Interactive Transcript
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Okay, so, um, HIE uh, ultrasounds can have a variety of,
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uh, appearances, right?
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So here's some kind of, you see
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that gray white interface, it's kind of blurred.
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And you've got slit ventricles. So this is a diffusely
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edematous brain, but the location's pretty good
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'cause we're now term, right?
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Here's one of the central injuries.
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So very echogenic basal ganglia compared
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to like the white matter.
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And then here's another one
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where you actually have almost like a super scan.
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So like you have diffuse kinda white matter injury here.
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Uh, and then it's actually kind of exaggerated contrast
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with the, the more ous gray matter.
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So you can have either decreased or increased contrast,
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but both are abnormal, right?
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And obviously you have to correct
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for ultrasound artifacts and gain and things.
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But again, like I think the clinical picture
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and then being able to really look at that gray,
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white distinction and so forth is helpful.
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Okay, so watershed
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injury, you know, just like adults, right?
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So these kinda like A-C-A-M-C, A PCA border zones, right?
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So the cortex, the white matter kind
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of paralleling the lateral ventricles
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here, restricted diffusion.
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You can see that the, the T two is, is sort of appreciable,
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uh, edema on top of an already watery brain,
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but it's not as easy to appreciate.
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So having, it's all about timing, right?
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Um, and then late, so this is called dula gyus.
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So, uh, the medullary arteries are penetrating in, uh,
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to the, um, you know, to these kind of like deep, deep sci.
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And so it's kind of a watershed area if, if you're getting
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that, um, uh, you know, low flow, uh, from cerebral artery.
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So basically you get the selective kind of injury
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to the deep ssci with relative span of surface of gyre.
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So it's like, uh, Latin from mushroom gyre.
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And so we're not talking like your American mushrooms.
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It's like, uh, not, not the straw mushrooms.
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It's like those Asian oyster mushrooms
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that have like really long stems and like tiny little tops.
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So that's what this eulo gyre is.
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And this is, this is a risk factor
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for seizures, for example.
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So you can see the border zone appearance, uh,
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on follow-up can be, uh, bilateral,
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but it can also often be asymmetric, right?
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So these, all of these cases, uh, uh, have some level
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of asymmetry, but there is actually bilateral
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involvement watershed.
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And this is, this just shows you that, you know,
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although watershed injuries usually partial hypoxia
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of its prolonging, you actually have pretty severe sequelae.
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Okay? The central injury here, uh, so this is, uh, the a DC,
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and you're seeing the restriction in
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these critical areas, right?
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High flow areas. So the corticospinal tracts,
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the basal ganglia, um, classically the areas
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that are selectively vulnerable
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and the term infant are gonna be the, um, the, uh,
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posterior pertamina right here.
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And then the, uh, ventral lateral thalami.
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So like these part of the thalami.
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So when you see that pattern, that's pretty specific
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for term HIE.
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And so here, this is a little tricky,
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but see, uh, the clicks, uh,
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they're a little bit like, they're a little bit faded.
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You're not seeing that T two darkness
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for like a third to a half of it.
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It's kind of blurred out.
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There's maybe a little bit too much edema here.
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And then the vent lateral thal line,
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the posterior peri are actually a bit too T one, right?
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So they're approaching the level of the clicks, right?
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So something's not quite right
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In this whole central area.
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And then the a SL perfusion, she says that we have, uh,
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re like essentially a reactive hyperperfusion in those same
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injured areas because basically they have the ischemia now
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they're trying to rebound, but you see
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that they're actually stealing
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blood from the rest of the brain.
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The rest of the brain has pretty slow flowing.
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You have excessive perfusion to these injured areas.
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So that's that secondary energy failure
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and it steals from the rest of the brain.
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And that's what we're trying to blunt with the cooling.
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So late findings, so here you see the cystic degeneration.
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So now like very, very bright, uh, posterior pertamina
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and ventral lateral alm I with some cystic degeneration,
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very specific for, uh, neonatal HIE.
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And then here, uh, this is older, uh, patient,
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but you see again that posterior
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pertamina ventral later thalami.
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So if you see this in an adult or an older child
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or whatever, and there's no history you can call it, right?
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Because nothing else does this.
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Um, and you can have as asymmetric, right?
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So hemiplegia, uh,
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you can have asymmetric central injury as well.
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So this person, you know, uh, right hemisphere involvement,
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they're gonna have more left-sided symptoms, okay?
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You can have large, uh, large artery infarcts,
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uh, in term babies.
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Um, it's not too common, not like adults,
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right, who have strokes all the time.
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But again, on the MCA stroke,
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on the ultrasound restricted diffusion edema, again,
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edema on top of a watery brain can be
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hard to see if it's more subtle.
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Um, interestingly, we usually don't find a, a clot, right?
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Like there's nothing for neural ir to do.
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It's usually the theory is
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that maybe there's some placental emboli.
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They kinda like flicked off and occluded
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and then they kind of cleared out.
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So we usually don't find the actual clot,
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but you see there's restricted diffusion,
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but on the a SL, there's actually a, a luxury perfusion,
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and that mc is actually more hyperemic.
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So again, that's that secondary energy failure.
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So that's flooding the area with free radicals
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and causing additional injury on top
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of the original ischemia.
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And so again, in the late phase, you can get, you know,
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porn cephalic and eulogy in those mc distributions.
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And so again, if you're seeing eLog gyri, that's pretty,
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that's quite specific.
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That pattern. Uh, those mushroom gyri
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or cystic porn cephalic, it means
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that they had a pretty early insulin,
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not necessarily perinatal,
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but at least in the, you know,
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first one max two years of life, right?
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When they didn't have mature astrocytes.
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So you can, you can, again, you can call it,
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this is not an adult mc in far, this is definitely,
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even if you had no priors,
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you'd know this was earlier in life and then global injury.
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Um, so, uh, these are tricky, right?
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Because, uh, this, uh, here are some cases
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where I think they were out outside the hypothermic window,
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like they got transferred in, it was more than six hours.
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So there was no point in starting the hypo in this
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heart, starting the cooling.
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But you do see there's some restricted diffusion centrally,
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but there's some little spots peripherally too.
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This is a little too emini.
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And then you're losing the clicks, you're getting
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that bright basal ganglia.
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Too much edema here. So on follow up,
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it's actually bloomed, right?
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So this was like one or two days, this was five days.
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And so you see that doing it too early, right?
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Doing the imaging too early can actually really
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underestimate the degree of, of, uh, end stage injury.
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So here, yes, there's central pattern,
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but there's really diffuse
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Diffusion restriction.
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Profound basal ganglia, really diffuse edema.
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You lose that gray, white distinction.
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Here's another example with a SL.
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So again, you see some central restriction,
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but it's a little too emus out here as well.
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So it's really both central and peripheral patterns.
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You see that rebound hyperperfusion
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of the injured basal ganglia,
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and then it's stealing from the surrounding brain.
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You're losing the clicks.
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And then here, uh, so you know, at day four or five, right?
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You have profound blooms. So the entire brain is restricted.
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The profusion actually is,
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is more consistent between the two.
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So it's been a better prognostic factor, right?
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So you're still getting a, a ton
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of rebound hyperperfusion, right?
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Um, and, and then in the end stage right,
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you essentially have this like cystic HIE, right?
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Very swollen and it all shrinks down.