. But a hole-in-horse plaque can fade over time. And then this is an example of the platelet-fibrin embolus. And that'll just fill the whole vessel, cause an arterial obstruction. It can be several dyspneamiders in length. So the most common symptom for a central artery occlusion is patients that come in with sudden vision loss, no pain, they can't see it all. They'll often have episodes of amirosis perceiving it about a quarter of a time. And on exam, you'll see this cherry red spot. Does anybody know what the cherry red spot's from? Why we see the cherry red spot? It's like the underlying core. So you don't have like the pigment in that area? Exactly, cause the ganglion cell layers that are there and then your fibro-layer layers that are there. So you're seeing the normal corporeal vasculature and everywhere else is edematous and opaque from ischemia. Mule, that edema in the cherry red spot will fade over a month and then you're left with a really pale nerve, really slurotic-continuated blood vessels. Initially, you'll see that box-carrying of the vessels where you see kind of the blood flow. On Fluorescena angiogram, you'll have a delay in arm-de-retina time, often, you know, 40 seconds until you're getting flow through the retinal arteries and then delay in the AB transit as well. So for a central retinal artery occlusion, basically the thrombosis gets... Sorry. There's a thrombosis, or an embolus, sorry, not a thrombosis, but an embolus just right at the lamina corposa and you'll get irreversible retinal damage after 90 to 100 minutes. This is why it's hard to do any treatments or trials or studies because patients don't usually present that quickly. You know, you guys probably see them quicker than I do, usually I see them after they've already had their work up, to be honest. What's happening in this picture, couldn't even tell? It looks like retinal edema. Yeah, so this is actually a siliorretinal artery occlusion in the setting of a central retinal vein occlusion. So the most common cause of a siliorretinal artery occlusion is actually a CRBO. And so the idea is that there's a thrombosis at the CRBO side that leads to stasis in the siliorretinal artery and leads to an occlusion. What's something else to think about for a siliorretinal artery occlusion? That is the answer. Siliorretinal artery. So yeah, consider GCA. So the siliorretinal artery is coming from the posterior ciliary vessel so it's not coming from the central retinal artery. About a third of eyes will have a ciliary retinal artery and in about 15% it'll supply the macular circulation. So in this photograph this is kind of a cherry red spot right here with the central retinal artery occlusion and then there's a siliorretinal artery here that's perfusing this little tiny area of the macula. Unfortunately, it didn't go a little further over. So people have tried a lot of different things to restore vision from a central retinal artery. Nothing's really been shown to be that efficacious. But people have tried to lower the pressure doing AC taps. I've tried it. If they come in quick enough or massage you'll put like a contact lens on the eye and try and massage the eye. The idea is to dislodge the embolus allowed to move downstream and restore blood flow. I've seen patients that have had hyperbaric oxygen treatment. People have tried to do inter arterial TPA and capitalize the ophthalmic artery but that's a pretty high morbidity and mortality associated with it. I've seen people present trying to yag the embolus and restore blood flow that way. But nothing really works out well because they have irreversible ischemia after an hour and a half, 100 minutes. So it's hard to restore vision. About 15% of eyes will develop neovascularization and it typically will occur within one month. So it happens pretty quickly. I think that the biggest thing that we need to do for arterial occlusions is recognizing them and then doing the systemic work up and doing an expedited work up through neurology often. There's been a movement to start calling this acute retinal ischemia and to really push it into the neurology kind of stroke world. So people take it seriously. There's been a lot of studies that have shown that ophthalmologists and optometrists do see these and I don't think here but I have seen it in the community where we don't get that expedited work up to look for cerebral infarcts and the underlying cause. A few months ago I had a patient that was referred in for an arterial occlusion just a B.R.A.O. And they, I don't know, I guess the referring doctor didn't recognize the urgency of it and by the time they got to me three or four weeks later they'd had a massive stroke. They'd crotted into our rectum and I think that if we would have recognized the arterial occlusion and started the work up, got the C.E.A. before they had the stroke they would have had a better outcome. So there's a pretty high rate in central retinal artery occlusions of finding cerebral infarcts on MRI scans. So kind of the policy here and whenever I've had to coordinate this I found it to work pretty well with the inpatient stroke team but if it's been, if they've had vision loss less than seven days you're supposed to coordinate an expedited inpatient stroke work up and typically I call this stroke team on call and they usually admit them and get everything going and I really haven't had an issue. If it's been longer than seven days then the policy is that we're supposed to start the work up into the stroke team after that and kind of the work up you guys know the work up right what are they going to do? Chronic ultrasound they'll get like basic lab work echo yeah they'll do the bubble study and they'll rule out GCA and typically they'll start aspirin and a statin if it's not contraindicated oh I guess I should I wish I could do this live like a Bluetooth to there that would be cool we're not at that point are we? okay so that is the work up that we were just talking about but I found whenever I called the stroke neurology team I think they're really receptive to this have you guys had issues on call? yeah yeah it's been really usually we have a patient that comes in and I had two French red artists and they page you and then the neurology team pages me because they are like in the TPA especially they're in the TPA window yeah yeah I found him to be this is just a patient of mine I saw a couple weeks ago this was his initial of CT a year ago from his CREO and you can see that hyperreflectivity the edema lost the cellular details and then over a year this is what the OCTO look like and so it becomes really atrophic and then less commonly I actually don't know if I've ever seen an ophthalmicardic occlusion that I was trying to think if I've ever seen one I really don't think I have but their vision is worse than a CREO it's usually light perception or no light perception there's no choroidal or retinal feeling on the FA and the ERG will show an absent A and B way there's no cherry red spot the most common thing to cause this would be a giant cell but you could also see it with the internal carotid dissection mucor or complications of surgical intervention okay any questions on artery occlusions what do we have Cerebio what else would be in your differential for a Cerebio for sure the other things you want to consider d retinopathy often that will be bilateral ocular ischemic syndrome the difference with ocular ischemic syndrome is that typically the vessels aren't quite as dilated and tortuous and the hemorrhages are usually kind of deeper retinoletic layers and then this is a BRBO segmental hemorrhages at an AV crossing site typically you can often see cotton wool spots as well and then later stages of a BRBO and this isn't showing up as well but the big thing you know when you look and do an examination you can see these kind of what we call collateralization across the median ruffe so you'll see these blood vessels that start to cross over here and this is allowing another drainage site an outflow site this patient also had neobascarization of the disc with that attenuated vessel and you can kind of see here the sectoral PRP that was done for the neobascarization so a BRBO is basically compression of the retinal vein at the AV crossing site and there the arteries overline the vein in this common adventitial sheath and that thickened arterial wall the vein leads to turbulent flow into little damage and then the thrombosis you want to consider an inflammatory cause if it's not associated with an AV crossing site the most common quadrant that's affected in a vein occlusion is in a branched vein occlusion is superior temporal about 60% of the time and so this is kind of a typical BRBO superior temporal at this but you can see up at that AV crossing site you can see the artery in the vein where the occlusion starts so it does come it's kind of finicky so what are some risk factors for a vein occlusion the biggest thing is age, hypertension glaucoma diabetes is not an independent risk factor and that comes from the eye disease case control studies a little crop of bun O-cap so diabetes is not an independent risk factor for a branched vein occlusion but it is for central renal vein occlusion the vision loss acutely you'll see macular edema, hemorrhages ischemia that can lead to vision loss and then long term chronic vision loss can be related to sub renal fibrosis pigmentary changes it can develop epiretinal membrane formation glaucoma, vitreous hemorrhages so the outcome really depends on the severity often the resolution of the macular edema is associated with these formation of those collaterals and this floor scene shows pretty well this collateralization that's happening in the chronic BRVO and so these collaterals just allow another outflow system for the macular edema and improvement and vision so those patients actually do better if they have that collateral formation in a central renal vein occlusion the collaterals occur off the optic nerve and you'll see these collateral shunt vessels in a CRBO you're getting compression of the renal vein at the lamino crevosa and they get this increased renal capillary pressure with associated macular edema and renal hemorrhages just to compare the risk factors for a CRBO versus a BRVO the one kind of thing to keep in mind is diabetes was an independent risk factor for the renal vein occlusion when do we work up these patients so do you guys know when we typically would work up a CRBO or a BRVO what about like an age cut off usually if they're younger than 50 we do a work up to figure out why they had a vein occlusion if they're older than 50 ages a bit of this risk factor for a CRBO we kind of break it down into the non ischemic and the ischemic CRBOs so for the non ischemic CRBO they usually have better vision they have less ischemia they have a better visual outcome for an ischemic CRBO it's 10 disc diameters of non perfusion that you'll see on fluorescent angiography they'll often have an adherent pupillary defect and the ERG will show a reduced lower flat B wave does anyone know what this is hemirentinal vein occlusion so would we classify hemirentinal vein occlusion as a CRBO or a BRVO CRBO so what's happening in a hemirentinal vein occlusion it's basically an anatomic variation where the superior and the inferior draining retinal veins actually meet posterior to the lamina crevosa so it's actually happening at the optic nerve head behind the lamina crevosa and it actually has a higher risk of neobascular complication than a CRBO or a BRVO so we kind of manage a combination of the two but it is considered a CRBO so instead of these retinal veins meeting here at the optic nerve head they meet behind the lamina crevosa and you get an occlusion there behind the lamina crevosa and that leads to hemirentinal vein occlusion so things to consider so vein occlusions when they come to our clinic most of us will start check the blood pressure right away often it's high kind of with a primary care doctor to control the blood pressure evaluating for glaucoma working with the glaucoma doctor primary eye position and then like I said under 50 do a workup I think the other thing that we'll see a lot of kind of younger women they're often on either estrogen or contraceptives or hormone replacement therapies I think that's an important thing to keep in mind and see if that's something they're able to come off of because that can increase their risk of vascular or occlusion disease this is kind of like a starting point for doing a hypercoagulable workup obviously but protein C protein S homeless esteem CBC cholesterol panel and then if you really aren't getting an answer I've ended up referring patients to HEMOC to help do a workup too if I can get to the bottom of it so I think the hardest thing about vein occlusions is the studies and these are always going to come up on OCAPs and it's trying to keep them straight and what they are right so there's really like the three main these are like the landmark vein occlusion studies that you've got to know I'll tell you how I remember them I don't know if it'll help you guys but the oldest study is the one that got the BVO and the CBO in the name right it's the oldest study so the oldest thing we were doing for vein occlusions laser so those are the laser studies so they got the name, they're the laser studies they're from like the 80's and 90's so that's how I remember the BVO and CBO score does anyone know what score is in the name like core corticosteroids that's how I remember it that's the corticosteroids study so that's how I remember it and then Bravo and Cruz, does anyone it's anti-vegeta it's randomism map and so I remember it B for BRBO, R for randomism map C is CRBO, R randomism map so that's the first kind of anti-vegeta those are the ones that tend to crop up on the test the most because they're the landmark studies so BVOS this was in like the mid 80's and there was two questions basically is there a reason to do macular grid for macular edema due to a BRBO and then the second question a benefit to PRP for neobascular disease so basically they found that macular grid improved two lines of vision in the majority of patients and treated like eyes were more likely to have vision better at three years they started the laser treatment at three months after presentation and then for PRP sectoral PRP reduced the risk of hemorrhage and neobascular complications after the development of neobascular disease so we don't do it for the ischemia but once neobascular disease develops like here then we would start sectoral PRP so that's the BVOS CBOS same questions it was like five or six years later early 90's photo coagulation reduced neobascular complications and then macular grid does that help macular edema from a CRDO they also will follow the natural history so from the CBOS macular grid really didn't help improve vision so that's why often we don't do grid laser for a CRDO it did PRP did help after neobascularization develop so we don't treat just ischemia but we treat neobascularization so BVOS BRBO you'll treat macular edema with grid this was our gold standard until the next studies came out treat neobascularization after develops from the CBOS no macular grid laser for macular dema and a CRDO so the score study this is a corticosteroid study and it compared standard of care which was laser versus one milligram and four milligrams of IVT so for the score BRBO study basically there was no difference between the three groups and the steroid groups were more likely to have complications like high pressure and cataract formation so after the score BRBO study we didn't change much what we were doing we kept doing macular grid and that remained the standard of care this was different from the score CRBO so before steroids we were just doing laser for neobascular complications we weren't really doing much for these patients at all because macular grid laser didn't work we didn't have antipagefs so these patients were really just two different doses of steroids versus observation and the steroids did better than doing nothing so for BRBO grid laser remained the standard from score and CRBO do steroids don't do nothing and then BRABO so this was our ranivizumab study and this led to ranivizumab getting an FDA approval for BRBOs and the ranivizumab patients did significantly better than sham so just remember this is ranivizumab where antipagefs became kind of our standard of care crews same thing patients did better with antipagefs than nothing at this point like we weren't even really doing steroids so they were able to just do sham so it's like two doses of ranivizumab versus sham and obviously the ranivizumab patients did better so really the big drawback to the antipagefs is that we just have to keep doing it ongoing I have CRBOs that I've been treating for seven years and I try and spread them out one week beyond 11 weeks they get macular edema they lose vision and we go back it's just crazy but we just can't just keep doing it so there's other treatments we do obviously now they're studies for these also but they're not kind of the key core landmark studies in vein occlusions the Azardex study was called Geneva I think the big thing to remember is the ILP speak with Azardex occurs more around eight weeks where IVT you see it usually around a month but the Azardex patients did really well and then ILEA had to get to do their studies to get their FDA approval as well and those are called Galeo and Copernicus for CRBOs and the Vibrant study for BRBOs but those don't tend to get tested on quite as much so really kind of our standard that you'll see us do for vein occlusions is start with anti-begeuffs monthly then try and treat and extend we'll add in steroids whether that's IVTs or Azardex and then we can add in laser grid if we're unable to extend or also if we're worried about poor follow-up as far as veneovascular complications this can be pretty complicated to treat we're lucky here to have really good glaucoma colleagues to help us with some of these neovascular complications in the retina clinic we're usually using a combination of anti-begeuffs with pan-retinal photocoagulation often they'll go on to need Ahmed valves or tubes to control the glaucoma or perhaps even a diode laser the nice thing about the anti-begeuffs is you can see the effects very quickly but the PRP will give you your longer duration of effect to control the neovascular complications so I think kind of historically people have tried to do a lot of other things for vein occlusions that have been pretty interesting not anything has worked really as well as anti-vegeuffs or steroids but they're kind of historically interesting so I mentioned that people did pretty well if they developed those collateral either across the ROFE or the optociliary shunt vessels so people have tried to surgically create these anastomoses and people have tried to do really hot laser burns in each quadrant to stimulate the retina to create these anastomoses or people will surgically go in and basically just kind of use a blade to create an incision at the venous congestions to allow an anastomoses it didn't work very well and it's pretty high risk people have also tried to go in with a retinal vein occlusion and I mentioned how the occlusion happens at that sheath where the AV crossing site is so people would go in and try to open up that sheath and allow outflow sheath and allow outflow and then also there's been reports of people using robotic surgery to cannulate the central retinal vein and allow an improvement in outflow and this is an interesting surgical procedure that people did and obviously this was before anti-vegeta before steroids but you have these horrible central retinal vein occlusions that you couldn't control and people would basically go in and I did this when I was a fellow so it's not that old but they did not do well but basically you do have a tractomy you take your MBR blade and then you go in at the optic nerve and take your MBR billiard and stab it into the optic nerve to the level of the laminate crevosa and making a big incision and the idea is just to allow drainage you have so much blood you gotta turn up the pressure really high but then they would end up having a lot of hemorrhage in the eye afterwards as well and we didn't really have anti-vegeta to control it, it was just crazy but I did do that when I was a fellow so I don't do it anymore I don't even know but those patients probably aren't around anymore they were do you guys have questions about vein occlusions, the vein studies are you gonna keep them straight? does that help at all? what was the way you remembered the BVOS and CVOS? so I figure like that's practically the name of the disease right? so it's B-O-B-O, C-R-B-O they got the name of the disease so it's the oldest study and the oldest treatment was laser so it's the oldest study, they got the name so that's how I remember it I don't know if that helps I think that's like the worst part of writing a book is just all the freaking studies studies I know but I feel like those three and they're like so old, we don't hear so anymore it's true, but the BVOS and CVOS was important because it kind of was in the natural history for us but I just remember because it has the name of the disease and the title so it's the oldest one and then score for quarter costeroids and then Bravo crews they have the R in their name for randomism I know, but it is a hard thing about the retina book is all the studies you know, marine, anchor, but that's what you know, I don't think you need to remember like Geneva, that's not as critical as score okay you guys look tired but I bore you to death with the retina I have a few questions, let's see if you know these, or if you paid attention I don't know so what has the highest rate of neovascularization of the iris hemirentinal vein occlusion but then after that it's CRBO but I mean we don't see hemirentinal vein occlusion that much when does the neovascularization occur after CRBO yeah and then what about a CRBO one month okay, you did listen does anyone know, I didn't say this does anybody know what this is oh, susan yes you get consults for it all the time do you really? I did when I was on consults last year how often do you see it? I saw it I've seen one patient that would say tally's patient oh yeah, I think I've seen my tally's patient that has it yeah, we've probably lost okay, see I'm an old patient, central retinal artery occlusion you can't see an embolist yes okay, most common quadrant for a BRBO yes super temporal, about 60% of the time okay, laser treatment for retinal vein occlusions, landmark study BVO yes, yeah just group yeah, group them together okay, CRBO what part of the ERD B-wave, ophthalmic artery occlusion yes yeah, AMB wave that's absent A waves okay, how many minutes perfect okay, you guys listen even though you look so tired she's so tired face that sucks, the 7am lecture well, that's a little bit because you have so many lectures I'm sorry yeah so after you have like a branch retinal vein occlusion or how long does it take before like findings in the retina like go away or what will I see like after the patients had one second so we had a patient in clinic yesterday actually that presented a little bit late but she had an episode of hypertension of the lidocaine occlusion over like 200 systolic and then about like the next week she noticed that her retina was blurry all over she'd already been dilated so I could check for an APB chest, robotic meridus so it was like 6 weeks later that I saw her so I was like thinking I was like I don't know the progression of like a resolution well, if she didn't have any treatment you know, so if it's a mild vein occlusion it could resolve over almost several months but usually there would still be some findings you could also have hypertension written off of these that could cause more acute hypertensive changes that could resolve what's resolution of blood pressure did you, you didn't have any findings on exams? no, so I didn't find anything so I was like looking and I was like and I checked her, she had an optic meridus in the eye so she had normal color vision and no red g-sat, no pain and then her vision was just a little reduced and she had a slight visual acuity to compare to so Dr. Lange just thought it was her cataracts but I was like, wondering about I mean, usually if it's been 6 weeks and they had her true ischemic event vein occlusion, you would see something you know, you would see sheathing of the vessels some retinal hemorrhages you know, long term a severe BRBO I mean, I'll look in a retina you'll see that collateralization across the median refabe to develop though and you can see that and you'll be like oh, they had a vein occlusion years ago and I'll still look in an eye and you can tell based on the shump vessels that it did happen unless it was a really mild event it wouldn't resolve that quickly I wouldn't think, usually there's something I mean, because I'll see those like dot hemorrhages from PDPs that you can treat and they're still there so next time I'm supposed to talk about oh, yeah, this is what we're supposed to talk about but I'm supposed to talk about ocular ischemic syndrome hypertension, sickle cell coats, macriannurisms do you guys want me to just prepare the lecture and we just talk and do some questions I mean, I know we're supposed to be doing this like flipped classroom, do you want to do it where we break it up and do some cases or what's better for you guys I favor ounce format okay okay we'll do it that way so you guys don't want to repair it yeah, I'll look I mean the hardest ones to find is going to be the sickle cell I'm going to have to take those from Julia I'm sure she has one I know that's the hardest but yeah, okay, we'll do a more like cafe round something good and go around and talk about cases is everybody okay with that all right cool, thanks guys