 Okay, so we'll get started. We're doing a retinal vascular disease, part two. So this is excluding diabetic retinopathy. Last week, for those of you that weren't here, we did venous and arterial occlusions. And I think Nico got the PowerPoints if you need them. It kind of goes over all the studies that you would need to know. So this week, it's really kind of a hodgepodge of vascular disease in the retina that we're supposed to cover. It's really all coming out of, I think, mostly chapter six in your book. So, ocular schemics syndrome, hypertensive retinopathy, sickle cell coats, macranurisms, juxtaphoial telangiectasia, radiation retinopathy, valsalva, tercins, perches. So it's like this big bag of stuff. And we'll try and get through it all and kind of get the salient points in for you guys. What's supporting? So, first we'll cover ocular schemics syndrome, and is this, sorry, is it going on its own? Let me see. What's that? It's kind of just going on its own. Do you know how to? Should I present your view? That's what I was doing. And it was just kind of, is there a way to, I feel like it's... Play form start as well. Yes, you have notes. Yeah, I have some notes, but they'll come up, so. Oh, okay. Okay, hopefully it doesn't zoom along. Okay, it's zooming along. How do I, do you know? Oh, is it moving by itself? Yeah, yeah, I've seen, okay. Huh, we'll see if it wants to move by itself. I don't know why it's doing that. Okay, sorry, technical issues. So, ocular schemic syndrome is characterized by reduced blood flow to the eye, and this leads to ischemia, both the anterior and posterior segments, and it's caused by severe carotid occlusion. Typically, patients are complaining of vision loss that's very slow over weeks to months, and they'll often complain of pain. The pain often gets better when they're laying down just because then they get improved perfusion to the eye when they lay down. You'll typically see it in older men. The ratio of men to women is about two to one, and it can be bilateral, but it's not very common. It's pretty rare, but it's thought that these numbers are an underestimate, underestimate, and it can often be confused with the vein occlusion or diabetic retinopathy. So those are the two things to really keep in mind and to rule out, and we'll go over those. So, the findings you'll see on the anterior segment, the classic thing is neovascularization of the iris, cell and flare of the anterior chamber. You can get corneal edema, and often you'll see an asymmetric cataract. The iris findings, they'll have synechia with the fixed pupil and iris atrophy, and they'll often have elevation of the intracular pressure. They can develop neovascular glaucoma. And then on the posterior segment findings, the really classic thing are these midperforal dot blot hemorrhages. You might see optic nerve pallor or optic nerve edema. They can also have macular edema or vitreous hemorrhages, neovascularization of the posterior segment as well. So, typically you'll find greater than 90% stenosis of that ipsilateral carotid artery, and this can often be the initial manifestation of carotid occlusive disease. These are gonna be your typical kind of vascular pass at the VA, ischemic heart disease. They've had CVA's, peripheral vascular disease, hypertension, diabetes, and it's an important diagnosis to make because they do have a higher mortality rate and a high rate of stroke. So you wanna make sure you're not missing this and calling it diabetes or vein occlusion when it's really this because it can impact their life. So this is really our typical fundus findings, these midperforal blot hemorrhages. And I think really of note is looking at the vasculature here, and you can see that the vessels are pretty straight. They're not dilated, they're not tortuous, and that'll help you distinguish that from a vein occlusion. You also don't see a lot of beating like you would see with a diabetic. One way to help make the diagnosis is with ophthalmodynomemometry. And so what you're doing here is you're trying to estimate the pressure in the ophthalmic artery at the site of the central retinal artery. And so what you'll do is just gently apply pressure to the globe and you'll start to see the arterial pulsations. You shouldn't really be able to cause that winking just with your finger when you're doing an indirect exam. And if you can start seeing those pulsations, you know that they have this reduced perfusion pressure and they're more likely to have ocular schemic syndrome. So I'll have to do that just when I'm doing indirect ophthalmoscopy. Just press on the globe and you'll start to see this blinking of the vessels. And that can help you differentiate this from a central vein occlusion as well. So imaging findings, the most specific sign is delayed caroidal filling. Most commonly you're going to see the prolongation of the AV transit time in 95% of patients. You'll also see vascular staining and a small percentage of patients will have macular demo with angiographic leakage. So the caroid, you should know this, but it'll fill within five seconds of the initial dye appearance in the caroidal vessels. But an ocular schemic syndrome, it can take up to a minute or longer for the caroid to fill. So this just shows this vascular staining that you can see in the peripheral vessels there. And then the mid peripheral kind of Doppler hemorrhages. And there's not a lot of pathology in the posterior pole. You'll notice. So to help make the diagnosis, really the first test we're gonna get is the carotid Doppler. That's the least expensive, the least invasive and the less risk. And you can often make the diagnosis with that. If that's equivocal, then you'll move to an MR angiogram or a CT angiogram. The last test we'll order, if those don't give you the diagnosis would be a carotid angiogram. That's really the gold standard to make the diagnosis. However, it's not really ideal because it's costly and there's a high risk of complications, including stroke, cerebral infarct, and about a 1% mortality rate. So we don't do that commonly, but if you can't get the diagnosis any other way, then that's what you would move to. So this table came from a review article in Survey of Ophthalmology from 2010. And I think this is a really, it's a busy table, but it really kind of helps highlight the findings and the difference between ocular schemic syndrome, evane occlusion, and diabetic retinopathy. I know it's busy. So, but I think just kind of looking through it, looking at the vasculature. So in ocular schemic syndrome, they're not really torturous. They might be dilated, but they're not torturous. Vaniclusion, they're gonna be dilated and torturous. And in diabetes, they're dilated and they're beating. So that'll help you. The location of the hemorrhages. So like I said, ocular schemic syndrome, they have these mid-perforal kind of blot hemorrhages. They really don't have a lot of flame hemorrhages like you would see with the vein occlusion. Diabetes, the location of the hemorrhages, they're involving the posterior pole and the mid-perforate, where in ocular schemic syndrome, they're just, they're really not in the posterior pole. Other changes with the vein occlusion, you might see shunt vessels at the optic nerve. You won't see that with ocular schemic syndrome. Exudates are not really present in ocular schemic syndrome, but they are very common in diabetes and rarely in a vein occlusion. And then the optic nerve can be normal. It might be pellar demidus, but it's most often normal in ocular schemic syndrome. Vain occlusion, you'll have in a demidus nerve. And diabetic retinopathy can be a demidus if you have like a diabetic papillopathy picture, but that's not common. And then we talked about the perfusion pressure and that's decreased and that's one of the distinguishing characteristics that you can do in your exam chair to help you kind of make that diagnosis. But if you have a doubt, you know, it doesn't hurt you. If you have like a mild non-eschemic vein occlusion and you're not sure, you can get a carotid Doppler to kind of rule this out. And then imaging changes, you know, the crudal filling being patching to late is a common in ocular schemic syndrome. And then in vessel staining for ocular schemic syndrome, you typically see arterial staining more than veins, whereas in a vein occlusion, your C vein is staining more than arteries. Diabetic retinopathy, neither of them will stain. So I know that's a lot, but it is helpful I think to kind of differentiate those three diagnoses. So the prognosis is pretty poor, actually. If they have neovascularization of the iris, 90% are legally blind within one year. PRP is pretty effective in treating neovascularization, but they do have a high mortality rate with a 40% mortality rate at five years due to ischemic cardiovascular disease. So treatment, working with the vascular surgeon for carotid artery stenting, or I don't know why it's skipping ahead, sorry. And our direct to me, I've had patients that have been sent directly from radiology straight to the vascular surgeon because they've had such severe stenosis. And then for treating the ocular disease, anti-vegeta agents are useful for neovascularization of the iris or neovascular glaucoma, pan-retinal photocoagulation, and then working with your glaucoma specialist if they need glaucoma surgery, such as a tube or a shunt, depending on how severe glaucoma could be. Do you guys have questions about ocular schemic syndrome? Okay. So we'll move on to hypertensive retinopathy. So really, the majority of patients that have mild to moderate hypertension, they really don't have fundus findings or ocular complaints, but you'll see in really severe hypertension or acute malignant hypertension, you can see severe vision loss and ophthalmic signs. So this is classified by the modified Shea classification. Grade zero is a normal fundus exam. Grade one, arterial narrowing. Grade two, you'll see narrowing with focal irregularities. And grade three is grade two plus retinal hemorrhages or exudates. And then grade four, you'll also see optic nerve swelling. The effects of high blood pressure can be seen at any layer at the retina of the cord, the optic nerve. And if you see AV-nicking, it doesn't really predict what the blood pressure could be. If you check it in the clinic, it might be normal, but they could have chronic high blood pressure problems. There's not a great correlation. So what grade is this? Anybody? Three. So you see they have severe hypertensive retinopathy. They have immacular star, cotton wool spot hemorrhages, but there's no optic nerve edema, as opposed to this would be four with severe optic nerve edema hemorrhages. The changes in the coroids are often seen in younger patients that have acute hypertension. So these are the eclamptic women, people with fiochromosatomia or renal hypotension. So you'll see this kind of tan lobular patch of the coriocapularis from ischemia, and then this turns into this pigmented spot that you can see here, and this is called an L-Schnick spot. The other kind of characteristic finding is called a segris streak, and this is this linear pigmentation that follows the coriolardary seen in acute hypertension. I don't see that commonly. I think the thing I see more often, my eclamptic women often come in with this exudative detachments that are involving the macula, kind of a central serocyte picture, and you follow those, they manage their blood pressure, they have their baby, the eclampsia goes away, and it often resolves on their own. So the most important thing, checking the blood pressure in the clinic, if it's very high, I've sent them to the emergency room, if it's moderately high, you'll kind of work with their primary care doctor, kind of depending on the urgency of the situation, but the treatments to get the blood pressure controlled, obviously. So, moving on to sickle cell disease, which is rarely seen here, but will be on the O-caps, regardless. Sickle cell, this has been on your board type tests you've been doing for years, but it's a valine substitution for glutamate, resulted in adenine instead of thymine, and then you get this reduced solubility with the sickling of the red blood cells in the vessels. Hemoglobin C is a lysine substitution for glutamate. So, sickle cell trade is seen in 8% of African-Americans, sickle cell, 0.4% disease, and then hemoglobin S-C disease is in 0.2% of African-Americans. I think this is more commonly on your O-caps, which is which one has the highest rate of systemic complications versus ocular complications. So, systemic complications, the highest rate is in sickle cell disease, and they rarely get proliferative sickle retinopathy. The higher rates of ocular disease are gonna be in the S-C and the S-thalassemia trade disease. So, what's happening is you get sickling of these blood cells that leads to hemostasis and thrombosis, and then you get peripheral occlusion and non-perfusion, and then in response, you'll get retinal neovascularization at the border of this perfused and non-perfused retina. Kind of our common non-proliferative findings are the salmon patch hemorrhage, and so this is intraretinal hemorrhage downstream of a retinal arterial occlusion. Initially, it'll be bright red, and then as those RBCs are hemolyzed, it becomes this kind of pinkish salmon color, and then as it becomes further broken down, you'll get these refractile deposits, and that's absorbed heme underneath the ILM, and then further downstream from that, you'll develop this black sunburst lesion, which is basically a pigmentation moving into that area of hemorrhage under the RPE. Yeah, the salmon patch hemorrhage is intraretinal, yeah. It's more long-standing, so the blood is starting to get hemolyzed. So initially, it's bright red, and then as the blood cells get broken down, it becomes pink, and then it becomes pigmented. The salmon patch, I know. The other thing that's common in sickle cell disease as well as sickle trait are angioed streaks, and this occurs in about 6% of these patients, and this is thought that there's occlusions in the caroidal circulation that are happening, and then subsequently develop breaks in Brooks membrane, and often you'll get caroidal neobascular membranes that can occur in association with angioed streaks. How commonly do you see sickle? Yeah, yeah, here maybe a couple of patients are kind of around with it, but it's pretty uncommon here, but you're probably dealing with it all constantly. So stages of proliferative retinopathy. The first thing you'll find is peripheral occlusions that lead to non-perfusion, and then you'll develop these hairpin loops or AV and astimoses, and these are occurring peripherally in the areas where you see that distinction from the perfused to the non-perfused retina, and then after that you'll get these peripheral C-fans, which are neobascular blood vessels, and then those can hemorrhage and then often lead to fractional detachments. The location of the neobascularization and distinction to diabetes, these C-fans are occurring in the peripheral retina, whereas when we look at diabetic retinopathy, they're often along the posterior pole, along the arcades and the optic nerve. Frequently, these C-fans can auto-infarct, and you'll see these kind of white C-fan picture. So this is an active C-fan, an attractional detachment, and then this is auto-infarcted here. And then this is a wide-filled imaging showing these peripheral C-fans, and you can see the edge of the perfused to the non-perfused retina, and that's where these C-fans are developing. As opposed to the fluorescein you'd see in diabetes, you would see the neobascularization occurring along these arcades, the optic nerve, and nasally, typically. And this just shows you, this is a diabetic, so you can see the location of the neobascularization is completely different than what you see with the sickle cell disease. Other findings are these comma-shaped vessels on the inferior forenecks in the bulbar conjunctiva from sickling. So I think considerations for patients that are African-American that present with hyphemia should consider screening for sickle cell disease. They can have more difficulty getting their pressure control, they're frequently rebleed, and an earlier AC washout is recommended. You don't wanna use carbonic and hydrous inhibitors because this can worsen the sickling. For patients with sickle cell disease, they should get twice-yearly dilated examinations to monitor for proliferative disease. And you wanna consider doing a baseline fluorescein angiogram to document and to evaluate for peripheral non-profusion. There are some emerging potential therapies to prevent proliferative disease, and the idea is to kinda stimulate this fetal hemoglobin with hydroxycarbomide treatment of children or perhaps reducing the sickle cell cells via exchange transfusion or hyperbaric oxygen. As far as laser treatment, some advocate for feeder vessel closure of the C-fans, and others do kinda peripheral scatter laser to the areas of non-profusion to cause regression. Either way, you wanna be cautious and judicious in when you do laser and how intense the laser is because laser's been known to precipitate retinal tears and retinal detachments more commonly than it would in diabetic patients. And then there might be some role for anti-veg-f agents as well. Do you use anti-veg-f agents in these patients or laser? So, perioperatively, when they develop detachments, tractional detachments or combined tractional regimenotogenist detachments, when you're planning surgery, you wanna avoid encircling elements. The idea is that those encircling elements can lead to anterior segment ischemia, so you can do segmental elements, but you wanna avoid those 360 elements. You wanna be careful with your cryopexy because you don't wanna promote that anterior segment ischemia, and you don't wanna use epinephrine in your anesthetics. And then for the systemic control, you wanna make sure they're adequately hydrated, nasal oxygen, and then be careful with your gas use. And then you wanna really be careful with their intracular pressure postoperatively so they don't develop vascular occlusions or anterior segment ischemia. So, the detachment often begins in the ischemic retina that's in the periphery, and it can be brought on by laser, and the tears will be just at the base of a C-fan. They have a pretty high rate of complications and some authors report recurrent detachments as high as 40 to 50% in proliferative sickle cell disease. So, when you're evaluating a patient with peripheral neovascularization, there's a pretty broad differential. This is coming from Table 6-2 in your book. So, you wanna keep in mind diabetes, vein inclusions, arterial occlusions, sickle cells, C-C fistulas, Irvan, do you guys know what Irvan is? Anybody? Brian? No? Idiopathic retinal vasculitis, aneurysms, and neuro-retinitis. So, it's pretty uncommon, but it would be on your differential, I don't know, maybe that, it's kind of falls more into your UVitis lecture so I didn't talk about it today. ROP fever, hyperviscose syndrome, ULZ disease, ocular schemic syndrome, and then inflammatory diseases can also lead to neovascularization. Commonly you'll see that with parisplanitis. Chronic detachments and melanomas can also lead to neovascularization. So, moving on to coats disease. This is characterized by these retinal telangiectasia and then you get these ectatic arterioles, microaneurysms, venous dilation, and then you get massive exudation and you can get these massive exudative detachments. They can be peripheral or in the macula. There's a pretty wide presentation clinically. Irleast taught that it's unilateral, but there's more and more evidence that this could be a bilateral disease just based on wide-filled imaging. But on your tests it's unilateral and typically male. There's a worse prognosis when these present at a younger age. Coats disease obviously is in your differential for leukocoria. I couldn't remember, do you guys have a mnemonic? Is there some mnemonic for leukocoria? You just have to know it. Just know it, okay. You just have to know it. Okay, so for leukocoria, coats disease, ROP, retinoblastoma is really the big one. Fever, toxocara, parisplanitis, eels, persistent fetal vasculature, metastatic disease, Norie's disease. So if you find calcium on your ultrasound or your CT scan, calcium is coats, no, retinoblastoma. So if you see calcium, that's retinoblastoma, not coats disease. There are these staging systems for coats disease and there's these two different staging systems. I've never seen anybody test on this stage one through five and they're both pretty similar just that they begin with sort of mild vascular changes that progress to partial detachments, total detachments and then complications include neovascular glaucoma and these eyes when very severe can progress to this kind of blind, painful eye and can require enucleations ultimately in very severe cases. Usually laser and cryo are pretty successful in controlling the exudative disease. Rarely you might have to progress to doing surgery, including buckles or protractomies and then like I said, the worst case would be going to an enucleation for a painful blind eye. Often the patients that present younger have a worse prognosis and have more severe disease and those are the ones that are more likely to progress to these really large retinal detachments. When they're older, it's usually milder and it can often regress on its own even. So macular telangiectasia, it's also called paraffovial telangiectasia or juxtaphuvial telangiectasia. It's characterized by focal retinal gliosis and telangiectasias. There's really three types. Type one is fairly uncommon but that's one is for unilateral, often seen in males and then type two is the most common type and so if you hear someone say MacTel they're probably just talking about type two is sort of the nomenclature and then type three is incredibly rare. I don't even know if I've ever seen a case of it to be honest but it's bilateral with retinal capillary obliteration on histology. The structural abnormalities in macular telangiectasia is actually similar to diabetes and they're getting deposits of excess basement membrane in the retinal capillaries. So this is a case of macular telangiectasia type one. This is thought to be a variant of Coates disease in older men. It's also known as Lieber's milliary aneurysms and they have these one to two disc diameters of exudates and telangiectasias in the temporal macula, what this kind of ring of exudates and the macular edema kind of waxes and wanes without treatment on its own. And so often these patients will retain excellent vision despite this type of picture. Here's another example of type one A and then an angiogram with this temporal leakage and these kind of focal telangiectatic vessels that leak late. Type one B is also unilateral middle-aged men. They can complain usually of some mild metamorphopsias and then they'll have this kind of focal telangiectatic vessel just right in the foveal avascular zone. They often have vision better than 2025 and just based on the location of this, it's not recommended to really do any treatments or any laser because they retain good vision anyways. It has a pretty good prognosis. And then type two Mac tel which we see a lot of here and this is Dr. Bernstein's big thing is studying macular tel, Mac tel, studying the carotenoids and the pigmentation and he's involved in a big international consortium to better understand Mac tel. It's characterized by these right angle venules that then become pigmented. You can often see crystal and retinopathy or these kind of glistening white dots which are called singerman spots. They can later develop chordal neobascular membrane. It's typically bilateral but asymmetric and your patients that present with this are usually kind of in their mid-50s when they come in. These are the stages of Mac tel type two. So first stage you'll have a totally normal exam but you might see a little bit of staining on your fluorescein angiogram. And then in stage two you'll start to get this kind of grayish sheen to the fovea and mild vessels in that temporal region. And then stage three you'll get those vessels that start to dive in at this right angle into the perifovial retina. And then in stage four you'll start to get these pigmented plaques develop around those vessels and then stage five is a chordal neobascular membrane. Patients typically are symptomatic in stages three through five. Most patients have pretty good vision 2030 to 2040 but they do complain of visual distortions but they do retain pretty good vision. And then you can see crystal and deposits pretty much stage two through stage five they'll get this crystal and retinopathy so that would be on your differential for crystal deposits in the retina. This just shows the loss of the luteal pigment. And this is a case report that has some really nice imaging that shows what the images look like in Mac tel. You get this crystal and retinopathy that develops. This is the fundus autofluorescence with loss of that normal hypo-autofluorescence in the center. And then on the angiogram in the early phases you'll get these temporal telangiectetic vessels and then those leak late in the angiogram. And this is really a pretty typical OCT. You can see these inner and outer systoid spaces in the retina loss of the outer nuclear layers here. And then this inner kind of lamellar defect is often in this parallel axis to the retina. And then this would be called like this ILM drape that you can see kind of covering that systoid space. And this is more advanced disease stage four and then stage five with the development of a net. Type three, like I said, is very rare. I don't think I've ever seen a case but it can occur in men and women, it's idiopathic and they have pretty severe vision loss with capillary occlusion and later they develop telangiectetic vessels. For treatment options, type one you can consider laser photocoagulation, just kind of a focal laser to the areas of leaky vessels. Type two, it's really not any great treatment. People have tried laser, people have tried anti-vegeths. Just for those cystic changes, people have tried steroids, PDT, nothing really works well. But if they do develop a CNBM then you wanna treat them with anti-vegeth agents. And like I said, they usually retain pretty good vision regardless of what you do. Unless they develop a CNBM, then they can lose vision. Any questions on MacTel? Sorry, I feel like we're like diving all over the book here because now we're gonna talk about macroinversals. So this is something to keep in mind when you see hemorrhage in every layer of the retina. There's not many things that can do that, but a macaroneurism is something that could cause hemorrhage in the vitreous, in the retina, pre-retinal, sub-retinal. So keep that in mind when you see some unexplained hemorrhage. Often as the hemorrhage clears you'll see this dilated macaroneurism underneath the blood. Often they can sclerose on their own, seeing here it's starting to sclerose on its own and then it will rarely rebleed. You typically see it in elderly women and often in this temporal arcade. It's typically associated with hypertension or you might see it following a vascular occlusion. This is kind of your typical fluorescent angiogram. So you see this hemorrhage that's sub-retinal and some intra-retinal heme. And then on your fluorescent angiogram you get this kind of bright white bulb that lights up, but not your macaroneurism. As far as treatments go, some advocate trying to close the macaroneurism directly with laser and that works. There is a risk that it can get downstream occlusion of that blood vessel and cause an arterial occlusion potentially. Others advocate for kind of this ring of laser around the macaroneurism to reduce the exudations in the macular edema. And radiation written up at the, so this is someone that had a plaque treatment to this melanoma and then you can see subsequently they've developed this severe radiation retinopathy with macular edema and exudates, evane occlusion and hemorrhages in the retina. Radiation retinopathy does resemble diabetic retinopathy with these microangiopathic changes and we do treat it like diabetic retinopathy. It's typically a delayed onset. So a year and a half or so after external beam radiation and then with like a plaque brachytherapy, it'll present earlier. Treatment options, focal, PRP, anti-vegia for steroids. You can also, you might need to do of atrectomy as well for hemorrhages or tractional detachments that can occur. You know, our typical exposure is 30 to 35 graze but it has been seen in as little as 15 graze of exposure. Valsalva retinopathy is, can be pretty mild. In some cases it's more severe. Often you'll see this in somebody after they've had food poisoning and they've just been vomiting. You can also see it with strenuous exercise. I've seen it with patients with severe constipation but typically this has a really good prognosis. What's thought to happen is there's a sudden rise of intratheurastic pressure and then it ruptures these small capillaries in the macula and the blood is typically under the ILM but you can also see vitreous hemorrhages as well. You wanna make sure that you're not missing a tear in the peripheral retina or perhaps a macoraneurism. And usually these patients are pretty healthy. You know, they come in and just under had this sudden vision loss and there's usually a reason for it. And then perturge retinopathy, this is typically seen in compression injuries. I was initially described in a man who fell from a tree and then suffered a brain trauma and you'll see these kind of large cotton wool spots and hemorrhages surrounding the optic nerve. It's thought to be due to the injury inducing complement activation and then you get granulocyte aggregation and leukoembolization. It may cause permanent vision loss and is often bilateral. The vision loss usually presents one to two days after the initial trauma. They can often have an afferent pupillary defect as well and optic nerve edema. It's kind of characterized by what's called percher fleckin. I don't know if you've heard that term. But it's this kind of polygonal area of retinal whitening and it's hard to see here but there's kind of a clear demarcation between that whitening and the vessel of about 50 microns. When these findings occur without trauma, we call it percher-like retinopathy and this can be caused most commonly from pancreatitis but also fat embolism, amniotic fluid embolism, retro-bulbar injections can cause this as well as autoimmune disease. As far as treatment goes, the treatments to kind of treat the underlying conditions, some people have tried high-dose steroids with some varying degrees of success. And then Tursan syndrome is intracal hemorrhage associated with an intracranial hemorrhage and it's thought that there's this acute rise in the intracular venous pressure that then ruptures the retinal vessels. So it's thought that about 30% of patients with a subarachnoid or subdural hemorrhage have intracular hemorrhage and this often improves on its own. If it doesn't improve, typically we'll watch these for several months but if it doesn't improve, you might need to do vitrectomy and perhaps even younger and young kids that have a Tursan syndrome. Typically, it's pre-retinal sub-ILM hemorrhages. There can be sub-retinal hemorrhages as well. Yeah, they're pretty close around the nerve, exactly. Yeah, they're not usually kind of in the periphery. It's poster pull. And then it's characterized by what's called this double ring sign of hemorrhage that you can see. So the inner ring is sub-ILM blood and then the outer ring is sub-hyloid. And it can occur within hours of the intracranial hemorrhage. It might go unnoticed because these patients have other systemic things happening and potentially can't be dilated and they're not complaining of vision loss because they're in the ICU. But that's why you guys end up getting called for a lot of these. All right. So I kind of got through that whirlwind tour of retinal vascular disease. Do you guys have questions? No, I know it's kind of, I don't know. When I was putting the lecture together, I felt like I was all over the place, but.