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Make sure the boys stay away. Right. Yes, we've gotten the screen. Um All right on. Um So this is Doctor Julie Thompson. She's a ophthalmologist at Kings Smith. She's a consultant and she's kindly agreed to do this session with us. Um And I'm handing it over to Doctor Thompson. Hello, everyone. So thank you for inviting me to speak with you today. Um I've been asked to um do an overview of ophthalmology with you. I've got an hour and 15 minutes. I've been given 36 conditions. Um So I'm gonna be going through an awful lot of slides. Um So please do say um because, you know, I don't, I don't, it's better to understand a few things in more detail than, than everything. But before I started, I wanted just to step back and give an overall um view to you all. Um for some tips, not so a lot of people are fazed by ophthalmology because they feel it's so super specialized, but it needs to be approached in the same way as any medical or surgical um examination. So, history is very important. Presenting complaint, history, presenting complaint, be guided by the symptoms that they give you previous medical history. Very important. For example, if the patient has diabetes, hypertension or atherosclerosis, they associated with a lot of conditions, the extra part of the history within ophthalmology um is the previous ocular history. So it's important to ask the patient if they've ever had any previous eye or eyelid surgery, whether they've had any history of ocular trauma, it may have been years previously, but can then lead to a chronic condition when they present to you. Also, if they have amblyopia or a lazy eye, which could account for reduced vision in one of the eyes, which is nothing to do with what they're presenting with. Whether they have hypertrophia, which is long sightedness that can be associated, for example, with angle glaucoma or if they're short sighted or myopic, which can be associated with an early posterior vitreous detachment or because myopic eyes are much larger than in general. These patients are at more risk of retinal tears because the retinas stretched more thinly family history should always include any hereditary eye disorders and also any other eye conditions. For example, glaucoma in a first degree relative, you've got a 10 times greater chance of developing glaucoma. So it's important to have regular intraocular pressure checks at the opticians at an earlier age work history. There's many, many drugs that is an exhaustive list. Um but they can affect the eye directly. For example, amiodarone can leave corneal deposits, also steroid use. Um for example, um patients who've been on long term steroid inhalers for asthma. Um they're at risk of um developing earlier cataracts and also they can have a steroid induced increase in ocular pressure. It's always important to ask about allergies and in the systems review that's important in ophthalmology also, for example. Um again, it's a, it's an exhaustive list but you know, there may be an association between rheumatoid arthritis and Sjogren's syndrome or Lyme disease syphilis. TB toxicara toxoplasma, et cetera can all lead to uveitis or a chorioretinitis for the examination and ophthalmology. All patients have a visual acuity um assessment first and this may include a color vision assessment and then I would suggest using AAA sort of a a standard front to back method so that you don't miss anything out. So start with the lids, then the conjunctiva, then the cornea, it's very important doing a corneal examination to put a drop of fluorescein in the eye and then examine with a blue light. And what this does is the fluorescein is taken up by any epithelial defect and will reflect as a sort of greenish yellow stain. So this can pick up corneal abrasions, ulcers, any ocular surface disorders such as dry eye disease or rosacea keratitis, then you move backwards to the anterior chamber, intraocular pressure, check the pupil reactions for both light and near um reactions and for an R APD then moving backwards to the vitreous. Um without a slit lamp, you'll be using your ophthalmoscope. So you'd only really be able to pick out big vitreous opacities. But it's important to mention it. Then the retina along with the retinal vessels, the optic disc itself. And depending on what the pre patients presented with, you may want to do an orbital or an extraocular movement examination, ophthalmological investigations. Again, just um think logically. Um so the investigations that are available to us are visual field testing, which can be automated or to confrontation, ocular coherence tomography, which gives a a sort of a three dimensional slice um through the eye, which can be used to examine the macular or the optic disc in more detail, fundus fluorescein angiography or FFA, which is where we inject fluorescein into a vein which then goes around the vessels in the body, including the back of the eye. And we take a series of photographs using a fundus camera to show where there's leaky areas in the vessels of the retina electrophysiological testing can be used. For example, electroretinograms, X rays, CT scans, which are good for bony structures and MRI scans for soft tissues. And don't forget the sort of generalized um investigations such as taking a temperature, blood test, including blood cultures, conjunctival swabs for bacteria, viruses and chlamydia and corneal scrapes of any ulcers to be sent to microbiology for testing. A nice little list of five things to look for is always worth bearing in mind. For optic nerve dysfunction. Again, there's this isn't an exhaustive list for optic nerve dysfunction can happen in many cases. For example, optic neuritis, optic neuropathy, advanced glaucoma arteritic ischemic optic neuropathy, thyroid eye disease, and papilledema. Um but there are many, many more and there's five particular things that you need to look for to establish if a patient has optic nerve dis dysfunction. The first one is visual acuity. The second is color vision, which is ideally done with the Ishihara charts, but red desaturation works just as well. Um So it can be as simple as just taking the top of a red biro, get the patient to cover one eye in turn and look at the red top and see whether the red is as red in each eye in optic nerve dysfunction, that red will look a bit pink or pale or more washed out. So it's a good um it's a good way of sort of checking the progress of optic neuritis, for example, checking for the presence of an R APD visual field testing and looking at the optic disc itself. So looking for example, for any swelling like in papilledema or any atrophy, which is where the the disc is more pale. It's got pallor, which um is a sign that it's had a problem in the past. So those five things again, just to reiterate for optic nerve dysfunction, any condition involving the optic nerve, check the vision, the color vision for an R APD for fish fields and for the optic disc itself. Another overview I just wanted to give you also was, you know, you'll be ophthalmology involves a lot of conditions which have huge lists of causes, um which you don't want to be memorized. If you asked any question in ophthalmology, the same as in medicine and surgery need a step back, think more holistically. So, you know, the causes of any condition, think of idiopathic causes. So a lot of uveitis is idiopathic. We don't know why it happens but tends to be a recurrent um condition, iatrogenic. So for example, uveitis can be caused by um you know, if you've had cataract surgery, an intervention by a doctor. Um and you get a postoperative um uveitis, hereditary conditions, for example, retinitis, pigmentosa, metabolic conditions, for example, diabetes can cause many ophthalmological problems, traumatic causes. So you can get a uveitis from trauma or cataract from trauma infective. We've already talked about Lyme disease. Um TB syphilis, toxoplasma, toxic car, et cetera, inflammatory processes. Neoplastic processes are more important nowadays because of the aging population, just general degenerative um conditions, we're all living older. Um And you know, there's a higher prevalence of cataracts and age related macular degeneration. So again, take a step back, if you can't think of anything, you know, if somebody asks you the causes of uveitis, just think of those more generalized um sections to to, to fit it into and it will, it will prompt you to think of um more particulars. So, if I could have the first slide, please. Now, um I've got about 60 slidess, so it is going to be a bit of a gallop. So bear with me if any of you want to see anything again or want to ask any particular questions, please do. Oh, that's what I was gonna say. That's not a very clear screen, but it's come clear now. OK. So the first slide were I'm just going to do like I say a gallop through the all the conditions that I was asked to um discuss with you. So the first condition um is on the eyelid. So one of the conditions for an eyelid is a stye. It's very common, particularly in general practice, a stye is actually due to an infected lash follicle. So the treatment is to remove the lash that's involved with it, use hot compresses to draw the um infection out and you can use antibiotic ointments. Another lid um condition that's very common is alain, which is otherwise known as a mym cyst. So within the lids, we have myb glands which produce a thick lipid material which when we blink, it spreads it over our tear film to give it stability. And in lots of patients, they have my bland dysfunction where these glands get blocked and that can lead to um inflammation of the eyelid, otherwise known as blepharitis. You can get crusting of the um, lids and if the gland is blocked and the secretions can't get out at all, um, they can fill up and cause this cyst, which is a Chalian, which may become secondarily infected the way that we treat Cal Asians, they, they tend to resolve themselves with hot compresses and lid hygiene. So 70% will resolve within seven months. But if it's infected or if it's persistent, despite conservative measures, then a referral to ophthalmology for us to turn the lid over and make a little nick under local anesthetic vertically um inside the lid where we open up that um block duct and we scoop out all the sort of cheesy material that's gathered. There may be indicated next slide, please. So other eyelid disorders, there can be eyelid position disorders. So, an entropion is an interning lid, that's the top slide. And as you this, this tends to be due to age um resulting in lid laxity and overriding of the orbicularis. It's um brought on by blinking but can be there all the time and the lid turns in on itself and the lashes as you can see are rubbing the eye. So it's quite a nasty condition because the patient feels like they've got an eye full of sand all the time and it can abrade the cornea which um puts you at risk of infection on the bottom. Um picture. There's a, a slide of an ectropion which is an out turning lid again. This is also due to horizontal lid laxity, which tends to be due to age, but the lid flops outwards and the sort of bright red area that you can see is the tarsal conjunctiva, which is normally up against the globe and nicely lubricated. But because it's turned out, it tends to dry out and desiccate. So it's very important in these patients to give them adequate lubrication to prevent that both of these conditions can be um referred to ophthalmology for lid tightening procedures, which would address the underlying cause of it. Um But for both, also, lubricants can help to protect the eye and keep it hydrated. Um and lid taping measures to tape the eyelashes away from abrade in the eye can also be a good temporizing measure next slide, please. So, subconjunctival hemorrhage. Um I've got a couple of pictures off the internet. So, subconjunctival hemorrhage is where you get a, a bright red area underneath the conjunctiva. It's due to one of the little vessels within the conjunctiva bursting, it can be due to trauma. Um but if there's no obvious trauma, it can have been induced by um sort of increased pressure. For example, after a sneeze or straining, the important thing to do for anybody with a subconjunctival hemorrhage is to rule out hypertension. So check the BP and also check for any underlying clotting disorders. Otherwise, just reassurance um is, is needed that this is something that's like a bruise and it will just resolve with time. So the subconjunctival hemorrhage does tend to have very well demarcated edges that you can see. The only reason when you would worry is if the patient had had a significant head injury and you couldn't see the posterior edge of the subconjunctival hemorrhage, um that may be indicative of a a skull fracture and would need um further imaging. Otherwise patient is just reassured if it's a normal con subconjunctival hemorrhage, that you can see all the edges of next slide, please. So, conjunctivitis, um there's three main types of, well, four main types of conjunctivitis. So we can have bacterial conjunctivitis, which is the one that we're all familiar with where you get a greenish yellowish sticky discharge that your eyes are matted together in the morning. It's very common in Children gets passed around. Um It is self limiting. Although using an antibiotic like chlorophen ointment or drops can speed up the recovery. But again, eyelid hygiene and preventing spread of infection is most important. Conjunctivitis can also be viral. A very important um viral conjunctivitis, adenoviral conjunctivitis, which is otherwise known as the pink eye disease. This is very highly contagious and in 60% of cases will be bilateral. It comes on acutely with watering redness and discomfort and can be associated with upper respiratory tract infection. Treatment of viral conjunctivitis is symptomatic. So, um keeping the eye nice and clean and avoiding sharing towels and flannels and ocular lubricants if needed for comfort. Another conjunctivitis um that we shouldn't forget is chlamydial conjunctivitis, which um is associated with a mucopurulent discharge. And if chlamydial conjunctivitis is isolated, it's treated with tetracycline. And a referral to the genu clinic is mandatory allergic conjunctivitis, um causes a watery um sometimes mucoid discharge and the particular um symptom is itch. So a patient who has an itchy red eye um often with chemosis of the conjunctiva, but that's where the um conjunctiva becomes edematous. So some people can have an allergy so bad that they have um what seems like bags of fluid hanging down over their cheeks. Um Treatment for that is remove the allergen if possible if you're able to isolate it. Um and cold compresses. Um getting rid of the allergen that's gone in the eye by um rinsing the eye out with plenty of water. I've known people who've got really severe bilateral allergic conjunctivitis just stick their heads in a bucket of water to uh to get instant relief. Next slide, please. Oh, sorry. No, you've already gone on to the next slide. Is, is that clear for everybody that slide? Cos it's a bit blurry for me. Can everybody see the slide? OK. It's blurry, right. I don't know if anybody uh can do anything about the blurriness of the slide cos I can't read the writing. So I'm sure you can't either. Is anybody there from the uh support side. So the slides have disappeared. Can, can you all hear me? And what I'll do is just um talk generally around what I know the next slides are while we wait for them to be set up again. Brilliant. So somebody said, yes, we can hear you. So until, until I get the slides back. Um So I know that the next slide is about watery eyes. So there will be a diagram for you to have a look at. Um And I know you will get to see these slides afterwards anyway. Um Oh here it comes again. It's still a little bit blurry, but we, I can just about read it now. OK. So um a watery eye. So the, the, there's a diagram there which shows where the lacrimal gland is supra temporal to the eye which produces the aqueous part of the tears. They come down some ducts and then when we blink it, it, it washes the fluid over towards the drainage ducts. So, in our eyelids, if we look in the mirror, we can see a little hole at the uh medial side at the top and the bottom lid, these are the punct and the tears go through these punc ti and they go through the um canaliculi which then join into the lacrimal sac. Um the lacrimal sac then goes into the nasolacrimal duct which passes through the bone of the nose and comes out inside the nose. And this is why when we overproduce tears, for example, when we cry, we get a runny nose. Um so there can the, the, the nasolacrimal duct um opens up it quite later on in utero. But sometimes babies are born when it's not completely patent and there's little membranes still blocking it. This is known as congenital nasolacrimal duct blockage and can be a cause of watering and stickiness in the eyes because the tears can't drain away. And so they become infected in the lacrimal sac and regurgitate out into the patient's eyes like you can see in this baby. So the treatment is massage initially over the lacrimal sac area. Um and it normally recanalize by itself. But if it hasn't recanalized by the age of 12 months, then we do a syringe and probing under general anesthetic, which is a picture of at the bottom where this metal probe is passed through that um lacrimal system and just pops the membrane and then the tears should flow again. Next slide, please. So in adults, this nasolacrimal duct can get um blocked and that can result in a condition called acute dacryocystitis. So where you see this um picture on, on the slide of a swelling to the side of the patient's nose, that's actually over the area of the lacrimal sac. So if the patient has got a blocked duct, the tears can't get anywhere, um it stagnates in the lacrimal sac and can get secondarily infected and cause this abscess. It's really important in acute dacryocystitis that this abscess isn't um incised because if you incise it to drain the pus, then a fistula can form. So the, the, the way to treat it is with hot compresses with antibiotics such as Augmentin, which if, if it has spread to become a preseptal cellulitis may require to be intravenous until the infection is settled and then to refer to ophthalmology for consideration of lacrimal surgery. So this is something called DCR surgery, dacryocystorhinostomy where a bypass system is made um to recannulate that nasolacrimal duct. Next slide, please. So dry eyes, dry eyes are, are, are very common um condition in patients that causes irritation, burning and grittiness. The shermer test is where there's a little strip of filter paper that before you put anesthetic in the patient's eye, you, you fold it over and place it just in the inferior fornix and then you measure how much wetting of that paper happens over five minutes. And if it's less than five millimeters, that's a severe dry eye, we can also check for tier break up time. So if you put a drop of fluorescein in the patient's eyes and get them to blink and then to keep their eyes open and you count the number of seconds it takes for that fluoresce to start to break up. So it should last um you know, about 10 seconds in, in a normal patient. Um if the tears start. If the fluoresce starts to break up um earlier than that, then you know that the patient's got an instable tear film, dry eyes can be um brought on by age. They can be increased by smoking, they can be increased by pollution. They can be increased by being in a dry windy environment or an air conditioned office. It can be related to hormones, for example. Um menopause is a very common condition of dry eye. In older women, the treatment for dry eye and dry eyes can also be associated. We talked earlier. Um severe dry eyes can be associated with systemic conditions like rheumatoid arthritis. So, treatment is uh with the use of artificial tears which range from um aqueous tears to more complex um sodium hyaluronate um formulations. Um cycloSPORINE immunosuppressive drops known as I called eye curvus can be used in very severe dry eye. PP stands for punctal plugs. So, in patients um who've got a tear deficiency if you put little silicone plugs in our punct eye, which are the little drainage dots that stops um the drainage of the tears that you are producing. So it maximizes the um effect in the eyes. It's not such a good idea to put punctal plugs in patients who've got inflammatory dry eye disease though because it keeps those inflammatory factors um in contact with the eye longer. They're the patients who are more likely to need um cycloSPORINE. Yeah, next slide please. So corneal abrasion is a very common condition. Um Any sort of scratch on the eye will show up um as a an epithelial defect with fluorescein. So as we said, any epithelial defect will take up the stain and with the blue light will shine yellow, as shown in the, in the screen, it's very, very painful, very painful. So the cornea has got one of the highest sort of um number of nerve endings in the body. Um So, you know, the patients are likely to be um photophobic, they're likely to have a watery eye um and be in quite a lot of distress. The good news is that the cornea tends to re epithelialize itself within 24 hours. But the use of topical antibiotics can prevent secondary infection. Uh sequela of having a, a large corneal abrasion can be a recurrent corneal um um corneal erosion syndrome. So, typically, um corneal erosion syndrome happens after a large abrasion, for example, a toddler scratching a parent's um eye with a fingernail. Um And it's due to the sort of deep connections of the cornea and not forming enough before the surface is taken off. So, within 24 hours, it will re epithelialize, but it does take um 3 to 6 weeks for it to actually form deeper connections. Typically during the night when you've got your eyes closed, uh when you wake in the morning and open the eyes, the that that very unstable uh re epithelial area can rip off again, which is like having the corneal abrasion all over again. So it's something to be aware of. There are things in ophthalmology we can do to help patients like this. But just to be aware that if somebody's got a history of a large corneal abrasion and they wake up with painful eyes every day and then when you examine them the next day, there's nothing to be seen. It could be recurrent corneal erosion. Next slide, please. So, corneal ulcers, uh microbial keratitis. So these can be bacterial which cause uh an acute infection. They're often contact lens related cause a very painful red eye, um decreased vision. If the infection is very bad, you can have a hypopen, which is uh which you can see in the lower picture. It's where there's a, a level of pus seen within the anterior chamber. Um You can actually see, you know, the, the fluid level of the pus, it's important to do corneal scrapes and plate them out and center microbiology for culture and sensitivity. So, if they don't react, um if they don't improve on the broad spectrum antibiotic that we start them on, um We usually give a fluoroquinolone like ofloxacin or levofloxacin um for these conditions. Um four times a day for very small ulcers or hourly for more severe ulcers. If the ulcer is not improving or the patient's not compliant or they aren't able to instill the drops themselves they may even require to be um admitted as an inpatient for um frequent cefuroxime and gentamicin drops. Cycloplegics can also help because it's a very painful condition. Um the iris will be inflamed. And if we give a cycloplegic such as cyclopentolate, it fixes the pupil dilated. So it's a bit like splinting a broken leg to stop it from moving around and causing more pain. Next slide, please. Corneal ulcers can also be due to fungi. So this te tends to come from organic um matter sort of in agricultural workers. Um Aspergillus and Candida are the most common species. Um treatments are topical antifungals and sometimes it may require oral um antifungals such as fluconazole. I don't know why. II presume you're aware that this is blurry when it first comes on and then it's and then it becomes clear. So um that would be great if we could do something about that, but that's a lot clearer. Now, thank you. Next slide. So, a viral corneal also the most common one that you'll come across is the herpes simplex, um dendritic ulcer. So this stains with fluorescein in this typical branching dendritic pattern with sort of bulbous ends on the dendrites. Um These are treated with topical antiviral um ointment. For example, acyclovir 3% 5 times a day. Again, this is as a corneal condition. It is ex extremely painful. Next slide, please. So, herpes zoster ophthalmicus um is when we get shingles in the first division of the trigeminal nerve. So typically, it's, it's dermatomal as shingles, um affects a particular dermatome. So the V one actually um supplies the scalp, the eyelids and the side of the nose. So there tends to be a prodromal um period of a couple of days, um where you get a sort of tingling sensation in the distribution of where the rash will be. And when the rash appears, it tends to be vesicular at first and then becomes pustular and then scabs. There's an important sign in herpes zoster VCU um called Hutchinson's sign. And what this is if, if the patient has lesions down the the on the tip of the nose. So if the patient has lesions on the tip of the nose, that means the nasociliary branch of the um nerve is affected and that also supplies the eye. So if the Hutchinson sign is positive, um there's likely to be ocular involvement, for example, um corneal um changes uveitis or increased intraocular pressure. The treatment for this is 800 mg of acyclovir five times a day. Another important thing about shingles or herpes atrophicus is it can lead a lot to a lot of post herpetic pain which can sometimes be so bad, it drives patients to suicide. Um So, amitriptyline and gabapentin are known sort of neuropathic relieving agents that can be prescribed if this becomes the case. Next slide, please. So, episcleritis and scleritis, episcleritis is literally inflammation of the episclera, which is the layer that overlies the sclera. So this can be distinguished from the more serious scleritis um by if you get a cotton bud and you can actually move the area. Um if it's in the episclera over the sclera and a blanching agent, such as 10% phenylephrine can be dropped in the eye and left for 10 minutes. And that will blanch superficial episcleral vessels, but it won't blanch the deeper scleral vessels. So that's a good way of distinguishing between the two episcleritis doesn't particularly need any treatment. Although lubricants can be used for comfort, but scleritis um is a little bit more serious. As you can see from the picture, the eye has a sort of a deeper sort of violaceous hue to it. Um And as I said, it'll non blunt with phenylephrine. Uh One of the treatments for scleritis can be topical steroids. Um Although the most important thing is to look for any underlying um systemic disorders that can be associated. Um for example, connective tissue disorders. Next slide, please. So, acute anterior uveitis, this can cause a a very painful red photophobic eye vision can range from mild blurring to severe loss of vision. It's very suggestive of uveitis if they've had previous uveitis in the same or a fellow eye patients who've had pre previous uveitis, know what it feels like they will tell you that this is my uveitis has flared up again. Uh There may be associated systemic symptoms such as low back pain. For example, if the uveitis is an HLA B 27 associated disorder such as enclosing spondylitis, next slide, please. So, signs of um anterior uveitis are circumcorneal injection, otherwise known as limbal injection. So if you look at the picture, the limbus is the area between the iris and the white sclera. And so if you can see the actual um hi inflammation, the redness of the eye is circumferential around that limbus. You may also get Katic precipitates known as K PS, which are um depositions of white cells on the endothelium of the cornea. They tend to be seen inferiorly. Um and you can see those with your ophthalmoscope. If the patient, um if you have it on high magnification, anterior chamber activity can include flare due to the presence of proteins or inflammatory cells themselves. The patient may develop posterior sine. And what that is is the um iris itself becomes very inflamed and so it becomes sticky and can stick down to the lens and cause an adhesion. So it's very important um to treat these patients early with cycloplegic drops to dilate the pupil out of the way. So it doesn't stick down sometimes if um a patient's had previous uveitis and they've not been dilated and they've developed sykia that can be a cause of an irregular pupil that doesn't react as you'd expect it to. As we said before, this can be associated with systemic disease such as ankylosing spondylitis treatment is with um regular topical steroids such as Maxidex and also cycloplegics. Um That's for um prevention of the posterior sa and also for that splinting effect that I talked about before because it will be very painful for the eye to um dilate and restrict. Um So having the cyplegin there would prevent that next slide, please. So a couple of pictures just to show um on the top one is some endothelial dusting. So that's just with some inflammatory material dusting. The inner layer of the cornea and the Katic precipitates which are a little bit bigger which are the depositions of the white cells can be seen next slide, please. So, acute angle closure, glaucoma. Um So the symptoms of angle closure, glaucoma are a rapid uh loss of vision, severe pain and congestion or redness of the eye, nausea and vomiting. And also um patients can complain of abdominal pain. And I've heard of patients before who have um come into hospital with nausea and vomiting and abdominal pain and had a an exploratory laparos, laparotomy, um found nothing and then lost their vision and they were found to have angle closure, glaucoma. It can be as severe as that. There can often be a a history of halos and headaches. So in the initial um in the initial phases of it, um seeing halos around lights um can be a uh can be a problem and headaches particularly on the brown forehead, on the side that the um angle closure is happening. So angle closure glaucoma um tends to be due to um patients who have a shallow anterior chamber. For example, the the lens is very big and pushing forwards or it can be that the patient is very long sighted. So they have a very small eye and all the structures are crammed in together. And this can have an effect on the drainage of the normal drainage of the fluid in the eye, the aqueous through the trabecular meshwork and once that closes off, it's like a a positive reinforcement. So the pressure goes up, which makes it worse and makes the pressure go up even more until the pressure reaches a very high level, which is when we get symptoms. So we've got a picture here. Um If you just go back a slide, did we have the signs of the angle closure? Um So we had the symptoms, but if we miss the signs, here's the signs, here we go. So I thought we'd miss that. So, yes, you can have a ciliary flush, which is that um sort of um inflammation around the um limbus. Again, the intraocular pressure is very high. Now, out in general practice or in other specialties, other than ophthalmology, you may not have access to check the pressure. Um but you can use your, your finger so you can check it digitally. So, um if you press your eye with the lid closed, the consistency of your eye should be around about the same as the tip of your nose, just that sort of squashy sensation with a bit of G. Um So you can check, you can check it against your nose to see what it, it should be or even easier. You can check it with the patient's fellow eye if they've only got unilateral. So just press your finger over uh on the normal eye and then press it on the um eye that you suspect angle closure glaucoma. And the pressure is high enough that the eye will feel rock hard. As we've mentioned, the anterior chamber is shallow and it will tend to be shallow in the fellow eye as well. Um For whatever mechanism has triggered the um angle closure, glaucoma, the cornea will be edematous. So it will have a, a sort of a hazy um appearance and the pupil tends to be oval, vertically, oval, fixed, semi dilated. So if we could go to the pictures now on the next slide. So this shows the um the fixed semi dilated pupil. It shows the hazy cornea, it shows the ciliary flush on the conjunctiva. Um and it shows the um shallow anterior chamber where you see the slip beam. Um You can appreciate that the depth of the anterior chamber isn't normal. Next slide, please. So, a differential for angle closure glaucoma, as I mentioned before, the shallow ac may be due to a what we call an intumescent lens. So, if a cataract um has developed, for example, due to trauma and it's swelled up in size, the lens is swelled up in size that can take um space in the anterior chamber and cause an acute rise in intraocular pressure, also neovascular glaucoma. So this is a glaucoma that occurs um due to the formation of new blood vessels over the iris and trabecular meshwork known as rubeosis. This can happen in patients who have an ischemic drive um from, for example, um diabetic retinopathy or from central retinal vein occlusion and it can cause an acute rise in pressure. So the management of angle closure glaucoma is intravenous Diamox, which is acetaZOLAMIDE. Um use of beta blocker drops. Um sympathomimetic drops, steroid drops at least six times a day and pilocarpine drops to make the pupil meos or go smaller and that can break the cycle. It's important to do um yag laser iridotomy in both eyes. So you may have got a chance to see some laser treatments on your ophthalmology attachments. Um But basically what this is is we fire a laser on the peripheral part of the iris to to punch a hole through it. And that gives an alternative pathway for the the fluid to flow. So it's important to do that in the fellow eye even though um it hasn't got angle closure, glaucoma to prevent it from happening in future. Sometimes in the eye that's affected, you have to wait until the actual um angle closure. Glaucoma attack has settled because the cornea haze may be so bad that you can't see clearly enough to do the laser treatment, but it's important to do the fellow eye in the meantime, next slide, please. So signs of a, a patient who's had a resolved angle closure, glaucoma, the top slide is something called glaucoma, which um I think you can appreciate on the lens, there's some deposits there. So that's an indication that they've had um angle closure, glaucoma before the picture at the bottom just shows what Rubios looks like. So the um if you look at the iris, you can see those vessels that are coming um out from, you know, they're, they're quite disorganized, thicker vessels and are normal for, for an iris. So if you see something like that, the chances are the trabecular meshwork has got a fibrovascular membrane over it also. Um So have a high suspicion of rubeotic glaucoma. Next slide, please. So, primary open angle glaucoma, this is AAA chronic degenerative optic neuropathy. Um and typically it's due to the pressure in the eye being high. So we have a, a guideline cut off of 21 millimeters of mercury um as as being a high pressure, although it does rely on a number of other factors. For example, the corneal thickness uh which affects the, the true reading of the of the pressure. Some patients may have something called a normal pressure, glaucoma when the pressure isn't high, but they've still got signs of open angle glaucoma. But in general, the pressure is greater than 21 there's a family history, it's not direct but you are more likely to get glaucoma if you've got a first degree relative with it. Other risk factors can include vascular disorders, migraines and Raynaud's, in particular for the normal pressure. Glaucoma. Glaucoma causes as long as it's not the acute angle closure, glaucoma, open angle, glaucoma causes a slow progressive visual loss. And many patients don't realize that they're getting this visual loss because it tends to come peripherally. And so it can be blinding if it's not picked up and treated early. Early detection is really important because by the time the patient has noticed visual field loss, that loss is irreversible. So we can prevent it from getting worse. Um But that's why there's lots of screening in at opticians for high intraocular pressure and referral to ophthalmology to catch it early. So a sign of open angle glaucoma is cupping of the disc. So when you look at an optic disc, there's a a paler area in the center and if that area gets bigger and it becomes paler, that can be a sign that there's glaucomatous changes, visual field defects. Um You can see on the chart below um tend to be arcuate. So they, they, they can um you see that ar pattern in the one on the top right, there can also be nasal steps. So in the top right, you can see that little area um in the nasal part of the visual field that looks like a little step and these can get worse and worse as it progresses. As you can see in the diagram until you've almost got just a an end stage, central island of vision left. Um And quite often that will be the level that patients will get to if, if they've not, um you know, been screened and not picked up earlier. The picture above just compares the healthy optic nerve with its its normal color with the sort of paler color with the bigger optic disc um seen in glaucoma treatment of glaucoma. Um is generally with intraocular lowering drops which can be used on their own or in combination if necessary um laser treatment. So, um SLT is the laser that we we use for glaucoma. What that is is um a laser that is aimed at the trabecular meshwork which helps to increase um the drainage system through the eye surgical treatment is Trabeculectomy where a little trap door is made in the sclera so that fluid can pass through and collect under a bleb in the conjunctival where it's reabsorbed into the choroidal circulation. There are more treatments nowadays coming through which are minimally invasive treatments and some of you may have seen this um on your attachments, they can be done in combination with cataract surgery and they involve the insertion of tiny devices into the trabecular meshwork to help with drainage and can be done as part of the cataract operation. Next slide, please. So, posterior vitreous detachment or PVD is a degenerative process. So as we get older, our vitreous tends to liquify a a process known as sinesis. Um and this causes the vitreous to separate from the retina. This is a normal process. It happens in, in almost all of us by the age of 65. Um although it happens in um at a younger age in patients who are myopic because they've got larger eyes with. Um so they're more, more inclined for the vitreous to come away. People with PVD S can see flashes and floaters because it can cause traction on the retina, um which is perceived as flashing lights. The floaty bits within the retina are the condensations of the col collagenous parts of the vitreous. Um But they can also um if there is a little hemorrhages formed. So, for example, as the vitreous is coming away, if it pulls on one of the vessels and ss it, you may get a vitreous hemorrhage which you'd see as a little shower of, of black specks if the traction is such that it pulls a tear in the retina, um that can be very serious because if there, if it is not picked up and there's a tear in the retina fluid can come from the um vitreous that can actually go in underneath the retina and peel the retina off. Um a bit like wet wallpaper, peeling off. And that's a retinal detachment. Most retinal tears happen in the superior fundus which is dangerous because then gravity can assist with that peeling off of the retina. So any patients who experience flashes and floaters, although it's likely due to the PVD, it is important. They have a dilated fundoscopy examination to make sure that there's no sign of any retinal holes or tears that have been pulled. If there is a retinal tear, then we can perform what's called laser retina pexy, which is where we laser around the tear which spot welds that area to prevent the fluid from um seeping underneath the retina. Next slide, please. So this is just a pictorial version of the liquefaction that happens in all of us in the top left slide and it causes the vitreous then to collapse away from the back of the eye. The bottom left picture is where you can see that it's caused a retinal tear. So the yellow layer is the retina and you can see where it's torn and some hemorrhage has gone into the eye. And the bottom right slide just shows an A VS vessel. So you can just see a little vessel that's pulled away and it's called the vitreous hemorrhage. Next slide, please. So for a a posterior vitreous detachment. As long as we've ruled out um any, any retinal tears, then we just reassure the patient, this is a normal aging process and just give them retinal detachment warnings. So advise them that if they have sudden, more repeated flashes of light or they have a sudden flurry of floaters or they experience a, a an effect like a curtain coming down, that that could be a sign of a retinal detachment and they should seek help again. Otherwise, they just need to be reassured after they've had a peripheral fundus examination. As I said, if you do find a tear, which is a nice picture of, of a retinal tear in the diagram there, then we laser around that tear. It's also important to examine both eyes because if you know, if they've had APD in one, they're likely to have had one in the other and they may have had an asymptomatic small tear next slide, please. So retinal detachment, um as we've mentioned, a, a cause of this is posterior vitreous detachment. If it pulls on the back of the eye, it's more common in myopic eyes. As we said, the myopic eyes are bigger, so they've got thinner retinas. It's more common if you've had previous intraocular surgery such as cataracts, or if you have a history of trauma and the symptoms and signs are a curtain across the eye, sudden loss of vision and a great pupillary reflex. Um As A as an extra part here. This this retinal detachment that we're talking about at the moment is what's known as the rhegmatogenous retinal detachment, which is due to the fluid getting behind the retina. There are another couple of common causes of retinal detachment known as exudative retinal detachment, and tractional retinal detachment. Now, tractional retinal detachment is due to pulling on the retina for, for example, from um a fibrovascular cause such as um in diabetes or sickle cell disease. An exudate detachment is when something is behind the retina from the choroid, pushing it forwards. So for example, a choroidal tumor. So it's just to make you aware of the different kinds of retinal detachments. Rhegmatogenous is the one that we're all familiar with due to a retinal tear. Tractional is due to pull on the retina and exudative is due to pushing on the retina. Next slide, please. So, again, just a couple of pictures you can see um here, the retinal tear with the um detachment around it and the slide on the right, you can see that sort of um wafting um sheet of retina that's, that's floating and you can see that the vessels are raised that's due to a Rous detachment. Next slide, please. So, moving on to the um anterior ischemic optic neuropathy. So there's two types, there's the arteritic type and the non arteritic, I don't have slides on the nonarteritic, but basically uh nonarteritic optic neuropathy um tends to be due to hypertension and diabetes as commonest causes. And it's due to ischemia of the posterior ciliary arteries which supply the optic nerve and can cause an optic neuropathy. So, that's all I'm going to say on the non arteritic. Um So the systemic factors obviously would need to be addressed, but the arteritic is very important. This is a common cause of sudden visual loss in the elderly. So the features of arteritic um optic neuropathy or headaches, jaw claudication, which is when you're eating, um it is a bit like having angina. So you, you get pain in the jaw which then when you stop um chewing, then the pain decreases again. But when you start using the jaw again, it increases, you can have scalp tenderness. Uh there can be a history of polymyalgia, rheumatica, um and the superficial temporal arteritis. So it's important to examine the temporal arteries themselves. So, on either side of your temples, to feel where the temporal artery is, whether it's um pulse t, whether it's got any nodules there and whether it's painful to the touch. Investigations um include E SR and C RP. Also a full blood count is useful because if there's increased platelets that can be suggestive also. But E SR and C RP are the standards. If um suspicions are raised. A temporal artery biopsy should be done. So this is a surgical operation where we remove a section of the temporal artery, you need to take at least two centimeters because temporal arteritis lesions are known as skip lesions. Um so they tend to occur in a sporadic fashion. Um And so it's very easy to take a section of artery that doesn't actually include the pathology. But if you take a section that's two centimeters long, that should include um one of the skip lesions. Treatment is with systemic steroids. Um So high dose oral steroids or we could use um pulsed intravenous methylprednisolone. It's important to start treatment straight away as this is not only a sight threatening condition but can be a life threatening condition. And also the fellow eye um is at risk. So don't put off um starting steroids until you've done a temporal artery biopsy. If the blood results have come back and the history and examination are suggestive, start it straight away and the temporal artery biopsy should still give positive results um up to a week afterwards. So if we say anything up to a week, we can still do a temporal artery biopsy. Next slide, please. So this is just a picture of of um the signs of um arteritic ischemic optic neuropathy. So the swelling of the disc and um engorgement of the vessels next time, please. So this is just a diagram of the thickened temporal artery that I was talking about. And um a picture of the histology of giant cell arteritis uh which is um when we send the temporal artery to the lab. This is what they they would see next slide, please. So, age related macular degeneration, um a leading cause of blindness in the West over the age of 60 years. So, you know, we've had an explosion of age related macular degeneration because of our aging population. There's two main types, there's a dry type and a wet type. The wet type is due to new vessels forming underneath the retina and these can hemorrhage 10 to 15% of the wet type are treatable. Um A lot of you may have experienced watching the intravitreal injections that we do in clinic. So the anti vegf injections, so the anti vegf injections will are done on a monthly basis directly into the vitreous of the eye. Um and they help to reverse this leak leakiness. Um and then allow the retina itself to reabsorb the fluid. Uh once the the leaking tap has been switched off as it were. So, did we skip a slide then? Was the one previous to that? No, that's fine. Thank you. Next slide. So just some pictures of some dry age related macular degeneration. So, macular degeneration affects the macular, which is the part of the eye that we see um sort of used for our close vision um and resolution um and discriminating. So for the central vision, if you're looking, you tend to miss people's faces. So if you're talking to somebody, you'll actually be missing their face, which is very distressing. Um a good way of monitoring, macular degeneration is with an Amsler grid which you've probably all seen. It's AAA piece of paper that we give the patient has a grid on it with a spot in the center and they can monitor their sort of distorted vision or metamorphopsia by looking at that spot and drawing around the area of distortion and see whether it gets bigger or not. Um If significantly bigger, that could be a sign that the dry has changed to wet. Um But the um fundal view of dry A MD um shows typically these drews in which are are little sort of deposits um on the back of the um on the back of the retina. Next slide, please. So wet ad this is a typical picture of a wet A MD. You see a sort of greenish gray membrane, there may be hemorrhage around it in the macular area. Um Anything looking like this, you would send for further investigations with OCT possible FFA um to a specialized macular clinic for consideration of intravitreal injections. Next slide, please. So some more different presentations of wet A and D. So um top left, you've got the um hemorrhaging and the top right. There's the hemorrhage is a bit deeper. So that subretinal hemorrhage, there's more extensive retina hemorrhage in the bottom left and in the bottom right, there's an area of scar, this is known as a sort of disy form scar So this is a sign of sort of burnt out wet A MD. Next slide please. So as I said, treatment with the intravitreal anti vegf drugs. This is just AAA quick slide to show the fluid that you can see within the retina in the layers on the OCT scan before treatment and then after treatment, you can see those pockets of fluids have gone. Next slide, please. So uh there are other causes of subretinal neovascular membranes other than wet A MD, this can be high myopia. So you can get a myopic srn VM choroidal tears can cause it and pseudo exanthema or elasticum. Next slide, please. So, moving on to arterial occlusions. So central retinal artery occlusion and branch retinal artery occlusion. So, occlusion of the arteries um tends to be caused by arteriosclerotic changes. It can also be caused by an embolus directly from the heart or from the carotid artery or more rarely, it can be caused to, to inflammation. The history is a sudden painless visual loss and the clue is in the painless visual loss which could be complete if it's a central occlusion or partially. If it's a branch occlusion, patients usually have a history of high BP or heart disease. So, in the picture on the left of the central retinal artery occlusion, you can see that the um retina itself is very pale edematous and swollen. But you've got this typical cherry red spot at the fovea and that's because at the fovea, the LEV the the thickness of the retina is much reduced. What you're seeing there is the um reflectance of the choroidal, the choroid behind it, you can see the redness of the choroid behind shining through. Whereas the rest of the choroid is missing where the retina is thicker. So it's a typical um pale retina with a cherry red spot at the center, the branch vein, a branch artery occlusion on the right, you can see that it's AAA sector. So that that sort of edematous area is in that bottom left sector. Next slide, please. So, vision's obviously reduced in central retinal artery, but it can be normal in the branch retinal artery occlusion. It's only affecting part of the eye. A relative afferent pupil defect will be present with a central retinal artery occlusion cos the majority of the retina is affected. The retinal arteries are very narrow or attenuated or collapsed in the central retinal artery occlusion. The fovea shows that cherry red spot against the white infarcted retina and in branch artery occlusion, the white infarcted retina corresponds to the occluded retina emboli can actually be seen. They can actually be visualized in the arteries if the cause is embolic. So just have a look in the vessels to see if you can see any emboli. Next slide, please. So management, um this is a uh an ophthalmic emergency. So the patient needs to be referred immediately. Um if they're caught within the first hour. There's a reasonable chance that the vision can be restored. Um But we would try anything up to six hours afterwards and even up to 24 hours afterwards. For example, if it's a young patient or an only eye as it may restore some more, most of the function. So, treatment involves the use of intravenous acetaZOLAMIDE known as Diamox that reduces the pressure, also massage of the globe. So literally just using your thumb to massage it. And this can also help to lower the intraocular pressure and hopefully reestablish the arterial flow, breathing in and out of a paper bag can sometimes help also as that will cause the um cause the arteries to um dilate. And so that allows um an embolus if it's stuck there to move on a little bit further. So for example, you could convert a central artery occlusion and move it further along and maybe it'll end up as a branch vein occlusion. Or if you're very lucky, if it's very small, it it would um resolve. The further management really is to aim to uncover underlying diseases like hypertension, cardiac or carotid thrombus. Um Next slide please. So, moving on to venous occlusion again, this can be a central venous occlusion or a branch venous occlusion. Next slide. So the visual acuity is reduced in central vein occlusion, but the reduction is dependent on the severity in branch vein occlusion. The vision can be normal. If the phobia is not involved. Next slide, please, there may be a relative afferent pupil defect um in patients with a severe central vein occlusion. Looking with the ophthalmoscope, as you saw on the picture a couple of slides ago, there's extensive intra retinal and preretinal hemorrhage in all four quadrants with distended veins and a swollen disc. Next slide, please. So for any venous occlusion, you need to refer to ophthalmology. We'd examine the vision. We'd look at the iris for any new vessels. We'd check for intraocular pressure. We'd do a fundus examination and an oct scan to look for any um intraretinal fluid, which if it's present can be treated with anti vegf injections. If there are any new vessels, then we can uh on the retina due to the vein occlusion. Then P RP laser as we do for diabetes can be performed. Next slide, please. So again, here's a picture of um crv O before and after treatment on the bottom is the oct scan where you can say see the significant intraretinal and subretinal fluid which then decreases after anti vegf treatment. Next slide please. And a branch retinal vein occlusion before and after treatment. Again, you can see that sectoral hemorrhage and you can see the resolution of the fluid on the oct scan. Next slide, please. So briefly, retinitis, pigmentosa is a degenerative condition of photoreceptors. It is a genetic condition which can be autosomal recessive or dominant. The features are these bony spicule pigmentation. So if you look around the periphery, that's a typical um bony spicule pigmentation that you can see the vessels in the retina are attenuated. So that if you look at them, they look very narrow and thready, there's optic atrophy. So the optic disc tends to have this sort of pale waxy appearance and you can have equatorial field defects. So it tends to come from the periphery and restrict the vision more and more until eventually you end up with some tunnel vision. So there used to be no treatment for this at all. But now there's lots of advances in gene therapy, which I won't go into any further. But there, there, there's a lot of work being done on gene therapy and trials under undergoing next slide, please. Optic neuritis. Um this is a condition um of the optic nerve which um can be at the front of the optic nerve and you can see the nerve is swollen. That's when it's called papillitis. Sometimes though there can be no signs at all because the optic neuritis is a retrobulbar neuritis. So all the inflammation is in the optic nerve behind the part that you can visualize with the ophthalmoscope. So if somebody presents with symptoms, suggestive of it, you don't necessarily need um a swollen disc. Next slide, please. So the condition typically affects patients in the um younger age group 20 to 45. It's more common in women and presents with impaired vision. It tends to come on over a couple of days. The vision gets worse and worse and can result in a central field defect. Next slide, please. So the visual acuity can be as poor as perception of light. Central scotoma is typical, impaired color discrimination um is present as we said, one of the things, uh one of the key examination features for optic nerve dysfunction is color vision. So here it says about best demonstrated with a red object. So the affected eye will see the red object less bright than the unaffected. There should be a relative afferent pupillary defect of the affected eye and there should be in particular pain on eye movement, especially on adduction. The fundus examination can be normal as some are retrobulbar neuritis. So if you see a patient who's got optic nerve dysfunction, particularly if they've got a history of MS and they've got pain and eye movement, it's likely optic neuritis. There isn't any um treatment. Um A lot of people advocated at one stage about giving high dose steroids, but it doesn't seem to um make a difference to the overall prognosis. And so the risks and benefits um really didn't, you know, weighing up the risks and benefits. It didn't show to be beneficial to give high dose steroids. Most patients will start to recover after approximately two weeks and it can be amazing seeing a patient who's totally lost vision, very unnerving and you sit tight and actually, you know, the vision does gradually come back. Um It's important if you are concerned if they have more than one episode of optic neuritis, it's important to do an MRI scan to show for any demyelinating lesions as it may be the first presentation of MS. Next slide, please. Oh, I've just seen a question. Is optic neuritis painful. Yes, it is. Um, it causes pain on eye movement. So the management refer the patient within 24 hours near a normal vision usually returns within six weeks. Treatment does not affect the outcome. Um Yeah, so follow up is important. Um Again, MRI scan may be indicated if you need to exclude a compressive lesion if spontaneous recovery doesn't happen. Next slide, please. So a little bit about visual field defects. Um So I've just gone for the most common one I II. It's just much too much for an hour and 15 minutes to go through all of them. But a bitemporal hemianopia is one that you should all know about. Um So this is due to um a pituitary tumor which you can see on the right, which is pressing on the chiasm, the optic chiasm and as you know, the the temporal fibers cross over in the optic chiasm. So you'd end up with this typical bitemporal hemianopia in general for visual field defects. Um sort of neurologically um is that the more back the lesion, the the more congruous. It is. Um so if they match exactly, it's likely due, you know, further back at the occiput. If it comes coming forwards along the optic radiations, the lateral geniculate nucleus, the optic tract s um it's more incongruent. So that, that's just the basic thing to pick up on it. We don't have to go through all the visual defects. Next slide, please. Next slides. Thank you. So, orbital cellulitis, um I'm just going to touch on the differences differences between preseptal cellulitis and orbital cellulitis. So within the eye, which you'll see a picture in a moment. Anything anterior to the rectum ie underneath the skin involving the litis treated with antibiotics, either oral or intravenous depending on how the severity orbital cellulitis is more serious. It's an ophthalmic emergency. It tends to be sinus related. It typically affects Children and young adults and can cause compression of the optic nerve. So again, remember those five things for examining an optic nerve before monitoring somebody with orbital cellulitis. A CT scan is mandatory as you can often have a subperiosteal abscess which may need surgical drainage and IV antibiotics. So, in slide, please. So the diagram of the eye upon the um top left, you can see um I can't point this out to you cos I don't have a pointer but um the orbital septum, you can see how that separates the skin and muscle um from the front with the deeper orbital structures at the back. So, preseptal cellulite is unlikely to have complications. It's likely due to an external source such as a uh an injury or an insect bite. Um orbital cellulitis, however, is very serious. It can progress the loss of vision, a brain abscess that's associated with paranasal sinusitis. Um The features are listed below. I'm going to leave that for you to read at your own leisure later because I'm aware I'm running out of time. But if you imagine the infection behind the septum, using that picture, you can see why it may cause interruption to the extraocular muscle movements and thus diplopia, you can see why it may cause the eye to bulge forward in a proptosis. Um So, next slide, please. So just a couple of pictures of orbital cellulitis where you can see the key swelling um around the eye. You can see on the top left one that you know, um where there's been a penetrating site um that's allowed bacteria to get into the skin and that's gone through the septum. Next slide, please. So just a couple of pictures of trauma, I was asked to cover ocular trauma. So uh picture top left. Um There's a corneal um laceration and you can see that some of the iris is prolapsing out of that which is distorting the pupil on the top left. There's a uh what was called an iridodialysis, which is where the Irish root has been pulled out. Um And so you can see that sort of black um gap. The slide at the bottom shows a um hemorrhage into the anterior chamber. Next slide, please. How much time do I have left? Because I saw there was a, a thing saying that could we extend the session? Has that been agreed? Cos I'm just aware that it is 330. Would you like me to continue? So, a diabetic retinopathy, um background diabetic retinopathy. Um This diagram shows your typical microaneurysms, cotton wool spots and exudates the bottom, right? Picture shows some maculopathy which is where there's a leaking area which has caused this sort of ring of cerinate exudates around the macular. Next slide, please. I'm also going to skip over these. You can look at them yourselves at home. I'm sure you've all done diabetic retinopathy. But there's a sign of uh a picture of preproliferative. And then there's a picture showing new vessels on the disc on the bottom left. So these new vessels are little tiny, fragile ones that have grown in response to the ischemic drive. And these are the ones that are, are very likely to bleed and cause a vitreous hemorrhage. Um And doing P RP laser destroys the peripheral retina to take away that ischemic drive, which then means that um you're sacrificing your peripheral vision, but to save your central vision. So the new vessels elsewhere, um you can see those little tiny um vessels growing off the, the peripheral retinal vessels and they've got little tiny bulbs ends, they're, they're very typical. Once you've seen the clump of these um new vessels, you'll be able to spot them again. Next slide, please. This is just a picture to show what it looks like what a retina looks like when they've had pan retinal photocoagulation or PRP laser. Um So you can see uh what I was talking about how you sacrifice the peripheral retina in order to save the central retina. And that helps to reduce the ischemic drive. Next slide, please. So, diabetes can also cause diabetic macular edema. Now, we used to treat this with laser, but now nowadays, we can treat with um anti vegf injections like Eylea. So again, you can see on the fungal pictures, these um cerinate deposits which is suggested there's fluid leaking somewhere. Um And the oct scan shows the um intraretinal fluid that you can get with diabetes and also a picture of it after it's been treated with Eylea. Next slide, please. So cataracts, what are cataracts? It's a clouding of the lens leading to decreased vision. Um I'm not going to go in more detail, cos of time restrictions. So, next slide please. So the main cause of cataract is age. So um you know that you can have senile or congenital. Next slide, please. So we've just got a few pictures of various types of cataracts. The one on the top right is quite interesting because it shows the natural sutures within your lens. Um The one on the bottom left is a posterior polar cataract, which is um commoner in Children. Um And that cataract is quite a difficult one to remove without damaging the posterior capsule cos the posterior polar cataract tends to adhere to the capsule. Next slide, please, cataracts can also be caused by trauma. So, um you can see in the bottom left slide where there's some corneal um sutures where there's been a laceration and and whatever's gone into the eyes touched the lens and caused it to turn cloudy. The one on the bottom, right shows that iridodialysis where the Irish root has been torn away. Again. Next slide, please. So, metabolic cataracts can include diabetic cataracts which tend to look snow flakey or Wilson's disease, which gives this typical sunflower cataract. Next slide, please. Cataract can also be secondary to inflammation such as anterior uveitis. We've seen a picture previously of the glaucoma fleck and cataract. Due to angle closure, glaucoma, myopia can predispose to a hereditary fundus dystrophy and various drugs such as steroids. Next slide please. The effect of cataract is to um prevent the light from coming to a a focus on the retina. So you get more scattered light which gives that appearance of blurred vision. Next slide, please. Ok. Again, management, I'm gonna just trot over this. So we do a pre op assessment of patients to make sure they're suitable for surgery. We, we do biometry, which is measurements of the um size of the eye and the refraction of the eye so that we can choose the lens, the artificial lens strength that we're going to put in um, the eye when we do cataract surgery. Next slide, please. Um So this was about the cataract surgery, which I was hoping to talk you through. But again, there's some lovely videos on the internet if you would like to watch those, I don't think we've got time at the moment. So next slide please. Complications of cataract surgery can be posterior capsule opacification which is occurs in about 15% of patients after they've had cataract surgery when the capsule that's left behind opacities and this is treated with laser yag capsulotomy complications during the surgery can be vitreous loss can be retinal detachment, endophthalmitis, which is infection inside the eye and cystoid macular edema, which is fluid at the macular next slide, please. So, ocular trauma can result from fights, falls, foreign bodies at work or in road traffic accidents. It's important to differentiate from blunt, from penetrating trauma and ocular trauma often has medico legal implications. So it's important to keep a very good record, including the visual acuity when they presented next slide, please. So, blunt trauma is usually from a fist or a, a sports injury like a tennis ball or a squash ball depending on the type that what's been used. Um will depend on what sort of injury you have. So a tennis ball doesn't fit in the orbit. So you're more likely to get a, an orbital fracture. Whereas a squash ball fits nicely inside the eye. So you're more likely to get high femur and cataract. The black eye that you get is common due to the skin ecchymosis or bruising. And the painful eye results from any corneal abrasion. And sometimes um trauma can lead to inocular pressure, rays, vision can be reduced due to high femur, which is bleeding within the anterior chamber. Again, like the hypopen you saw in corneal ulcers, you can see a fluid level of the blood within the anterior chamber, which is known as a high femur. You can also get retinal contusions and double vision can occur because of blowout fractures. So, a blowout fracture tends to um be due to the inferior orbital wall, which is the weakest. Um if the pressure goes up suddenly that wall can fracture out and the um extraocular muscle can go through that and get trapped. Which means that when you try to look up, the eye doesn't move and you get the double vision next slide, please. So again, some views of trauma. So there's some hemorrhage within the eye. There's the iridodialysis, there's a picture on the bottom left of the blowout fracture. So you see when the patient's trying to look up, that left eye is stuck, so that patient's going to have double vision and there's some corneal foreign bodies on the bottom. Right next slide, please. So double vision patients may actually complain of blurred vision or headache. Um If the double vision is binocular, you need, you need to find out if it's binocular or monocular. So you get the patient to cover one of their eyes and see if the double vision resolves. So if it's binocular and they cover an eye, the double vision will go. Whereas if it's monocular and they cover the fellow eye, it will continue. So it's important to determine if the double vision is vertical or horizontal. Cos that will let you know which um extraocular muscles are involved and it's important to look for associated signs. So for example, the presence of ptosis, which is a droopy lid or a dilated pupil, which can suggest a third nerve palsy double vision can be associated with systemic diseases such as hypertension, diabetes or intracranial lesions. Next slide, please. So management, if it's binocular, the patient needs to be referred and they'll be evaluated by our orthoptic department and maybe prescribe prisms, they may need neuroimaging if there's any concern that the double vision is due to something happening inside the head. If the double vision is monocular causes of monocular double vision um can be refractive. So they um advise to see their optician um if it's not refractive and they need to come to clinic because there may be a problem with the cornea or with the development of a cataract. Next slide, please. So um a little slide about an isochor, I was asked to talk about pupils. So um the one on the left is a third nerve palsy. You can see the left eye is in these down and out position, the lids having to be held up because there's a ptosis and the pupil is dilated. The one on the bottom right is a Horner's syndrome. The patient has a meos pupil, so it's smaller than the opposite side and there's a partial ptosis or a partial droopy lid. Next slide, please. Brilliant. That's the end of the show. Um Just a couple more minutes though, if that's OK because I'm not quite at the extra 15 that that was agreed. So just about an isochor again, um I didn't do a slide on this, but just to try and make it a little bit easier for you. I only had those two pictures. So an isochor um it can be broken down into physiological. So a lot of us have um different size pupils, but we'd have normal response to light and near and no symptoms. It can be due to Iris pathology. So for example, as we saw earlier, if they've had previous uveitis and there's posterior si that might result in the pupils being unequal, it can be pharmacological. So for example, if the patients had an opioid overdose, they may have small pupils or if they've had um mydriatic drops in still, they could have large pupils. It can be due to the sympathetic chain. So this is uh the sympathetic chain is what causes the Horners syndrome. So without going into too much detail, Horners, the sympathetic chain goes from the head centrally down to the um spinal column where it synapses. So the central um fibers go from the brain to the spinal cord, then it synapses and the preganglionic fibers then go up, they swing through the chest and up through the neck um to synapse in the cervical ganglion, then they continue on with the carotid artery and enter the skull again from there and therefore into the orbit and they're the post ganglionic fibers. So, the investigations that you do for Horners syndrome will depend on which part um has caused this. So the patient may need an MRI scan of the head or the neck or a chest X ray or CT. If you're suspecting a pancoast tumor, et cetera, an isochor can also be caused due to parasympathetic pathway problems such as a DD tonic pupil. This is thought to be due to a a virus, a viral denervation with aberrant regeneration. So the Aedes tonic pupil is dilated and you tend to see these vermiform like worm like movements of the iris. If you look closely at it, if the um Aedes pupils associated with loss of deep tendon reflexes, that's what's known as the Holmes Ad syndrome. I was also asked to talk about Argil Robertson, but I don't think that's very important nowadays because that is, um, something that you get in the tertiary stage of neurosyphilis, which is almost wiped out now due to the use of penicillin. But if you did see anybody with Argil Robertson pupil, you would refer to a G clinic for penicillin treatment. It tends to be a unilateral problem followed by a bilateral problem. Um, and basically, um they're irregular meos pupils um that um react poorly to light and have light nerd association. But it's academic nowadays. But I think that that broad categories have been isochor breaking it down into the physiological, the Iris pathology, pharmacological due to the sympathetic Ie Horner syndrome or due to parasympathetic, like the A tonic. Um is the important thing. Does anybody have any questions? Oh, I've got one. What are the risks of complete vision loss in optic neuritis? Um I'm not quite sure what the exact question is. So patients with optic neuritis can present with total loss of vision which then can gradually come back. Um And although the vision might not come back to what it was exactly before, um there usually is improvement of vision. So if the patient had lost vision completely and it never came back, you need to be thinking of, of alternative diagnoses. I don't know if that's answered your question. Um Hi, Doctor Julie. Thank you so much for that. That was really really informative. Like, I think you covered almost all the topics and offer that we require. I hope it wasn't information overload. But, um, no, no, and we're putting it read over the leisure in future. Yeah. And we're putting it online anyway. So anyone can, like, go and visit it and see it again when required. But that was really good. Thank you so much. No problem. Um Right. So we're just gonna take a five, I think, I think we're gonna take a five minute break and then uh we're gonna probably start the next session. Uh, but thank you so much. We're putting feedbacks on the chat. So please do fill it up. Thank you very much, Doctor Thompson. No problem. Mhm. Yes.