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Uh Today, I'm gonna be covering kind of the common conditions and emergencies you see in ophthalmology. Uh This is just following the first session we had where we're looking at the anatomy and kind of hi everyone. Thank you for joining us today. So again, as a mentioned, she's gonna be talking about the clinical conditions. So, uh while he runs us through that, I just wanted to talk to you guys about the certificates as well. So I will be sending in feedback forms at the end of the session. So if you fill this in, you'll be able to receive your tenon certificates and also discount codes for uh PO RC and teach me surgery as well. If you guys have any questions, feel free to pop them in the chart during the session and while we get through it during the session and yeah, without any further to do, we pass it on to Abby. Thank you. So, first I just wanted to have, oh, well, thank you to our partners as well. Um And I just wanted to have a quick recap of the anatomy. So you've got from the outside, you've got your six extraocular muscles, they attach to the sclera. You've got the cornea, the clear dome shaped portion at the front here and that focuses light kind of 70% of the job is done by the cornea. Um And then behind that, you've got the anterior chamber here with the aqueous humor and we'll be having a closer look at that, uh particularly in relation to glaucoma. Um But we'll get onto that, uh, the iris, which is uh basically the muscles that can um that contract or um dilate your pupil. Um And the main, the main job of that is just to control how much light gets in. Then you've got the lens which is also for focusing light and that's for uh kind of 30% of it. But also the minute changes with these um sus suspensory ligaments and muscles attached there controlling the shape. Then you've got your retina which has the rods for your black and white and cone for your color vision kind of respectively. Um And yeah, you've got the, you've got the specific parts of the choroid and the fovea, which you'll see on fundoscopy and then you've got your optic nerve which uh connects to the visual cortex. So, starting off, I wanted to talk about diabetic retinopathy. So, di diabetic retinopathy is kind of that eye disease that you classically see in diabe diabetic patients. Uh This is particularly kind of one of the first things that goes away because of the um kind of size and delicacy of the vessels within your eye. So, particularly hyperglycemia causes uh increased retinal blood flow and abnormal metabolism. This affects the cells around it. So this is particularly the endothelial cells and the parasites. So the endothelial dysfunction leads to kind of vascular permeability. And that kind of lets you that kind of explains what you classically see on fundoscopy. So on the back of the eye, you'll see these kind of exudates, these these small yellow dots and that's kind of fat and stuff from the blood coming out and building up on the retina. Then you've got your parasite uh dysfunction, which is kind of the cause for microaneurysm. So you'll kind of see blot hemorrhages is classically what we're looking for. And then the more concerning sign is uh neovascularization and that's uh caused by the production of growth factors, which is in response to the ischemia caused by these uh cell dysfunctions. And um although that you would think that's a good thing, the new cells that are the new vessels that are produced are quite weak and leak out. And so it actually turns out to be worse most of the time. So, uh diabetic retinopathy is mainly split into two types and that's non proliferative and proliferative. The one you want to be more concerned about is proliferative. But first, we look at non pro proliferative because that's more commonly, what you will see in your diabetic clinics. So that's split into mild, which includes microaneurysms. And so that's kind of, you know, just what you would see a bit more blood in the retina and kind of bleeding out. Um, with moderate, you're gonna see block hemorrhages which are marked here, there's these kind of big red dots where the, the leaking has occurred, then you've got hard exudates. These are these bright yellow, er, dots, they're not necessarily um, points of ischemia. So it's not the pale retina coming through there, it's actual fatty deposits. Uh compared to that, there's cotton wool spots. So that's these kind of wider areas less well demarcated and generally less yellow and bright. And so that's where you, you tend to see more ischemia, that's where blood is not reaching. Then you've got intraretinal microvascular abnormalities, which I'll just call uh Ir Ma from now on. But it's um it's quite similar to neovascularization in that there are quote unquote new vessels, but these aren't actual vessels. They are more like shunts between um vessels that are already there. So as you see more fundoscopy images, you'll start to notice where it's normal to see vessels and where it's not. Uh these aren't, you know, this is not something you need to learn at your level. But um you are generally seeing these blue areas of shown, you'll see these kind of vessels that go across towards these kind of larger vessels which are normally there. And so that kind of shunting is what, what is considered I RMA. Um And yeah, that's kind of as close to neovascularization as you can get before we classify it as neovascularization. So it's not really new vessels, but rather connections between um vessels that are already there and then severe which we use the 41 rule. So you split it into quadrants and there's diffuse hemorrhages in all four quadrants, two or more quadrants have venous beating, which is um basically uh constriction or dilation of the uh venous system in the retina. And so I don't know, it's quite small there if you can see, but the size of this vessel here gets a lot smaller points. I'm sorry, I should have got a better image uh closer, but you'll, you'll notice it where it's also also called v uh nipping as well as another term for it where they've crossed over each other and they constrict at those points as well. And then you want one or more quadrants of Ir Ma. So here, this is, this is quite a classic example of a severe nonproliferative, but generally tho those cases are not as concerning until you get to the severe part. Here, proliferative is far more concerning and it's more common in uh type one diabetics because they tend to have uh far worse controlled diabetes. Um You've got retinal neovascularization. So those are those new vessels and as you notice, they are quite small and they are not, they are not like these large vessels. So that's typically what you see kind of this um spider Nevi almost um appearance where the vessels are small, they are sprawling out randomly and yeah, it's not a good sign. And then there's also the more obvious sign of vitreous hemorrhages. This is, you know, kind of because it's taking up such an area, you might not see those other signs. And so this would point towards proliferative diabetic retinopathy. Obviously, this is all in the context of the patient. So this is done in their diabetes check. So you check their HBA1C, their um blood glucose levels and then if it's high, it's more likely to point towards this. So a diag a diagnosis is done with slit lamp fundoscopy, which is just a more um detailed and easier view of the fundus rather than, you know, using your um classic handheld one. And that's usually done in clinics for their normal diabetic screening and retinal assessment. Um generally, that's enough to form a diagnosis, but in cases where, you know, you're not too sure you can do fluorescein angiography. And that's just the classic, you know, using a stain to follow the vessels and then seeing where you might see more neovascularization. So in terms of management, uh we're not too worried about the non proliferative, it's just kind of diabetic control, close monitoring and you consider treatment when it's getting towards the severe stage. Um that kind of treatment is more linked to proliferative. So, in pro proliferative, we're more worried about those new vessels. And so we use photocoagulation across the retina and it produces this very striking uh fundus. And if you saw this, you might be thinking, oh, this person has parasitic eggs in the back of their eye or something like that. But no, this is, this is just a a case of someone who has had pan retinal photocoagulation. So it's good to learn this one as well. Just so you're not thrown off in a, in an exam or anything like that. There's also the option of um anti uh anti vascular endothelial growth factor medication. Um So that's particularly um targeting that growth factor which is released when ischemia is there that produces the neovascularization and that's more done as an injection into the eye. Um And that's just an example of the kind of drugs, but you generally don't need to know the names of the drugs as long as you understand that it's anti vegf. And then there's also the um the option of vitrectomy, which is just a, a surgery to um basically try and cut out parts of the retina which are considered too far gone. So then we're going to move on to uh age related macular degeneration. Now, this is the most common cause of blindness in the UK. And it's kind of, it's kind of related to diabetic retinopathy because diabetic retinopathy is the most common cause of blindness for uh working age people, whereas age related is more for older people, but is also the most common cause. Generally speaking. So that's something to consider. If you have a patient of a certain age group, you can kind of take a guess at which one of the two they are likely to have. So a a clear feature that is shown here is a scotoma which is a loss of visual field in the center. Um and changes are usually bilateral. So this is, you know, an older patient who's come in and noticed that their central vision is really poor. Um a classic sign which we see on fundoscopy is the DRS drusen are these hard uh nodules of fat, which you see kind of similar to a hard exudates, but they tend to be more all across the retina because it's a systemic cause you, you know, you're more likely to see it across the retina. And yeah, it's more common with advancing age and it's more common with females. Some other risk factors include uh smoking, family history, and ischemic uh cardiovascular disease history. So any kind of um high BP or anything like that will will increase the likelihood of someone having um age related macular degeneration. So, yeah, it, it presents with gradual loss of central vision, reduced visual acuity, uh a crooked or wavy appearance in straight lines which we'll have a look at later. Uh night blindness is a common, a common thing that, you know, in GPA, a patient will come in and say, oh doctor, I can't see you when I, when it's at night at all. And you know, this, this will kind of point you towards that kind of um idea. Um And then something called Charles Bonnet syndrome, which is basically patients with low vision, actually have visual hallucinations as the brain tries to fill in the gaps or, you know, attempt to make more out of the limited visual stimuli that they actually get. Uh this also is classified into two and one is more concerning than the other. But here we have dry, which is where it's drusen is the main sign you'll see and the loss in vision tends to be more gradual um wet. On the other hand is where you, you've again got that worrying sign of neovascularization. And generally speaking, the visual acuity, acuity loss is more acute and you know, they'll start coming in with symptoms and they're more likely to notice as well because they, they notice that their vision is getting so poor, whereas dry is kind of a offhand comment when they come in to see the doctor. So again, uh investigations always do your slit lamp, uh having a look at that retina. Sorry, I'll just go back to show you the what you'll be looking for. Um You're looking for these yellow marks and kind of all around the retina with a wet, you know, you're going to have that central area where you've got that neovascularization. There's also something you can use called Amsler grid testing. And so that's here in the bottom left where um you ask the patient to look at the grid and then you ask them to describe what changes there are and they might, you might have another, another grid where they draw what changes are different there. Or you can just, you can just discuss it because you don't need an accurate representation of where exactly it is. Um And so in people with scotoma, they will obviously talk about their blind spot in the middle and slight waving of the lines. But also you can just have patients with um distorted or wavy lines. And these are both signs for age related macular degeneration. Again, angiography is always an option. If you're not too sure about neovascularization, there's also the option of OCT which is optical coherence tomography. And so this is kind of when you still suspect macular degeneration, but there's no visual changes on any of the other options there. And so this is the bottom right here where you've got this kind of side view image of the back of the eye. And so if I just go back one slide you'll see here is a is a kind of drawing showing that um drusen coming here and the uh new vessel formation And so that is basically a, a cartoon version of this. And so with a, that's what you would expect to see in um wet because you've got your neovascularization there. B is actually dry, but the DRS aren't very clear, it will just be these little bumpy parts here. But this is a classic case of where CT might be beneficial. And then C is just a more a clearer case of, of DRS. These are quite large and that's, that's kind of typical of what you'd see in dry in terms of management, dry is something you just want to monitor similar to non proliferative diabetic retinopathy. But there are, there have been trials done which show that vitamins supplementation help a lot. And so that's in particular, there was a certain mix in the trial which was zinc, vitamin AC and E and those were shown to stop the progression of age related macular degeneration or at least slow down with that uh with that where it's classically anti vegf injections. And that, that tends to work quite well if it's not too late stage. Moving on, we're talking about glaucoma. Glaucoma is uh optic nerve damage caused by a rise in intraocular pressure. This is caused by a blockage of the aqueous humor trying to uh escape that eye. So if you remember, we talked about the anterior chamber here and uh aqueous humor is always produced and then filling up. But you need a place for it to go away. And so that's through the trabecular meshwork and the canal uh of Schlemm. And so your normal eye pressure is 10 to 21. Um in Glaucoma above 24 is usually when you're worried and, you know, you want to um actually, you know, try and try and change the pressure there. So here is the normal aqueous humor flow. Um and it goes through the trabecular meshwork which provides some resistance. So you're not just always on the low side of uh your intraocular pressure. Um And then it goes through the canal sle which connects to the general um the general uh blood work. So, you know, your, your uh aqueous humor will just flow back into your, into your bloodstream and you know, you're not losing any kind of um any kind of moisture in that regard. So there's two types which we'll go on to. But uh so one type is blocking the Trabeum meshwork and the other one is actually here where the iris is pushed forward and completely blocking the area. So some risk factors include increasing age as always uh family history, uh Black ethnic origin and myopia or nearsightedness. The presentation is classic blurry vision, uh tunnel vision in particular. So, uh compared to age related macular degeneration, it's gonna be the outside rather than the middle uh fluctuating pain. This this comes in the form of headaches, but also in the eye and the classic sign, which they'll, they'll usually talk about in the exam is halos around the light. So that's typically what the patient will see when they look at a, a any sort of light. Uh This is just an image showing cupping in glaucoma. So uh your optic disc here is larger than 0.5 but we'll, we'll have a look at that in the next slide. Yeah. So it's classified into two types. So open angle, this is where it's a gradual increase because of the uh resistance of the trabecular meshwork. And this slowly builds up pressure. A queue is uh obviously where the symptoms come suddenly. And that's because the iris has bulged forward and sealed off the trabecular meshwork. Um and this is considered an ophthalmic emergency. So it's something that you need to, you need to look out for the presentation tends to be a bit more severe. So you'll see the patient with a red eye, they might have a hazy cornea, their pupil size will be fixed and mid dilated. So that's a classic way to tell between the two. If, if a patient comes in with red eye and dilated pupil, you're gonna start thinking acute ankle, uh glaucoma compared to other presentations of red eye and with acute angle, the pressure difference is so severe, you can actually just press on their eyeball and you'll feel how hard it is. I've seen, I've seen a, a doctor on a emergency care. Do that before. So in terms of investigations, it's got a Goldman applanation tonometry, which is this machine here, which applies pressure usually through air and we will get a reading back. So you don't actually have to touch the patient's eye and that's the gold standard. Um obviously you do your slit lamp, so that's checking the cup disc ratio. So there um in a normal eye, you would have this less than this wider area, less than 0.5. Uh you know, in terms of width of the uh macular, the you can also do a visual field assessment just to understand that there is peripheral vision loss if the patient hasn't come in with that. And there's also the option of G gonioscopy, sorry. And this is here where um you basically again having another side angle look at the um at the angle of the glaucoma. So if you, if you can see the iris blocking and so here, if you actually look closely again, sorry, the image is quite small, you can see the trabecular meshwork there. And so the fact that it's still visible means that it's open, open angle if the pressure is still high. Whereas here you can't see anything, it's just going from your iris to to the side of the eye, which, which is, which is not what you want to see. Um You can also do a central corneal thickness assessment and that's just to check if it's being pushed out or not. But again, that's, that's kind of a last last minute option or just, you know, depending on what's accessible in your, in your clinic. So the treatment is quite complex because there's quite a few uh number of options. But generally speaking, you start treatment at above uh 24 millimeters of mercury. So the first line is uh Prostaglandin. So Latanoprost is the, is usually the go to. Um and I think it's quite important to know the side effects of this because they are quite strange and, you know, they like to throw that in exams. So it includes eyelash growth, eyelid, eyelid pigmentation and iris pigmentation. Um, so you tend to get more brown eyes from it. And so that's something to keep in mind. Uh, I've also put how, how each of these medications work here, but I would, I would just say go over that in your own time. But the, the, the idea is that all of them reduce the, um, the interocular pressure. So Timolol is usually second line and then you have these as other options. Uh, sometimes these medications don't work. Um, I've seen it in clinic before where you've tried all of them and they haven't worked. So, uh, that's where surgical comes into play. Um, you can use 360 degree selective laser trabeculosa, sorry, um, to clear out the meshwork and repeat procedures if the person keeps developing a, a blocked meshwork and that's basically just removing, you know, that part which blocks how much is removed. Um You can also do Trabeculectomy uh which will create a new canal off the side here in this image and have a bleb at the top. And it's quite interesting when you see a patient with a bleb. Um And yeah, that would, that would basically just avoids the whole problem as is uh the canal phlegm is completely avoided. So you don't have to worry about it anymore. Um And then you can also have stents. Um It's quite new. Uh A lot of, a lot of research is being done on what's optimal with this. By an example is eye stents, which is a type of modified heart stents and that's basically just putting a stent there. So to stop any of these issues from developing. Um So this is all kind of generally speaking, um tackling open angle glaucoma in acute, you obviously need to tackle the issue a lot more quickly. Uh And so you go straight to Pilocarpine which is a muscle uh contraction to open up the pathway. Um And that, that just basically forces it open. Uh it can be quite painful for some patients. So it's something you, you need to confirm that it's acute angle um glaucoma before you start that, uh another, another option is IV um uh option of the previous medication that we use. And again, it does the same thing of reducing production uh but it's just a stronger, stronger version. And finally, the kind of definitive management is laser iridotomy. And that's just basically punching a hole through um through the um iris to basically release the pressure. And yeah, it's, it's uh quite effective. So that's usually what you would want to go for. Then we've got cataracts, which I'm sure you've all heard of before. But it's basically where the eye lens gets progressively more opaque and reduces, you know, the amount of light that goes through, thereby decreasing visual acuity. Uh cataracts are actually more common in women than in men. And it also again, increases with age but not as much as some of the other conditions mentioned. So, you know, you, you can see um cataracts in people just above 40 years old, there's also the case of congenital cataracts. So, Children born with cataracts as well. And one study showed that 30% of individuals age uh uh above 65 actually have a visually impairing cataract in one eye at least. And so some other factors, smoking, alcohol, diabetes, uh steroidss and hypocalcemia. Uh they're usually asymmetrical because they develop on their own unless there's a systemic cause. Um and it, it typically presents with the reduction in visual curry, um progressive blurring, uh colors become more faded. So here's an example of that where um they come more brown and yellow whereas they previously, again, it's very, it's a very slow change. So patients won't often notice and it's only after a while, maybe if they look at something that they saw in the past and realize it looks different. Uh again, light is affected. So starburst is the classic sign. And the main thing you want to look for is the loss of red reflex as well. And the reason why we look for that is because it's quite easy to, to look for as well. So, again, classic uh ophthalmoscopy or fundoscopy. So it should be a normal fundus after you have a deeper look at the retina, if any retinal changes would probably point you towards something else. And then slit lamp will have allow you to actually see the cataract in, in quite obvious detail. So in terms of management, uh surgery is the only effective management, unfortunately, but a lot of people do use um glasses up until a point where, you know, they're no longer working or the strength is too much. And so, um uh generally surgery is only used when the cataracts are impacting the quality of life for the for the patient. Um And it basically uh works by breaking the lens uh with uh with a kind of uh sound, sound, uh sound waves and a kind of earthquake effect. Um And then you can remove the pieces because they've been made smaller with just classic suction. And then here at the bottom, you can see they, they implant a folded lens and then will, will manually uh unfold it or move it into place and it, and it works very well. It's one of the earliest op down surgeries. Um, it's quite important to know the POSTOP care because that's, that's probably the part you're more likely to be dealing with as a doctor. Um And so you've got your antibiotic, antiinflammatory and lubricating uh eye drops. Um It's also important to instruct the patient about good eye hygiene as you want to uh avoid the chance of infection. So now we're just going to move on to ocular emergencies. So, here's one talking about chemical eye burns and see, I've chosen some quite er extreme examples. Uh It's unlikely to be this bad. These are, these are kind of grade four deeper chemical burns, but generally speaking, the person is gonna come in with severe pain, red eye, uh overflowing tears, um kind of blepharospasm. So that's where the muscles around your eyes are spasming and it basically doesn't let the patient open their eyes. So they're obviously in pain. So they don't want to open their eye anyway. But even if you ask them to, they won't be able to, and you may need to force it open to get a good look and of course uh reduced visual acuity. Uh there will also be usually some, you know, uh history, the patient will say something got in my eye or they might work in a job. So, uh I saw a case recently where I was on burns. Uh A patient didn't describe their job to us and was purposely avoiding it because they knew that was the cause of the burn. So, um, initial management is the same as any other burn. You've got to irrigate it as much as you can. So at least 20 minutes is recommended, but really you could, you could do it for longer. There's no, there's no, um there's no trouble in doing that uh test the ph. So this can be done with a basic litmus strip. It, it doesn't need any special kind of test and you'll just see what kind of ph they they have. And um the one you're more worried about is actually alkali uh because uh alkali is liquifying and will continue going to deeper, deeper layers. So that's why irrigation is so important. You need to wash it out, whereas a acidic will, will stop itself. It's self limiting in cases where you have irrigated and the PH is still abnormal. So that's out of the, the 8 to 6 range. Um You can use Diphoterine, which is a amphoteric buffer. And so what that means is it works both ways. It doesn't matter if it's acidic or alkali, it will bring it back to seven and it's very effective. It's, it's taken with ambulances generally if it's available, uh there's something called the Roper Hall classification for treatment. It's, it's quite detailed and II don't think you need to know it, um, for med school level but it, it's just something to keep in mind if someone ever tells you. Oh, yeah, this chemical I burn was a grade 1 to 4. Then you have an idea of, uh, four is really bad. One is not too bad at all. Again, this, um, post, post assessment care is quite important. So, um, stronger eye antibiotic, eye drops are used because um if it's a deep bone, you can get to get to quite um important structures of the eyes and you really don't want them infected. So they, they tend to use stronger um eye drops there, steroids. So that helps uh calm infection uh because of the inflammation that will just do more damage to the structures. And you generally want to avoid that uh artificial tears for comfort. You would generally see that in a lot of things and then here where you've got. So this, this kind of first one is a grade one, grade two chemical eye burn here. We've got a clear grade four in both of these. And so you start to see this hazing of the cornea. Um you see this necrotic tissue here. And so this, this one on the right is a clear example of where you would need surgical debridement uh to remove the tissue there because unfortunately, that tissue isn't going to isn't going to come back any time soon, even with any kind of management. So, OK, next, we have uh central retinal artery occlusion. Uh So this is a classic presentation where a patient comes in with sudden painless loss of vision with um relevant afferent pupillary defect. And so what that means is uh when you shine a light in the affected eye, the other eye does not, the the other eye does not um contract. So usually what you would have is if one eye contracts to light, the other one will do it um automatically. And so here, because the central retina artery has been occluded, they cannot sense that change in light in the affected eye. And so you'll see, let's say they had it in their right eye. That means if you shine a light in their right eye, the left eye will not um contract, the people won't contract. Uh This is commonly secondary to atherosclerosis and giant cell arthritis. Uh fundoscopy is a classic image which you need to learn. So it's a pale retina and you're gonna see that cherry red spot classically. Uh unfortunately, the management is quite uh conservative. It's similar to, you know, um it, it's basically a complex form of stroke. And so you, you likely refer it to the stroke clinic more than anything. But some um some options include uh ocular massage and that's just to dislodge the emboli um kind of naturally because um thankfully, it's not gonna go anywhere where, where it's more severe. And So you can actually do that. Um But studies have shown more extreme interventions that lead to worse outcomes. Um The exception of this obviously is giant cell arthritis. So, uh that is where you can just use high dose steroids and that, that should hopefully fix it because that obviously um stops the contraction of the, of the uh arteries there. And generally, the focus is long term improvement of their cardiovascular health. Another painless er loss, er vision loss, one is retinal detachment and so you need to be able to discern between these two. So classically retinal detachment will present with a, a kind of curtain or a shadow forming across the vision. And here's just an image showing that you're also going to see um flashes and floaters in particular. So that's something that's also different because this is this is affecting your actual perception. Whereas the other one is um sorry, this, this one is affecting your um intake of the light, whereas the other one is affecting your actual perception. So this is often due to trauma and diabetes. Again, diabetic retinopathy, the patient isn't likely to come in with any symptoms. So they, this is a classic emergency where they come in and then you suddenly realize they have diabetic retinopathy and that's the cause of the retinal detachment, but also less commonly retinal malignancy. Um and it can be secondary to retinal tear, which is, which is basically just a tear in the retina and that, that can cause it to detach. So, a management of uh the tears include laser therapy and cryotherapy. That's just to join it back up together. And uh management of the detachment is usually forms of surgery uh which you don't need to know too much about. But VOM is basically going to the back of the eye and fixing it. Uh scleral buckling is applying these bands around your eyeball and basically forcing it back together and hoping that it, it goes, it, it sticks back on. And pneumatic retinopexy, I believe is where you put pressure in the eye. And that basically like a balloon forces the, the retina back into place. But again, you don't need to know too much details about that as long as you understand that it's a surgical management. Uh Finally, I wanted to talk about orbital compartment syndrome. So this is usually uh secondary to trauma and orbital fracture. So you, you'll learn about how to um you know, look out for orbital fractures and what you're really concerned about there. But here is something that needs to be fixed as soon as possible because uh the intraorbital pressure excess will actually cut off the blood supply completely. And once once all those cells are dead, they're not going to come back. So you need to, you need to remove the pressure as quickly as possible. Um It's a clinical diagnosis. So, you know, a history of trauma and sometimes it will just be obvious like here where you can see the eyeball bulging in, in ways around the iris. It's just not possible any other way. So, you know, that that's how you know that this is an option. But another good part is the management uh lateral canthotomy and cantholysis are both um you know, ways to release the pressure quickly, but they don't have any kind of negative. So it's this kind of external part, you're not actually affecting the um the important structures of the eye. Um And so um actually attempting this, you know, if you do some training, you, there's a lot of good training sessions um being done around the country. And so if you get a if you get an opportunity, I highly recommend learning this just so you have that knowledge of how to do the procedure and hopefully um help a person out when this happens. I think that's everything. If there are any questions, feel free to put them in the chat. Thank you very much for listening. Thank you, Audia. I think that was a really helpful session for everyone here today. So I'll put the feedback form in the chart for all of you. So if the if you fill those in, you'll get a certificate and also discount codes, we will be releasing the recordings and the slides soon after the session. And yeah, thank you all for joining us today. If you have any questions, put them in the chart, we'll stick around for a little bit. Otherwise we're good to end the session here. Thank you, everyone.