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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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Vocabolario e note di pronuncia per questa lezione
Questa lezione di conversazione si basa sul video “Retinal Vascular Disorders - CRASH! Medical Review Series”. Le parole che ritornano più spesso: artery, retinal, occlusion, patient, vein. Questo video contiene 234 frasi e 3050 parole da ripetere con lo shadowing. Il parlato dura 22:30. Chi parla mantiene un ritmo costante di circa 136 parole al minuto, comodo per lo shadowing. Solo il 75% delle parole rientra nelle 3.000 più comuni dell’inglese, quindi il lessico è impegnativo.
Vocaboli chiave di questo video
15 parole del video che vale la pena imparare, con pronuncia e significato:
| Parola | Pronuncia | Significato |
|---|---|---|
| artery sostantivo | /ˈɑɹ.təɹ.i/ | arteria |
| vein sostantivo | /veɪn/ | vena |
| temporal aggettivo | /ˈtɛm.pə.ɹəl/ | temporale |
| diabetes sostantivo | /ˌdaɪəˈbiːtiːz/ | diabete |
| symptom sostantivo | /ˈsɪm(p)təm/ | sintomo |
| consistent aggettivo | /kənˈsɪs.tənt/ | costante, continuo |
| sudden aggettivo | /ˈsʌd.ən/ | improvviso |
| twin sostantivo | /twɪn/ | gemello, gemella |
| diagnosis sostantivo | /daɪəɡˈnəʊsɪs/ | diagnosi |
| underlying aggettivo | sottostante | |
| obesity sostantivo | /ə(ʊ)ˈbiːsɪti/ | obesità |
| plaque sostantivo | /plæk/ | placca, piastrina |
| prominent aggettivo | /ˈpɹɑmɪnənt/ | prominente, rilevante |
| cherry sostantivo | /ˈt͡ʃɛɹi/ | ciliegia |
| acquire verbo | /əˈkwaɪɚ/ | acquisire |
I phrasal verb che sentirai
| Parola | Pronuncia | Significato |
|---|---|---|
| give off verbo | /ɡɪv ɒf/ | emettere |
| take out verbo | cavare, cacciare |
La grammatica di questo video
Le strutture che chi parla usa di più, con le parole esatte del video:
| Struttura | Nel video |
|---|---|
| Forma passiva be + participio passato — conta ciò che accade, non chi lo fa | is blocked · would be considered · is mentioned |
| Present perfect have/has + participio passato — un’azione passata che conta ancora adesso | has been shown · haven't been diagnosed · have never had |
| Frasi relative who / which + frase — un’informazione in più su una persona o una cosa | beat, which can · pallor, which makes |
Pronuncia a cui fare attenzione
Chi parla usa 40 contrazioni e forme ridotte, come you're, I'm, you'll. Pronunciale nella forma breve, così come le senti.
- I suoni “th”: gather /ˈɡæðɚ/, ophthalmologist /ˌɔf.θə(l)ˈmɑ.lə.d͡ʒɪst/, ophthalmology /ˌɒfθə(l)ˈmɒləd͡ʒi/, antithrombin /ˌæntɪˈθɹɒmbɪn/
- I suoni “sh” e “zh”: inflammation /ɪnfləˈmeɪ̯ʃən/, deficiency /dɪˈfɪʃənsi/, concentration /ˌkɑn.sənˈtɹeɪ.ʃən/, examination /ɪɡˌzæm.ɪˈneɪ.ʃən/, preservation /ˌpɹɛz.əˈveɪ.ʃən/
- Parole lunghe — attenzione all’accento: obesity /ə(ʊ)ˈbiːsɪti/, inflammation /ɪnfləˈmeɪ̯ʃən/, deficiency /dɪˈfɪʃənsi/, concentration /ˌkɑn.sənˈtɹeɪ.ʃən/, examination /ɪɡˌzæm.ɪˈneɪ.ʃən/
I suoni difficili per chi parla italiano:
- /h/ — va soffiata, non è muta: whereas /(h)wɛɹˈæz/, highlight /ˈhaɪˌlaɪt/, headache /ˈhɛdeɪk/, hemorrhage /ˈhɛm(ə)ɹɪd͡ʒ/, inhale /ɪnˈheɪl/
- Consonante finale — senza aggiungere una vocale dopo: diabetes /ˌdaɪəˈbiːtiːz/, consistent /kənˈsɪs.tənt/, diagnosis /daɪəɡˈnəʊsɪs/, plaque /plæk/, prominent /ˈpɹɑmɪnənt/
- /æ/ — più aperta della “e”: plaque /plæk/, lab /læːb/, whereas /(h)wɛɹˈæz/, examination /ɪɡˌzæm.ɪˈneɪ.ʃən/, gather /ˈɡæðɚ/
Come esercitarsi con questo video
- Ascolta tutto il video una volta senza parlare e annota le parole che non conosci.
- Fai shadowing frase per frase a velocità normale, ripetendo ognuna finché il tuo ritmo coincide con quello di chi parla.
- Registrati e confronta con l’originale, facendo attenzione a parole come artery, vein, temporal.
Cos'è la tecnica dello Shadowing?
Shadowing è una tecnica di apprendimento delle lingue supportata da studi scientifici, originariamente sviluppata per la formazione dei traduttori professionisti e resa popolare dal poliglotta Dr. Alexander Arguelles. Il metodo è semplice ma potente: ascolti un audio in inglese di madrelingua e lo ripeti immediatamente ad alta voce — come un'ombra che segue il parlante con un ritardo di solo 1–2 secondi. A differenza dell'ascolto passivo o degli esercizi di grammatica, lo shadowing costringe il tuo cervello e i muscoli della bocca a elaborare e riprodurre simultaneamente i modelli di discorso reale. La ricerca dimostra che migliora significativamente la precisione della pronuncia, l'intonazione, il ritmo, il discorso connesso, la comprensione dell'ascolto e la fluidità del parlato — rendendolo uno dei metodi più efficaci per la preparazione alla prova di speaking dell'IELTS e per la comunicazione reale in inglese.