Stroke
Stroke is an umbrella term, that means loss of neural tissue its not very helpful because it doesn't tell you anything about the etiology, or the management. So I'm going to start off by talking about the different types of strokes because it's obligatory, and then focus this lesson on what I call obstruction strokes, those that are amenable to IV tPA alteplace and treatable with endovascular thrombectomy. And you're going to see that it goes from high yield to low yield left to right. And it goes from high level to more detail left to right. So let's start off with the different types of strokes. Illustrating why stroke as a term is unhelpful. The usual distinction is that between hemorrhagic and ischemic and hemorrhagic stroke is a brain bleed that is going to be managed by neurosurgery and see subspecialty surgery for more details. You're certainly not going to treat a hemorrhagic stroke with TPA or thrombectomy. In fact, that is the risk of giving or using those therapies. So above this line is hemorrhagic and below this line, ischemic. The first of the ischemic strokes is global hypoperfusion. As occurs from hypotension, shock, cardiac arrest, also not treated with IV tPA, or thrombectomy. This is going to affect the watershed areas, territories between national territories the third and fourth are the ones that matter for this lesson. rupture and thrombosis. That is atherosclerosis rupture of an atherosclerotic plaque, thrombosis of the vessel and an embolism specifically, an embolism of a thrombus. Because there are other emboli, like septic embolism. Also not treated with IV tPA, or thrombectomy. So, I chose to use a term that sounds funny, but one that was not taken by word that sounds like it. Obstruction strokes. Obstruction strokes are defined by the ability to treat with IV tPA and mechanical thrombectomy. And that's what we're going to talk about in this lesson. Much like a heart attack, an obstruction stroke is an acute change, and it becomes a supply ischemia issue. Because technically, a hypoperfusion is a supply ischemia issue as well. An obstruction stroke is specifically supply ischemia caused by a focal blockage. And most of the time, the patients who get obstruction strokes are those who have cerebral vascular disease or disease of vessels leading to the brain. And so atherosclerosis is the predominating feature. There are non modifiable and modifiable risk factors for atherosclerosis and non modifiable are going to be age and sex 45 For males, 55 females and a family history. The modifiable risk factors are going to be diabetes, chronic kidney disease, and atherosclerosis somewhere else, which is why if you have atherosclerosis somewhere else, you get heart and brain prophylaxis. These three are coronary artery disease equivalents. Other ones are hypertension, dyslipidemia, obesity, and smoking tobacco. And in addition, because there's more than just rupture and thrombosis, you might have not this substrate, but have something that puts them at risk for a thrombus which is Afib. The brain, cerebellum brainstem, when there is an infarction, or stroke, there's going to be the tissue that's lost. That's the core. In addition, there's going it'd be a territory around it, that if you don't do anything, it will die. But that's tissue that can be saved. That's the penumbra. And when we intervene, what we're trying to do is save the penumbra. The core is the risk by reperfusing or giving a clot buster that you can turn that infected area into a hemorrhagic stroke. A patient with a stroke can present with any focal neurologic deficit, because an infarction can occur anywhere, and there's neural tissue, I want you though, to start thinking about only the cerebral vasculature. And what that does is gives us several vascular territories. The first distinction is anterior versus posterior, we're looking at the circle of Willis. The posterior circulation comes from the basilar artery which comes up to the circle of Willis and then bifurcates to form the two posterior cerebral arteries, the left right, then, the anterior circulation is going to be two vessels. The first is going to be the left internal carotid artery. As it gives off the branch, the left anterior cerebral artery, the left internal carotid artery becomes and continues as the left middle cerebral artery. But on the other side, it was the right internal carotid. It branches the right anterior cerebral artery in the right internal carotid continues as right middle cerebral artery. Now of course there are communicating arteries between them between the anterior cerebral arteries and between the middle and posterior cerebral arteries but because they're connecting branches, they're tiny slivers and strokes occur distal to the blockage. Once you start thinking about three territories ACA, MCA PCA, and then left versus right, right side stroke left sided symptoms. So while any focal neurologic deficit can be indicative of a stroke, you should identify three syndromes an ACA stroke, which is going to have sensory and motor deficits of the feet and legs. The middle cerebral artery stroke which is going to have sensory and motor deficits of the face, hands and tongue, which means issues with swallowing. And if it is in the dominant hemisphere, issues with speech, both formation and interpretation. And lastly, the posterior cerebral artery stroke syndrome is going to be mainly vision changes and sometimes syncope. But any focal logic deficit can trigger the stroke workup. And if the focal illogic deficit is determined to be a stroke and the stroke button is pushed, the workup includes the following. The first thing you're going to do the noncontrast CT of the head you're gonna rule out a brain bleed because if it's brain bleed, you don't follow anything else that's going to come on this board. Then you're going to get a CT angiogram. And I want you to see this together with the perfusion study, usually CT. These are going to be used in the workflow to determine thrombectomy noncoding CT head rolls out bleed, thus opening the door for TPA. And then ultimately, usually not involved in the first day. The best radiographic test is an MRI, specifically the diffusion weighted images. And as we go through the board, I'll go into more details but the treatment for stroke begins with Can you give TPA that is intravenous all to place the clot buster separately independently, but also considered the same time do you perform an endovascular thrombectomy? There's going to be some consideration for blood pressure. If you do not intervene, there's going to be permissive hypertension to 20 over 120 For the first 24 hours, versus controlling the blood pressure in order to give intervention such as delta plays. To start, you need to get it to 185 over 110. And then to continue it, it's 180 over 105. And also the anti platelet it's going to be aspirin 325, then 81, when you give it is going to be dependent on whether or not they're getting all the place. Because it increases the risk of bleeding, but get the aspirin 325 on as soon as you possibly can. This is sort of the acute management. There's other things that matter though. But I'm gonna put them in the follow up category. You're going to work on these things, even as you're considering the GPA and the endovascular back to be, et cetera. But these are things that are essentially cooking in the background. You want to consider radiology things like afib, getting telemetry, a mural thrombus, getting an echo, and working up a carotid artery stenosis, which can be achieved with the CTA, or a duplex ultrasound. functional status is very important, and you're going to achieve their understanding of their functional status by consulting specialists, physical therapy, occupational therapy and speech therapy, they'll help determine functional loss and disposition for rehab. And if it is a stroke, you want to do secondary prevention. And since most strokes are cerebral vascular disease, or atherosclerosis, you're going to do atherosclerotic treatments in any other artery, which is platelet mono therapy. Either put aspirin 81, or clopidogrel 75, a high potency statin turista and receive a statin and risk factor control. You control of blood pressure, blood glucose, rent progression of CKD and smoking cessation. And the main risk of treatment is hemorrhagic conversion. If you don't treat, you condemn them to permanent neurologic disability, if you do treat, there's the hope of recovering all of that deficit. But at the same time, there's also a risk of causing a brain bleed, which is generally worse than the initial stroke. And so the last thing before we get into the details is grading a stroke on the NIH Stroke Scale. This is a score of zero to 32. With 32 being worse, zero being no deficit, the cut off is five. The closer to 32 you get the worse you are the more likely you are to have permanent deficit and the more likely for hemorrhagic conversion. But five is the cutoff for consideration. below five is considered a non disabling stroke and five or more disabling and being disabling means it is a candidate for TPA and thrown back to me. Now you may only have a sliver of a defect, but if a singer has lost their voice that might be worth the risk. The details we're gonna get into and you're gonna see it's very individualized per patient at your level of training, crosses five is disabling is a candidate. Okay, so getting into the details, the first question is, is it a bleed? Because if it is, none of the things we're going to talk about matter. The only tests you need to give IV tPA is a non con CT of the head and the blood glucose. In reality person persons with the stroke button they get wheeled into the ER 37 People are doing things telemetry wires, IV started saline running, moving to the scanner. So the labs are going to come back by the time they're back from the scanner. But technically, all you needed these two things not hyperglycemia now to bleed can give TPA non con CT shows you two things. blood and bone are bright white. And the brain parenchyma is gray. lighter gray than the dark grey of the ventricles but certainly darker gray than bright white. See bright white where they're supposed to be brain parenchyma that's the brain bleed And this next piece sometimes screws up new learners. A hemorrhagic stroke is bright white on non con CT. When there is ischemia that is not yet infarction, the CT is going to be normal. If you do nothing, you don't intervene, and it turns into an infarction, there is a stereotyped behavior on the CT, first you're going to see is blurring of the gray white junction. Then, as cells die infarction, you're going to see evidence of cytotoxic edema. edema is fluid, and fluid is dark gray. By the time you see obvious evidence of infarction, it is way too late. This is an old infarct, and one that has an increased risk of hemorrhagic conversion. The ischemic stroke you want to intervene on is either going to be stone cold, normal word only beginning the signs of infarction. So it's not the hemorrhagic strokes or bright white and ischemic strokes or dark gray. It's what is white old infarct is dark gray. If you decided it's not a bleed, the second thing you want to ask is, can we give IV tPA. And the TPA that's available now is Ulta place. If yes, all the places given as an infusion that's in the ICU. And in a very close monitoring both of the neurologic status and of the blood pressure. In order to start all the plays, in order to reduce the risk of hemorrhage or conversion, you got to get the blood pressure below 185 over 110. And then to continue it's below one ad over 105. And what agent you use doesn't matter. All the usual antihypertensive infusions can be chosen. And you choose to give it based on the last known normal. That is, when was the last time they were known to have no neurologic dysfunction. There is going to be talk about four and a half hours versus three hours. Four and a half is what most centers go on. There's a lot of evidence of safety at three, but four and a half. And for a licensing exam, a test question if they want you to give TPA, it's going to be below three hours so that there's no question it's the right thing to do. However, modern practice involves not only time, but also imaging, whether it's the CT Nan con or perfusion study. It's getting more sophisticated, it used to be hard cut off. If you went to sleep, your last no normal was eight hours ago, you're excluded from TPA. Now as we'll talk about the end of the week, upstrokes is more of a combination of everything and how disabling and how, what's the risk, it's not a hard cut off. But for your licensing exam, it will be and so you don't give it to a TA that is a symptoms that are getting better on their own. And because of the risk of hemorrhage or conversion, you don't give it to non disabling strokes. And most importantly, you don't give it to anyone who has an exclusion criteria. And when you do this for real, there's going to be a literal checklist. So committing to memory all the reasons not to give it and their time relative to the stroke, not worth the squeeze. If a licensing exam wants you to exclude the patient from getting TPA, whatever the contraindication is, is going to be obvious and recent. But you should know some of them to have a sense for what they are. That is time. The presence of anticoagulation and a reason to have a clot that will cause them to bleed out. We just talked about the four and a half versus three hours and or evidence on imaging. If it's dark gray, chances are it's going to bleed collegues if the patients on warfarin and the INR is over 1.7 If they're on the noec DNA inhibitor, or thrombin inhibitor and they've taken it within 48 hours What if they've received therapeutic? heparin DVT prophylaxis doesn't count, if they've ever had a brain bleed, don't give it and then recent trauma or recent surgery, or GI bleed, you don't want to give the TPA because all of the clients that are associated with that will open up the patient bleed out. So give it if there's going to be recovery, it's a disabling stroke and the risk of hemorrhage conversion is low. All the place is really good at getting these small and distal clots those that are hard to reach with thrombectomy which is good because the next consideration endovascular thrombectomy. is really good at getting proximal and large. Because it involves getting the thrombectomy device into a blood vessel in the skull, it can be used only on large vessel occlusion collusions. And only in the anterior circulation is where we have good safety data. That means distal internal carotids proximal MCA ACA the decision to do thrombectomy is completely independent of TPA that can be used together or one not the other. So much to say that if a patient's at a critical access hospital without opportunity for endovascular thrombectomy, TPA can be started their patient put an ambulance and send it to a tertiary center to be evaluated for thrombectomy. You can do both. The CT angiogram is practically achieved the same time as the non con CT they're in the scanner. Push the contrast scan again. So practically speaking, non con CT and CTA get done at the same time. But in terms of the work of the reason you do the CT angiogram and you do it of the head, neck and top of the chest is to determine access. Can interventionalist get from the aorta to the occlusion? Is it practical? And the perfusion study is done. To answer is it worth it to try? Last Known normal. Six hours is the cut off. And you can use thrombectomy up to 24 hours. You're always going to use the CT angiogram to determine if there's the ability to get to the clot. Within this first six hours, you don't need the perfusion study. It is safe and worth it. Between six and 24 is how you help answer what is the risk of conversion. And how much of a number is left to save. You won't have to interpret this just know that you do need it between six and 24 hours. It's very complicated. Patients take different paths and with a number of imaging modalities, we're able to see how much brain has died, how much is left to save. And is it worth it to do the thrombectomy these things are the hyperacute decisions you're going to make. The fourth thing will be worked up in tandem that is the etiology. What caused the stroke and the events organizer I use is a question mark with the dot being the heart, heart, neck head is it cerebrovascular disease? This can be answered with the CT angiogram or Mr. angiogram is it carotid artery stenosis? We're going to talk about carotid artery stenosis in detail in the surgery subspecialty surgery Of course, you work up carotid artery stenosis with the CT angiogram. If you didn't get it, duplex ultrasound, it is known in treating carotid artery stenosis for stroke. A carotid endarterectomy is very much preferred over carotid artery stenting because it was a stroke, symptomatic enough to intervene on it, and the timing is also important. Stroke happened and they've stabilized. Surgery should be done between two days for eight hours after stabilization. But before the end of two weeks, it used to be wait at least two weeks now it's known that if there's a TIA or stroke, and there's 50%, more stenosis, you should intervene early, but not during the evolution of the stroke, increased risk of hemorrhagic conversion. And the heart is there to remind us of a couple of things. A thin human worked out up with a 24 hour telemetry that's gonna start as soon as they walk in the door. And then you're looking for thrombus whether it's mural thrombus, whether it's atrial appendage, vegetation, whatever, you look for that thrombus with an echocardiogram. And then almost never do you consider a patent foramen OMalley been framed volley found a lot of echoes, it's usually not a paradoxical stroke. However, in very specific patients, that is those who are young, and who don't have any of this, right, there's no reason for them to have a stroke, no hypercoagulable disorder, it's called cryptogenic. It might be worth it in this specific patient population, because they have so long to live to do a bubble study. That is unique, a cardiogram really takes some saline agitated, injected, you see the bubbles go from the right atrium to the left atrium almost instantly. In patients who were young with cryptogenic stroke, and to paint frame and volley on a public study, consider closure. But in general, don't go after PFOA don't do closure, but there's maybe a subset of patients where it's beneficial. All right. Even deeper, things of lower yield, but still important. You might get to the point where you ask, is it even the stroke, either the patient got better or you didn't intervene. The best chance to tell if it's a stroke or not, is an MRI. And again, diffusion weighted imaging, it takes a while to do the MRI. So generally it's the CT scans that are used for the hyper acute management. If you've had a resolution of symptoms in the MRI is negative, then you've had a transient ischemic attack. You have said both resolution the symptoms and evidence of infarct on the MRI. If the with a diagnosis of TIA is the only time you're going to see DAPT near stroke, dual antiplatelet therapy is given for 21 days to reduce the chance of this Tia becoming a full blown stroke while you work it up, find out what the cause is and fix it. If the MRI is positive, and you've had a cerebrovascular accident, and what you do about the cerebrovascular accident is dependent on whether or not you did an intervention if there's not going to be an intervention. The patient gets aspirin 325. The first day rectally, orally, however it's going in, get the aspirin on board, and you do permissive hypertension. To 2120 You're still going to do neuro checks are still likely put them in the ICU because you don't want the blood pressure to go up. And the stroke head is evolution a stroke that's done, it's over and already stabilized. That's different. If there is intervention, handling the way of TPA you're still going to do aspirin 325 score measure but you're going to do it only after 24 hours and a repeat CT of the head. If you get TPA, you get an encore on CT to make sure there's no evidence of bleed and the blood pressure is kept one at one time. Even after the alteplase is stopped Do you evaluate the patient for the risk of bleeding, but if they do bleed you have to know what to do. The good news is not hard to spot, the patient is going to have any focal neurologic deficit, yet TPA have resolution of their symptoms. And because you're doing Q one our neuro checks in the ICU, there's going to be any, it can be new, be the same one, it can be something different. Any neurologic deficit or headache, it is unlikely that they're going to read thrombose in the exact same spot. The bleed can happen anywhere generally in the spot that had infected but it can happen anywhere, and it's going to cause compressive symptoms. So any new deficit a headache or herniation syndrome, initiates diagnostic CT, non con CT to find evidence of the bleed and before they're headed to the scanner. If it's running, you stop Multiplus. When you diagnose the brain bleed, you call neurosurgery. See subspecialty surgery. And lastly, things that matter but don't warrant deep discussion. Other stuff. There was once consideration for seizure prophylaxis, especially in bleeds, do treat seizures do not prophylaxis them. The patients and two biggest risk for hemorrhagic conversion are also at biggest risk for deep vein thrombosis. That is the worst the stroke the more disabling the more bed bound they become and the more at risk for a DVT they become. And people are worried about hemorrhagic conversion in the heparin definitely do STDs and get them on low molecular weight heparin as soon as possible. Of course, if they didn't have a disabling stroke or they got better ambulation is the answer. But don't be afraid of low molecular weight heparin, not a criteria to avoid the TPA, no need to avoid low molecular weight heparin, and a patient who has received alteplase. Patients who have disabling strokes are at risk for major depressive disorder. Definitely want to screen these patients not in the hospital but later and treat them if positive. However, do not do prophylaxis. Wake up strokes. It's all about last no normal. So you went to sleep woke up with symptoms you'd have to go to whenever the time was last, generally outside the window for TPA. As we said earlier, it's both the time and the imaging. Specifically for Wake Up strokes, it's likely that the symptoms started upon waking up. And so you use not only the time, but also imaging, whether that's the proof of an infarction that's old on the CT, or perfusion imaging showing that there's a lot of brain left to save. Wake up strokes are now no longer excluded from TPA. It's a more complicated decision to get there. And lastly, there is opportunity for recovery. And the biggest gains are going to be seen in the first week. But improvements persist up to a year. The brain is plastic and so the smaller the stroke, the areas around the stroke can take over responsibilities for it. Thus, ongoing rehabilitation is meaningful. Right we talked about the types of strokes, most of which are not those that respond to all the place or thrombectomy hemorrhagic stroke hypoperfusion or any of the others. Obstruction strokes is what this lesson was about. Destruction strokes are supply ischemia, focal blockage, generally the substrate is atherosclerosis, hypertension, diabetes, CKD, dyslipidemia, obesity age, any openlogic deficit, but I want you to recognize the Enter cerebral artery as feet and legs motor sensory MCA face hands swallowing speech, motor, sensory and PCA vision changes. The workup involves nonconscious CT to rule out a bleed bleed is white dark gray is old infarct, the one you want to intervene on is normal. Then CT angiogram and perfusion study. Practically you're going to get this NomCom CT and the CT angiogram at the same time, but you use the angiogram and perfusion study to determine do you do endovascular thrombectomy? No need for the perfusion study within six hours of onset. You're going to answer the question is do I do TPA? Get them under control the blood pressure. Look for excluding criteria. Then use imaging and time to decide and have acid thrombectomy Can you get to it with using the CT angiogram? Is it worth doing perfusion study control the blood pressure based on whether they receive TPA or not? To 20 over 120 from pretension, then 185 To 110 to continue 180 to 105 Getting an antiplatelet onboard it's aspirin 325 Then at one 325 comes first day for no Ulta place our 24 After a repeat CT with Ulta place and then all the while they're gonna be working up the etiology, telemetry and echocardiogram and either a CTA or duplex ultrasound for the carotid artery stenosis. Console PT ot speech therapy, it's atherosclerosis, so treat atherosclerosis platelet monotherapy high potency stat and again control the risk factors. Is it a bleed CT? IV tPA time and imaging endovasal thrombectomy. Can you reach it CT angiogram perfusion study? Is it worth it? etiology, CTA or an MRA duplex ultrasound can replace the CTA for carotid artery stenosis. Telemetry echo bubbles study only in very specific patient populations. MRI is the best test if a TIA dat for 21 days. If they do undergo hemorrhagic conversion your low because of a headache or new focal neurologic deficit. CT stopped the TPA called neurosurgery. And then don't do seizure prophylaxis don't do depression prophylaxis. Do do DVT prophylaxis and make sure you work up patients for major depressive disorder. Wake up strokes are now no longer excluded and recovery can continue for up to a year and that is stroke.