Intracerebral Hemorrhage (ICH): Etiology, Pathophysiology, Clinical Features, Diagnostics, Treatment

what's up ninja nerds in this video we're gonna be talking about intracerebral hemorrhage before we get started please continue to support us if you do really enjoy this video you like it it helps support us by hitting that like button commenting down in the comment section and most importantly subscribing all right ninja nerds let's get into it iron engineers let's start off talking about the etiology and pathophysiology of intracerebral hemorrhage so what causes it how do these particular causes lead to a bleed within the brain so first thing by far one of the most common causes of intracerebral hemorrhage is going to be hypertension so when we talk about intracerebral hemorrhage it's important to remember that there's actually kind of two subtypes there's a non-traumatic interest representation that's what we're primarily going to focus on in this lecture and there's also a traumatic interest reprehemous it's pretty obvious what the etiology is if it's traumatic there's some type of blunt force trauma penetrating trauma that's present let's focus on the non-traumatic causes that most common one being hypertension so how does hypertension cause interest reproduction it's really straightforward if someone has high blood pressure right really sustained high blood pressures that's going to exert a lot of forces on these blood vessel walls as you exert a lot of force on these blood vessel walls enough in particular areas of the brain where the vessels may be a little bit more weak or a little bit more susceptible to rupturing guess what happens these vessels will then rupture as a result of this maybe acute or sustained or very intensely elevated blood pressure and this can lead to these vessels rupturing and blood spilling out of these into the brain tissue and so that is an important thing to remember so very extremely elevated blood pressure can lead to bleeds within the brain via simple shear forces and stress on those vessel walls what's really important though is where these bleeds most commonly occur that's what i want you guys to remember the most common locations for hypertensive bleeds include first your basal ganglia so what are the different components of the basal ganglia so your internal capsule your putamen your globus politus which makes up the lentiform nucleus the caudate nucleus the thalamus a lot of those structures are components of your basal ganglia what's the next one the next one is here in your pons your pons is a very very important area and it is very prone to hypertensive bleeds as well another one is the cerebellum the cerebellum is extremely sensitive and has a very high risk of bleeds that are secondary to hypertension and the least common one is going to be bleeds that are near the actual cortex so bleeds that are near the cortex so cortical we also call this low bar and we say low bar because we're talking about is this the frontal lobe the parietal lobe the occipital lobe the temporal lobe where this bleed is occurring so by far most common locations include basal ganglia ponds cerebellum and low bar with low bar being the least likely another big thing to remember is that this is by far going to be one of the most common causes and patients usually less than 60 years of age okay boom roasted let's move on to the next one the next one is called cerebral amyloid angiopathy you're probably what the heck this is actually interesting so when you hear amyloid you probably think oh is this like dementia stuff yeah it definitely is amyloid proteins or amyloid beta peptides and what happens here here we're going to have let's say that here we have here's kind of like your proteins right so we're going to call this a beta amyloid peptide what happens is these beta amyloid peptides they deposit into the walls of these cerebral blood vessels near the cortex near the cortex they deposit into these blood vessels and when they deposit into the blood vessels they kind of weaken the blood vessels so imagine here i have a bunch of these little beta amyloid plaques that are developing within the blood vessel this weakens the blood vessel makes them very fragile and prone to little micro hemorrhages and small little ruptures where where is the most common location bleeds at the cortex i need you guys to remember that so where are these bleeds most common most common location for these are cortical bleeds and this is going to be low bar bleeds now when we talk about cortex this could be it's important to remember this one these bleeds we already concluded the cerebellum as a separate one when we talk about cerebral amyloid angiopathy this can happen in the cerebrum and it can happen in the cerebellum okay so very very important thing to remember here last but not least this is the most common cause of ich in patients greater than 60 years of age so most common when you're greater than 60 years of age especially if they have previous history of ich also there is a a component of dementia related to this so if the person also has maybe some dementia present take that into consideration as well so there is a dementia component present okay all right great so we have hypertension most common generally the most common cause especially in those who are usually like less than 60 or any age really but the most common cause greater than 60 cerebral amyloid angiopathy the next one that i want you guys to be thinking about here is coagulopathies so this is a big one there's a lot of drugs and medications that are involved in this so coagulopathy we particularly see this with anticoagulation or some type of measure that we'll talk about anti-thrombotic anti-platelet agents anticoagulants um fiber analytic medications we'll talk about all these but what happens is this coagulopathy usually you put someone on anticoagulants right so they're on anticoagulants let's just say here as the example anticoagulants is basically you're decreasing the coagulation cascade right so when you give someone anticoagulation you're decreasing the coagulation cascade if you will and if you decrease the coagulation cascade that is a component of what hemostasis so you decrease hemostasis let's say that someone has little micro tears just from the daily wear and tear on those blood vessels so they develop like little you know tiny little micro tears which is pretty common in individuals usually what happens is we have particular measures like hemostasis and the coagulation cascade that help to plug up those little holes but if someone's an anticoagulation especially if they're on super therapeutic levels this anticoagulants are going to affect them being able to properly plug up those holes and lead to hemorrhages or a little seeping of blood out of these blood vessels that's really important to remember so coagulopathy is another one and there's a bunch of different types of medications some that we'll talk about are going to be warfarin it's going to be a big one the other one is going to be heparin we'll talk about doax we'll talk about tpa and there's even the uh the last one which could be aspirin and clopidogrel okay which are your anti-platelet agents okay the last thing that you want to think about is if it's not anti-quack related is there a cirrhosis or liver injury or there is there acute liver failure chronic liver failure where they can't make pro coagulants so they can't make the coagulation protein so you're giving drugs that are inhibiting the pro-coagulants or the liver is not making the pro-coagulants so think about that as well if someone has liver failure that could lead to what a decrease in the pro coagulants okay so here we'll put that like this a decrease in pro coagulants like which ones factors two factor seven factor nine vector ten uh protein c protein has all of those and the same kind of process here occurs okay and so then you can get bleeds related to that so we have hypertension we have cerebral amyloid angiopathy and we have coagulopathies either related to anticoagulants or severe liver failure let's move on to the next one all right so what's another potential cause of interest rebel hemorrhage hemorrhagic transformation is a big one to be thinking about so we got hypertension we got cerebral amyloid angiopathy we got coagulopathies hemorrhagic transformation what could this be do too think about it simply someone had an ischemic stroke they had an ischemic stroke maybe they got tpa and what happened is they converted that ischemic infarct into a hemorrhagic infarct or they had an ischemic stroke they didn't get any intervention but they had such a big infarct that we re-perfused that area maybe by pushing their blood pressure up too high and we just converted that ischemic infarct into a hemorrhagic infarct by bleeding into that infarcted bed either way there's a transformation of an ischemic infarct into a hemorrhage so what does this usually do to someone had an ischemic stroke so we'll put an ischemic infarct and what happened is is that converted into an ich what could be the reasons for that one is maybe they got tpa and that tpa just was enough to kind of again weaken the integrity of those blood vessels enough that they couldn't actually uh sustain that and they cause a bleed right so it could just be from the tpa that caused that because again tpa is designed to be able to make the blood thin to break up clots and so they have a high bleeding risk when you give a jug like that the other thing is that they develop a re-perfusion injury so what happens is let's say that maybe they didn't get any tpa um or maybe they did get tpa and you just don't control their blood pressure as well and so what happens is the blood pressure is maybe a little bit too high and you push too much blood into an area where the vessels are already weak because of an underlying ischemia infarction will explain how that happens but the blood vessel is just really weak and you push the blood pressure a little bit too high into those weak vessels they rupture and cause a bleed into that infarcted bed so how does this kind of mechanism happen so really what happens is let's say here i have some neurons here so here i'm going to have maybe some neurons and these neurons become damaged because they had an ischemic infarct there what happens is they release a lot of inflammation this basically leads to a lot of inflammation right because of their injury there's a lot of inflammation and that inflammation causes like a lot of neutrophils to come to the area causes a lot of reactive oxygen species and free radicals and stuff like that to come to the area and that inflammation starts really acting and wreaking havoc on these vessel walls and so those vessel walls just become relatively weak then you give someone tpa after they've had an ischemic infarct so the ischemic infarct right of these neurons lead to inflammation lots of inflammation weakens the vessels you push the blood pressure a little bit too high into those weak vessels or you give them tpa and it just again causes more weakening of the vessels those little bad boys rupture and you bleed into that infarcted bed and that's where you can get a hemorrhagic transformation okay so we got hypertension cerebral amyloid we got coagulopathy we got hemorrhagic transformation the next one is malignancy there's some type of metastatic cause not usually usually the most common cause of these ichs is a metastatic cause rather than primary so malignancy you got to know where are these actual where these cancer cells coming from they started somewhere they got into the brain they broke down the blood-brain barrier i'll explain what that means which caused blood to seep into these areas around the tumor what are the tumors that you have to be thinking about that were the original source that spread to the brain big one papillary thyroid cancer so that's one so which one is it the first one here is going to be thinking about thyroid so papillary thyroid cancer is the first one the other one is lung cancer particularly small cell lung cancer the other one is renal cell carcinoma so renal cell carcinoma is another one the other one is melanoma melanoma melanoma's a son of a gun right so this one can really be a nasty type of cancer that can spread and then the last one here is choreocarcinoma so let's actually write this one out choreo carcinoma okay so this can definitely plague like the uterus and reproductive organs as well so what happens is these cancers right some of the cancer cells spread from these different primary locations and what they do is they actually infiltrate the brain tissue right so they're going to infiltrate the brain tissue when they infiltrate the brain tissue what they do is they disrupt the blood-brain barrier you guys remember what the blood-brain barrier is made up of you get the endothelial cells then you get the basal lamina and then what are those little glial cells the astrocytes right well what these guys do is they really damage and disrupt that blood-brain barrier and so now you don't have a proper blood-brain barrier and what is the blood-brain barrier designed to do control things leaving the blood and coming into the neural tissues if you don't have good control guess what's going to happen some things are going to leave the blood and enter into those neural tissues so you start kind of destroying that blood-brain barrier and blood can start seeping in around so imagine here would be the mass that came from one of these cancers there would be kind of a bleed that would surround that mass okay because of it disrupting the blood-brain barrier so what do these things do let's actually write that down they disrupt the blood brain barrier okay so that gives us the next cause which is malignancy let's move on the next one is cerebral venous sinus thrombosis that's a heck of a name also abbreviated cvst cerebral venous sinus thrombosis it's basically a dvt of the brain that's literally what it is so you have different types of veins in the brain right so you have like what's called the superior sagittal sinus the inferior sagittal sinus the transverse the sigmoid the straight sinus all of these crazy sinuses someone can develop a clot a venous clot within these veins and it can literally lead to a bleed i'll explain how that happens but generally what is a cerebral venous sinus thrombosis it is a clot in the uh the venous system of the brain okay how does this now okay let's talk about one more thing before that so we know it's a clot in the venous system what in the heck causes the clot in the venous system it's really any kind of like hypercoagulable condition whether that hypercoagulability so hyper coagulable condition so it's any kind of hypercoagulable condition this hypercoagulability it could be due to an underlying like inherited disorder so we're not going to write down all of them but for example this could be things like factor 5 leiden this could be things like anti-phospholipid syndrome this could be things like anti-thrombin 3 deficiency and so on and so forth but it could also be acquired things so sometimes if people are on oral contraceptives or if they're pregnant these are all things that can also kind of make them a little bit more hyper coagulable and at risk for forming clots within that venous system in the brain now let's talk about how these clots actually do lead to basically a hemorrhage so if you imagine here imagine there's like this arterial thing that's eventually feeding into this vein here right so they say that there's kind of like you'll have a capillary network but let's say that blood will come in through the artery and then leave out through the vein right if you have a clot that's obstructing the venous drainage sometimes what can happen is the blood is actually going to have to like so you might not be able to get blood past this and so what happens is this may plump up the vessels that are proximal to wherever that clot is in the venous system and these suckers may plump up a little bit enough that they can rupture and then what can happen is they can bleed into the brain tissue but it's usually near the edges of the brain tissue like near the edges of the cortex so usually whenever you see like a cerebral venous sinus thrombosis it produces a very characteristic bleed that's usually near the edges of the cortex so again that's kind of the basic way that cerebral venous sinus thrombosis leads to an ich or a basically an intracerebral hemorrhage there's a clot in the venous system venous congestion can lead to hemorrhaging of the venous system some of the arterial system there and bleeds near the cortical regions and it's usually due to some type of hypercoagulable type of condition there okay so that's cerebral venous sinus thrombosis so we got hypertension we got cerebral amyloid we got coagulopathy we have a hemorrhagic transformation malignancy dvt of the brain the last one is vascular abnormalities you see this in younger individuals so first things first is you see this in younger patients and this is actually a vascular malformation referred to as an avm so let's write this above it so that we know that this is in younger patients what is this thing here called this is called an a v m an arteriovenous malformation so this is present in younger individuals and it's basically this abnormal arterial capillary network so there's not a complete formation of that micro circulation so what happens is usually you have an arterial it branches into your capillaries goes into the capillary bed jane's into a venule and then to a vein this one you kind of have like this abnormal connection between the arterial and the vein and it creates like this abnormal ball or nitis that's just super susceptible to if there's any kind of increase in pressure it's going to rupture and so that can cause a bleed there as well so usually this is a kind of more commonly in younger individuals and it's basically an abnormality within their vascular channels okay the other abnormality here is something i want you guys to think about and this is what's called a microtic aneurysm so you can have ichs that can be due to aneurysms in general and there so if we had for example let's say that we had an aneurysm there's different types of aneurysms you can have saccular aneurysms fusiform aneurysms and microtic aneurysms so this is one that i really want you to remember we'll talk about aneurysms those rupturing and what's called subarachnoid hemorrhages aneurysmal subarachnoid hemorrhages but for right now the big aneurysm that i want you to remember that can cause ich is called a mycotic aneurysm and what happens with mycotic aneurysm is someone may have what's called infective endocarditis so what do we call this infective we'll put i endocarditis and in infective endocarditis they develop these kind of like vegetations like these little septic vegetations on the valves and what happens is these little vegetations can break off from the left atrium left ventricle into the aortic system go up through the carotid system so now follow this bad boy through into this actual cerebral circulation and go here where it kind of nestles into these vessels and what happens is this is basically little septic structures these little infective little vegetations that get lodged into the cerebral vessels and cause damage to those vessels and cause them to balloon up and then if someone has kind of this little ballooning and weakening of the blood vessel what can happen if maybe there's just a little brief rise in pressure these little bad boys can rupture and lead to bleeding into the brain tissue which is going to cause their ich okay and so usually mycotic aneurysms are secondary to an effective endocarditis so now let's talk about the clinical features of intracerebral hemorrhage so the first one and probably one of the most common symptoms is especially if there's a cortical bleed right or a low bar bleed they can present with a headache the reason why is if the bleed's near the cortex under the lobe like it's involving particularly a cortical region or a low bar region it's close to the meninges and they can agitate the meninges you know the meninges are supplied by cranial nerves like the trigeminal nerve and so that can send signals via the sensory fibers of the trigeminal nerve to the trigeminal nucleus up via the trigeminal thalamus tract and cause this pain basically within the head region so headache is a very common clinical manifestation or clinical feature that can be seen in individuals with ich especially if the bleed is cortical or low bar and again that mechanism is via agitation of the meninges activation of the sensory fibers of particular cranial nerves activating the trigeminal thalamic tract now we're not going to go through all of the different types of neurodeficits because we talk about that in stroke syndromes because it's the same kind of concept if someone has a bleed in a particular area where they also maybe comparatively had an ischemic stroke they can present somewhat similar so if you guys want to know more about these focal neural deficits go check out our video we're gonna have a link up here to go watch the stroke syndromes okay but they will have different types of focal neural deficits maybe aphasia maybe weakness on one side maybe gaze preferences maybe sensory loss so on and so forth okay the next particular clinical feature that i want you guys to be aware of is that these individuals can also have high intracranial pressure whenever you have a bleed there's something called the monroe kelly doctrine where inside of the skull the skull is kind of a fixed thing it doesn't really expand you have brain blood and csf if you have more of one of those things it's going to increase the space now crowded within that skull and the pressure inside of the cranium is going to increase if we got a lot of blood more blood than we should have inside of that skull it's going to increase the intracranial pressure so you can develop symptoms from this bleed okay so this is going to cause high intracranial pressure what are some of the symptoms of high intracranial pressure they're relatively generic but one of the big ones is nausea and vomiting okay and this may be due to like a stimulation or compression of things in like the the chemo trigger zone the area post stream which is in the brain stem so maybe some brainstem compression this also could lead to kind of a decreasing level of consciousness so l-o-c so maybe like an altered mental status they're really becoming sleepy you're trying to say hey you know wake up wake up wake up when you're trying to examine them and they're just not waking up as well the other thing is they can start to have cranial nerve deficits what do i mean maybe their pupils are starting to become ones larger than the other maybe it's not reactive to light maybe you're testing their corner reflexes they're not reacting maybe you're trying to see if they have a cough reflex and it's not there and the other thing is they may start showing signs of posturing so you have the different things like the cerebral posturing decorticate posturing that may become a little bit more evident with high intracranial pressures and the last thing is you guys already know this there's a particular triad called the cushing's triad what is the cushing's triad i want you guys to remember that it's a high bp it is a low heart rate and it's a low respiratory rate or irregular respirations as well okay that gives us the big clinical features now that we understand how interest reprehensive can present to us let's now talk about how we diagnose it so first thing the most important if you only had one kind of test that you could use to determine if someone has an ich it's a image a stat ct scan of the head so by far the most important thing to obtain is a stat ct of the head so stat ct generally like a non-contrast ct scan of the head and this will help you to identify if there is a bleed present so i can tell you if there's an ich it can tell you if there's any midline shift what does that mean so some of the brain so from this bleed you start having some of the brain tissue pushing to the opposite side maybe causing like herniation syndromes to be present you also want to note is there any hydrocephalus so sometimes when you get a lot these bleeds you can get hydrocephalus because some of the blood from here starts extending into the ventricles and so they get what's called hydrocephalus due to ivh or intraventricular hemorrhage so that's one thing we could do you could get a ct angio if you want to look for like a vascular like a cta mra something like that if you're looking for vascular abnormalities so that could be another image you could obtain is maybe a cta or an mra if you're looking for particular types of like vascular causes like you know anomalies of some form for example you're maybe looking for a mycotic aneurysm maybe you're looking for maybe some type of avm or something like that you can also do like angiography as well but the cta is a pretty quick one relatively easy especially if you're getting a ct scan the other thing that you can do is an mri this is actually a relatively significant thing that you should be able to obtain after you've you know pretty much you got the first diagnosis with the ct later on after you stabilize them you can get an mri and an mri also mrv you should add on okay and we'll explain why in a second mri what i like to look for is i look at pretty much like one sequence really i look at the swi so the swi is a particular sequence that tells me if there's any like iron or blood that's kind of sitting in a particular area of the brain and so an swi will come up basically showing like these like black spots really so it'll show like little black holes if you will that tell me that there was blood there's blood in this area there is a hemorrhage in this area and that is important if you're trying to really see okay do they have a hemorrhage you can obviously tell that from a ct scan but remember i told you there was a particular thing called cerebral amyloid angiopathy you want to get a swi because if someone has tons and i mean tons and tons and tons of little bleeds all over their cortex and their cerebellum and they're older greater than 60 what do you think that could be indicative of cerebral amyloid angiopathy and the other thing we said is an mrv why is an mrv going to be helpful for me what was that condition so we have an mri it just kind of gives us a look at the brain no contrast there's no you're not filling the vessels cta mra you can fill the arteries to look at those to see if there's any abnormalities there mrv is you're feeling contrast through the cerebral veins what was one of the etiologies as a potential cause of hemorrhage cerebral venous sinus thrombosis right so look there to find any cerebral venous sinus thrombosis all right i think that's a pretty good start when you all right let's move on we got our imaging the big imaging next thing we found an ich we've looked for some vascular anomalies to help us to find the cause we did like some other mri studies to look to see if there is an ich cerebro amyloid cvst all that good stuff what was another particular cause malignancy so sometimes what i may do is i can obviously maybe get an ultrasound of the thyroid i could do that to look to see if there's any mass there but the common biggest thing to look for here is to do what's called a ct you can do what's called a ct of the chest can help you to look at the the lungs to look to see if there is any particular like lung mass there you can get a ct and this is all one order so for example you would get a ct at the chest abdomen and of the pelvis and if you see as you know a mass within the lungs that could be a cause a mass within the kidneys that could be a cause a mass within the uterus or other reproductive organs that could be a cause of their malignancy so if they have a bleed and they're imaging and you go and you find a mass somewhere else that it metastasized from you now have a cause or primary source and again check their skin from melanoma you know palpate and do ultrasound for the thyroid as well so i think that's a pretty good kind of test for that what else could we do we could get an echo you get an echo why why do i want to get an echo zach so remember we said infective endocarditis you form little infective vegetations on those valves they bust off they get stuck in a cerebral vessel cause a mycotic aneurysm look for that do an echo so we can do a trans thoracic echo or we can do a trans-esophageal echo and what we're looking for is is there any kind of like septic emboli that's present and we'll talk later because the other thing that we can add on to help an aiding in our diagnosis is did the person have a fever so what could add to that did they have a fever do they have any iv drug abuse and then check the blood cultures because usually blood cultures are positive okay and then if they have a murmur do they have a new murmur that you're whenever you're auscultating them so i think this is kind of the big stuff to think about is images ct you can get arterial images venous images a big thing is mri looking at that swi you suspect malignancy ct of the chest abdomen pelvis you suspect a septic emboli infective endocarditis echo with the other associated blood cultures that we'll talk about in a second let's talk about some labs that can help us so now we got our images let's talk about some labs that we'd want to order and what these things could tell us and help aiding and our diagnosis and maybe more specifically the etiology the causes of this diagnosis because really the main thing about the diagnosis we get a ct that's going to tell us what we need figuring out the etiology of the ich is kind of going to be the extra things that we can get from other images and labs so labs what do we do well it's important because you want to be holistic you want to see cbc right start off with a cbc why a cbc because this can tell you if the person has any severe anemia right anemia if they're maybe they're bleeding a lot do they have any thrombo cytopenia so basically do they have any very low platelets that's another thing that could be important from this as well another lab that i would obtain is a cmp so a cmp is going to be helpful it'll tell you remember we said that one of the things could be coagulopathies so coagulopathy could be due to the anticoagulation we'd have to ask them about their history do you guys take any anticoagulation but the other thing about a cmp is it's going to tell us is there any elevation in their ast their alt they're alphos and maybe this is the reason why they have a coagulopathy because they have severe liver failure and they're not making pro coagulants so something to think about the other thing is for the most part it shouldn't always determine whether or not you add contrast in a study if you need the contrast it's important for the study you should get it but sometimes a cmp is helpful because it tells you about your renal function tells you if there's any elevated bun tells you if there's any elevated creatinine because that could come into play whenever you're going to give them contrast but again don't get too bogged down in that okay the other thing is coags we should check a pt we should check up ptt and we should check an inr right these are things that are important because if someone has maybe an elevated ptt we got to figure out why do they have an elevated ptt or if they have an elevated inr why do they have an elevated inr is it due to a coagulopathy or is it due because they're taking warfarin do they have an elevated ptt because they're on heparin and they were just on too much heparin and that's why they bled thinking about those potential causes thinking about these from the labs can be helpful in aiding in what the cause is and how you're going to treat them okay so we got a cbc we got a cmp we got some coags there it's also important remember we were talking about someone having infective endocarditis and also there's another risk factor we didn't talk about some of the risk factors but there is risk factors for ich any time someone is on any kind of like drug like cocaine any methamphetamines alcohol itself really is a risk factor for bleeds to happen so it's important to also obtain a urine drug screen and someone for a couple reasons one it's important just to make sure that there is no thing uh there's nothing that you're missing as potential risk factors that way if they do recover and they do recover from this bleed you can try to prevent them from developing a bleed in the future by addressing these issues like avoiding things like methamphetamines and and so on and so forth so basically looking for any tox stuff so for example are they on cocaine because that is a very important risk factor was it positive for alcohol because that's another important risk factor okay the other thing that you should always obtain it's a quick little easy test is a point of care glucose a point of care glucose is a quick little easy thing to look to see if they have any hypoglycemia so point of care glucose it's important to obtain to look to see if they have any low glucose hypoglycemia or high glucose hyperglycemia okay what else a blood culture that's oh that's another reason you should get a urine drug screen because what if somebody is an iv drug abuser and you don't actually know it because it's not someone that's not told to you or the person's basically non-responsive and they can't tell you that they use drugs or you just can't find it maybe on the top screen they're positive for heroin that could maybe lead you to think oh do they have infective endocarditis maybe that's the cause for their bleed and the same time you should also get blood cultures especially if they were fibril especially if they have a new murmur especially if your echoes suggest potentially some vegetations there so definitely doing something like that like obtaining blood cultures may be helpful to rule out infective endocarditis as a cause for those septic emboli the other thing is remember we said that cerebral venous sinus thrombosis we may be able to pick it up from the mrv but the thing that we got to think about is what was the cause of someone developing cerebral venous sinus thrombosis hypercoagulable conditions right and so maybe doing a hypercoagulable workup may be somewhat beneficial in this scenario as well so checking for hypercoagulable work up and we are not going to go through all of these what you can do is we'll mention a couple you can check the factor 5 levels you can check their anti-thrombin 3 levels you can check their protein c and s and there's so many other ones that you can check we won't go through all of these but checking some of those levels to look to see is there hypercoagulable condition that is causing them to form a basically a dvt in the brain and that's why they developed a bleed okay so that can aid in your diagnosis as well particularly the causes the other thing and kind of the last thing we didn't really mention it as causes because they're really really really relatively rare and it kind of goes along with the vascular malformations the two big ones that i wanted you to know was the avms and the kind of like aneurysms like mycotic aneurysms barrier aneurysms but another really low in the differential it should really be low is any kind of cause of vasculitis so sometimes vasculitis are also susceptible to the blood vessels kind of rupturing as well so is there you know a suspected vasculitis and so again autoimmune cause what can you do for that one check an esr check a crp check an anchor checking a a so on and so forth we can do there right is it infectious how do i determine if it's infectious well think about the causes look for tb look for syphilis look for varicella zoster virus right so you can do like the interferon assays you can check the vdrl rpr you can check a pcr for vzv and then the other one is is there like a primary cns vasculitis that is the cause of this one and this actually would somewhat require a biopsy to kind of confirm that so these are things to be thinking about of how you're going to go about diagnosing ich and figuring out the causes of ich i hope this helps now let's move on to the treatment all right ninja so now let's talk about the treatment of intracerebral hemorrhage so this is the biggest you know really really kind of like you need to know this stuff you have to have this part down so first thing when someone has a really big whopping ich that has midline shift and increased intracranial pressures there's always the concern can they protect their airway especially if they have this declining level of consciousness and they're not able to kind of like follow commands and you know really they aren't completely oriented to person place time and things like that so you should have a very low threshold for intubating somebody especially if they have a very very large bleed with a declining mental status so airway in every emergent situation abcs right so airway breathing circulation is always kind of the best steps here so why is an airway a problem well think about this you have all these respiratory centers here in your brain stem right pons medulla and these basically are important because the nerves that are coming from here via the intercostal nerves and the phrenic nerve supply muscles that help to aid in breathing via your respiratory rate and your respiratory depth if there is compression because there's high icps maybe you have a bleed right here and this bleed is causing some some compression of that brain stem that's going to injure these areas and decrease your ability to generate respiratory you know breaths particularly rates and and depth so important to think about that so when someone has these large bleeds you need to protect their airway how do we do that have a low threshold for intubation so sometimes intubation may be a very important thing to do in these patients and when you intubate them and you put them on a mechanical ventilator there's different types of modes there's all these different types of modes we'll cover this in another lecture but maybe cmv maybe asv so continuous mechanical ventilation adaptive support ventilation but the biggest thing is that you want to control their ability to breathe and so we set particular things in settings here so you set like your fio2 you set your peep and these two things control your oxygen saturation you can also control your tidal volume you control your respiratory rates which helps you to determine your co2 concentrations so very important thing to be thinking about whenever you're intubating somebody also when you're intubating somebody it helps because high intracranial pressures you want to control their breathing and you also want to try to sedate these patients a little bit because these sedation meds also help to lower basal metabolic rates lower the actual oxygen consumption of the brain so sometimes intubation allows for someone to be able to be sedated because you can protect their airway so allowing for sedation is also helpful so things like propofol or versed also known as midazolam let's write that down here midazolam can be helpful to kind of really sedate the patient keep them comfortable and help to control their uh potentially elevated intracranial pressures so protecting their airway with mechanical ventilation is very important what's the next thing so after we've stabilized the airway it's kind of and they're in their breathing it's circulation so blood pressure is a huge thing it is definitely one of the big most most important things to control so when someone has a bleed you want to prevent the expansion of that already present bleed so keeping a blood pressure goal systolic blood pressure less than 160 millimeters of mercury sometimes it can be even if you want to have a more stringent goal less than 140 millimeters of mercury but we're controlling their blood pressure with particular antihypertensives so things that are going to be like what well the best thing to be thinking about is nicardipine nocardipine you have very good control over blood pressure other things are going to be things like libado law so the beta law is a a so nocartipine is a calcium channel blocker labatal is a beta blocker you also can use things like enalapril okay and actually it's called a naloprenet and this is also iv so all of these are these iv forms you want to use iv forms and when someone's this sick so that you get very good better blood pressure control also there's other drugs that you can give sometimes you can even give furosemide especially if someone is actually volume overloaded that may also be helpful in iv form as well so either way controlling the blood pressure by whatever means you can particularly be these iv methods and then later you can use oral antihypertensives so anti hypertension meds once you kind of get them a little bit more stable so you have a plethora of options ace inhibitors arbs you have also your dihydropyridine calcium channel blockers like amlodipine nephetipine you have other drugs like beta blockers so beta blockers things like labetalol or other options and then you even have alpha 2 agonists things like clonidine so it's important to get good control of their blood pressure less than 160 and again you can use iv drugs and then once able oral antihypertensive medications for prolonged blood pressure control is also very important okay what else so control their airway intubate mechanically ventilate sedate blood pressure control less than 160 more stringent goals say even less than 140. the next thing is do they have a coagulopathy so reversal of an underlying coagulopathy is extremely high yield so think about the anticoagulation right so first thing are they taking a particular medication like warfarin if they're taking warfarin you need to know the reversal agent what is the reversal agent for warfarin well the first thing is you need to give iv vitamin k generally you give this like 10 so you're going to give 10 milligrams of iv vitamin k the other thing that you give is what's called p c c prothrombin complex concentrate and it's important to remember that this is based on the inr we're not going to go and write all of these down i'll quickly list like for example if the inr is between 1.5 to 1.9 you get 15 units per kg if it's 2 to 4 you give 25 units per kg if it's 4 to 6 you get 35 units per kg and if it's greater than 6 inr you give 50 units per kg of pcc another option is that there's another other option of what's called f f p fresh frozen plasma but generally pcc is preferred so warfarin what do you do again remember you reverse it with iv vitamin k and pcc based upon their inr the next one is heparin so if someone is on a heparin infusion particularly they have a hepa infusion within the past three hours you can give a drug called protamine sulfate and protamine sulfate you can give this there's a particular conversion factor for this one generally it's like a 50 milligram kind of max that you can give and that can reverse the heparin especially if they've kind of finished this within the past or they've been on it with at least the past three hours the next one is your do axe and there's a couple different types of doax or no wax if you want to know them but the big thing to remember is apixaban and rivaroxaban and there's also a doxaband but these two drugs you reverse these there is no like specific reversal agent as compared to these other ones up here but we've seen somewhat of a decent efficacy reversing these with pcc so prothrombin complex concentrate and again this one ranges as well this can go anywhere from 20 to 50 units per kg but that's one option the other option is there is somewhat of a newer drug there's not a ton of evidence to support its use but indexing that alpha is believed to be a drug that can reverse these dough acts as well there's one more dough act that you have to remember because it does have a very specific type of reversal agent so the other one is called debigatran so uh apixaban rivaroxaban if you really want to remember these are 10a inhibitors factor 10a inhibitors de bigatran is a factor 2a inhibitor or also known as a thrombin inhibitor and this one you actually reverse with a very specific like a monoclonal antibody called ioda richisumab okay so warfarin reverse with iv vitamin k pcc or ffp heparin protamine sulfate dox if it's the 10a inhibitors it's pcc or indexing at alpha if it's the bigatran which is a thrombin inhibitor it's idler kisumab alright what about tpa well if you guys watched our ischemic stroke lecture you already know what we do for tpa if they're still getting the tpa infusion you stop the tpa infusion but you give them what's called tran examic acid also known as txa a one gram bolus and then maybe another gram eight hours later you can also give what's called cryo precipitate maybe up to 10 units plus or minus platelets that can be transfused in these patients okay the next thing is if there wasn't enough already is if someone is on anti-platelet agents now here's the last thing with these anti-platelet uh platelet agents include which ones so this is your aspirin which is a pretty common one in clopidogrel all right which is also known as plavix so these two agents there's actually not a lot of evidence to support the use of platelet transfusions okay the only time where platelet transfusions may be utilized is if the person is getting a neurosurgical intervention so neurosurgical interventions you actually want to have platelets that are greater than a hundred thousand so if they have less than a hundred thousand they've been on anti-platelet agents you can consider giving like a platelet transfusion another option besides this is also there's what's called a ddavp which is also known as desmopressin so this is another option to give in someone who is anti-platelet agents big big big thing to remember there's not a lot of evidence to suggest actually using these things if someone took an anti-platelet agent and they developed a bleed it's mainly the ones above that we would reverse this one not a lot of evidence to support okay we've so we've supported their airway we've controlled their blood pressure we've reversed the coagulopathy now what let's control the cerebral edema and elevated intracranial pressures all right so now let's talk about how we treat cerebral edema elevated intracranial pressure that's seen in ichs so whenever someone has an ich they have probably a big midline shift a big old pocket of blood it's important to know kind of the treatment measures that we would go about within this patient so what do we do so the first things you really really need to know is is sometimes neurosurgical intervention is the big big thing here um intervention so what are these neurosurgical interventions that we could employ for this patient so the first thing is so sometimes if you have a pretty decent sized bleed right sometimes what we we don't want is we don't want this bleed causing so much midline shift that you start trying to push parts of the brain tissue downwards onto the brainstem causing herniation so what we do is is take the bone off where that bleed maybe is near that area so that the brain can actually swell outside of that actual calvaria bone flap area and not downwards onto the brain stem so we can do kind of a decompressive craney okay now if the bleed is super tentorial there's been a couple different trials like the stitch trials that look at blood within the super tintorial so above the tentorium up in the this portion of the cerebrum versus impertintorial kind of like posterior fossa where the cerebellum and brainstem is there's not a lot of support to say you can you know evacuate and pull out blood within the super tentorial region but sometimes it's still done there's a lot more support for saying pull and evacuate out the blood that is actually within the infra-tintorial region because it's such a small space and it can smash on the brain stem and cause really significant hydrocephalus so sometimes not only you can decompress them but you can sometimes evacuate some of that actual blood the other thing is if this this blood extends into those little cavities right so you have the different cavities let's just say i draw a cavity here this cavity let's just say is the fourth ventricle some of that blood coming from that hemorrhage can extend into these ventricles and block up the flow of cerebral spinal fluid and so that that cerebrospinal fluid can actually back up and start causing those ventricles to balloon up and that can cause hydrocephalus so sometimes putting in what's called an external ventricular drain and evd can help with the hydrocephalus so this is important in situations with ivh intraventricular hemorrhage and hydro the next thing is we can employ particular medical management so there's some medical kind of like interventions that we can employ for these patients so one of the things that we can do is we can make the blood really salty and just dehydrate the crap out of the normal healthy brain tissue to just decrease the amount of space inside of the brain and so we can use different types of salty kind of measures so we can use drugs like three percent hypertonic saline or 23.4 percent hypertonic saline and really make the blood salty maybe you approach a sodium goal of like 150 to 155 and that's your goal to make the blood so salty that you draw water out of maybe this area here where there's healthy brain tissue and an intact blood brand barrier another medication that we can give besides like these hypertonic salines is there's also the option of mannitol okay so mannitol generally like it's a 25 solution and this comes in various different doses that you can give but mannitol is another drug that you can give to kind of again dehydrate the brain pulling some of the fluid away from this healthy brain tissues to kind of dehydrate the brain a little bit so these are kind of the basic measurements that you can utilize for cerebral edema and increase icp the next thing that i want us to talk about here is seizures man oh man bleeds that are near the cortex are very high risk for seizures so these bleeds create a very significant kind of epileptogenic focus that can lead to maybe focal seizures so these individuals can maybe develop focal seizures and depending upon where that is it could be very specific so for example if it was like in the left like uh front like maybe to the frontal or parietal lobe maybe you start developing like some twitching on that right side of the body or something of that nature so that you can develop focal seizures now sometimes these focal seizures can actually generalize and you can develop generalized seizures that are full on like tonic clonic okay another thing is sometimes these bleeds can not only cause focal seizures generalized tonic clonic seizures but they can cause these types of seizures that are really not that obvious they're not just flailing around or twitching certain parts of their body it can lead to what's called non-convulsive status epilepticus and this is one where they just really are just kind of like a decreased mental status they're not super involved they're not really maybe a phasing maybe they have gaze preferences and stuff like that and you actually need a continuous eeg to really kind of diagnose this type either way it's really important to treat these seizures with anti-epileptic medications okay and so there's many different types we're not going to go through all of them but i want you to know that there's some medications that we can give such as phenytoin phosphonotoine valproate levitarazetam lucosamite and we can even accelerate that to really intense sedation agents like propofol and midazolam and even if we have to uh barbiturates in those situations as well okay so that covers the seizures the last thing that i want us to well as we get towards the last thing is kind of the ich prevention so there's different things that we've talked about as potential causes of ich that we want to prevent from happening in the future and what are those things and what do we say is the most common cause of someone developing an ich hypertension right so we need to have better um so control of someone's hypertension and so it's very simple just maximize their anti-hypertensive meds and so that's very very important because if you have someone who develops a bleed and it was due to hypertension you really want to maximize their antihypertensive medicines to keep their blood pressure lower so they don't develop another bleed somewhere the other thing that you want to be thinking about here is what if somebody had an ischemic infarct that can transformed or kind of converted into a hemorrhagic bleed and it was due to an embolic source so you want to be thinking about anticoagulation sometimes in those situations so sometimes sometimes anticoagulation may be needed but here's the big reason why there's really one condition that i want us to know this for anticoagulation there's a thrombus that forms within your veins what was that called cerebral venous sinus thrombosis so cerebral venous sinus thrombosis you have to anticoagulate even if the person does develop a bleedbeak from that you have to prevent that clot from continuing to develop so you want to start breaking down that clot preventing future clots with giving them anticoagulation like heparin or different types of heparin there's unfractionated there's low molecular weight heparin and sometimes even treating them with different types of dough acts as well so it's important to remember anticoagulation is very important for these individuals especially if they have a hyper coagulable condition underlying there and then again if they have um risk so let's say that this person has atrial fibrillation so they have atrial fibrillation that is causing their ischemic infarct you don't want to give them that anticoagulation while they're bleeding you want to give it time you need to give the person time for that bleed to heal so for afib you might start this maybe you know two months to three months later you'll start their anticoagulation but you definitely want to restart that and the reason why is if they go on and develop an ischemic and fart they're going to develop a stroke because of that so you want to anticoagulate them if they have some type of cardio embolic source i'm just putting afib as an example here sometime later after their bleed heals and it starts to clear some of that clot you want to put them back on their anticoagulation if they were on that okay but give it some time for that bleed to heal and recover before you do that the next thing that i want to think about let's just keep the blue marker here is infective endocarditis that was a potential cause right so infective endocarditis what do you do for this antibiotics right so you're going to put these individuals on broad spectrum antibiotics until you obtain their blood cultures and find out what exactly they're on so maybe start them on vancomycin and cefepime and then adjust based upon whatever comes back from their blood cultures okay so that and then sometimes infective endocarditis if it causes mycotic aneurysms sometimes there is potential in indication for coiling so coiling that actual area where the mycotic aneurysm is to prevent that from continuously bleeding into that cerebral tissue okay last but not least is vascular abnormalities so you know that goes back to your vasculitis that goes back to your avms and things like that the big one that i want you to remember is the avm so avm sometimes you don't touch them you don't even mess with them but if they're really becoming problematic what you can do is you can actually develop kind of you can literally clot off the blood flow to these these avms and so cause these little avms to pretty much like die down so they're not even getting any blood's even going to them anymore so that way if you know if you develop kind of another brief rise in pressure sometime in the future you don't rupture those anymore because again we're embolizing them so that no more blood actually goes to these avms so sometimes there may be an indication for what's called avm embolization and that will cover everything that we need to know about intracerebral hemorrhage [Music] you

Channel: Ninja Nerd

Views: 41,190

Keywords: Ninja Nerd Lectures, Ninja Nerd, Ninja Nerd Science, education, whiteboard lectures, medicine, science, intracerebral hemorrhage, strokes, CVA, cerebrovascular accident, ICH, hemorrhage, hemorrhages

Id: 4NKx7lE3INw

Length: 62min 3sec (3723 seconds)

Published: Thu Jul 22 2021