Cram The Pance - S1E42 Stroke

Episode Date: January 14, 2022

Stroke review for your Pance, Panre, and Eor's. ►Paypal Donation Link: https://bit.ly/3dxmTql (Thank you!)--- Support this podcast: https://anchor.fm/scott--shapiro/supportIncluded in review: Ischemic stroke, hemorrhagic stroke, TPA (thrombolytics), middle cerebral artery, posterior cerebral artery, anterior cerebral artery, TIA (transient ischemic attack), subarachnoid hemorrhage, subdural hematoma, epidural hematoma, intracerebral hemorrhage, mechanical thrombectomy.Become a supporter of this podcast: https://www.spreaker.com/podcast/cram-the-pance--5520744/support.

All right, so this podcast is going to be on stroke. I have a few mnemonics in there to help you remember the things you need to know for your exam. And of course, I'll try to keep it as brief as I can just to focus on the things you really need to know for your exam questions. As always, thank you so much for all of the really nice comments. I truly do appreciate that. So thank you for that. Let's go ahead and get started with stroke. We'll start with our TIA, our transient ischemic attack.

Keep this part brief. There's not a lot of high-yield stuff from TIA. Just a few things that you need to know of. So, first, what is it TIA? So TIA is a transient episode. of neurologic dysfunction caused by focal brain, spinal cord, or retinal o'schemia without acute infarction. That's the official definition from the American Heart Association and the American Stroke Association. So a TIA, it's a clinical diagnosis. It's often not the easiest diagnosis to make because a presentation can be highly variable.

There's many differentials to consider and often by the time the patient presents to you, their symptoms are already gone. But essentially a TIA looks exactly like a stroke in presentation, but the symptoms resolve, they get better. That's the key. There's no tissue infarction. There's no tissue injury. So to put it really simply, TIA, there's a clot in a vessel, causes some transient symptoms, but it dissolved fast enough. The clot dissolved fast enough that it didn't lead to the death of brain tissue. I wanted to talk a little bit about the time-based TIA. So you may have heard that a TIA is described as a focal neurologic signs or symptoms lasting less than 24 hours. You may still hear about that in clinicals, your preceptor. It's something that we used to use a while. ago before we had MRI neuroimaging. The de-emphasis really came after multiple studies showed that up to

half of classically defined time-based TIAs showed brain injury on MRI. So you had these patients, their symptoms resolved in less than 24 hours. So time-based definition of a TIA, but then when they actually had an MRI done, they showed stroke on their MRI and infarct. So just be aware of that. Kind of try to get that time-based definition out of your head. Focus on the tissue-based definition of a TIA, which is lack of tissue infarction, visualized on neuroimaging, MRI, etc. Now, history and exam with the TIA, usually the symptoms are really brief. They're only going to last a few minutes, maybe up to a half hour or an hour or so. Often by the time these patients get to your office or the ER to see you, the symptoms are already

gone. So a lot of the actual exam is getting a good history. We'll talk more about the specific symptoms when we talk about stroke in a minute. But for TIA, there's really two things you should be familiar with that always seem to come up on exam questions and that's amorosis fugax and carotid brewie. So ambrosis fugax, it's a transient monocular vision loss. This one's really big. It always seems to come up on exam questions when we're talking about TIAs. There's obviously other causes, but if you see an exam question right away, be thinking of a TIA. So what happens is you have an occlusion or stenosis of the internal carotid

artery circulation. This leads to hypoporfusion of the ocular arterial circulation. So basically your carotids are clogged, your eyes aren't getting perfused, and this temporarily shuts off the lights. That's Amorosis Fugax. In the vignette, the way you'll see it described is as a curtain coming down in front of their eyes, a generalized darkening or shadow in one eye. It can last a few seconds up to around 30 minutes. If you see it on a vignette, right away be thinking of a TAA. The other thing, carotid brew, so on physical exam, you oscillate the carotids. You hear this turbulent flow through the carotids, and this is due to atherosclerotic plaque in the carotic arteries causing stenosis.

and it can be a major cause of not only just a TIA, but also an ischemic stroke. All right. Now let's talk about diagnosis. I'm going to briefly run through the diagnostic test because the thing is the workup, it's very much the same as in stroke, which I'm going to go over next in more detail. The idea is, though, with the TIA, is you start with your neuroimaging and suspect TIA patients. So MRI CT. So early brain imaging with MRI or CT is indicated for all patients with suspected TIA.

MRI does have greater sensitivity than CT, but the problem with MRI is it's time consuming, it's expensive, there's contraindications. So CTT is often used more often than MRI, but if MRI is available, it is the better test of the two. So that's your brain imaging. Then we talk about neurovascular imaging. So MRI, CCA, carotid ultrasound, it's really important in patients with the TIA to rule out an obstructive lesion in a large artery supplying the affected territory. So you image the vessels of the brain, the neck. You're looking for your source, essentially. Do you have an intracranial atherosclerotic disease? Do you have carotid stenosis? Because once you find your source, you can direct your secondary prevention at that atherosclerotic disease, or you can

intervene even with like a carotid endartorectomy, for instance. So that's really the cornerstone of your diagnostic workup for TIA. That's what I'd memorize. Your neuroimaging with CT or MRI and your neurovascular imaging, MRI, CTA, etc. You also have your ancillary test. These aren't as important, but I'm going to talk about them just so you have an idea. So ECG to rule out, say, AFIB, echo cardiogram, where you're looking for your cardiombollic source for the TIA, lab tests, rule out metabolic and hematologic causes. But the main workup is going to be your brain imaging, your neurovascular imaging. So focus on those, but be aware of the EKG, the echo, the lab testing, you rule out low blood sugar and those types of things. Now, treatment,

there's a few things that you need to know. So anti-platelet treatment, this one's really important. So aspirin or a combination of aspirin and clopidigril. This is probably the most important intervention to remember for TIA. So for almost all patients with the TIA who do not have a known cardiomabolic source, so this isn't from like a fib throwing a clot. We start with antiplatelith therapy. So this can be aspirin as monotherapy or dual antipatleth therapy, aspirin and clopidigral. You decide that depending on their risk score, which we'll talk about in a little bit.

So remember that antipatelet treatment for almost. all TIA patients. Now, if they have a cardiombolyx source, you're going to use anticoagulation. So if they have, like I said before, they have AFIB. You're going to start them on oral anticoagulation with warfarin or a direct oral anticoagulant to prevent future emboli. So if it's a cardiomabolic source, your treatment's a little bit different. And then you have your little bit more invasive treatments. So carotid endartorectomy or carotid artery stenting. So if you see a neurovascular imaging, the patient has significant carotid artery stenosis. Specifically, what we're looking for is internal

carotid artery stenosis 50 to 99%. You're going to intervene with revascularization of the carotidid is, which can be done via an endarid rectomy or crudid artery stenting. So you're looking for stenosis 50 to 99 percent. And then also in the guidelines, it says the patient should have a life expectancy of over five years. All an endaridrectomy is, is you basically cut open that carotid artery that has the stenosis in it. You pull out the plaque, you suture it back up. That's what an enderatorectomy is. Or you have the option with stenting as well. Then finally for treatment, this is important too. So your intensive risk factor management, hyperlipidemia, hypertension, diabetes, smoking cessation. So the big thing with the TIA is the patient

got a warning sign. Not everybody's going to get that lucky. So these patients need to make some significant lifestyle changes to prevent recurrence. So effectively treating their hypertension, getting started on high intensity statin therapy to lower their LDL, smoking cessation. Citation, limiting alcohol consumption, if they're diabetic, improving their glycemic control, reducing their modifiable risk factors to help reduce their future stroke risk. I don't necessarily think that'll be an exam question because it's kind of hard to ask that, but in generally you need to be aware of that because that's really important for treating these patients. So for treatment overall, the two most important things to remember is your anti-platelet treatment.

So that's aspirin clopidigrope, that's going to be most of your patients with the TIA. And then remember, reduce those modifiable risk factors. That's the cornerstone of TAA long-term management. Let's talk about one last thing for TIA. So there's something for your stroke risk called your ABCD squared. And I'm quoting up to date here, but up to date calls the ABCD Squared score a simple but suboptimal assessment tool. So the test is far from perfect, but it's still being used. You'll likely hear about it.

So let's go over what it is, what it's designed to be used for. So the ABCD Squared Score helps you determine a few things. So a patient that has a TIA is at a much higher risk for stroke in the future. So this calculator helps you to determine, one, how high the risk is for stroke in the near future. This test also helps determine how aggressive the treatment needs to be in these patients. So for instance, it helps determine whether or not we're going to use just monotherapy with just aspirin or dual antiplatelet therapy with aspirin and clopidigrope, all depending on their score. And then finally, it helps you determine is the patient that's present in your office today in the ER going to get the

full million dollar TIA workup or do they maybe just have complicated migraine? Maybe we don't need to do every diagnostic test in the book. So how high is the risk? So this calculator helps guide you with these types of things. So again, the assessment tool is known as the ABCD Square tool. Do not memorize it. Just be aware that it exists for stroke risk stratification. And then I'm going to briefly go over it. But again, I repeat, don't memorize this. Just be aware of it. So if it comes up, your preceptor mentions this, you kind of have an idea of what it is. like, oh yeah, that's the stroke risk assessment tool. So just be aware of it. I'm going to briefly go over it. So ABCD squared stands for age, 60 or over. That gives you one point.

Blood pressure, 140. Sistolic or 90 or higher diastolic. That's another point. Clinical features depending on what their features are. Unilateral weaknesses, two points. Isolated speech disturbance is one point. The duration of your TIA symptoms all gives you more or less points. And then if they have diabetes, that also gives you another point. How high their score is. is the higher risk of their two-day stroke risk, you know, and you can look all those things up if you want the specifics. Again, I don't think you need to memorize that, but just be aware of it. What do you need to know for your TIA? There's three things I would say to take away if you're going to forget everything else. Remember what a TIA is. It's a transient episode of neurologic

dysfunction caused by ischemia without acute infarction. Remember amaurosis fugax. It's probably the most important clinical manifestation. And then for treatment, I'd say the one thing you should definitely remember is your antipalate treatment with aspirin. All right. So that's your TIA. Let's move on to stroke. All right. So for stroke, there's two types of stroke. There's ischemic and hemorrhagic. So, ischemic, that's going to be your most common type, around 75 to 80% of all strokes.

And that's the one that we'll really focus on, as most of your questions are going to come from this. Hemorrhagic, like I said, it's much less common. We'll touch on that at the end. So ischemic stroke. Let's start with ischemic strokes. This is the one you need to focus on. An ischemic stroke is a sudden loss of blood circulation to an area of the brain leading to death of tissue and loss of neurologic. function. So ischemic stroke is a compromised blood vessel leading to decreased profusion,

resulting in death of brain tissue. So remember in a TIA, the clot dissolved fast enough, so there was no brain death and stroke. That's not the case. We have death of brain tissue. That's the key. Now there's two types of ischemic stroke. There's thrombotic and there's embolic. So thrombotic is going to be by far your most common. So most common type. And what happens is you have a thrombus that forms in the artery walls. And this generally happens. when you have atherosclerosis in the vessel. So you have a plaque in the vessel. Something causes the fibers cap of the plaque to shear off. So it opens up. And then once this happens, platelets come in to plug up that little fibers cap that popped off. And when that happens,

all the platelets come in to plug it up and a thrombus forms around the plaque. This leads to occlusion of the blood flow distal to this area, which leads to the stroke. Second type is embolic. So embolic means the clock came from somewhere else in the body. It traveled from a distal site, got lodged in the vessel of the brain, and included the vessel. Common cause of embolic stroke is aphib. Patient has aphib throws a clot from the heart. The clock gets lodged in the vessels of the brain, leaving the stroke. If you ever forget which is which, like is a thrombotic or embolic the one where the cloth traveling from somewhere else, the way that I remember that is embolic starts with an E. E stands for elsewhere, aka the clot came

from elsewhere in the body. Just a little tip to remember which is which. Clinical manifestations. All right, so different arteries supply blood to different parts of the brain. Different parts of the brain, as we know, control different parts of the body. So you need to have a very basic understanding of occlusion of which vessel is going to lead to a deficit in which part of the body. This is important because it's likely going to come up. I had this on an Oski question. I had an exam question. They're going to give you the patient presentation.

Maybe they'll give you a left, lower leg weakness. And then they're going to ask you which type of stroke is this. Middle cerebral, anterior anterior cerebral, et cetera. I do have a couple tricks for you to remember. this. I'm not going to list every single symptom or deficit for each different artery. I'm going to stick to just the very basics, enough for you to pick it out in a vignette. So let's talk about first our anterior cerebral artery stroke. All right, with an anterior cerebral artery stroke, there's one thing you need to be looking for, and that's contralateral involvement of the feet and legs. This is the most common area to be involved. Contrilateral, meaning if it's the left anterior cerebral artery involved, the right leg or right foot will be affected. There's obviously other possible presentation. patient's urinary continence, it's possible to have weakness in the upper extremities, but the most common, what's going to be on the vignette where you need to focus on is some kind of deficit in the lower extremities. So paralysis and sensory loss and the contralateral leg and foot. So how do you remember that? Antire cerebral artery stroke. As soon as you see anterior cerebral artery stroke, I want you to think of the first three letters, which is ant. And I want you to think of an ant. What do you do when you see an ant on the floor? You lift your leg and you step on it with your foot. interior cerebral artery stroke most commonly affects the contralateral leg and foot so when you see anterior cerebral artery stroke think of an ant on the floor lifting your leg stepping it on with your

foot most commonly affects the contral lateral leg and foot that's how you remember the most common presentation of anterior cerebral artery stroke think of an ant stepping in it with lifting up your leg stepping in it with your foot that's anterior cerebral artery stroke let's move on to middle cerebral artery stroke now middle cerebral artery stroke is the most common artery to be involved in an ischemic stroke. The way that you remember that is middle cerebral artery, MCA, also stands for most common artery. So that's how you remember the MCA, the middle cerebral artery, is the most common artery to be involved in an ischemic stroke. What you're looking for in the vignette is contralateral face and arm involvement as well as aphasia. So paralysis

and sensory loss is going to be greatest on the contralateral side of the face and the arm verse the lower extremities, and you also may see aphasia in middle cerebral artery stroke. Ephesia remember is difficulty producing or understanding speech. The way that I always remembered this was instead of remembering middle cerebral artery, M-I-D-D-L-E, instead of middle- cerebral artery, I remembered madal cerebral artery, aka M-A-D-D-L-I-D-L-I-D-L-I-D-L-I-Soreoreore stroke. So instead of middle- cerebral artery, think of mad-Maddle-Corebral artery. artery and think of somebody that's very mad. Think of like that cartoon image. Whenever you think of

like a cartoon character being mad, what do they do? Their face gets all red. They raise their arms up in the air and like shake it and then they like scream. They're like ah. So that's what I want you to think of. Middle cerebral artery. Think of mad dull cerebral artery and think of that cartoon character. His face is red and his face is red because remember it uncommonly involves the face, the contralateral side of the face. It helps remember that. And then remember the arms are up in the air. They're shaking their arms in the air remember most commonly affects the contralateral arm that's their arms in their face being red, and then they're yelling, they're screaming because they're so mad. And that helps to remember not necessarily that the patient with middle cerebral artery stroke is going to be yelling,

but it helps to remember okay, the voice is involved and then helps you remember epasias. So remember middle cerebral artery stroke, think of mad old cerebral artery stroke. Somebody's very mad, arms are up in the air, shaking them up in the air, that helps you remember the contralateral arm involvement. Their face is all red because they're angry. That helps remember the contralateral side of the face. And then they're yelling. They're screaming that helps remember the aphasia, the voice involvement. All right, so let's move on to our posterior circulation, specifically the posterior cerebral artery and the vertebro basler artery. In general, if they mention any kind of visual changes, you should be thinking posterior circulation.

I wanted to break it down a little bit further, though, each individual vessel, and we'll discuss the unique presentation scene with each. So let's start with our posterior cerebral artery stroke. So two common things in a PCA stroke that you should be aware for the exam. First one is homonymous hemianopia. So that normally spares the macula because the macula is perfused from collateral flow from the middle cerebral artery. So again, homonymous hemianopia. So what this is, you can also see this in an MCA stroke, just an FYI, but it's much more common in a PCA stroke. So it's a visual defect involving the contralateral side.

So either the two right or the two left halves of the visual fields of the eye. So basically half of the visual field is not being processed. You can just think of like half of the vision on one eye is just completely blacked out. So the visual field is blacked out on the contralateral side. That is homonymous amoeia. And remember that for your PCA stroke. They may mention that it spares the macula again because remember that's perfused from the middle cerebral artery. The second thing that you need to know for your PCA stroke is something known as Alexia without a graphia,

which means they cannot read, but they can write. So they cannot read, but they can write. So they can write out a whole story, but they can't read it back to you. And the way that I used to remember these two, let's talk about that. So the first thing is, this works much better with a visual like I have on YouTube, but I'll try to explain it. So basically, when you think of your posterior cerebral artery stroke, and when you think of like a P on its side, and if you think of a P on its side, it kind of looks like glasses. And I have a picture of this. It obviously works and makes it much easier.

But if you think of two peas on their sides, they basically look like glasses. And that always helped me to remember. I just have this visual of two peas on their sides like glasses that it involves the eyes. The homonymous hemianopia that helps me remember two pieces, glasses, posterior, it starts with the P, posterior cerebral artery. And then the second thing is Alexia without a graphia. The way that I used to remember that is posterior cerebral artery, PCA. Alexia is your personal computer assistant because Alexia sounds like alexia.

Alexa, like Amazon Alexa, and Amazon Alexa is a personal computer assistant. So Alexia is your personal computer assistant that helps me remember Alexia without a graphia. All right, so I know those aren't the best mnemonics, but that's the way that I used to remember it. Let's move on to the last thing, which is going to be our vertebral basler artery stroke. Now, the good thing about vertebral basle or artery stroke is most of the things you'll see in a vignette, most of the clinical manifestations all start with a V, and vertebral basler artery stroke also starts with a V. So as soon as you see vertebral basler artery stroke, think of all of your V clinical clinical manifestations. That's going to be vertigo, visual changes like diplopia, vomiting.

And then the last one, I kind of made this up on my own, but vibrating eyes, because nystagmus is another possible presentation of vertebral basler artery stroke. And if you ever look at nystagnus, basically the eyes are like shaking and vibrating off to the side. So that's how I remember that. Vertigo, visual changes, vomiting, vibrating eyes, vertebral, basal, artery stroke. Remember, they all start with viz. Those are your clinical manifestations. If you remember that, you'll likely be able to pick it out on a vignette. Let's talk about diagnosis.

This is obviously going to be pretty similar to the TIA workup. Going a little bit more depth, though. So when making the diagnosis in a patient with suspected stroke, the initial test, like right when they come in the door, that's going to include a finger stick blood glucose, oxygen saturation, and a non-contrast CT. Those are the main diagnostic tests to guide acute therapy. The finger stick, it's important because you want to make sure the presentation isn't due to hypoglycemia. Hypoglycemia can cause focal neurologic deficits that mimic a stroke. So you must roll

that out right away because that's really important to make sure this patient you think has a stroke doesn't just have low blood sugar. So that's important as well. All right, let's talk about your CT head non-contrast. So CT of the head non-contrast. You're going to do a CT of the head in any patient you suspect a stroke. This is your initial test of choice. Now, is a CT of the head used to make the diagnosis of an ischemic stroke? It's actually not. And that's a common misconception. The main purpose of a non-contrast CT is basically to tell us one thing. Is there blood?

Is there no blood? Is this a hemorrhagic stroke or is it not? Because if there's blood present and this is a hemorrhagic stroke, we know that reperfusion therapy with intravenous thrombolysis like TPA, it's off the table. So again, CT initial test of choice used basically to guide treatment in regards to TPA and let us know whether or not this is a hemorrhagic stroke. It can pick up some early signs of acute ischemic stroke, but really, the best way to look for acute eschemic stroke is going to be with an MRI, like I talked about

before when we were talking about our TIA. So MRI is a better test than a CT. It does a much better job at determining acute infarction. But the reason why we use CT compared to MRI more commonly is because MRI is time consuming. CT just takes a few minutes. MRI is not available at every institution. MRI has a bunch of contradictions. So basically, again, like I went over before TIA, MRI is a better test, but it's not used as often most of the time, non-concuitions. contrast CT. It's going to be your answer. It's what you'll probably use in real life. All right. So once you've done your neuroimaging, you've done a finger stick, make sure this patient's presentation isn't due to severe hypoglycemia. You have some additional tests as part of

your workup. Let's first talk about your EKG. So you get an EKG because you want to know, does this patient have an arrhythmia? Do they have a fib, a flutter, which may have been the cause of an embolic stroke? And is this patient going to be started on anticoagulation to prevent future strokes from this cardiomboleic source. Another thing you're going to use as your ancillary testing is an echo. So echo cardiogram. So with your echo, you're looking to detect cardiogenic and aortic sources of cerebral embolism. So basically you're looking, is there another bullet left in the chamber? Does this patient have another clot in the heart that could potentially lead to another stroke? Is there vegetation's on the heart valves from endocarditis, etc? So echo cardiogram is another

important test. And then neurovascular imaging like we talked about before, CTA, MRA. main thing is you want to rule out a large artery occlusion, make sure this patient isn't a candidate for something called a mechanical thrombectomy, which we'll go over in a minute. So those are your ancillary test, your E.K.G. Your neurovascular imaging. The main diagnostic test, though, focus on your non-contrast CT. That's going to be the one you get when they first come in. Treatment, acute treatment, there's two things that you need to know. TPA, that's the really big one, and then mechanical thrombectomy. All right, let's start with our thrombolytics, Altaplase, aka TPA. to place is a thrombolytic drug, it's a clobuster, and its first-line therapy for acute ischemic stroke patients if it's initiated within 4.5 hours of symptom onset. And after 4.5 hours, there's really no point. The risks are actually going to outweigh the benefit of using

TPA. There are some exceptions to the time that I'm going to go over in a minute, but most patients are going to be within that 4.5 hours of onset. Then the other thing is that you want make sure is that this patient doesn't have any contraindications to TPA. There's a whole laundry list. I wouldn't recommend memorizing them, but if you want to remember a few of the important ones, I do have a little mnemonic. So instead of remembering TPA, I want you to add on a couple letters and make it T-Pain, aka the rapper. I'm going to buy you a drink. So remember T-Pain instead of T-Pay, and remember T-Pain is 45. That's how you're used to remember some of the main contraindications for TPA. So T pain is 45. What that stands for, the T stands for trauma to the head in the last

three months. So any kind of severe head trauma in the last three months is going to be a contraindication of TPA. The P stands for platelet count less than 100,000. A stands for active internal bleeding. The I stands for intracranial hemorrhage ever in their lives. The N stands for neurosurgery in the last three months. So any kind of intracranial or intrasinal surgery. The eye and T-pane is stands for intestinal malignancy or intestinal hemorrhage in the last 21 days. The S stands for stroke. Specifically, we're talking about an ischemic stroke in the last three months. And then the 45, T-pane is 45, stands for then 4.5 hours.

Let's talk about the 4.5 hours for a minute. So there's a few warnings, not absolute contradictions to the 4.5 hour window, where you have to weigh the benefit versus risk. So in certain patients, this 4.5 hour, it's car. caution that maybe it shouldn't be 4.5, but maybe three in certain patient population. So these patients are patients that are over 80, patients that have a severe stroke classified by the NIHSS score, patients that are on oral anticoagulants, or patients that have a combination of both previous ischemic stroke and diabetes mellitis.

Then generally, it's safer to be within three hours, but not an absolute contraindication. You kind of have to weigh the benefit versus risk. So that's just something to consider. Most patients will be within that 4.5 hours. Those other patients, you just want to kind of weigh the benefit versus risk, see maybe should they be within maybe a three-hour window. Second treatment that I wanted to talk about is a mechanical thrombectomy. So mechanical thrombectomy, you have an interventional radiologist

or another type of surgeon that goes in and literally just pulls the clot out. Works great. It can be done in up to 24 hours compared to 4.5 hours, the restriction with TPA. But the problem is not every hospital is equipped to perform this type of procedure and it can only be used in patients that have a large artery occlusion in the anterior circulation. So other patients aren't going to be eligible. It is a great alternative to TPA because obviously there's way less risk with this. It's a minimally invasive procedure.

But the problem is it's not going to work with every patient. You have those exclusions that I talked about there. Okay, so those are your main treatment options. Let's talk about blood pressure for a minute because blood pressure is interesting. So in patients with an ischemic stroke, you don't touch their blood pressure unless their blood pressure is 220 over 120. So either a systolic over 220 or a diastolic over 120, or if you're giving them TPA, then you have to make sure you manage their blood pressure once it reaches a point of 185 or

higher or 110 or higher. So let's talk about that again. So blood pressure in patients with ischemic stroke, if they're getting TPA, you want their blood pressure less than or equal to 185 and diastolic blood pressure should be less than or equal to 110. That wasn't in the pneumonic, so just be aware of that as well. If they're not getting TPA, you can actually let their blood pressure ride all the way up to 220 over 120 before you have to intervene. So why is that? Well, let's think about that. Well, you have this clogged up cerebral artery. There's not much blood getting past the secluded area and profusion pressure distal to that obstructive

vessel is actually really low. So this elevation and blood pressure, it's actually helping to maintain brain profusion past this point in those ischemic areas. So most of the time, you actually don't want to turn down the pressure in an ischemic stroke. Some of your adjunct and your long-term management treatment options, let's talk about that too. So in addition to TPA, you're throwing back to me, there's an amount of interventions for schemic stroke that reduces the complications and it reduces stroke recurrence. So one, just like in our TIA, we have our anti-platelet therapy aspirin. and clopidigro. If they didn't get TPA, they need antiplatelets. General, it's going to be 325 milligrams of aspirin. If they had TPA, you have to wait at least 24 hours before you give

them anti-platelets. Also, statin therapy, this one's really important. There's clear evidence in studies that long-term invasive statin therapy is associated with a reduced risk of recurrent ischemic stroke. And then, of course, lifestyle changes, smoking cessation, exercise, weight reduction, controlling blood pressure, controlling diabetes, etc., to produce, to reduce the risk of a future stroke. All right, so that was our ischemic stroke. So let's talk a little bit about our intracranial hemorrhages, our hemorrhagic strokes. I wanted to briefly touch on some of these intracranial hemorrhages, including some of the causes of our hemorrhagic strokes. I'm just going to focus on the basics. I'm going to give you some mnemonics.

Diagnosis is pretty similar across the board for these with the CTMO's cases. Treatment is generally not going to be tested on can range from supportive measures clips and coils all the way up to craniotomy in severe cases okay so let's start with epidural hematoma so an epidural hematoma is bleeding between the skull and duramatter so it's a collection of blood that forms between your skull and the and the dora matter middle menigial artery so bleeding typically arises from the middle menedial artery and a lot of times it's associated with a temporal skull fracture particularly seen in children more common. Lucid interval.

In the vignette and epidural hematoma, they're always going to mention the patient had this loss of consciousness, then it was followed by this lucid interval where they had this transient recovery. So this lucid interval where they got a bit better for a period of time. That's the key to look out for the end of the vignette.

If you see lucid interval, right away be thinking of an epidural hematoma. On your CT, you're going to have a convex-shaped bleed, so you're going to have this bleeding that the outline or the surface This is kind of curved like the exterior of a circle or a sphere. It's hard to describe these things without visuals. So really there's three things that you have to know.

You need to remember your middle menageral artery tear. You have to remember the convex bleeding on the CT and be able to recognize that on a CT image. And then you need to remember that lucid interval. The way that you remember that is when you think of epidural hematoma. I want you to think about those first three letters in epidural hematoma. So EPI, if you rearrange those letters, you have the word, You can also, the second two letters, P-I is spelled pi like P-I, like the mathematical term pie. So however you get there, as soon as you see epidural hematoma, I want you to think of a pie.

And I want you to think of this sentence, mm-a-lulu-lemon-pie. Mm-a-a-lulu-lemon-Py. So what does that stands for? So M-M-A stands for middle meningial artery. So M-A. And then Lulu-Lemmon pie. I'm sure you've all heard of Lul-L-Lon-Lon. And that's like the athletic company that makes the leggings and stuff.

So Lulu Lemon. Lulu stands for lucid interval. So LULU, as soon as you see Lulu, think of lucid interval. That's associated with your epidural hematoma. And then lemon is actually because, and this makes sense when you look at the CT image. But if you look at a CT image, you have a convex shaped bleed. It looks exactly like the side of a lemon. And I have a picture on my YouTube channel.

You can see it. But the bleed, as soon as you see a CT image and it looks like there's like half a lemon on the CT sticking out, you'll be thinking of an epidural hematoma. So that's why I have lemon pie. So as soon as you see epidural hematoma right away be thinking of pie, epi, epi-epi-eepioreal hematoma, M.A. Lulooleum A, middle menageal artery, lucid. That's going to be your lulu. And then lemon, think of your lemon or convex shake bleed on the CT.

All right. So that is your epidural hematoma. Let's move on to our subdural hematoma. So this is bleeding that forms between the dora and the arachnoid membranes overlying the brain. Bridging veins tear. So an acute subdural hematoma is usually caused by tearing of the bridging veins located between the arachnoid membranes and the dura. So bridging veins, remember that. That's really important for subdural hematoma that will likely come up.

Now, as far as the patients are going to see this in, elderly alcoholics. So in a vignette, the patient will likely be elderly or an alcoholic who had some kind of trauma, a fall, a motor vehicle accident. The reason that we see this more commonly in this patient population is because cerebral atrophy is common in both older adults and those with the history of chronic alcohol abuse. Cerebral atrophy results in this larger space between the dural membrane and the cortical surface of the brain, and that increases tension on these bridging veins. So when these patients fall, they have a traumatic brain injury, like in an MVA, these bridges. veins, they're more susceptible to tearing because they're stretched and pulled across this greater distance. On CT, you're going to have a crescent-shaped hematoma, so crescent-shaped appearance because the bleeding follows the contour of the overlying dura. And it looks, I'm sure we've all

seen a crescent moon, just that little sliver of moon. That's what it looks like on a CT. So the way that you remember the things that you need to know for your subdural hematoma is instead of subdural, as in D-U-R, so sub-dural hematoma. I remember sub-dural hematoma, so S-U-B-D-O-O-R-all, so sub-dur-all hematoma. And then door stands for drunk, old, overpass, because an overpass is another way of saying bridge, and that helps you remember your bridging veins. And then the R in-door is the second letter in Crescent. So sub-dural hematoma, drunk-old, that's your patient's that you'll see.

in overpass, that's your bridging veins. And then Crescent, the R in Dore is the second letter in Crescent because you have a crescent shaped hematoma on CT. So that is your subdoral hematomas. Let's move on to our subarachnoid hemorrhage. So a few things you need to know about subaractnoin hemorrh. So this is going to be an extravization of blood into the subaractoid space between the Pia and the arachnoid membranes. You're bleeding within the meninges into the ventricles. Berry aneurysm rupture is going to be your most common cause. So a rupture of a berry aneurysm, which is also known as a sacular aneurysm, it's going to be your most common cause of a subaractoine hemorrhage. Presentation, this is important severe headache, aka worst headache of my life.

So subaractnoin hemorrhage has a very specific clinical presentation. I'm sure most of you have heard of this before, probably even before PA school. So a patient with a subaractnoin hemorrhage will often describe having the worst headache of their life. It's also known as a thunder clap headache because all of a sudden when they have this headache, the severe headache, It's not an insidious onset. This patient is feeling completely normal. And then all of a sudden, they have this 10 out of 10 headache in a matter of minutes. So the same way like thunder all of a sudden just hits out of nowhere, that's the severe headache.

That's also known as a thunder clap headache. Menindial symptoms. So this is really important as well because these patients may have symptoms of menigial irritation, which is also known as meningismus. So you look for nucal rigidity, photophobia, lower back pain. It can occur in as many as 80% of patients. And it's from the breakdown of blood products in the CSF, which leads to this aseptic meningitis. And then finally, the diagnosis is a little bit different with the subaractnoid, because we always talked about the CT. I talked about that earlier.

But with a patient with a subaractoid hemorrhage, you want to consider a lumbar puncture. Now, you're going to get your CT like you did, and all of your other types we went over. But in a patient with a negative CT that you really suspect may have a subarachnoid hemorrhage, you have to go a little bit further. You have to get a lumbar puncture. And this is going to be on your vignette. What you look for in the lumbar puncture is something known as xanthochromia. And it's this yellow tinged CSF, which is from Billy Rubin and the CSF indicating old blood. So if both the CT and the LP are negative, you've essentially rolled out a subarachnoid,

but you need both to say definitively in patients with a high clinical suspicion because this can be fatal, so you don't want to miss it. Intrace cerebral hemorrhage is the last one I'll go over. There's very little to know for this. There's not really much unique about it. it and most things that don't have a lot unique about them are often not tested on. But in intrastrebral hemorrhage, it's bleeding into the brain parenkima. It's the second most common cause of stroke after a schemic stroke. And then what you need to be looking for is an older patient, an older age and

hypertensive. So the risk for intrastrebral hemorrhage increases with advancing age. In addition, the most common etiology of a spontaneous intrastrebral hemorrhage is hypertension. So look out for that. So elderly patients, hypertension, those are the main ones you need to know of and then be aware of some of the other causes that are also common as well. So amyloid angiopathy, ruptured vascular malformation, but focus on hypertension. That's the most common etiology. All right, so that is stroke. Let's do five quick questions. See what you've retained. So question one. Sixty-seven-year-old male with history of hypertension and hyperlipedemia arrives to the emergency department accompanied by his wife and daughter.

His family members state he is unable to speak and he has not been able to lift his right arm. When you ask the patient to pop out his cheeks and smile, you know prominent drooping on the right side of the face. This patient likely has a stroke of which cerebral artery. So that is going to be your middle cerebral artery. So left sided specifically as we see contralateral involvement of the right upper extremities, we see contralateral involvement in the right side of the face and then aphasia. Remember your middle cerebral artery, you're mad, your maddle cerebral artery. You're raising your arms up in the air.

This patient has right arm involvement. Your face is red. This patient has drooping in the right side of the face. And then you're yelling. Remember your aphasia. This patient has trouble speaking. So middle cerebral artery, left side specifically in this patient. Question two.

63-year-old male presents today to the emergency department complaining of neck stiffness and a sudden onset, severe headache unlike any other he has had before. This past medical history includes only hypertension. While speaking to him, you notice he is squintinging his eyes. and asks if you can dim the lights. You order a CT of the head, which is negative, which additional test should be performed for the suspected diagnosis.

So that is going to be a lumbar puncture. This patient has a history of a severe headache, which he describes came on suddenly. That's our thunderclap headache. In addition, he has meningial symptoms. So photophobia, remember he's asking the doctor to turn on the lights, nukeal rigidity, that stiffness of the pain of the neck. No history of migraines.

So we should be suspecting a subaractoid hemorrhage in this patient. And you start with your non-contrast CT if that's negative, You have a high degree of suspicion for subarachnoid. You need to also order your lumbar puncture, which will be looking for again, xanthochromia, which is from the breakdown of the red blood cells in the CSF. Question three, 76-year-old male accompanied by his daughter, has been diagnosed with an acute ischemic stroke. His blood pressure is 168 over 92, oxygen saturation 96%, pulse 88, 88,

temperature 98.3. He was known to be well two hours ago when his daughter spoke to him by phone. she states he has a history of hypertension, type 2 diabetes, and celiac disease. She's very worried about him as stating this is his second Schemic stroke in the last three months. Would this patient be an ideal candidate for TPA? If not, why? So that's going to be no, because he has a history of is hechemic stroke in the last three months. Schemic stroke in the last three months is part of the exclusion criteria for IV thrombolysis TPA.

It's one of the many. Again, I don't expect you to remember all of them, but this is one of the important ones. And just remember, T-pane is 45. You can remember the important ones. Question four, which artery is the most common to be involved in an ischemic stroke? So that is going to be your middle cerebral artery. Remember middle cerebral artery, MCA, most common artery. And that's going to be in around 70% of the cases.

It's going to be your MCA that's going to be involved in an ischemic stroke. Question five, patient being treated for is greeted by the treating physician who informs him they're going to administer a medication called nicartapine into his IV to start lowering his blood pressure. is unable to receive TPA due to gastrointestinal malignancy. The blood pressure in this patient has likely exceeded what systolic and or diastolic level. So that is going to be systolic over 220 and a diastolic over 120. So patients with the schemic stroke were not going to be treated with thrombolytic therapy. We stated this patient is not.

It's not a candidate due to the GI malignancy. We don't need to worry about those BP guidelines. But this patient that's not going to be treated with TPA should not have their blood pressure treated acutely. unless the hypertension is extreme, that's going to be a systolic blood pressure over 220 and or diastolic blood pressure over 120. So remember, in these patients with ischemic stroke, the perfusion pressure distal to the obstructed vessel is low, so we need to keep that pressure high enough to maintain brain perfusion only if it's systolic over 220 and or diastolic over 120 do we treat like in this patient.

All right, so that was your stroke. Hopefully that was helpful. Thank you so much for listening. And thank you, as always, for all of the really nice comments. I do appreciate it. and good luck in PA school, your pants, your pandery, and your EORs.