Shadowing Practice: Retinal Vascular Disorders - CRASH! Medical Review Series - Learn English Speaking with Video
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Retinovascular disorders is going to be the topic of this lecture
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and by retinovascular disorders I'm referring to the central retinal artery occlusion
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and the central retinal vein occlusion
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so you have a central retinal artery the retinal artery is
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is the first artery off of the internal carotid artery in most people
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and that's going to branch into several branches smaller branches
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that then go off to different parts of the retina now
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if the entire retinal artery is blocked before it gives off tributaries branches then it's considered a central retinal artery occlusion.
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If it's just a branch that's blocked, that can cause symptoms, but that would be considered just a branch retinal artery occlusion.
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And it works the same way with the veins.
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If the main vein that's leaving the eye is blocked, then it's a central retinal vein occlusion.
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If it's just a tributary of that vein, then it's a branch retinal vein occlusion.
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So hopefully that makes sense.
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Okay, so the central retinal artery occlusion is an occlusion of the retinal artery, is mentioned.
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It's the first artery coming off of the internal carotid
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and it presents as a sudden profound monocular loss of vision without pain or redness.
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So this is just like having a stroke to the eye.
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And about one to two percent of patients will present with bilateral CRAO, but that's pretty unusual.
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The incidence is one in 10 ,000 and the average age of onset is in the 60s.
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So this is a disease of the elderly.
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However, if you do see this in somebody who's in their 30s or 40s, you should be highly suspicious of something like a thrombophilia.
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In many cases, the patient will have a history of giant cell arteritis, whether that's diagnosed or not diagnosed.
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That's also called temporal arteritis.
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And this is a big risk factor for central retinal artery occlusion
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so that branch retinal artery occlusion as was mentioned I'm not going to spend a whole slide talking about it
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but this is just a similar process due to similar causes
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but it's a smaller clot and it affects a downstream vessel
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and so it doesn't affect as much of the retina as a central retinal artery occlusion
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so this is much further downstream and
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so it affects a smaller part of the retina
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and the symptoms will be similar
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but it will only affect the part of the visual field that that obstructive segment supplied
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okay so what are the risk factors hypercholesterolemia of course that's a risk factor for clotting obesity
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Obesity, advanced age, diabetes mellitus, and all of these three things,
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maybe not hypercholesterolemia, but obesity and advanced age, those certainly play into diabetes mellitus.
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But just having diabetes mellitus by itself, even if you're not obese and you're not advanced age, that is a risk factor too
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and then temporal arteritis is a big risk factor for artery occlusion
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and so what is temporal arteritis again I address this in a different lecture in the medical section
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but temporal arteritis happens to people 55 years of age
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or older it involves a headache scalp tenderness and thickening
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or tenderness of the superficial temporal artery you should be able to feel pulse over
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that artery and it's right over the temple
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if you feel your own superficial temporal artery you feel your temple you should be able to palpate
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that artery patients with temporal arteritis they usually have this this inflamed firm cord
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and you can't feel the pulse because the artery is
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so inflamed so what does this lead to especially the hypercholesterolemia the obesity the diabetes
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and the fact of being old those all can lead to
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or increase your risk of carotid artery stenosis and of atrial fibrillation
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because of small undetected heart attacks and those things carotid artery stenosis
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because you're gathering plaque and atrial fibrillation because you can develop a clot
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because of a lack of a lack of appropriate contraction both of those things you can develop a clot
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or release a clot or release a plaque and
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that can be the embolus that's needed that can go in to the into the retinal artery
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and so this is how central retinal artery occlusion and
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if it's a smaller plaque
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or a smaller clot that's how a branch retinal artery occlusion can happen other risk factors include
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congenital or acquired thrombophilia you can acquire thrombophilia by taking birth control pills
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and so those would be something you would look for in younger patients who don't have these risk factors.
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And there's other risk factors in addition to these, but these are some of the most common that you'll see.
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So as mentioned, this is painless, sudden, and often this is a profound loss of vision.
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98 to 99 % are monocular.
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The symptoms are sudden loss of vision.
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Acuity is typically worse than 2200, which is the cutoff point for being legally blind
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and a lot of times they won't even be able to tell you how many fingers
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you're putting up in front of their face even
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if you get really close there may be some preservation in the temporal field I'm assuming that's
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because there may be some additional there may be some additional circulation coming from somewhere else
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but I'm not exactly sure but the literature does say
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that there may be some preservation in temporal fields and
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that is certainly the case
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so some of the things you're going to want to know from the patient
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or at least know on the question
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that's going to help you with the diagnosis is how long have the symptoms been present usually
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when somebody loses their vision they're going to get to the er as quickly as possible
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you also want to know
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if they have any past medical history of ocular problems you'll want to know if the patient has a high cholesterol,
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if you ask the patient that or if you look in their charts, do they have a history of diabetes?
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Certainly both of those would increase the risk of this being a central retinal artery occlusion.
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And do they have any history of stroke or TIA?
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That would lead you to believe that perhaps there's a carotid artery stenosis
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and that's a big contributor to retinal artery occlusion
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now I just want to right now differentiate central retinal artery occlusion from something else
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which is called amaurosis fugax and with amaurosis fugax you get a temporary loss of vision
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that usually lasts a few minutes
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and then your vision comes back with central retinal artery occlusion you have a loss of vision
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and it stays at least until you get treated on On physical examination,
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you want to document their visual fields and then get their visual acuity, even though it's probably going to be 2200 or worse,
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just to compare it to baseline and document it on the records.
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Look for signs of temporal arteritis, especially in older patients, because that contributes, that strengthens your diagnosis.
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You should also check their pupils for an afferent pupillary defect or the Marcus Gunn pupil.
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Ocultate for a carotid brui, and then ocultate the heart for murmurs, and especially an irregular beat, which can be consistent with atrial fibrillation.
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For diagnosis, you'll want to get routine labs,
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and that's great, but all patients with acute loss of vision should be referred to ophthalmology for a formal ophthalmoscopy,
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highlighting the fact here that CRAO, as in a lot of cases of vision loss,
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cannot be diagnosed with a simple handheld ophthalmoscope.
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You'll need to do a dilated exam and have the optometrist use their equipment.
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So findings consistent on indirect ophthalmoscopy, consistent with CRAO, includes retinal pallor, which makes sense because it's not getting enough blood,
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a prominent cherry red macula, and that is actually because the fovea,
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the macula, gets its vascularization elsewhere from the choriocapularis.
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And then attenuated arteries may be present, as well as a boxcar appearance of veins.
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But what you're really going to notice is the retinal pallor and the prominent cherry red macula.
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So here's a normal posterior pole.
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Here's your optic disc and in the center here is your macula.
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Now the macula is red but it's a lot different in comparison than when we see the retinal artery occlusion.
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So here's an example of a central retinal artery occlusion and as you can see there's pallor here.
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This is much more pale.
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Now, every ophthalmoscope uses slightly different lighting,
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but you can see that there's a much more contrast between the macula and the rest of the retina,
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whereas here, the macula and the retina weren't as contrasted.
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You also see that you don't have a whole lot of vasculature around the macula,
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whereas on a normal visualization, you do have vasculature around the macula.
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So here's another one, again the macula is much more prominent, that cherry red macula.
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See the same here too.
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So this is a branch retinal artery occlusion.
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So you can see that it's normal on the top here, but it's abnormal on the bottom.
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If the rest of the retina was like this on the bottom, then you'd have a central retinal artery occlusion you'd be able
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to see this macula very distinguished from the rest of the retina
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but it's only distinguished from this retina here on the bottom
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which is the diseased retina that's not getting enough blood
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and then here's another one here above the above the macula
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so the treatment the patient is going to need admission through
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ophthalmology the treatment is going to be under the guidance of an ophthalmologist.
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So I don't expect ever you'll be required to know how to do this
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or exactly how to treat them in the ER or as an internist or even as a surgeon.
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But you do need to know that they need to be admitted and it's worth knowing some of the things that
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ophthalmologists use.
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So presently there's controversy in the exact management for patients with CRAO, but most ophthalmologists agree with some basic principles.
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So high concentration inhaled 100 % oxygen, that's something you can start in the ER.
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So that's something you should know.
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IV acetazolamide, IV corticosteroids, those are done,
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the IV corticosteroids are done to reduce the inflammation and
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that is expected to help with with maintaining vision reducing the inflammation
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and then treatment of the underlying cause as the internist this is going to be your concern finding
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and treating the underlying cause right some ophthalmologists use intra arterial thrombolytics
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and they inject those thrombolytics into the retinal artery system that's not universal
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but this has been shown to be effective by the EGLE study
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so you can look look up more on that if you want
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but high high concentration inhaled oxygen acetazolamide corticosteroids
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and treatment of the underlying cause
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so upon diagnosis it's going to be your responsibility to work
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the patient up for underlying causes these don't just happen on their own
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so the patient will have something wrong with them
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that put them at predisposition all patients regardless of their age should get a carotid artery duplex ultrasound
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they should get an echocardiogram to look for atrial fibrillation
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or any other kind of abnormality valvular abnormalities that can gather clots
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and then and then release them they should get an EKG routine labs that's usually done anyway
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when you're first investigating the patient an ESR is useful
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and that's kind of to look more towards the temporal arteritis
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that would be elevated a fasting blood glucose is useful to work them up for diabetes
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if they haven't been diagnosed with diabetes and then coagulation studies younger patients
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or older patients who have normal results after this workup should get a workup for any kind of congenital
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or acquired thrombophilia so factor V Leiden antithrombin 3 deficiency protein C deficiency protein S deficiency
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and so forth oh and then elevated homocysteine
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that was another one I wanted to add to and that's another congenital thing older
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Older patients should follow up regularly, patients with CRAO have a 56 % mortality rate within 9 years
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and that's compared to 27 % in aged match patients who have never had CRAO.
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So that's a big deal when you think about it.
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Somebody who's older and has the same,
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let's say you've got two twins and one twin develops a CRAO and the other twin doesn't,
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That twin that developed the CRAO is two times more likely to die within the next nine years.
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And that shows that it's likely due to the fact that there's some level of increased thrombosis.
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The plaque is not stabilized but it's important to remember that patients who have CRAO,
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really what this was, was a stroke that just happened to go the right way.
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Rather than go up to the brain, it went to the retinal artery.
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And so rather than having a debilitating or deadly stroke, you just got your eye taken out.
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And I mean, neither of those are good, but this is the same pathologic process that causes a stroke.
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So it's important that patients are aware that they are at imminent risk of stroke and that you take interventions as necessary,
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as if the patient had had a stroke.
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Okay, so central retinal vein occlusion is occlusion of the retinal vein.
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And this presents a little bit differently.
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So initially, the patient will present with sudden monocular loss of vision without pain or redness,
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but it's usually not as severe as the central retinal artery occlusion.
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But this is a more progressive disease, and the vision will worsen with time.
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And eventually, pain erythema and watering can develop.
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So this is less severe usually when it presents, but with time, when it's diagnosed with time, if it's not treated, it gets worse.
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The symptoms have a tendency to be noticed on wakening.
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I'm not sure why.
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The lifetime incidence is 2 to 5 per 1000
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and 90 % of cases are seen over the age of 50
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so again this has a preponderance in the elderly and there's a slight male preponderance.
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The equivalent branch retinal vein occlusion is a similar process
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but it affects a downstream vein and
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so it does not affect as much of the retina
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and the ophthalmoscopic findings will be localized so
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when we look at what the ophthalmoscopic findings of central retinal
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vein occlusion are you're only going to find them in one part of the retina with the BRVOs.
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BRVOs are thought to be most commonly caused by a mechanical compression on the branch vein by an artery
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but there are other possible causes systemic hypertension is considered the most significant major risk factor in BRVOs.
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So back on the CRVOs they're very similar as far as risk factors go
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but other risk factors with CRVO can include primary glaucoma probably because of the elevated pressure,
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alcohol consumption, head trauma, and excessive physical activity.
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Symptoms include as mentioned progressive visual impairment.
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The natural progression includes worsening of vision to the point of blindness, pain, photophobia, redness, and eye watering.
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All suspected cases of loss of vision, as mentioned, should be referred to an ophthalmologist for formal indirect ophthalmoscopy.
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And the findings on ophthalmoscopy depend on how progressed the CRVO is.
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So typically with CRVO, we see a certain degree of optic disc swelling there's going to be a certain amount of hemorrhages
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and you may see some tortuous veins
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but as it progresses you're going to see a more swelled optic disc you're going to see more
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and more and larger hemorrhages
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and a lot of times the hemorrhages get in the way to where you can't see the veins even
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if they are tortuous so i'll show you some examples
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further tests to evaluate the CRVO include fluorescein angiography
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when to do this test is at the discretion of the ophthalmologist
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so here is a case of what would be considered early CRVO
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so the you can see there's some hemorrhaging here on these early veins
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and then you also have this tortuosity this would be probably a little bit later
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so you've got more hemorrhages here and this is much later too
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because the hemorrhages are much further out okay
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so this is a branch retinal vein occlusion so you can see here
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that the veins and arteries are normal but here you have this localized area of hemorrhage
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So this was found to be a branch retinal vein occlusion.
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Here's another one.
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Now just looking at the results of an ophthalmoscope, it isn't going to tell you what the disease is.
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You always have to include it in the clinical picture of the patient.
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Any radiologist would tell you that.
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But with a patient with consistent symptoms, this is certainly a branch retinal vein occlusion, as is this.
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So patients with central retinal vein occlusions should be worked up for diabetes, hyperlipidemia.
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So both of those are easy.
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You can get them in the morning, get a fasting blood glucose level, get a lipid panel.
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They should also be worked up for thrombophilia markers such as factor V Leiden, protein C, etc. and then be worked up for an elevated homocysteine.
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For treatment, unfortunately there is no available effective medical treatment for CRVO.
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Various treatment modalities are under investigation, however, and they may be performed by the ophthalmologist.
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Some patients can get enrolled in studies, but you won't be responsible for knowing any of this on the USMLE
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but some of those modalities include intravitreal administration of anti -VEGF inhibitors
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so remember that VEGF is a protein that stimulates angiogenesis and
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so this will reduce the development of more arteries
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which is the classic response
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when there's ischemia there's also intravitreal administration of corticosteroids to reduce some of the inflammation
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that invariably happens with this the use of locally injected tpa and then plasmapheresis
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complications include neovascular glaucoma panretinal photocoagulation can be performed either prophylactically in crvo
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or as soon as there's signs of neovascularization
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and macular edema is another complication for that laser photocoagulation can be effective but only if it's due from BRVO.
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It has not been shown to be effective in CRVO.
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So if you have any questions, feel free to leave a message below.
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Bu dersin kelimeleri ve konuşma notları
Bu konuşma dersi “Retinal Vascular Disorders - CRASH! Medical Review Series” videosuna dayanıyor. En çok tekrarlanan kelimeler: artery, retinal, occlusion, patient, vein. Bu videoda gölgeleme çalışması için 234 cümle ve 3050 kelime var. Konuşma bölümü 22:30 sürüyor. Konuşmacı dakikada yaklaşık 136 kelimelik dengeli bir hızla konuşuyor; gölgeleme için rahat bir tempo. Kelimelerin yalnızca %75’i İngilizcede en sık kullanılan 3.000 kelime arasında, bu yüzden kelime dağarcığı zorlayıcı.
Bu videodaki önemli kelimeler
Videodan öğrenmeye değer 15 kelime, telaffuzu ve anlamıyla:
| Kelime | Telaffuz | Anlam |
|---|---|---|
| artery isim | /ˈɑɹ.təɹ.i/ | arter, atardamar |
| vein isim | /veɪn/ | damar |
| temporal sıfat | /ˈtɛm.pə.ɹəl/ | cismani, dünyevi |
| diabetes isim | /ˌdaɪəˈbiːtiːz/ | diyabet, şeker hastalığı |
| symptom isim | /ˈsɪm(p)təm/ | semptom, belgi |
| sudden sıfat | /ˈsʌd.ən/ | ani |
| twin isim | /twɪn/ | ikiz |
| diagnosis isim | /daɪəɡˈnəʊsɪs/ | tanı, teşhis |
| obesity isim | /ə(ʊ)ˈbiːsɪti/ | obezite |
| prominent sıfat | /ˈpɹɑmɪnənt/ | önde gelen |
| cherry isim | /ˈt͡ʃɛɹi/ | kiraz, vişne |
| acquire fiil | /əˈkwaɪɚ/ | edinmek |
| disk isim | /dɪsk/ | disk, ağırşak |
| inflammation isim | /ɪnfləˈmeɪ̯ʃən/ | enflamasyon, iltihap |
| formal sıfat | /ˈfɔɹməl/ | resmi |
Duyacağınız deyimsel fiiller
| Kelime | Telaffuz | Anlam |
|---|---|---|
| give off fiil | /ɡɪv ɒf/ | yaymak, saçmak |
| look up fiil | /ˌlʊk ˈʌp/ | yukarı bakmak |
| take out fiil | çıkarmak |
Bu videodaki dil bilgisi
Konuşmacının en çok kullandığı yapılar, videodaki sözcüklerin aynısıyla:
| Yapı | Videoda |
|---|---|
| Edilgen yapı be + fiilin üçüncü hâli — kimin yaptığı değil, ne olduğu önemli | is blocked · would be considered · is mentioned |
| Present perfect have/has + fiilin üçüncü hâli — geçmişte olan ama şimdi de önemli olan bir eylem | has been shown · haven't been diagnosed · have never had |
| İlgi cümlecikleri who / which + cümle — bir kişi ya da şey hakkında ek bilgi | beat, which can · pallor, which makes |
Dikkat edilecek telaffuzlar
Konuşmacı you're, I'm, you'll gibi kısaltılmış biçimleri 40 kez kullanıyor. Bunları duyduğunuz gibi kısa söyleyin.
- “th” sesleri: gather /ˈɡæðɚ/, ophthalmologist /ˌɔf.θə(l)ˈmɑ.lə.d͡ʒɪst/, ophthalmology /ˌɒfθə(l)ˈmɒləd͡ʒi/, antithrombin /ˌæntɪˈθɹɒmbɪn/
- “sh” ve “zh” sesleri: inflammation /ɪnfləˈmeɪ̯ʃən/, deficiency /dɪˈfɪʃənsi/, concentration /ˌkɑn.sənˈtɹeɪ.ʃən/, examination /ɪɡˌzæm.ɪˈneɪ.ʃən/, preservation /ˌpɹɛz.əˈveɪ.ʃən/
- Uzun kelimeler — vurguyu doğru yere koyun: obesity /ə(ʊ)ˈbiːsɪti/, inflammation /ɪnfləˈmeɪ̯ʃən/, deficiency /dɪˈfɪʃənsi/, concentration /ˌkɑn.sənˈtɹeɪ.ʃən/, examination /ɪɡˌzæm.ɪˈneɪ.ʃən/
Türkçe konuşanların zorlandığı sesler:
- /w/ — dudaklar yuvarlak, /v/ değil: twin /twɪn/, acquire /əˈkwaɪɚ/, whereas /(h)wɛɹˈæz/, distinguish /dɪˈstɪŋ.ɡwɪʃ/, swell /swɛl/
- Kelime başındaki ünsüz kümesi — araya ünlü eklemeyin: twin /twɪn/, plaque /plæk/, prominent /ˈpɹɑmɪnənt/, whereas /(h)wɛɹˈæz/, progressive /pɹəˈɡɹɛsɪv/
- /æ/ — “e”den daha açık: plaque /plæk/, lab /læːb/, whereas /(h)wɛɹˈæz/, examination /ɪɡˌzæm.ɪˈneɪ.ʃən/, gather /ˈɡæðɚ/
Bu videoyla nasıl çalışılır
- Videonun tamamını konuşmadan bir kez dinleyin ve bilmediğiniz kelimeleri not edin.
- Normal hızda cümle cümle tekrar edin; ritminiz konuşmacıyla aynı olana kadar her cümleyi yineleyin.
- Kendinizi kaydedin ve orijinaliyle karşılaştırın; artery, vein, temporal gibi kelimelere özellikle dikkat edin.
Gölgeleme Tekniği Nedir?
Gölgeleme, başlangıçta profesyonel tercüman eğitimi için geliştirilen ve çok dilli Dr. Alexander Arguelles tarafından popüler hale getirilen, bilim destekli bir dil öğrenme tekniğidir. Yöntem basit ama güçlüdür: ana dili İngilizce olan bir sesi dinler ve hemen yüksek sesle tekrar edersiniz — konuşmacıyı 1-2 saniye gecikmeyle takip eden bir gölge gibi. Pasif dinleme veya dilbilgisi alıştırmalarının aksine, gölgeleme beyninizi ve ağız kaslarınızı gerçek konuşma kalıplarını eşzamanlı olarak işlemeye ve yeniden üretmeye zorlar. Araştırmalar, telaffuz doğruluğu, tonlama, ritim, bağlı konuşma, dinleme anlama ve konuşma akıcılığını önemli ölçüde geliştirdiğini göstermektedir — bu da onu IELTS Konuşma hazırlığı ve gerçek dünya İngilizce iletişimi için en etkili yöntemlerden biri yapar.