Acute Ischemic Stroke: Etiology, Pathophysiology, Clinical Features, Diagnostics, Treatment

what's up ninja nerds in this video we're going to be talking about acute ischemic strokes before we get started it's very important for you guys to continue to support us by hitting that like button commenting down in the comment section and please subscribe also we're going to have a link right here where you guys should click we're gonna have comprehensive notes illustrations on acute ischemic stroke that'll aid in your academic understanding of this topic so let's dive into it all right so let's start talking about acute ischemic stroke particularly we have to talk about the

causes of it the etiology and then how those particular causes lead to acute ischemic stroke the pathophysiology what we're going to do is we're going to talk about the causes in different categories if you will so i like to break them down into global hypoperfusion you're not getting enough oxygen or blood flow to the brain second one is there's thrombotic causes there's a clot within a vessel that's actually occluding blood flow the third one is symbolic there was a clot somewhere where there was in the heart another blood vessel somewhere that broke off from that

location and circulated up and got stuck somewhere in the cerebral vessels the next are the other causes which aren't the super common ones and that includes vasculitis dissection and hypercoagulable states and we'll go through each one of these in great detail the first one that we have here on the docket is global hypoperfusion so these are very commonly known to lead to what's called watershed infarcts and i'll explain what that means a little bit later so first things first what are causes for global hypoperfusion the big things that you guys really want to remember here

is when someone has significant and i mean significant cardiogenic like shock or failure or cardiac arrest is kind of like the best thing to say so let's say that we talk about cardiac arrest when someone goes into cardiac arrest their heart is not pumping any blood out right if you don't pump blood out of the heart your cardiac output is pretty much null you don't perfuse your mean arterial pressure is going to be low if it's and actually maybe no and then that means that you're not going to provide oxygen and blood flow to the

cerebrum as well as other organs in that case if you don't get blood flow to the cerebrum for a prolonged period of time it can lead to ischemia if not corrected infarction so it's important to remember that cardiac arrest the whole concept behind this is that there may be a significantly low cardiac output that leads to a significantly low mean arterial pressure and if you have a very very low mean arterial pressure are you going to perfuse the brain as well their other organs no and if that happens over a long period of time ischemia

infarction can progress the other thing to think about here is what if somebody not only had let's say that they actually have blood flow to the brain but you don't have any oxygen going to the brain and so maybe someone is in severe acute respiratory failure and they're not actually ventilating putting oxygen through their lungs and into the pulmonary capillary blood to come back to the heart and then push blood up to the cerebral circulation that could be another one so acute respiratory failure if you will and the whole concept behind this is that there

is significantly low oxygen if there's significantly low oxygen that's going to lead to ischemia even if you have regular blood flow if you don't have a good oxygen carrying capacity from a severe hypoxemic hypoxia that's going to lead to ischemia and if not treated infarction okay another potential cause of global hypoperfusion besides cardiac arrest and acute respiratory failure would be something where let's say someone has a really like pretty significant carotid stenosis so they have a big fatty plaque within their internal carotid artery so here let's put i c a stenosis so they have a

really bad critical ica stenosis like let's say greater than 70 of it's like clogged with a big fat plaque and very little blood flow is getting past that you know your icas supply your anterior circulation and supply blood to the brain let's say that now you're already getting very little blood because of this bad stenosis on top of that you have low blood pressure so let's add on to that and you have something where that causes your blood pressure to drop so you develop low blood pressure okay and what would i mean by this so

for example this can happen when someone is getting their blood pressure dropped too quickly too abruptly maybe they came in with high blood pressure you gave them anti-hypertensives and tanked their pressure so low that they don't have enough pressure to push through those little little narrow stenotic areas of their carotids and so that could be a cause so too much anti-hypertension meds okay another thing is if they go into like a shock like a cardiogenic shock a septic shock something some kind of shock where they're not able to give good maps good perfusion and on

top of having low maps or low perfusion you also have a big fatty plaque that's already obstructing that perfusion that makes it worse so if someone goes into some type of shocky state and again that could be septic shock cardiogenic shock doesn't really matter either way there's a drop in blood pressure another common scenario is cardiac surgeries so sometimes this is a kind of common on your boards so think about cardiac surgeries as another potential indication so sometimes within these cardiac surgeries you can also have these events especially if you have a critical ica stenosis

all right so the next one that we want to talk about here is thrombus right so thrombotic causes of intra acute ischemic strokes so thrombotic causes here's what i want you to remember there is risk factors for thrombotic strokes and we'll talk about those in a second but what i want you to know before that is where these thrombi are prone to forming so let's talk about that so these thrombi that we're going to discuss are very common in what's called large vessels and we'll denote which ones i mean by these large vessels these large

vessels that can form thrombus a large vessel will put large vessel thrombi or thrombus is usually going to be your internal carotid artery and you know your internal carotid artery there's actually two parts of it there's ones that actually are outside of the skull the extra cranial ica and then the ones that are inside of the skull the intracranial ica so remember both of those are large vessels another one is the middle cerebral artery but particularly we got to denote that it's more particularly the proximal portion of the mc like the m1 segment not the

m2 m3s those are less common to deform these form these plaques and thrombi and the next one here is your posterior circulation so your vertebrals and your basilar arteries these can form these nice fatty plaques there from a couple different risk factors we'll discuss and then they can rupture a fish or open form thrombi on them so remember these particular large vessel thrombi particularly with these vessels the other ones are your small vessel thrombi these are not as high yield but you should remember them they're these tiny little vessels these tiny little vessels that come

off of the middle cerebral artery and supply your basal ganglia you guys know what they're called they got one heck of a name they're called the lenticulostriate arteries what are they called they're called the lenticulostriate arteries they're these tiny little vessels that feed the basal ganglia they can get a lot of plaques within them that can fish or rupture and form a thrombus or a clot there and decrease blood flow to the basal ganglia leading to strokes the other one's not as significant but you have these small pontine branches these small little pontine branches are

prone to a lot of these plaques to develop and again form thrombi leading to tiny little strokes within the ponds as well okay so these are the big things to remember thrombotic causes can affect large vessels those are the ones i really want you to remember ica extracranial intracranial proximal mca vertebral basilar small vessels that can form thrombi is lenticular stripe more significant one lesser degree small little pontine perforators we have to explain particularly now what causes these thrombite to form we didn't talk about that yet so there's particular things called risk factors so i

want to talk about primarily the risk factors that you can modify okay because that's the things that we can treat later on and those particular risk factors that can lead to thrombi is hypertension is going to be the most common cause i want you to remember that okay the second one that i want you guys to remember is diabetes so diabetes mellitus whether it be type 1 or type 2 that hyperglycemia is no bueno another one is hyperlipidemia hyperlipidemia can also lead to fatty plaques the other is smoking and last but not least as modifiable

risk factors is obesity if you guys want to know the most important and common non-modifiable risk factor is old age greater than 65 years of age as well as being male having a family history things like that and adding on to that hyperlipidemia can be acquired and it also could be genetic too so another potential non-modifiable risk factor for the most part is maybe some type of genetic hyperlipidemia that's really difficult to control with statins and other medications so again we know thrombotic causes are really due to these particular risk factors and these thrombotic vessels

are particularly these vessels now we have to explain how these risk factors lead to thrombi so what happens here these things here that we all talked about here these risk factors what they do is they lead to these atherosclerotic plaques these atherosclerotic plaques you see here within the vessels they lead to this fat little cheesy material that really accumulates here and starts to kind of cause stenosis and somewhat of an occlusion of the cerebral vessels okay what happens is that maybe because of you having some high blood pressure something like that you fissure a little

bit or rupture or break off a piece of that kind of covering of the plaque and expose the inner cheesy material of that plaque and you know this inner cheesy material it's super thrombotic crazy thrombotic little platelets love to adhere to this and that's what will happen platelets will start to adhere to that little cheesy material there and start to cause a lot of platelets to adhere here and then on top of that what starts to hold and kind of anchor down that platelet plug your fibrin right so then you get that fibrin mesh that

also forms on top of that so these risk factors lead to atherosclerotic plaques if the plaque rips fissures ruptures opens up exposes that cheesy material platelets adhere form a platelet plug fibrin covers it now look what you got you got a clot on top of the thrombus can i get blood flow if i had a neuron a little baby neuron just sitting right here waiting for oxygen hey give me oxygen no you can't get it buddy because i got this big whopping thrombus there blocking the blood flow there so that is the thrombotic causes that's

a big one right all right the next one that you guys need to remember is the embolic causes embolic causes are by far going to be the most common causes for acute ischemic strokes and they can be broken down into three different categories the first one is arterial to arterial emboli it's very simple you have two big vessels okay that are extra cranial your extracranial ica let's denote this one here this guy right here is your extracranial internal carotid artery and then this bad boy right here that you have coming up here is your aortic

arch so over here you're going to have your aortic arch what can happen is that you see these little plaques here that they have these plaques let's say that again similar concept you risk rep rupture you fissure you break off a piece of that plaque now that plaque that was stuck and adhered to the wall is now freely circulating what is that called an embolus and so now that can go up through your cerebral circulation via your ica or via your vertebral circulation and get stuck in one of these vessels lead to ischemia if not

treated infarction same concept here in the ica what happens you break off a piece of that plaque it then freely circulates as an imblus gets stuck in a further cerebral vessel important to remember so arterial to arterial emboli they're not as common but what happens is this could be due to an i c a plaque or less common it could be due to an aortic arch plaque and all that happens with these is that you have the plaque on that vessel wall the plaque that's on the vessel wall will rupture off a piece of the

plaque so you'll get a piece of plaque that's going to be freely circulating now and then that is going to get stuck in a vessel and that's going to lead to eventually if untreated and infarct to that cerebral tissue all right but boom we killed that one the next symbolic cause very very important one that you guys need to remember if you guys don't remember all of these please for the love of goodness remember the cardiac embolus causes cardiac emboli what are the big ones think about the atria think about the ventricle and then think

about the valve all right so let's write that down then so let's think about the left atria the left ventricle and then the valves so we'll put down here left atrial thrombi that form there so you form like a left atrial thrombus that occurs here somewhere in the atria and then eventually it breaks off and then freely circulates becomes an imbalance what are potential reasons that you can form a thrombus somewhere within the atria think about it what if someone has a very dilated atria and they have like this quivering kind of activity there that

they're not actually completely pushing blood out of the atria into the ventricles so there's not an effective atrial contraction because there's an arrhythmia there i'm already giving away right so atrial fibrillation we'll denote that as a fib or atrial flutter to some degree as well okay the other thing is what if there's a problem with the valve so you've got a valvular issue there and there's a cloth that's kind of forming near on the inner surface the atrial surface of that valve what could be a potential reason there what if you have a mechanical valve

that could be a potential cause so if you have a mechanical valve oh man that's that's definitely problematic what if you have like some type of rheumatic heart disease and these valves are like super prone to forming clots as well or you have infective endocarditis because you are an iv drug user or you got a dental work and you ended up with an infection that spread to the heart okay these are all potential indications of forming a left atrial thrombus anything that leads to stasis of blood flow hypercoagulability or endothelial dysfunction increases the risk of

colossus called verticos triad right what else left ventricular thrombi so this one is kind of again similar what if somebody had a really bad mi they had a significant myocardial infarction they knocked out a good chunk of that that left ventricle and it starts to become weak and then it forms like a little like little sac if you will like for example here let's say that for example when someone has a really bad mi they kind of develop this little divot here where it's easy and prone for a lot of clots to form within that

divot what could that be called a left ventricular aneurysm so if someone has what's called a left ventricular aneurysm that could definitely be a cause another thing is what if their ventricles they had a significant mi that knocked out a good chunk of their entire like anterior and lateral portion of the heart so they had a very significant maybe anterior and lateral mi that's going to cause a stasis of blood flow because that controls like what's almost 60 to 70 percent of your pumping function if you can't pump 60 to 70 of the blood out

of your left ventricle blood's going to sit there and it's going to lead to clots forming and the other thing is what if you have heart failure and you have chf so you have what's called heart failure with a reduced ejection fraction and particularly i'm talking low efs for example maybe we're talking like uh like 30 to 35 percent usually less than that is where you start having increased risk of thrawn by forming because you're not ejecting enough of the blood out of the heart okay so these are just some of the many kinds of

different causes but these are the big ones that i want you to think about how does this happen it's very simple here's a clot here that's in the left atrium for some reason that breaks off goes into the left ventricle or the clot in the left ventricle or here it's either in the atria it's on the valve these break off they come into the left ventricle or the clot from the left ventricle breaks off where does the blood from the left ventricle go up into the aorta where can it go from the aorta can go

up through the carotid system get stuck into a cerebral vessel cause ischemia if not treated infarction but boo we got it okay last embolic cause here is a very interesting one called a paradoxical embolus so this one is actually due to what's called a an atrial defect it's the basic way of saying it so this is caused by an atrial septal defect of some kind right and there's really the most common one is a pfo so a patent foramen ovale another one could be what's called an atrial septal aneurysm but by far the one that

i want you to remember here is going to be the pfo all right so what happens with these there's a hole an abnormal hole that forms between the atrial between the right atrium and the left atrium there shouldn't be a hole there what's the structure called that's usually between there the fosso valves right let's say that someone develops a a dvt right so they get a dvt which is a clot within the lower extremity that clot breaks off from one of the vessels in the deep veins of the leg within the deep veins of the

leg they eventually will come up via the ivc via the ivc they will enter into the right atrium normally what does dvt's lead to pes but if someone has a pfo or an atrial septal aneurysm these can just go right into that little hole there within the atrial septum and then come over here from the right atrium whoop and to the left atrium from the left atrium it's just as if a thrombus was forming there and now this can float down float up get stuck in the cerebral circulation and lead to an ischemic stroke so

it's important to remember these as potential causes last thing i need you guys to know is that we talked about locations for thrombotic causes the large vessels small vessels we've talked about how global hyperperfusion affects watershed reasons regions the embolic causes so embolic locations if you will are very important to remember so usually embolic locations include your mca okay so the middle cerebral artery usually it can be like the proximal stem of it for example like the m1 segment the proximal stem limit of it you can also get this in your pca okay and this

could be in the main part of the pca but here's where it gets a little bit interesting they could also branch down further into the further segments of the mca and the pca so the smaller segments so for example just as an example your mca has like m2 m3 like you know different types of segments that you could actually throw a little clawed into that thrombotic causes don't usually occur in these tiny little cortical vessels or maybe a p1 or a p2 vessel that they get stuck in so it's kind of just that kind of

example it's little small cortical vessels that are extreme small branches of these large vessels okay so very important to remember that lymbolic locations you can have to a couple of things one in these locations and also you could have a stroke an mca and a pca because when you have emboli you could have multiple emboli that go and decide to float into the mca circulation and maybe another one decides to float into the pca circulation so if you see someone with a stroke on their imaging and they got strokes all over the place potentially think

about an embolic cause okay anyway off our soap box into the other rare causes that we should just think about but don't dwell on them all right the other causes that i want you guys to be thinking about is the other rare causes so vasculitis dissection and hypercoagulable disorders you should think about it because you don't want to miss it in case it's not one of these so vasculitis so there's a couple different types right so when we talk about vasculitis it could be autoimmune okay so there's a couple different types of autoimmune vasculitises think

about takayasu's think about giants arteritis right the other thing is it could be infectious and so when we talk about infectious there's mainly three types there tuberculosis varicella zoster virus and syphilis syphilis can do really anything okay and then the last thing is if it's just what's called a primary cns vasculitis and so don't worry too much about that one that usually requires a lot more thorough evaluation but big thing is these three particular types of vasculitis these are the causes now how does vasculitis lead to a stroke i guess is a good question right

so what happens with any of these causes whether it be due to let's say we have like here we have like a pathogen of some kind or we have like antibodies from an autoimmune cause these love to attack the cerebral vessels right and what happens is when you attack these cerebral vessels it leads to inflammation that inflammation does what well sometimes it can just basically if you have a really thick inflamed vessel wall on both sides it could narrow the vessel a little bit and they kind of really narrow the lumen but another thing is

think about this when you injure endothelium because that's what you will do with this pathogens or with these antibodies what are you going to do if you injure the endothelial cells you increase the risk of clots and so if you form a clot on this like vasculitic kind of bed here what can happen you can occlude the actual blood flow beyond that and lead to some ischemia and if not treated or you know reversed infarction okay what's another cause dissection so dissection is usually kind of due to trauma so it's usually some kind of traumatic

event and this can occur you know in your vertebrals this can occur in the uh the carotids very common locations for those to occur if it's smaller ones like really really tiny ones it's usually an iatrogenic cause so for example if you're going in to retrieve a clot from somebody and you start threading that catheter down further and maybe you just accidentally like hit like the endothelial lining and tear it well then you can create a dissection and that can allow for blood to kind of track between the endothelial layer and the tiny little muscle

layer there the other one as you think about connective tissue diseases if there really is risk there the connective tissue the internal elastic lamina and the different types of tissues there are a little bit like not present or they're defective there could be a little bit more risk of you actually easily rupturing those vessels so think about things like marfan syndrome ehlers-danlos syndrome things like that but how does this happen so again it's very simple whether it's any of these things you kind of just break through that kind of vessel wall lining the endothelial lining

the tunica internal intima and allow for blood to track in through that in between the media and the intima so it can actually kind of move like side to side in this area here and if blood kind of like sits in between the tunica media and the tunica and turner and it just kind of accumulates think about it just like you're filling a balloon it's going to bub and eventually this whole thing is going to include this lining there as blood kind of fills within that little space there and that can lead to a scheme

if not corrected infarction last but not least is your hypercoagulable disorders so hypercoagulability is you increase the risk of forming clots right so there's your hypercoagulable cause within that vertos triad so when we talk about these they aren't too common and actually believe it or not they're more likely to cause venous clots than they are likely to cause arterial clots but you should still think of them because they can cause acute catastrophic arterial clots so what would be a some of the causes here i don't want you to get bogged down on them but a

couple of them include factor 5 leiden so it's called factor 5 leiden is a very common one another one is called protein c and s deficiency another one is called anti-thrombin iii deficiency another one is called the pro-thrombin gene mutation now there's so many dang things here right so pro-thrombin mutation and another one is called like anti-phospholipid syndrome so there's another one a couple extra other kind of rare ones is like polycythemia so in this kind of condition you make a little bit too many red blood cells and you can really make the blood viscous

and clot up those vessels you know if someone gets heparin is what's called heparin induced thrombocytopenia that also can lead to like this paradoxical clotting that can occur even though it doesn't make sense sometimes that's why it's called paradoxical so heparin-induced thrombocytopenia is another hyper-coagulable cause and that gives us what we need to understand the ethiology and pathophysiology of acute ischemic strokes now let's go over and briefly talk about the clinical features all right so let's talk about the clinical features involved in acute scheming stroke now we're not going to go into crazy detail because

if you guys haven't already please for the love of goodness go watch our video on stroke syndromes we thoroughly evaluate all of the neural deficits that come from acute ischemic strokes that's going to be really really important okay so please check that out we'll have a link right here to go check that out okay all right but to breeze over that because you guys have already watched that clinical feature is dependent upon the vascular territory that gets hit for example if you knock out this portion here you're the anterior cerebral artery syndrome there's particular symptoms

the mca syndrome the pca syndrome and a little bit of the combination the ica syndrome that you can get kind of a mixed mca and aca as well as the amarosis fugax that we talked about the other ones that i did want to kind of briefly talk about because we talked a little bit about them with global hypoperfusion is watershed areas and that's basically these areas where the mca and the pca meet called the mca pca watershed zone sometimes in global hypoperfusion it can knock out that area or the mca aca watershed zone can get

knocked out in global hypoperfusion we also in that video talked about the stroke syndromes involved within the brain stem remember pca syndrome can involve the midbrain the basilar artery syndrome can hit your ponds and then there's little feeders that come off of it called the ica and the superior cerebellar artery that involve the cerebellum the superior and anterior portion of the cerebellum and then your vertebral arteries are going to be involved if they get hit that can affect the portions within the medulla as well as the feeders that come off of that which include your

pica which hits that posterior and inferior portion of the cerebellum as well so again watch that video on stroke syndromes it'll give you a nice little recap of that if you guys need to to understand the clinical features now that we have a basic rundown of clinical features let's run through the really important stuff i don't want us to get bogged down in all this excessive details i want us to think about these other things but the most important thing you need to do when someone you suspect has an acute ischemic stroke is get some

imaging what imaging do you need the big thing to obtain is a stat ct scan and particularly in like a non-contrast you don't really need contrast unless you really want to we can talk about why you could get that but a stat ct scan and really what i want to do is if someone had comes in with neurodeficits or strokes you guys need to remember that strokes there's not just ischemic strokes there's hemorrhagic strokes so intracerebral hemorrhage subarachnoid hemorrhages those can also present like a stroke so it's important to remember we get a stat ct

scan to rule out that this stroke is not due to an ich or it's not due to a subarachnoid hemorrhage the second thing is if we do get the stat ct and you're good at reading ct scans you may be able to pick up something some things called hyper dense signs and these can show up as a hyper dense mca like a fresh cloth that shows up bright on the ct scan within the mca or within the basilar artery okay other things that you could look for and again this is for the vessels when someone's

in farc they have an ischemic infarct and let's say that they have these neurodeficits and it's a little bit later and that infarct has already completely like hit that entire territory and it's evolved it may show hypodensities um as the infarct okay to the tissue the cerebral tissue it may show darker than other parts on the ct scan i did say that you can get other images called a cta and we'll call that a ct angiogram which is basically a ct scan with contrast all that does is it fills up and brightens up those vessels

in the brain and the reason why you would do that is if you find out that they don't have an ich or a subarachnoid hemorrhage then what can you do if maybe if you don't pick up the hyperdense sign maybe if you're not good enough to pick up the hypodensities you push contrast through those vessels you'll see where the contrast can't get past that clot and so this will show you like a filling defect maybe or like where the occlusion is and that can key to oh that's where it is and that tells me where

it is as well is it in the mca the aca the ica so on and so forth so it's a pretty good thing to think about afterwards you shouldn't do this acutely this is the big big stuff if there's anything that you take away from the diagnosis for the love of goodness don't forget this but afterwards after they they're like they've been treated acutely later you can obtain an mri mris are good for giving you a little bit more sensitivity and definitive diagnosis of the infarcts ctas are great but mris will be very helpful and

the reason why is there's two parts to that and there's the dwi sequence and the adc sequence within the mri of the brain what the dwi shows is that if you have an ischemic infarct it'll show up bright so we call that hyper now get ready we call it hyper and hypodense for ct we call it hyperintense on an mri on the adc it shows up dark where the infarct is and it should correlate to the same location you see on the dwi and if it's dark here what do you think is going to be

here if it's bright there it's going to be dark here in the adc so hypo intense so again to recap that dwi where the infarct is it'll show up bright hyper intense look at the adc in that same area where it was hyper intense on the adc sequence it should show up dark or hypo intense okay that's our soapbox for the ct cta mri those are the big images that you need what are some of the other stuff okay once we've diagnosed this is basically we've diagnosed acute ischemic stroke at this point we could stop

and move on to the treatment but if we want to be true awesome ninjaners after we've diagnosed them and we started to acutely treat them we should start thinking about what caused their stroke because do we want them to have another stroke in the future no so we've got to find out what caused their stroke and that's where the rest of these diagnostics come into play so the next thing i would and encourage someone to do is to obtain a echo okay so to obtain what's called a trans esophageal echo that's kind of the ideal

scenario but transthoracic echo is also very valuable what does this do this gives you a look at the heart what should you think about when someone has a stroke what did i tell you is one of the most common causes embolic causes and where were those embolic ones that i told you if you don't remember it if you don't if you forget everything else please don't forget these ones cardio embolic so the echo looks at the heart and looks to see is there any atrial thrombin any ventricular thrombic is there any vegetations on the valve

so this will give me a good look do they have a fib right or i should actually be more specific do they have a left atrial thrombus that left atrial thrombus could be due to afib so do they have a left atrial thrombus and then another thing that helps us is is the atria dilated usually if the atria are dilated that's probably a good sign that this person has atrial fibrillation because dilating the atria definitely leads to atrial fibrillation but also do they have a left ventricular thrombus and another thing that's nice about this is

echoes will give your ejection fraction and look for motion wall motion abnormalities so is there any wall motion abnormalities because that may tell you that if they have a wall motion abnormality that maybe they had an infarct of that portion of the heart they had an ischemic attack there or it tells us our ejection fraction our ef and maybe this person's ef is really low and we use the example of 30 to 35 percent as we get less than 35 percent it's getting a little low maybe that's the reason for their cardio-embolic cause boom roasted

move on another thing that we can think about it just helps in aiding in the cardio-embolic cause because that's one of the most common ones to think about is getting an ekg correlate your echo with your ekg or your halter monitor or your telemetry readings think about these so if someone has on their ekg so let's say that you obtain a 12 lead ekg maybe you don't pick it up on that maybe you put them on a continuous monitor like a halter or a telemetry monitor and you pick up oh i see that they got

a-fib or oh i see that they got atrial flutter or oh i see that they got maybe like some n stemmy or maybe they got some q waves or maybe they even have a stem who knows but we kind of see oh i see some reasons of why they may have this cardio embolic cause it just aids in the diagnosis you know all right we hit these what are the other stuff that we should think about let's get into the quick little easy labs all right so remember at this point we've obtained the most important

kind of imaging which is that stat ct we got the cta we got an mri a little bit later we later on we got an echo we got our ekgs to kind of help to assist in what was the cause of the stroke but that ct scan and the cta were really the most important things and the same thing for the labs there's a really important lab that you need to get really kind of two labs really if you really want to take it to the extra mile but really important one that you cannot forget

to do is what's called a point of care glucose and all that means is you just tell the nurse hey can you go into the room use that glucometer and tell me what their glucose is the reason why is we want to know are they low glucose hypoglycemia or are they high glucose hyperglycemia the reason why is that sometimes hypoglycemia into a lesser degree hyperglycemia can present a stroke mimics got to make sure that before i give them tpa are they actually having these kind of weird symptoms because they're hypoglycemic also another important thing is

that if someone has low glucose you need to make sure that before you give them tpa you correct the glucose okay you can have hypoglycemia before you give tpa it's just a part of the requirements the other things that you'd want to do a little bit less significant i think this is a really really big one but another thing is check their inr and the reason why is you can check the other coags for example you can check pt inr and you can even check a ptt but really the most important one out of these

is your inr so if someone has an inr that's technically greater than 1.7 and let's say that they're taking warfarin we can you know we have to take that into consideration when we give tpa because if they're being anticoagulated and i give them tpa that may increase their risk of bleeding so i have to think about that so sometimes getting an inr may be helpful as a part of your coagulation studies the other thing to think about here is maybe obtaining a cbc so a cbc the only reason i think that this would be a

helpful one is to really see if the person's like bleeding maybe you don't see a visible bleed but you check their cbc and they're significantly anemic that may be an indication also if you want to take it the extra mile what was the hypercoagulable cause that's the exact opposite of anemia polycythemia that may help you in your diagnosis again not big important thing to do right away but a little bit later getting that cbc cbc for anemia is the big thing because maybe they're bleeding so that can affect tpa but polycythemia may be a diagnosis

for their cause of stroke the other thing is thrombocytopenia so do they have low platelets okay because having low platelets like less than a hundred thousand can also be somewhat of a contraindication to giving tpa so it's something to think about as well so the big things for these labs is checking to make sure they're hypoglycemic because it can cause a stroke mimic also when you give tpa you can't be hypoglycemic also coag's getting that making sure that they're not hyper having elevated inr so that they're at a high bleeding risk from maybe taking warfarin

or like a liver coagulopathy checking your cbc to look to see if they're bleeding maybe you can see some signs of anemia or low platelets thrombocytopenia because that can affect giving tpa low on the list of tests not super concerned because some don't even really consider this at all is checking a bmp and the reason why is to look to see if someone has a high creatinine or high buin the only reason why is that this may determine whether or not you give someone contrast but if you're going to give some a contrast because they

need the study to determine if they're having a stroke i think that supersedes a a you know their elevator creatinine bun so again these are some of the basic tests to think about the other ones i think that you should be aware of a little bit later after you've acutely treated them and stabilized them maybe if someone is having like a stemi or an end stemi and stuff like that they're having some signs of ischemia from the heart their heart may be leaking particular cardiac markers that could be another sign aiding in maybe a cardioembolic

cause and that would be where you want to be tracking troponins or checking ck and b but mainly the troponins and seeing if these bad boys are elevated because maybe you're leaking these types of things from the actual heart tissue because you damage the heart tissue that could potentially aid in the diagnosis the other thing that's actually really interesting was taught to me by an attending was that sometimes if someone doesn't have afib that's on their ekg on their halter you don't see like a dilated atrium you don't see any thrombi in the heart check

a tsh and the reason why is sometimes if someone has a low tsh but a high free t4 they have what's called hyperthyroidism but we'll call this thyrotoxicosis when someone has really really bad hyperthyroidism that really can stimulate the heart and put it into overdrive and guess what it can do to the heart it can cause the heart to start developing these abnormal arrhythmias and leading to what's called atrial fibrillation so another thing to be thinking about is are they hyperthyroid and maybe they do have afib pretty cool thought so that covers that the last

thing that you should think about for the quick little easy labs here actually these are the big quick easy labs the other stuff is a little bit more kind of involved takes maybe take a little bit more time if you think for example they're young so you have like a patient like less than 50 years old and they have this acute ischemic stroke um and they have had a history of multiple dvts or they had a history of multiple hormonal embolisms or things like that they're just you think that there's something weird they may have

a hyper coagulable condition do a hypercoagulable workup so what does that include oh we don't want to go through all of these do we we won't we're going to mention a couple see if you guys can remember what was the big one that i want you guys to remember factor five do they have low factor five what was the other big one i want you to remember maybe protein c and s right is that one low do they have low antithrombin three they have anti-phospholipid syndrome so on and so forth and there's other ones right

we said heparin induced thrombocytopenia polycythemia prothrombin gene mutation all of these different things that we can order but do it if you suspect it because they're younger and they're they're throwing other clots in other areas of their body particularly like venus clots the other stuff is more uh again this one's a little bit less you know this should this last kind of workup should really really be low on your differential and your work up here but this one's a kind of an important one so what's causing their plaques do you guys remember or the risk

factors hypertension you could just check their blood pressure when they're coming in if they're really high that could be a risk factor we're already going to notate that but what else what if you check their hemoglobin a1c and they have a very very nasty hemoglobin a1c and they haven't had very good blood sugar control maybe that keys into that and them having diabetes and you need to think about that as the reason why they're developing these big old fatty plaques in their vessels and then when it ruptures and fissures it leads to those thrombotic causes

other things is check a lipid panel do they have a lipid panel like one of our engineer co-founders rob where they have elevated ldls or they have maybe low hdl which again they're not able to pull those plaques from the vessels and sometimes there could be a hereditary causes so maybe throw in like a lipoprotein a as a potential cause for like a hereditary thing but i think these are some of the big things so do they smoke are they obese things like that those are other risk factors but these are the ones you can

get quick little labs on some people even order like homocysteine levels as well i think these are the big things to think about hemoglobin a1c lipid panel for the other stuff is your vasculitis and this is why i was saying this should really be low i don't really want you guys to spend a lot of time to be honest if you guys want to skip to the next part of the video i'm fine with that but vasculitis is really low on your differential the ways that you can kind of go about checking this one is

start off is it autoimmune maybe you just start off with an esr and a crp and those are elevated okay well maybe i'll take it to the next level and i'll check check like some anchors and i'll do like an a a panel and stuff like that for autoimmune causes maybe you suspect infectious causes so maybe you go ahead and you go straight for you know they have a abnormal like sexual history and you want to check for syphilis vdrl rpr maybe you want to check for varicella zoster virus because they had a history of

shingles or something like that so you check a pcr of their varicella zoster maybe you suspect tb so you can go through all the tb tests maybe check a chest x-ray maybe you check the quantifier on assay and then primary cns vasculitis sometimes this requires a way more thorough work up and sometimes you really kind of need like a biopsy really to get to that point so again you can see why not too big but we need to be thorough here at engineer and really think about the causes but big things to take away stat

ct point of care glucose coags cbc are the big big diagnostic studies the other stuff will aid in thinking about the cause of the acute ischemic stroke let's hit treatment all right engineers with the last part of the lecture which is very important so we got to start acutely treating this patient who's coming in with some neural deficits okay we got that ct scan we found no bleed we suspected maybe a hyperdense sign we got the cta we found the occlusion now we got to start treating this person we made sure that they don't have

an ich we made sure that they don't have a subarachnoid hemorrhage we made sure that their glucose wasn't low and make sure that their coags were fine make sure they're not bleeding on their kind of labs there what do we got to do give them the tpa but when we give tpa what should be the reason why we give the tp let's think about this mechanistically tpa is kind of an activator of plasminogen what the heck is plasminogen so plasminogen is like a little enzyme right that's present kind of circulating in the blood and what

tpa does is it helps to convert plasminogen into an enzyme called plasmin and what plasmin does is it acts on the fibrin within the actual kind of blood clot and starts shiatsuing that fibrin and breaking down the clot to bust the clot up so again what is tpa really doing tpa is stimulating this process here so we know now how the tpa works because it activates plasminogen into plasmin plasmin breaks down the fibrin within the fibrin mesh helping to dissolve the clot now we have to think about indications when do you give the tpa all

right so indications to be giving tpa include having a neuro deficit we didn't talk about this but whenever you're doing a neuroexam and you're thinking about the person's clinical features you utilize what's called the nih stroke scale the nih ss and you're basically giving them particular scores on what deficits they have present the sometimes the guidelines say you need like an nih stroke scale score greater than four to really be able to get tpa but if you have neuro deficits that's really what i want you to know you have neuro deficits but nih stroke scale

scores sometimes greater than 4 is preferred so we look for them to really have neuro deficits i wouldn't get too caught up on the score okay second thing that you need is you need them to have no ich and subarachnoid hemorrhage on their ct scan their non-contrast ct scan that we had that's an important thing and the next most important thing is that you know their last known well this can sometimes be a little bit difficult and a little tough you need to know when was the patient normal they didn't have those neural deficits i

need to know the exact time the reason why is that there's two kind of categories for this there's less than three hours and generally within this we give the tpa no problem hit him with the tpa baby but if it's like three to four and a half hours we have to be a little bit more stringent with the tpa and so we need them to have no history of diabetes or a previous stroke we need them to be greater than 18 years old we need them to have this is where the nih stroke sales score

kind of comes in and they night stroke scale score of less than 25 and we need if they do have an infarct that's already kind of showing there it's less than one-third of the mca territory or if there's ischemia of that it's less than one-third of the mca territory if you meet all this criteria as well as the following above give them the tpa baby okay so that's the big things now there is a lot of other contraindications we kind of blew past them again making sure that their glucose isn't low if there is hypoglycemia

give them glucose making sure that they don't have any active bleeding from anywhere in their body whether it's in the brain whether it's from the gi tract whether it's from any other traumatic incident make sure that they're not bleeding because if they're bleeding you can't give them tpa another thing is blood pressure we'll talk about blood pressure control you prefer to give someone tpa with a blood pressure less than there's two different goals the a lot of the goals will say less than 185 over 110 some will even say 180 over 105. just go with

the less than 185 over 110 that's kind of like the standard number that would be another reason oh it's their blood pressure's too high lower it and then give them the tpa so there's a lot of contraindications to this but i think the biggest things to think about is do they have neural deficits do they have not have a bleed in their brain or any other blood coming from any other part of the body their last known well is well documented here give them the tpa okay i think that's the big thing to think about

here when you give tpa it's important to remember that when you give tpa the dosage is actually kind of a standard dosage like 0.9 milligrams per kilogram you give 10 percent as a bolus and then you get the remaining over like the remaining hour the other thing is again post tpa will talk about this blood pressure goals are very important but after someone has had like 24 hours post tpa we need them to obtain a ct scan because we want to make sure that they didn't like convert or we just want to have a good

a good idea of what their scan looks like after they stroked okay and then they probably need to go to an icu so they can have good monitoring and frequent neuro checks okay what is another treatment option so let's say that someone comes in they have neurodeficits they don't have an ich or subarachnoid hemorrhage on their ct scan they last known well um is a little bit beyond four and a half hours maybe we're at six hours so a mechanical thrombectomy is very interesting so basically what happens is this is an interventional radiology type of

procedure and what they do is they take and they feed like a catheter up here and they can do two things one is they can use this catheter and they can suck out that clot or they can put like a stent in there and then retrieve the clot so it's one of the other so either what's called a stent retriever or like an aspiration device but either way when someone's getting a mechanical thrombectomy the indications are pretty much relatively the same as the giving tpa we need neurodeficits to be present we also need no ich

or subarachnoid hemorrhage but we can also change our time frame okay there's two parts of the timeframe i'll explain what i mean if you're in six to 24 hours post should like last known well so six to 24 hours from the last known well you still fit within the window of getting a mechanical thrombectomy it is preferred that you try to get there less than six hours or at the six hour mark because time is tissue the longer you wait the more tissues being damaged and the less penumbra is present to be salvaged what the

what the heck is a penumbra zac you never talked about this so whenever you have ischemia you can infarct a particular like a core of the brain tissue around that core there may be still tissue that's ischemic and it's getting ready to infarct but if you give them tpa or if you do a thrombectomy and suck that clot out you can save the tissue that's really suffering right now and it's ischemic and hasn't infarcted yet so we prefer to keep it at that six hour range if you start pushing towards these longer times getting towards

like close to the 24 12 24 hour range we want to make sure and is there a salvageable penumbra such a weird name right and so this is where sometimes you can use what's called like um different types of perfusion scans like ct perfusion mr profusions sometimes people even use it called like aspect scores and things like that but we're using this to determine is there a number that we can even save the other reason that we would do a mechanical thrombectomy is someone can get a tp they can get tpa they have a stroke

but do they have a large vessel occlusion what the heck does that mean is there a clot in the mca the ica or in the vertebrobasilar system if there is a clot in any of those you can give tpa and do a mechanical thrombectomy okay so i think we have a pretty good idea now for mechanical thrombectomy tpa these are acute treatments get these things done and then some of the other stuff we can kind of figure out okay what's the next thing i kind of contradicted myself right tpa definitely mechanical thermoback to be very

important but always whenever you're treating somebody it's always abc's airway breathing circulation so if someone's coming in and they don't have a good airway you should obviously control their airway so airway breathing circulation first but you still want to give the tpa this is the acute treatment so when we talk about airway what do we mean if someone has a decreasing level of consciousness because of their stroke or because they aspirated because they have significant dysphagia from their stroke then what do we need to consider so if they have like a gcs that's less than

or equal to eight that may be an indication to intubate them and then responsively mechanically ventilate the patient to make sure that we're controlling their airway okay so very important to think about that the other really really big one is blood pressure control you need to have good blood pressure control and people who have strokes particularly post tpa or even if there's no intervention at all so let's write that down so if someone is status post tpa remember when they give tpa you have to be less than 185 over 110 after tpa usually for the

first 24 hours after tpa you particularly there's again different goals i'm going to write them both down um in an institution dependent like 185 over 110 is kind of one of the goals there 185 over 110 some will even say 180 over 105. the difference there is very minimal really but when we talk about these you want to have your blood pressure less than this after tpa for at least 24 hours after those 24 hours you can modulate it and it's modifiable there but how do we base this the next thing is what if there

is no tpa so they don't get tpa then what okay well then i just got to keep their blood pressure less than 220 systolic blood pressure i want that less than 220. that's good enough for me right if we start getting higher that's not that's not too great so less than 220 is the goal for no tpa if they're getting tpa 185 over 110 or 1 less than 185 over 105. how do we control their blood pressure there's so many drugs that you can give the preferable one within the first 24 hours because you get

the most control of it is nicardipine because it can come as an infusion and you get very good blood pressure control with this other options include iv labata law very relatively quick acting and then the other one is like hydralazine okay a little bit more variable in its effect but these are some of the drugs and there's other ones too like analoprolate also known as vasotec those are some other drugs that you can give but you want to control their blood pressure if they get tpa or if they don't get tpa based upon these goals

so we got airway we got breathing and circulation we gave them the emergent tpa or mechanical thrombectomy all the other stuff now is not as significant in the acute scenario it's things to prevent and help afterwards okay what's the next thing anticoagulation anticoagulation is important if somebody has a reason to be anticoagulated like they have a cardioembolic cause so cardio and violent causes are very important things to remember so if someone has a cardio embolic source of their acute ischemic stroke for example and we'll just throw in a couple of these maybe they have afib

maybe they have atrial flutter maybe they have a left ventricular aneurysm whatever they have one of these reasons and they need to be anticoagulated what do you do acutely if they're still like in the hospital you can you you know you get a little bit better like titration control with a heparin infusion but once you kind of like get a good control of their anticoagulation you can put them on something that's called a doac and this is like for example just put one of them like a pixaban another one is rivaroxaban or you can put

them on warfarin it kind of just depends on their cause like if someone has a mechanical valve or they have some type of valvular problem usually warfarin's a little bit more preferred over something like a pick savanna rivaroxaban but this is our anticoagulation now big thing to think about please don't forget this for the love of goodness if they have a huge mca infarct so let's say that they don't get tp they don't get ir and they end up like infarcting like their entire mca territory for the love of goodness don't give them anticoagulation even

if they have like really bad afib you can convert that infarct into a hemorrhagic bleed you don't want to do that so you might have to hold anticoagulation for a while and again you don't anticoagulate them immediately after they stroke you have to give it some time after they've gotten tpa or their intervention and then after they're stable you can give anticoagulation the next thing that was on the list was that paradoxical causes right so you have a paradoxical embolus due to like a pfo or an atrial septal aneurysm pfo is the big one i

want you guys to remember so with pfos sometimes there's like this this question of should we anticoagulate them sometimes you can give warfarin or aspirin one of the other there's actually there was a study that showed no superiority of warfarin over aspirin in these scenarios but what seems to be relatively helpful is doing what's called a percutaneous closure percutaneous closure of that pfo so that you don't have any risk so if they had a hole here and a hole there right a hole between the atria just take a little little thing there close it up

so that you can't allow for any clot to freely circulate there so that's something to think about there now we hit our embolic causes right for the most part the anticoagulation for cardioembolic and then the paradoxical one carotid revascularization is kind of revisiting those thrombotic causes so remember we talked about the internal carotid artery so this right here is our so this is our c c a common carotid artery and then this is going to branch into your e c a and into your ica where do we say that plaques like to form at that

bifurcation where you go into the ica or eca right there is where you start to form these like nice little plaques right now whenever someone has really bad stenosis like really really bad stenosis so what am i talking about so let's say that they had a stroke so let's actually write that down let's say that they have carotid stenosis and there's two things one is they had a stroke they had an acute ischemic stroke because of that and on top of that they have stenosis that is greater than like 70 sometimes people even do it

less than 70 but the best thing is if they have stenosis that's greater than 70 percent this they definitely need intervention and the two primary interventions to be thinking about here is if someone gets what's called a c e a i'm not going to spell this out it's just too long of a name carotid endarterectomy what does that what does that mean you basically cut the plaque out and that's all you're really doing you're just going in there and cutting that plaque off of the vessel wall the other one is going to be what's called

a carotid artery stent and this one's actually pretty simple i can actually spell this one out for you so carotid artery stent all you do is you take a catheter move this thing through the vessel and then put a balloon in there to really you know push that actual plaque down and then put a stent in there and that helps to control that as well now here's the big thing to think about what someone has carotid stenosis right really really bad one a critical stenosis like greater than 70 they have a stroke so they're symptomatic

they should get one of these procedures and there's different protocols and reasons why someone should get one over the other we'll talk about that in a video dedicated to carotid stenosis but for right now what i want you guys to think about is if someone gets like a stent placed there you need to be thinking about do they need to get antithrombotics so sometimes if they either are not getting treated or they're getting a stent sometimes you need to put them on anti platelet agents and we'll talk about that with the like some of the

risk factor modifications really but anti-platelet agents is a big thing to think about anti-platelets especially if they get stents there okay or if they don't get a stent they don't get any intervention sometimes you should give them anti-platelets because what is the cause a thrombus if that ruptures fissures what's going to happen they're going to form a thrombosis on top of them give them anti-platelets to prevent those platelets from adhering to the actual area where that a thrombogenic cheesy core is okay that hits the big stuff there the other stuff is playing into this kind

of like plaque stuff right so if someone has these this atherosclerotic cardiovascular disease and they have all these like nasty plaques within their vessel wall what do we say with the risk factors that we can actually treat and modify i know it's right here hypertension how do you treat hypertension i shouldn't have to write this down better blood pressure control how do you treat diabetes mellitus better insulin better control of their anti-diabetic medications hyperlipidemia put them on statins we'll write this one down here because this one is important to remember this one is statins okay

statins are very important you should remember there's a torvastatin or substation they need to be on high intensity statins smoking stop smoking obesity lose weight and anti-platelets going back to that anti-thrombotic thing think about aspirin or clopidogryl sometimes if they're having carotid artery stents or they have like a coronary artery disease with stents sometimes they'll put them on dual antiplatelets aspirin and clopidogrel but again thinking about these kinds of things is going to help you from preventing a future stroke remember airway breathing circulation acute treatment with tp or mechanical thrombectomy now let's talk about potential

complications that you have to be thinking about to treat all right so what else do we got to think about when we're treating someone for an acute aesthetic stroke well if you give them tpa if they're within the window you give them the tpa later on when they're in the icu and they're getting their neuro checks and they're getting all their post tps you know kind of criteria that you have to follow all of a sudden maybe they were moving their right arm they're not moving it anymore they work kind of communicating with you they're

not communicating within you anymore get a stat ct scan maybe that infarct from you giving them tpa convert it into a bleed and so get a ct scan so right away you get a ct scan you see this big whopping bleed in their brain now what do i do besides go to the bathroom and change your underwear you need to start getting quick interventions if they're on tpa still getting it stop the tpa infusion and if they're fibrinogen you should quickly throw in a fibrinogen level the reason why is if someone has low fibrinogen you

should reverse their tpa especially if it's like less than 180 if you really want to go there i'll write it down less than 180. milligrams per dl you should reverse it so how do we reverse tpa what are the things that we give the baseline stuff that you need to remember is you have to give what's called txa tranexamic acid you give it as one gram bolus and then another gram a little bit later and then the other one is cryoprecipitate okay some people may only give the txa but cryoprecipitate has fibrinogen in it so

that may help as well and sometimes the protocols even call for platelet transfusions so you can even consider that as well but these are the big things let's say you give someone tpa the neuroscience icu nurse comes and says hey zach they're really hypoxic now or hey they're having difficulty breathing or they're like their face is like swollen they look like shrek what do i do i need to think about angioedema this can happen post tpa not super common but think about it so if you have them you go in there and you see old

trekkie there what do you do you give them antihistamines because it's a histamine reaction right so give them antihistamines i just butchered the antihistamine so you give me antihistamines like benadryl right also known as diphenhydramine and you should also give them famotidine with that even though it's not an h1ra it's an h2ra but it's involved in the histamine reaction you should also give them iv steroids things like methylprednisolone 100 milligrams and have a very very low threshold to intubate them the reason why is think about it if there's so much edema around that larynx really

really edematous and you decide i think they're fine i don't need to intubate them you come back in later after you gave them the iv steroids and histamines and it's still swollen you're like oh crap we got to intubate and now you got to stick a tube through that big old fat larynx now that's all swollen are you going to be able to maybe get that tube down probably not so have a very low threshold to intubate the person as well next thing is cerebral edema icps this is common when you have very large hemispheric

infarcts so this is a little bit more common when you see someone with a very large hemispheric infarct primarily the most common one you're going to think about here is that mca and farc so they get a big old mca infarct they knock out that entire mca division what happens is they develop something called cytotoxic edema and that cytotoxic edema is basically the cells dying and just rupturing and spilling out water out of those cells and then what happens is as this kind of like swells over here it starts pushing starts uh the side the

brain tissue from this side to the opposite side and so you start getting something called midline shift across like this area where the septum pellucidum is you need to treat cerebral edema accordingly so what are the different types of treatment options there's neurosurgical options so surgery includes what's called a hemi craniectomy and what that means is you pop the skull off here and allow for that swollen brain to herniate through that bone flap rather than down on their brain stem the other thing is medical management so medications that you can use and these are kind

of temporizing measures they're not going to be effective like long term but they can't temporize the patient and this is things where you make them salty baby remember that make them salty so what are the different things that you can use there's what's called three percent hypertonic saline there's 23.4 percent hypertonic saline and then there's that good old mannitol the probably the most like significant one to remember though is this 23.4 percent the whole thing with these two the hypertonic salines is you want to approach a very salty goal so if you're trying to make

them salty aim for a salty goal of like 150 to 155 why am i saying all this here's some normal healthy tissue cells so this brain swelling right there's what's called the mondo kelly doctrine where you have blood csf and brain inside of the skull whenever one of those increases it starts to increase the intracranial pressure so shrink one of them what can i shrink shrink the brain tissue so how do i do that i come over here and make the blood really salty and yank water out of these normal healthy tissue cells to decrease

the size of the entire brain that's what we do when we give these kinds of medications okay seizures is another common complication that can arise whenever someone develops a infarct but it has to be really important to remember this it's usually a cortical infarct so it happens has to happen really kind of like near the cortex when someone has a cortical infarct that's where the cell bodies of the neurons are the gray matter of the cerebral cortex and what's really important to remember is that those neurons if they become injured or damaged later this can

become a focus of like an epileptic like source really and it can lead to things like seizures like focal seizures or maybe seizures that become like they're focal and then they generalize so generalized seizures what the heck does that mean they go full on tonic clonic like you know thrashing or they have what's called non-convulsive status epilepticus where they don't actually have any kind of really convulsions they have decreased mental status and gaze deviations just abnormal behavior so whenever you think about that you need to treat these patients with anti-epileptic drugs and there's so many

different types there or maybe you need to be a little bit more aggressive and you need these like really significant sedative medications so what do i mean by that sedative medications are anesthetic medications so things like propofol for example just mentioning one of them but aed's there's so many of these there's a valproade there's phosphonatoin phenytoin levator levitarazetam there's so many of them we're not going to talk about them right now but treat those if that happens so aspiration pneumonia this can happen because if someone has an infarct right within the brain tissue so let's

say here's the brain tissue you know nerves are going to be coming down here to control swallowing right so there's a lot of nerves that control swallowing and if you infarct a part of the brain tissue that is involved in that they can develop something called dysphagia and the problem with that is that if you infarct the ability to swallow what if you have a lot of these secretions that are kind of sitting here in the oral cavity usually what you want to happen is those to go down the esophagus but if you have difficulty

being able to swallow where am i those secretions may be where they go right down here into that larynx down into the lungs and start brewing and pneumonia that's where we don't want that to go right so what do we do to prevent this kind of thing from you know someone having dysphagia from their stroke one of the big things to do is to get what's called a speech evaluation to make sure that they actually have the ability to swallow if they don't pass their speech evaluation they maybe need a food like a feeding tube

so that you can feed them another way that we kind of bypass this kind of event happening and so maybe you have to put in like a peg tube or a feeding tube like a dob hover like a nasogastric tube now if they develop an infection though because of that aspiration what do you treat that with you give them antibiotics right broad special antibiotics until you get cultures back and figure out what the cause of it is and then narrow it down ninja nerds you beast we made it through acute ischemic stroke all right ninja

nerds in this monster of a video we talk about acute ischemic strokes i really really hope that it made sense and i hope that you guys did enjoy it and learn a lot from it all right ninja nerds thank you and as always until next time [Music] you