 and this is the little thing that they added on the hill behind the gardens in the back and I have no idea what that is. We walked through it we still have no idea what it is. They've got a little cafeteria in there where you can buy really expensive food that's not very good. Now this is the nice thing about the view this is the view from up there so here's the palace there's Vienna there's the gardens and you go up this hill and there's this pretty fountain and then this structure whatever it is but you get a nice view of Vienna from there. Here's a Schoenbrun palace kind of a copy of Versailles you know all palaces in Europe try to copy Versailles so they're always you know they're always in that vein but you guys don't know Sam Mascot but Sam Mascot's a surgeon from Southern California who knows wine and those museums and all and his response to Schoenbrun is well once you've seen Versailles so but it was kind of a nice palace once you're there and then this is as you go up into here and as I said this little cafeteria up there so not much exciting going on but I do like the you know the guardians here the you know eagles with armor and shields over there guarding the place. Okay so Catherine this is an intern question what do onions ogres and retinas have in common? Layers. Layers exactly they all have layers so we're going to sit and spend a little bit of time on the retinal layers because it's really important that you recognize each of the layers of the retina and what they do and why they're important so first off we're looking at a picture here of the retina and just a brief definition to the pathologists you know what is the definition of the macula to a pathologist? Oh it's the region between the arcades. That's the definition of the macula to a retina doctor. What's the definition to a pathologist? It's where I think the ganglion cell layer only has is only is thicker. Exactly so to a pathologist the definition of a macula is where the ganglion cell layer is more than one cell layer thick but fortunately it pretty much corresponds to the area inside the arcade so the definition that retina doctors use and pathologists use are pretty much the same. Okay so we're going to go ahead and we're going to talk a little bit about layers of the retina so the first thing we're going to do is we're just going to go and start naming them so I just want to go around the room so this is the vitreous. What's this layer right here? Okay and here? Good here. Alright there. Outer plexiform layer. Outer nuclear layer. Here. And last but not least back to Katherine. Alright exactly so those are all the layers of the retina so when you're talking about the retina you can talk about the anatomic layers but you can also talk about you know how a photon of light comes through and how it's processed and what it does and so I think we can kind of go ahead and do that two ways. So when we look at a close up of the retina here let's let's trace a photon of light so a photon of light is interesting it has to come through the retina and so you know to me the retina is kind of designed upside down it's weird because if I were designing something I'd have the photoreceptors out where the light comes through and it wouldn't have to go through the retina but what's critically important is photoreceptors are amazingly active cells and they take a lot of metabolism and so the reason why the photoreceptors are clear down here is because they have to be close to the quarry where they attain their nourishment so that's why the retina is kind of inside out if you will or upside down so a photon of light comes through a photon of light hits one of these areas here in the outer segments when you guys do retina you'll see what these look like on EM they look like a little stack of coins and so the membrane is right there and you've got all the rhodopsin that's there and so photon of light hits that rhodopsin it switches from cis to trans it changes the the potential in the membrane and it starts a hyperpolarization so it starts a polarization wave going and so then that transfers here and it goes to the outer nuclear layer which is where it is and then the axon comes here and then where does the axon link up or what cell does the axon link up to just keep going around okay so it links up to a bipolar cell and the bipolar cell body is here in the inner nuclear layer and the axon goes out here and then what does it link up to okay so it links up to a ganglion cell the ganglion cell layer body is right here in the ganglion cell okay and then the axon leaves that ganglion cell and where does that axon eventually synapse exactly so this is a really long axon it comes all the way from that ganglion cell to the lateral geniculate body and so that's a really long axon the problem is is anywhere that's interrupted anywhere along that could eventually cause death to that cell and so all the way from the lateral geniculate body forward ganglion cell nucleus it can cause problems there okay so now we're going to go ahead we're going to talk a little bit about what's in each cellular layer and kind of what each layer does so now we're going to start from into out so internal limiting membrane what is the internal limiting membrane exactly so it's really not a membrane like a basement membrane but the little muller cells have their foot plates on there and it's kind of a separation between the vitreous and the retina so we call it the internal limiting membrane but it's really not a true membrane itself all right and then where are we in the eye right now yeah true question when the macula why exactly because the ganglion cell layers multiple cell layers thick right here so that tells us that we're actually in the macula right here now this is an interesting cellular layer here the inner nuclear layer now the inner nuclear layer not only has the bipolar cells that we talked about but what other cells live in the inner nuclear layer so we have the apocrine cells cells another one muller cells muller cells and the last one well amicron I'm sorry I heard amicron it should have been amicron not apocrine cells amicron horizontal cells horizontal cells so this is a very busy cellular layer because not only do you have the bipolar which link it vertically if you will but you've got amicron and horizontal cells which kind of run horizontally they're very interesting cells because they've got their little processes go all over the place and we think that this is the beginning of where visual processing takes place and so you know if you think about it simplistically you say okay well one you know photon comes in and triggers one rod and then it goes through the lateral geniculate body but there is processing going on even in the inner nuclear layer and already it's starting to you know do on-off signals and process it and so when people are talking about putting little chips kind of on the surface of the retina and eventually connecting it to the brain it's a lot more complicated than that and the interconnections between the horizontal and the amicron cells are amazing Helga Cobb who's one of our PhDs here who's now emeritus she won the proctor prize for her work on this she's been a career looking at how these are all interconnected and has some amazing EM showing it so very very complex Mueller cells what the heck do they do they're kind of like scavenger cells or microglial cells okay so they're a microglial cells so they do scavenge but they also give some structural support because do that their cell bodies live in here but their little processes go all the way up here and all the way down here which is interesting so in one last little area right here people sometimes call this the outer limiting membrane right here with the here's the cell bodies of the rods and cones and then their inner and outer segments the heck is the outer limiting membrane what exactly forms it right here these are actually little tiny junctions and so when you look at the junctions in light microscopy it almost looks like it's a membrane so you may hear some people say outer limiting membrane it's not a membrane it's the little junction in the inner segments of the cells right there that form those little dots that looks like a membrane okay so now we want to talk about this area right here and I guess we'll just keep going watch what area is this okay so the retina does kind of part a little bit in the fovea because the fovea is the part of the macula that gives us our fine vision and so it really does thin out here such that the light doesn't have to pass through the entire retina but just that part of the retina and then it it hits right here now what kind of cells are predominant in the outer part of the fovea cones exactly so they the center of the fovea is very very cone-rich and the reason why you get a lot of fine vision at the fovea is when you look at the fovea one cone is attached to one ganglion cell and then goes back so it's a 1 to 1 to 1 ratio and so because of that you want to part the area to let the light come through so all these ganglion cells get stacked up way over here and so this rod this cone right here may link up to a ganglion cell right there and because of that the fibers right here tend to run in a more open show this nicely here well you kind of get the idea see those fibers running obliquely a little bit right there and so you know you have to have all those ganglion cells stacked up on the side and the fibers run obliquely what is this layer called right here henley's layer okay and why is that important exactly so that's where when you have sisterhood macular edema that's where the edema for you get that flower pedals because this layer of henley is the fibers going obliquely to get connected to those ganglion cells to go back now the peripheral retina is a little bit different the peripheral retina you may have a hundred rods hooked up to one single ganglion cell and the reason why we do that is why does why does nature do that yeah exactly so it summates it summates and so if you ever out on a you know like you're out on a night and it's dark and then you see a light out here and then you look at it the light disappears and that's not uncommon that you see that and so it's because it summates out here now that's important because teleologically you know you're out climbing through the tundra you know you want to see that sabertooth tiger that's going to try to eat you you know and so you want to be able to see things in the periphery and so the way nature does that is it gets summation so you may have a hundred rods going into a single cone and that'll show you movement it'll show you little lights out there where's the cones in the center are one to one because that's your fine vision that's your reading that's your visual recognition that's your fine vision so a little bit different the way the retinas wire okay now we want to talk about some specific pathologic entities that can affect the red so we'll go to Chris what are you looking at right here this is a pretty much in all layers so we see images more superficially so we see these kind of flame shaped images and we also see some deeper it's like little dot and black images and then over in the back you know we see it looks like some anxiety over here so what do you think this could be so I mean there's a lot of things you can do this I mean hypertension can do this bad diabetes can look something like this so exactly you can get hypertension look like this but remember diabetes can look like this too why are superficial hemorrhage is more flame shaped exactly so that nerve fiber layer you know that leaves the ganglion cell and then it turns perpendicular to the surface you know as it are actually parallel to the surfaces it runs into the optic nerve and so images that are superficial tend to have that flame shape images that are deeper tend to be more dot and blocked but if you look right here you can see that there are both dot block flame hemorrhages some macular exudate even maybe a little bit of ischemia right here and so the good guess would be hypertension and so this was a patient that came in actually a younger person came in and they had severe severe hypertension and it was interesting because they were seen in triage and they looked and said you know I don't know maybe this is you know central retinal vein occlusion or something and then you know we were looking at it and scratching our head saying what could this be and this was when the student said well did anybody check their blood pressure so of course we had to find a blood pressure cuff we checked that it was 200 over 100 and so off to the ER they went and so this is severe hypertensive retinopathy now what else could happen with hypertensive retinopathy Brad the heck is going on right here so it looks like some hard exudates have some like hemorrhages coming off of the disc as well flame shaped hemorrhages now why are the exudates this kind of star shape so exudates usually indicate prior edema and so like maybe some residual edema or why are they star-shaped though probably because of the layer that they're in which is I would say neurofiber layer no they're actually deeper in Henley's layer so you can see just like the flower panel for sister immaculate emo when you've got this hard exudate so hard exudate is protein rich it's lipid rich you know you've got leakage of fluid and then the fluid eventually gets reabsorbed but the stuff you know the the proteins the lipid end up staying there so you get these yellowish hard exudate the star shape is just indicative that it's in the macula now if you look real carefully Mike what's going on right here in the optic nerve there's some disc margin blurring so probably some I guess we can't technically call papillodema but disc edema exactly so be careful because papillodema by definition is increased pressure you know our swelling of the optic nerve due to increased cerebral spinal fluid pressure and so technically you can get in severe hypertension you can even get some swelling of the disc in hypertension so you end up getting some disc swelling there and that's what you're seeing there is some disc swelling and this is a severe case and so this is a patient who had severe hypertension you can see that almost looks like papillodema there's some ischemia here there's some tortuosity of the vessels there's these hemorrhages around here and so in a severe hypertensive crisis you can even get swelling of the optic nerves all right what are we seeing right here Tina degree of pallor just diffusely through the whole macula and then looking at the phobia you look like you have a cherry red spot in the middle so you'd be concerned about a central artery occlusion here okay so this is a classic central retinal artery occlusion why do you get a cherry red spot just the the pallor of the outside compared to the pigment in the macula creates that appearance rather than it actually truly being more red yeah it's not even so much so much that the you know the pigment in there but it's the fact that that you're actually kind of seeing through toward the coroid we still have decent blood supply and the phobia and of course the retina itself is all swollen so it turns white so this is the classic central retinal artery occlusion now are arteries more embolic or are they more thrombotic they tend to be more embolic more embolic so when you see someone with a central retinal artery you want to look for clots coming from somewhere cholesterol coming from somewhere you know you want to have them worked up for their carotids for their erotic arch even for their valves in the heart and so these are usually more embolic and that's the classic central retinal artery occlusion what do we see in here you see a more focal area of the the whitening of the ischemia and also perhaps like a cotton wool spot as well okay so maybe a little cotton wool spot focal what does that mean we have branch artery exactly so this isn't a branch artery occlusion rather than a central artery occlusion so this would be one where this one of these arterioles gets blocked off right there and you get this focal area of ischemia corresponding to it so it's the same process it's usually embolic but it's in it's further downstream and so it hasn't blocked off the entire central retinal artery it's blocked off one of its branches so this is a branch retinal artery occlusion and what are we showing right here all right so which vessel is this exactly so we're actually in the optic nerve and what i wanted to show you is the central retinal artery shares a common avaticial sheath with the central retinal vein and so look at that artery look at all of that cholesterol and lipid and all those crown burgers and moochies and all that good food that we eat you know and so you vegetarians your arteries don't look this way so you guys should be very good about this so look how narrow the lumen is there and so you don't usually get a central artery occlusion in a nice normal wide artery and so it's usually been narrowed from arterial sclerosis and then it's more susceptible to a little clot forming or little emboli forming but also look at that artery that big thickened juicy arteries pushing next to the vein next to it so this is why we always say the most common cause of a central artery occlusion is arterial sclerosis the most common cause of a central vein occlusion is arterial sclerosis because that sclerotic artery kind of pushes on the vein next to it can lead to stasis which can then lead to a central retinal vein occlusion all right so what am i what am i showing here it gets vile so you're showing that so when you look at the blood supply of the retina tell me how it's divided how's the blood supply of the retina divided so the inner two-thirds is supplied by the retinal vasculature and then from the coroid and so you kind of divide it by the form layer well what you see right here exactly at the inner two-thirds roughly of the retina we see this blood splash from central retinal artery the outer third from the corids if you look right here the corids still intact here and that outer third is is still intact but the inner two-thirds is wiped out and so there's still a tiny bit of the outer nuclear layer that gets its blood supply from the coroid so there's a little bit of the outer nuclear layer but the inner nuclear layer ganglion cell here totally wiped out so this is a central retinal artery occlusion all right what are we looking at right here it looks like and it's got some vessels that are kind of white as CRBO exactly so this is a little bit different than the central while a lot different than central retinal artery occlusion which is paleon ischemic this is where everything's backed up so you know you're driving in the snowstorm and there's a wreck on the freeway you know everything gets backed up and so central retinal vein occlusion you get backup of blood and all four quadrants all the way around and they call this the blood and thunder i don't know what thunder means but the blood and thunder right it just sounds cool blood and thunder and so rachel what is this one right here so branch retinal vein occlusion what's the most common cause of a branch retinal vein occlusion exactly so if you look at this arterial look at that they call that silver wiring and so that's actually even a sclerotic arterial right there and so right where the venial where the arterial or the the venial crosses over the artery you'll get some thinning and some sausageing of that vein and then eventually that vein will occlude and you'll get that focal branch vein occlusion so it's usually right at the crossing point where the arterial and the vein you'll cross over so but again it's it's arterial sclerosis here look at that silver wiring there so that's your arterial sclerosis that causes it and this is just an eye that's been cut in half sagittally and you can see that it will cover all four quadrants so it goes all the way from the optic nerve to the oracerata so central retinal artery or central retinal vein occlusion will do all the quadrants in you just get that backup of blood throughout all the layers this just shows it pathologically you can see the blood in all layers of the retina eventually you can get some shut vessels start to form you can start to drain that out and so when you get remote from a central retinal vein occlusion the hemorrhage will eventually reabsorb and it's almost like you know when there's a crash on the freeway you know you get off and you take the side streets and eventually get around the crash and that's what the blood does too and sometimes you'll even see little shunt vessels on the surface of the ret of the optic nerve as that blood finds different ways to get out of there in a central retinal vein occlusion what do we see in next year uh yeah so it's a little what the last picture I saw so this is um bonus photo uh right so here we see um a lot of anxiety in the macula we see hemorrhages again um some of the plantations look a little bit deeper and we see what is that common wall spots probably they're inferiorly as well so what else could this be what's the most common finding the most common disease for this finding yeah so uh again diabetes would probably be the most common hypertension like an aspirin should also look like this diabetes is pretty common so diabetes is common and unfortunately becoming more and more common and so as our society eats more and more cheeseburgers and and moochies um obesity has become a huge problem and as a result diabetes has become a huge problem so type two diabetes is just exploding now and so even I'm just a general ophthalmologist I see probably five diabetics in a half day every single day I mean there's just tons of diabetics now so you're going to see this more and more and more so first of all how do we subdivide diabetic retinopathy what's another word for non-perliferative some people call background so when you hear the term background retinopathy that's non-perliferative now remember there is an entity kind of in between people will call pre-perliferative all right so when we're looking at background retinopathy or non-perliferative retinopathy what am I looking at right here I guess Brett looking at here we're looking at um some what appears to be like um micro aneurysms exactly so this is uh uh trypsin digest this is where you put in a material that digest the tissue around the blood vessels and then you can get a view of just the blood vessels so this is a micro aneurysm so that's the first thing that we think happens the perisites you know are damaged from the ischemia and from the diabetes and then eventually they drop out and you'll get these little micro aneurysms you know these micro aneurysms make the vessel wall weaker they also make it so it leaks a little bit so in addition to the micro aneurysms you get dot hemorrhages blood hemorrhages even flame hemorrhages Mike what are we showing right here um so you have flame hemorrhages dot blood hemorrhages exudates and especially right there in the macula you just have a big patch of heart exudate exactly so now once we've got heart exudate in the macula you can imagine that's not really conducive for good vision so we really want to try to do what we can to prevent this from happening now you can't really laser that because you get damage some people have talked about the possibility of even using anti-veg F to try to get this to dry up and go away steroids can sometimes help to get this to go away but boy once you get all that heart exudate in there I mean that's really not conducive to good vision so you really want to treat it before it gets to the point where you get the severe heart exudate and you can see this is a path specimen of the retina and this is the heart exudate here so if you analyze that it's very protein rich it's very lipid rich and that's why it's yellow because of the lipid so this is the heart exudate that you can get a very good well Tina what am I what am I trying to show right here um for those cotton wool spots cotton wool spots and what are cotton wool spots the ischemia of the uh nerve fiber layer all right so it's an area of focal ischemia and so if you look this is actually not blood here these are actually swollen ganglion cells here in the nerve fiber layer so when you get focal ischemia you'll get swelling there now the cotton wool spots will eventually go away but it's not because you know that's because the swelling goes away but once that axon gets ischemic and gets permanently damaged it dies off so if you were able to do little pinpoint ERGs you would find focal areas of disruption where areas of big cotton wool spots work so focal ischemia here of the ganglion cells nerve fiber layer is the hallmark and here's a picture of it these are actually swollen ganglion cells here in the nerve fiber layer so that's why it looks like cotton wool on the surface of the IOL I mean surface sorry of the retina sorry IOL is on my brain and so it kind of obscures the retinal tissue underneath it so that's why it looks like this white fluffy you know cotton on the surface all right what are we seeing what are we seeing right here it's like a lot of diffuse hemorrhage and then also some exudates up towards the a lot of dilated tortures such as vessels neobascularizations of new vessel forming so what do we call this a proliferative diabetic right okay and then more specific how do we subdivide the neobascularization um it's either in the disc or elsewhere exactly so we kind of crudely divided into nvd neobascularization of the disc and nv e neobascularization elsewhere and so here's the neobascularization elsewhere of course we have the nvd neobascularization of the disc and so this is like remember greek mythology medusa that I've had all the snakes coming out of her head so this is a medusa disc and so you can see all of the abnormal blood vessels there growing out of the disc so what's the what's the underlying etiology for nvd or nvd and is he trying to create vessels to bring more oxygen to the areas essentially exactly so you get chronic ischemia and then the reaction is through various mediators one of which is VEGF is to get new blood vessels to grow the problem with these blood vessels is they're not competent blood vessels they don't have good parasites around and they leak like crazy and so one of the applications that you can run into is you can run into this what is exactly so those vessels can leak you get hemorrhage you get gliosis going on you get scarring you get tractional retinal detachments and then what's going on here so you can see this is a boat shaped hemorrhage what why is that right so it's between kind of the hyeloid face they call it so between the posterior vitrus and the retina you'll actually get hemorrhaging so on the top here you just get a fluid layer and then of course it's kind of shaped like a boat here and so that's pre-retinal but between the retina and the vitreous so it hasn't broken through to the vitreous yet it's in the layer in between you can see the neovascularization right here this is another complication of this neovascularization what are we looking at right here okay so look at all those vessels so we we so we call this condition rubiosus eridus you know literally red iris so we used to call it when it's bad like this rhodiosis because you know it looks like those big big red ropes in there but so this is severe rubiosus eridus neovascularization of the iris and again it's a response to chronic ischemia and that ischemia can even cause this now so the most common cause of rubiosus is is you know diabetic retinopathy what's another cause okay yep zero zero is second what would be third just ocular ischemic syndrome is kind of the third thing so think about it if they have severe ischemia to the eye itself you know say they had severe crota disease they had three muscle you know muscle surgery and took away all the you know blood from the anterior segment and so chronic ischemia inside the eye can cause the neovascularization on the surface of the iris and as we talked about last week you know when we looked at the you know causes of glaucoma here's the abnormal blood vessels on the surface of the iris what is going on right there i guess bratt next you're hiding behind right there sorry so you have kind of the urea coming into your to the iris so the ectropion urea so they call it ectropion urea it says that neovascularization on the surface of the iris contracts a little bit it literally pulls that pigment epithelium on the posterior surface kind of around the corner of the pupil and bends it around so you see a little dark area around the edge of the pupil ectropion urea and again as we showed last week these vessels can grow into the angle and cause secondary angle closure and there you see here's the iris plastered against the peripheral cornea closing off that angle now what else Mike what else happens to the iris here in chronic diabetics um so that just looks like the pigmented epithelial air uh there's just um vacuoles in it exactly so you get from the chronic ischemia you get what they call lacy evacuation now again they love showing obscure path pictures on boards and so this is one that they'll often put in there so you can get lacy evacuation of the of the iris pigment epithelium tina what are we showing right here first of all what what part of the eye are we looking at ciliary body the absence of make a step back what kind of stain is this oh this is a stain in the basement membrane so what stain does that um so it's pis yeah stain yeah stain stains basement membranes why wouldn't we be showing you one of those of the ciliary body so this is another finding and in diabetic eyes with the thickening of the basement membrane in the ciliary body exactly so this is a pis stain for basement membrane look at that thick one and so when i was i did a pre residency fellow like you guys fellowship like you guys are doing with dave apple and so he you know the american board said we need some path pictures from you and so david will always like shove it off on me see i learned that from him and so he said nick go take some good pictures send it to these guys i said okay here's a good picture i took a nice picture of ciliary body pis basement membrane thickening send it to them and so i'm taking boards now you know five years later and i sit down and sure enough there is my picture on the board exam you know saying what it is and i said oh man that's my picture i'm so smart diabetic great so now what you guys will learn when you take your ocaps is that there are no one part questions there's two part questions so they show you this you say ah diabetic man i'm smart i've got this nailed and then question a is a patient with this would have a glomerular filtration rate of perineal nerve velocity of and so you know yeah you know that kidneys are failing you know their nerves don't work well but shoot what's the real number so again two part question you may know the answer and still don't get it right so that's so don't feel bad when you walk out of ocaps and say oh my god i missed all of them because you always feel that way all right how do we treat perliferative diabetic retinopathy um a veg f intravitral injections okay what is this what is the older way to treat it it looks like prp or some type of laser to scar down the ischemic part of retina so when that the lasers first came out the very first laser wasn't an argon laser it was a xenon arc laser and my program was so you know so much in ancient times that our va we still had one of these in the back and it was like as big as a whole closet and it would put these thousand micron spots and it would just sizzle the tissue and so when these first came out people were saying well we're going to take the laser and we're going to treat those you know that new vascularization and that'll make it go down and so they were actually taking xenon arc lasers and blasting the new vascularization on the disc and so this is one of the first things by predecessor Dave Appel did in the 60s as they looked at pathology and they said wait a minute you're killing off the nerve fiber layer actually you know blinding the patient by doing the laser but at the same time they were that people would come in with extensive nv e and so they take this laser and they blast the peripheral retina then they'd say okay come back next month and we'll you know blast the optic nerve and they'd come back the next month and the vessels on the nerve would have regressed and so finally people said well wait a minute maybe if we treat the periphery we can save the center and that was the whole idea is you do panoramic photo coagulation of the peripheral retina first off it kills off ischemic retina but it also you know makes these laser spots that allows more oxygen to flow through and the proliferation on the disc would shrink down and go away and so you do panoretinal peripheral photo coagulation to make the neovascularization of the disc go away and now of course we can do anti-vegeta injections and do the same thing and here you see here's an actual laser spot so now we use argon laser the argon laser works by being absorbed by the pigment of the rpe so here's rpe here here's rpe here's a laser spot here and it's absorbed by the rpe pigment it kind of kills that off it kind of kills off some ischemic retina and it lets more oxygen flow from the core into the retina so again you treat the peripheral retina in order to save the center the heck are we looking at right here those have these like fronds and neonastorization there you look beyond it boy and that's not a film artifact that's just dark beyond there what could this be sickle cell disease exactly and so these are what they call c fans you know if you've seen that pictures of you know jacuzzo diving and you see these c fans that's what they look like and so you've got these fronds here and beyond that there's no good blood vessels so you get focal ischemia kind of wiping out peripheral retina and then again it tries to make new blood vessels to go across that and so this attempts to be a sickle cell patient so sickle cell will do that you can get a weird disease again they love asking this on boards yields disease again it's it's something that you see actually in southeast asia south asia and you'll get again this peripheral ischemia with these c fans trying to grow across it and this just shows you this is a patient with sickle cell and you can see the knobbiness of the vessels there because when the cells sickle they'll clump up in that area and then you get focal areas of ischemia so you don't see much sickle cell here in utah because you know a lot of utahs are caucasian but you see a lot of this in areas with a high african-american population you'll see a lot of sickle cell all right so now we're looking i guess okay yeah so there's a macular hole there but looks like there's a little bit of surrounding edema as well exactly so you see that's a full thickness macular hole and there's a little bit of edema around it and here you can see a close-up of that what is this thing right here exactly that's a fixation rod you know so i've had people say oh man it's a fold in the retina there and it's like that's just something because you know this is central you know a full thickness hole your vision drops to like 2200 and so it's hard for them to fixate and so this is actually fixation rod in there and so you see full thickness hole but there's a cuff of edema around it so sometimes even if it's a full thickness hole if you can get it to seal off surgically you can sometimes get that fluid to go down and the scatoma will shrink a little bit so here's the edge of a full thickness hole here's some edema next to it what do we think the cause of full thickness holes are or just macular holes in general it's actually focal vitro retinal traction so when you do the surgery you have to do have a tractomy peel off any traction then you put gas in their eye and then these poor patients have to you know sit face down for like seven to ten days it's just awful but eventually if you can get it to seal off their vision will improve all right what are we looking at right here so there's um like the vessels are slightly distorted centrally near the macula and there's a little ring maybe these vessels are kind of curvy there maybe they're pulled here like what do you think this could be exactly so this is an epiretinal memory now this one's a little bit more prominent you can see it here this would be one that maybe even an intern could see you know so here you can see that you've got all this wrinkling here and so this is an epiretinal membrane and then again we've got a fixational line this happens to be a red-free picture and this just kind of highlights how you've got the vessels being pulled in and so they're kind of straightened pulled in and so you can imagine this would cause distortion of vision metamorphopsia and then of course here's our what is this over here OCT exactly so look at the little wrinkling on the surface there so when you see the OCT you'll see this little wrinkling that's on there and this is thought to be due to the fact that um astrocytes that's another cell that can sometimes live in the retina in small numbers as astrocytes and once they gain access to the surface of the retina you know in front of the interlimiting membrane you can actually get growth right there and then you'll get this epiretinal membrane starting to form and again here's a OCT showing that epiretinal membrane very nicely there's the path wrinkling on the surface of the retina so epiretinal membrane all right what are we seeing right here um there's a lot of uh it looked like drusen to me in the magnolence kind of phobia okay where where are drusen located pathologically all right and this is where we want to talk a little bit now between the rpe and the coroid there's another structure that has layers so what is in between the rpe and the coroid uh brooks membrane how many layers does brooks membrane have five and what are they and how do we remember them uh so there's a couple of membranes this is that sandwich thing i think we've talked about yeah exactly the sandwich thing yeah so there's there's five so there's a there's a base of membrane of the rpe i think and there's what makes up the sandwich so there's that's the bread and then there's uh meat turkey turkey the cladge layer then there's uh cheese cheese cheese elastic elastic layer all right so brooks is a five layer so you've got the bread you've got the basement membrane of the rpe and the basic membrane of the cordial capillaries that's the bread then you got two pieces of cheese what is cheese cheese is elastic so you've got two elastic layers and then in the center you have that really collagenous you know thick turkey layer and so you've got meat two cheeses two breads and so brooks and so the point i was getting at here is technically the drusen are underneath the rpe but on top of brooks and so technically drusen are actually intro brooks so they're under the rpe basement membrane but they're on the surface of brooks membrane and so these are these deposits they're rich and lipo fusa they're really kind of waste products of all the metabolism that's going on in the rpe and eventually they get excreted and they build up in that area so these are drusen and here is you know we call this a big drusen you know giant drusen and if you can imagine that's going to disrupt the rpe overlying it it's going to cause areas where the retina degenerates when the rpe on top you know underneath that degenerates and so this is a large drusen and you can even get more what we call diffuse drusen so here's a patient with more you see those are looking bigger those are larger drusen they're more diffuse and you look at the pathology there this is just a big kind of confluent drusen over here loss of rpe overlying it you know while we're here on the rpe brad tell me some of the functions of the rpe so the rpe is responsible for recycling uh rodopsin yeah so it's it recycles it takes the the deesterified rodopsin it gathers it it reesterifies it it puts it back up into the outer retina mike another function of rpe they're the um the garbage people of the retina so it takes waste products and yeah it really does they kind of process waste products Tina what what's another function of the rpe provides a barrier it's like a barrier function so it is actually the we call it the outer you know blood retinal barrier and so there's tight junctions in the rpe and that just keeps fluid from flowing from the coroid into it directly and so um one other thing that the rpe does kathleen well we already kind of said it it's kind of a waste station it takes waste salt puts nutrients in not sure well the actual pigment and so because of the pigment there it makes it so that you're not really light sensitive and so when you take sand albino really a pure albino they've got no pigment in their rpe boy they're really really light sensitive so again it helps to absorb some of the pigment too all right now what are we looking at right here you see a lot of pigment but look at that kind of macula itself that looks yeah so the rpe in this place has been wiped out what do we call this type of macular degeneration exactly so ga or geographic atrophy so you can get in an end stage of dry macular degeneration you get the rpe wiped out you get so-called geographic atrophy and here's what it looks like here's brooks there's a few little cells here not many and you look the rpe is totally wiped out which means secondarily that the retina gets totally wiped out so that's so-called geographic atrophy what are we showing right here so retinal as well as sub-rpe in your vascularization the flame-shaped hemorrhage there's exactly so when you get hemorrhage under the retina just under the retina itself where it's broken through it can be read but when it's under the rpe where new vascularization first starts it looks kind of greenish grayish so this is what we call sub-retinal neo this is macular degeneration and then if you look i copied this out of a book i just don't have a beautiful picture like this here's brooks here's the rpe and look there's a little break right there and here's the blood vessels going through that break growing underneath the rpe here in the retina so sub-retinal neo vascularization and that's part of the amd and if you don't treat it you can get this so huge again sub-rpe sub-retinal hemorrhage huge here so we used to laser this and that's the problem is when you laser tissue you actually destroy overlying tissue so you would use quote light laser and you try to lightly laser it and obviously that would end up causing you know more damage to vision so now fortunately we do have the anti-veg F injections that we give that can make this regress and if it doesn't regress you end up with this which is a fibrotic we used to call this a discoformed scar so this gliotic i should say gliotic scar underneath the retina from neo vascularization bleeding under the retina what are we seeing right here so there's some focal areas that look like there's some scarring perhaps some infarct this i mean since they're focal or not i mean there's some of the macula but there's some off to some of the other vessels and so it could be an infectious cause and what infection looks like this exactly so you see there is a macular component in some of these but you get these peripheral they call these punched out lesions and they actually call this presumed ocular histone because it's very rare you can actually prove an actual bug in there so it's presumed ocular histone but people have blood tests showing that they had histone and it's in an area that's endemic to histone and so peripheral punched out lesions and then you can get macular lesions and even subretinal neo a lot like you get in in amd all right so we're looking right here we've kind of lost our foveal reflex there it's almost like it's it's gone but you look in there and something's just not right you just don't see a good foveal reflex what do you think that could be what's a test you want to do when you're looking and you're not seeing a good foveal reflex quite sure what's going on there you can do an oct or you can do this test all right so on f a what is this showing yeah so this is kind of what they call that flower petal that's a dangerous late leakage in the macular what causes that exactly systoid macular edema so remember it goes into those little cysts of henley's layer and you get these little flower petal patterns so this is systoid macular edema that's what it looks like pathologically sure enough we're in the macula here's the outer plexiform layer which we call henley's here and you can see the exudate in henley's and so anything that causes you know chronic inflammation in the eyes you can get it from uveitis you can get it after cataract surgery and so this is systoid macular edema all right what are we seeing right here kind of a funny looking macula again we'd really have a pretty poor foveal reflex wait that picture is not this picture i mean i know that sounds funny but but you have to come around here for a minute come look at this picture right here make a road trip come around here because no seriously because that that doesn't show it well you gotta write you guess can all come around if you want i mean this is definitely not that's that picture is not that it really isn't so it's not even fair but but please take a look at that i don't know why that's so what are we looking at there now so looking at it here it looks more kind of like a bullseye maculopathy exactly this is a bullseye maculopathy so you can't see it when you look up there because it's all kind of more sense of this is a bullseye maculopathy what are some of the causes of bullseye maculopathy so the big one we worry about is the black one on toxicity right so we look at a lot of patients in clinic with hydroxychloric when black window you worry about it now you want to catch it before it gets to this point because by this time there's a permanent damage done so usually it's medication some of the antipsychotics can do this a black window can do this and so bullseye maculopathy now you can get a bullseye appearance in some of the cone rod dystrophies too but this is kind of an end stage bullseye this was a black window patient when you look at the fluorescein instead of leakage you actually get window defects here so it doesn't like it bigger and bigger and bigger as time goes on these are actually window defects you can see the dark area around and this is actually the coroid shining through so this is a bullseye maculopathy all right i'm sorry we'll have to go quickly here what is this entity this is these are angioid streaks exactly so these are angioid streaks and they are actually under the retina in what layer the coroid no no yeah they're actually in brooks so you get a brittle brooks and you get these little formal breaks in brooks angioid why would i be showing you this lady's neck we're associated with chicken skin exactly chicken skin from pseudosanthoma elastica this is a so-called plucked chicken look so angioids you can sometimes also get them even in sickle cell too but angioid streaks pseudosanthoma elastica what are we looking at right here um oh so this is clarifying this photo the nerve looks uh has some power to it pale nerve the vessels are attenuated really attenuated vessels and then you have pigment clumping so it looks like rp exactly so this is retinitis pigment hosta and here's a close-up now why do you get this bony spicule pattern to the pigment you know i i don't know actually the pigment gets released from the rpe which gets chewed up and then it'll kind of diffuse around to the vessels it'll deposit around the vessels and that's why you get that bony spicule pattern and here you can see chewed up rpe pigment going up into the retina along the vessels so you get the bony spicule pattern but diffuse they call this chalky white pallor of the disc attenuated arterioles all right what the heck is this thing it's like a central right in the faux egg shapes okay so what disease gives you this this is best disease this is the only time you ever do an eog i don't think i've ever done that in my career but this eog and so you get this deposition of this material underneath now in kids they call it best sometimes in adults they call it adult the teleformed dystrophy and you get this deposition of this material again kind of underneath the rp now surprisingly they can have that big sunny side up egg in the middle of their fove and still have like 20 40 20 50 vision so it looks really dramatic but they can still have pretty good vision all right what are we looking at right here um you have some flex kind of radiating out from the this is where you have to be imaginative and i always say that the pathologist of sniff formalin but i don't know what the retinologist excuse is because fluorescein doesn't do anything to your brain so they call this pisiform or fish like and so this is actually if it affects the macula it's called stargardt syndrome if it's peripheral they call it fundus flavium aculatus and so you get these little deposits and these little fish like entities there and and the material is actually lipofucin so you get lipofucin deposited in the rpe cells and this is stargards and last but not least and this is not a blurry picture this is in focus so this this is actually an acute infection this is the so-called headlight in the fog and this is toxin so toxo is a you know choreo retinitis it's a retinitis actually and then it spills into the vitreous and so acute toxo you get a headlight in the fog but chronic toxo you get one of these burned out scars there's all these lacunae with this white sclera showing through on the broken up pigment so this is where you had a toxo infection this is often congenital you know you get it from uncooked meats and can even be passed on from the mom in you know intrauterol and you get these little toxo cysts here in the peripheral retina and this just shows you an area where you had some rpe here and retina here but then you come over here the rpe and the retina get wiped out by the chronic toxo and last but not least so this is your typical no-kentia picture ischemia exudate ischemia what is the classic one for this cmb and so cytomegalovirus and when we when unfortunately hiv was really exploding and we couldn't treat it well you would get a ton of this this cmb retinitis and you actually get in the ganglion cells in the retina you get intranuclear and intracelloplasmic inclusions so you get these inclusions in there and then we say goodbye to vienna next week is going to be optic nerve so please study up your optic nerve