Subarachnoid Hemorrhage | Etiology, Pathophysiology, Clinical Features, Treatment, Complications

what's up ninja nerds in this video we're going to be talking about sub arachnoid hemorrhage before we get started please support us and the best way that you guys can support us is by hitting that like button commenting down the comment section and most importantly subscribing all right ninja nerds let's get into it all right ninja nerds let's talk about what the heck is a subarachnoid hemorrhage it's it's very simple it's a hemorrhaging of the cerebral vessel primarily of the vessels of the circle of willis into the subarachnoid space that's all it is now sometimes it's very important to remember though that those circle willis or cerebral vessels not only can they rupture into the subarachnoid space but they can also rupture into the ventricles as well and cause intraventricular hemorrhage and we'll talk about that a little bit later but basic concept cerebral vessel ruptures into the subarachnoid space that is a subarachnoid hemorrhage now what's the causes of this the first and easiest one and the most common type is traumatic so there's some type of trauma and there's two types of trauma there is blunt force trauma so you basically get hit over the head with a bat or you have penetrating trauma so maybe you got jabbed in the head with a knife okay not funny but either way one of these two things lead to the injury of those cerebral vessels they rupture into the subarachnoid space causing a subarachnoid hemorrhage by far one of the more common causes the less common causes is non-traumatic and there's actually kind of like two particular types there that i want us to focus on one is aneurysmal and that's what we're going to talk about real quick so there's some type of aneurysmal cause now the first thing that we need to talk about here is aneurysms there's actually a bunch of different types of cerebral aneurysms that you could form what are these different types of cerebral aneurysms the first one that i want you guys to be able to recognize here is that whenever you have this asymmetric so imagine this little bump here is not present so just imagine that's gone for a second whenever you have kind of a ballooning or out pouching of the vessel that's asymmetric it's not the same on both sides that's saccular or a berry aneurysm so we call this one a saccular aneurysm also referred to as a berry aneurysm now this one is a saccular berry aneurysm but sometimes we call them giant sacular berry aneurysms we just like to add on to it so this one is a saccular aneurysm but we just add on the term a giant saccular aneurysm whenever it's greater than 2.5 centimeters so either way we can call this a saccular aneurysms but if it's greater than 2.5 we just call it a giant saccular aneurysm the other type of aneurysm that you can get which is less common is this type where you have symmetrical outpouching or dilation of the actual cerebral vessels and this is called fusiform so fusiform aneurysm or dolichoatic not writing that out so fusiform is a symmetrical dilation of the cerebral vessels the next one is actually not a true aneurysm actually called a pseudoaneurysm but really it's a dissection of the vessel and that dissection creates what looks like an aneurysm on imaging but it's not a real aneurysm it's a false aneurysm so we call it a pseudo aneurysm okay very important so the reason why really care quickly here is let's imagine blood flow is running through this vessel and as it runs through this vessel it tears through the intimal lining so you know you have a tunica intima or interna tunica media tunica externa if the blood slices and dices through that tunica intima our tunica interna and accumulates here inside the actual between the media and the intima it can kind of create an out pouching that is filled with blood that looks like an aneurysm but it's not it's a pseudo-aneurysm because there is a hole within the vessel wall that is allowing blood to accumulate in the vessel wall okay it's not a true aneurysm so that would be a dissection also known as a pseudoaneurysm the next type here that i want you guys to remember is actually kind of what looks like maybe a sacular aneurysm but it's actually infected it contains infectious material that is within that aneurysm and we call these mycotic aneurysms and so i just want you guys to remember kind of infectious in nature okay so big different types of aneurysms you have saccular aneurysm is the most common that's also known as a berry aneurysm fusiform also known as dilococtatic less common dissections are pseudo-aneurysms and then finally mycotic or infected aneurysms now these are the different types of aneurysms you can have now the first question that we should have is how do we form these aneurysms and then what causes those aneurysms to pop and rupture and bleed into the subarachnoid space so the first thing that you guys want to remember is that there's some type of stress on the vessel wall and so what happens is if you put if you have increased stress and we'll talk about the different types of stressors if you will that increase stress can actually weaken the vessel wall and we'll talk about how it actually does that in a second so increase stress on the vessel whether it be direct or kind of indirect mechanism weakens the vessel wall as you weaken it you increase the risk of it dilating and then popping the first one that i want you guys to remember here is hypertension so hypertension is a very big one the other one that i want you guys to remember is something that can kind of act like hypertension and this is sympathomimetics what the heck is this this is things like cocaine methamphetamines things that basically increase your sympathetic nervous system okay the other ones are smoking so smoking nicotine all that good stuff the other one here is ethanol so these are some of the big things to think about it's hypertension sympathetic smoking ethanol one more that i want you guys to remember here is oral contraceptives or we can even add down here pregnancy now let me explain how these things actually do this the big thing to remember is hypertension so hypertension can actually cause you have you have all this high blood pressure so hypertension sympathetic smoking oral contraceptives all of these things can actually increase your blood pressure and as you increase your blood pressure you put lots of stress on these vessel walls over time that can actually weaken these walls making them more susceptible to becoming dilated or having these out pouchings the second way that this can happen is hypertension and some of these other things here can act on these tiny little vessels that supply the tunica media of the vessel wall you know what these little vessels are called that supply the tunica media we call that the vasa vasorum so what happens is is you know what hypertension or sympathomimetics or smoking or ethanol or contraceptive pregnancy can do besides increase your blood pressure putting stress on the vessel wall it can also make these tiny little vessels of the vasophorum become arteriole it can cause high lying arteriosclerosis and as you cause that hyaline artery sclerosis that affects the blood flow to the tunica media so what can happen here you can develop what's called hyaline arteriolo sclerosis and what happens is you actually kind of like cause these little like plaques to develop within these tiny little vases of asorum vessels as those plaques develop you decrease the blood flow to the muscle the tunica media of the vessel and then that muscle if it doesn't get oxygen it dies and then you start causing weakening and ballooning and dilation of those vessels so that is what happens and that's what i want you guys to remember so big big quick quick recap here what things can increase stress on the vessel wall weakening it increasing the risk of dilation of it hypertension sympathetics like cocaine methamphetamine smoking ethanol oral contraceptives or pregnancy either direct shearing forces on the vessel wall putting stress on it weakening it or causing hyaline arterial sclerosis of those vasovasor vessels decreasing blood flow to the actual tunica media causing the tunica media to die and then leading to weakening of the vessel wall okay that's the big one there the next causes that i want you guys to be thinking about is going to be something that actually causes a genetic usually genetic causes that is actually there is a weakness in the vessel wall because of a connective tissue defect so there's actually some type of connective tissue defect and because of that connective tissue is very important for the entire structure of the vessel wall if you have a defect within that connective tissue that can weaken the vessel wall if you weaken the vessel wall it's prone to forming dilation out pouching and then rupturing what are the different types of connective tissue defects that you guys should be thinking about one the very important one here is going to be marfan syndrome so marfan syndrome is actually a deficiency or absence of the protein called fibrillin which is important for the elastic laminas the other one is called ehlers-danlos syndrome and the ehlers-danlos syndrome is actually a deficiency within collagen which is again important for that tunica media okay so collagen is deficient and then the last one here is called polycystic kidney disease which is an autosomal disorder usually the autosomal dominant type which is there's usually a defect within the polycystin proteins which are also incorporated into the vessel wall the whole basic concept is if these proteins aren't there you don't have a structural integrity of that vessel the vessel structure is very susceptible to dilation out pouching and then popping okay all right so the next thing that we want to remember besides direct stress connective tissue defects is there's another type of genetic cause where there is abnormal growth dysplasia if you will so there's abnormal growth or dysplasia of the smooth muscle within the vessel wall so dysplasia of smooth muscle and what does the smooth muscle make up within the vessel wall the tunica media if there's dysplasia of the actual smooth muscle this can lead to particular weakness in particular areas of the vessel which make it more susceptible to forming out pouches dilations and then popping what is this called this is called fibro muscular dysplasia this is a genetic condition usually it's more evident in at older ages because it takes time for it to actually start to develop and cause problems like subarachnoid hemorrhages but basically think of it like this what is dysplasia how do you determine again pleomorphism you make different smooth muscle cells in this case dysplasia smooth muscle so some smooth muscle cells are big some smooth muscle cells are small so in areas where the smooth muscle is less maybe that area where there's less smooth muscle is more susceptible to dilation or out pouchings and so areas here you'll have out pouches and then other areas where the smooth muscle is really thick you have increase in smooth muscle size those will actually be kind of like thickened areas so fibromuscular dysplasia is this different kind of formation of smooth muscle cells some big some small in different shapes and sizes that increase the risk of forming thin layers and thick layers and that is called fibromuscular dysplasia these vessels are out pouches they're thin the walls thin it's very susceptible to a change like a brief rise in blood pressure that'll pop these things and lead to a cerebral aneurysm that ruptures so that is the next one there that is a genetic cause again fibromuscular dysplasia pleomorphism the smooth muscle walls some areas are thin which can dilate and some areas are thick the last type of cause here is related to this last one here the mycotic aneurysm so in another condition where someone can have what's called infective endocarditis infective endocarditis infective endocarditis is usually wherever somebody has an infection off their endocardium and they form these little infective kind of vegetations usually on the valves of the left side of the heart usually the left atrium but it could be the right atrium if it's tricuspid valve but if it's mitral valve involvement or aortic valve involve involvement you'll form these little vegetations on those valves and what happens is if these vegetations that contain a lot of infected material break off and they flow up through the left ventricle into the aorta through your cerebral circulation and then guess what these little infective materials get stuck into these vessels and start actually degrading away at those vessel walls degrading them making them very thin increasing the risk of these out pouching and then what happens a change brief rise in blood pressure you pop those suckers so again infective endocarditis is a condition where you have infection of vegetations that form on usually the valves that break off these little things called septic emboli that gets stuck in cerebral vessels infecting the vessel wall making it thin making it susceptible to dilation out pouching and popping that covers the basic things that i want you guys to know as risk factors causes and the basic pathophysiology of aneurysms the next thing i want to talk about is we have a reason for these aneurysms forming right big quick recap stress on the vessel wall hypertension ethanol sympathetic smoking ocps pregnancy connective tissue defects like marfan ehlers-danlos polycystic kidney disease fibromuscular dysplasia and lastly infective endocarditis these are some of the reasons we can form aneurysms and how we have an increased risk of those aneurysms rupturing where can these aneurysms form within the circle of willis is another very very important point that we have to talk about so where are the most common locations where these aneurysms that we talked about with the most important one being saccular where can they form the first area that i want you guys to remember here is going to be the anterior communicating artery so the first one which is the most common is called the anterior communicating artery this one actually accounts for up to 30 percent of the the saccular aneurysms or berry aneurysms so that would be this one okay the second one that i want you guys to remember is the posterior communicating artery so the posterior communicating artery is another big one and this one accounts for about approximately 25 of the different types of sacular cerebral aneurysms the third one is the mca usually where it bifurcates so wherever bifurcates is a very high risk spot so what's called the mca bifurcation this one accounts for about approximately 20 percent of the cerebral aneurysms the fourth one that i want you guys to remember is right here what's this structure here called this is your internal carotid artery the terminus of it as it gives way to the aca and the mca and the p com so the ica terminus accounts for approximately 7.5 percent of the sacular cerebral aneurysms the next one is number five what is this vessel here this is the basilar comes all the way up here and gives way to the pca the basilar tip is another common location so the basilar tip accounts for about seven percent of the cerebral aneurysms that you can form what else do we have well think about what else do we got left here the next one is this guy up here six that's the anterior cerebral artery so the anterior cerebral artery accounts for about approximately four percent of the actual cerebral saccular aneurysms and the last one is this tiny little guy coming off of your vertebrals your pica so that's the last one which is going to be the pica and that counts for about three point five percent of your cerebranos the rest of them that makes up the last of the hundred percent is different miscellaneous locations that we're not going to talk about so big thing to remember if somebody asks you what is the most common location for these aneurysms to form and pop you would say anterior communicating arteries someone said the second one you would say the pecan someone said the third one you say mca bifurcation those are the big three that i want you guys to remember okay so we know now the types of aneurysms the causes of it how those causes lead to aneurysms and we know where those aneurysms can form most common locations the last thing that i want us to discuss is what is the reason why someone will actually pop these aneurysms so in other words we know the cause of them what forms them where they form but what causes them to eventually just rupture all of a sudden and that's a nice little discussion that we should talk about so the next little thing is what's the trigger and it's actually not that hard thank goodness it's a very simple straightforward thing what is the trigger and really the most common trigger is an acute rise in blood pressure that's going to be probably one of the most common causes the other one is some type of painful stimulus so maybe they have a painful stimulus of some kind and the last thing is they have some type of anger fit these are kind of the big big reasons why someone would actually have an acute trigger to eventually rupture these aneurysms that have been formed by the different reasons that we talked about how they form okay so we got traumatic subarachnoid hemorrhages we got aneurysmal subarachnoid hemorrhages with the different causes different types of aneurysms where they form and what triggers them to pop the last thing i need you guys to remember is what is the last potential cause of a non-traumatic subarachnoid hemorrhage and that last one is called an arterial venous malformation so an arterial venous malformation we also call these avms what's important to remember is that these are common usually in children so children adolescents younger individuals that we would see this more commonly in what is an avm and how does this actually become a problem well usually whenever you have a arterial so this is actually what's called an arterial right an arteriole will feed into what's called a venule via what's called a capillary bed so it'll actually branch off into these different capillaries that'll come back into the venule when someone has an avm they don't have a true capillary so there's actually no true capillary here so no true capillaries they just form kind of a direct connection between the arterial and the venule which leads to this big old nidus that you see here this big old ball of vasculature this big ball of vasculature is very susceptible to acute brief rises in blood pressure things like that and that sucker can pop leading to a subarachnoid hemorrhage okay so those are big things to remember here okay we talked about the causes we talked about the pathophysiology of these different things with subarachnoid hemorrhage the last thing that i want to talk about is going to be discussing a little bit more of the clinical features and the treatment so when we talk about subarachnoid hemorrhage where is the subarachnoid space where the blood accumulates well if you guys remember what is this part here this black layer is the brain tissue there's a piece of tissue that we're not showing here but it clings to the actual brain it's called the pia mater then there's another one this blue layer here that looks like a spider that's called the arachnoid mater then you have this kind of like maroon colored one which is just outside of the arachnoid mater that's called the inner meningeal layer of the dura mater and then you have this green layer which is the most outer part of the dura mater called the outer periosteal layer of the dura mater the subarachnoid space is located between the pia mater and the arachnoid model so what runs in this area if you imagine here let's say here's your anterior cerebral artery it runs within that subarachnoid space if you pop one of those aneurysms the blood will accumulate here in all of this subarachnoid space and that's where it can actually accumulate and form all that bloody area the other thing that i want you guys to remember is that sometimes you can actually have these aneurysms ruptured that not only does it fill within the subarachnoid spaces but the blood can actually extend into the ventricles if blood extends into the ventricles why is that a problem and i really want us to think about this logically where does csf flow let's see if you guys remember your anatomy and phys of the csf system it would start over here from your lateral ventricles and they would come down from the lateral ventricles into the third ventricle from the third ventricle had run down through the cerebral aqueduct and then into the fourth ventricle then from the fourth ventricles it would run over here into the subarachnoid space via the lateral apertures or the median apertures or go down into the central canal we know that's kind of the basic flow what if i had a hawking clot there from that blood from the subarachnoid hemorrhage that got stuck in the third ventricle could the csf move from the lateral ventricles into the cerebral aqueduct no and if the the csf can't move here what's going to happen to the size of these ventricles they're going to get bigger they're going to balloon up because of that backflow and as they balloon up because of that backflow what is that called hydrocephalus so what i want you guys to remember is that a subarachnoid hemorrhage can lead to what's called an intraventricular hemorrhage that intraventricular hemorrhage can lead to hydrocephalus but here's the next thing if the blood accumulates within the ventricles that's a called a hydrocephalus right because it's a blocking the it's obstructing the csf flow there's two different types of hydrocephalus one hydrocephalus is actually due to an obstruction of blood flow that's called the obstructive type that's the one we just discussed but there's one other type you know if you have blood within the subarachnoid space you know there's these little thingies here these little things called the arachnoid granulations or the arachnoid villi they suck some of the csf out of the subarachnoid space and then put it into the things called the dural sinuses right we know those structures we know that from our anatomy if there's a lot of blood within the subarachnoid space these arachnoid granulations they get stuck they get they're trying to pull all the csf but they're getting stuck and fill it up with blood and so they're not going to be able to drain that csf as well and so what happens is the csf that's not getting drained into the dural sinuses starts backing up in the same way so backing up from the subarachnoid space backing up into the ventricles and causing hydrocephalus what's that type of hydrocephalus very important name that's called a communicating hydrocephalus so it's a hydrocephalus but it's a problem with the communication between the subarachnoid space and the dural sinuses so we call that a communicating hydrocephalus the reason why this is important is that the obstructive one is usually more acute they communicating is a little bit more chronic okay important thing to remember so that is the last part of the etiology and pathophysiology that i want you guys to remember for subarachnoid hemorrhage now let's talk about the clinical features all right nigerians now let's talk about the clinical features of subarachnoid hemorrhage so the big thing to think about here is whenever that blood's in the subarachnoid space right whenever there's a rupture of the actual subarachnoid whenever there's a rupture of those cerebral vessels what happens is it can irritate the meninges whenever it irritates the meninges it can do two particular things what are those things that it can do the first one that i want you to remember is when it agitates the meninges there's a bunch of different cranial nerves including the trigeminal nerve that supplies the meninges if you agitate those meninges it's going to activate the trigeminal nerve whenever you activate the sensory fibers of the trigeminal nerve it can lead to the sensation of headaches so one of the big big kind of symptoms that you're going to see is a headache and what's really important what you guys need to remember is that this is kind of like the worst headache of the patient's life we also kind of use the term thunderclap headache as a pathomnemonic sign of someone having a subarachnoid hemorrhage the other thing that you want to remember is that whenever the blood's in the meninges it agitates the meninges irritates them and can produce particular types of meningeal signs what the heck does that mean so you know whenever someone has meningitis there's particular meningeal signs that we can see with those and those include photophobia so significant sensitivity to light they can also have neck stiffness or nuchal rigidity and they can also have those positive kind of physical exam tests that you could do which is called a positive kernigs or a positive brzezinskis okay that's kind of the big thing to think about so again thunderclap headache worse headache that they're live meningial signs the other thing that you guys need to be thinking about with this one is that remember the monroe kelly doctrine the monroe kelly doctrine says what as you have inside of the skull blood csf brain tissue if one of those increases the skull can't expand and so what happens is the intracranial pressure increases when one of those things increases so in this case what's increasing inside of the skull blood so because of that these individuals can also develop increased intracranial pressure and increased intracranial pressure also can present with headache but it also can present with nausea vomiting it can present with cranial nerve deficits like a blown pupil and also it can present with posturing so maybe they have decorticate maybe they have d cerebral posturing and it also can present which is very high yield for your exam cushing's triad which is a classic sign of increased blood pressure low heart rate and irregular respirations okay so this is kind of the classic things to be thinking about here the last thing that i want you guys to think about is that for example if the anterior communicating or the mca vessel ruptures the blood flow that's going to be going to the particular part of the brain is now lost and you can't supply blood to that part of the brain so what could you develop stroke symptoms and so another thing to be thinking about in these patients is that they can also develop focal deficits and so it may present like a stroke syndrome and that's where you guys need to go watch our video on stroke syndromes if you guys aren't completely familiar with all of the different types of stroke syndromes that'll help you with that okay so those are the basic clinical features to think about again what are they worst headache of the life meningeal science because of agitation of the meninges photophobia what else next stiffness nuclear rigidity positive brzezinski's kernigs also increase intracranial pressure because you have more blood in the cranium so that's going to present with nausea vomiting cranial nerve deficits posturing as well as the cushing stride and finally depending upon the vessel that's affected you may not supply a part of the brain leading to particular focal deficits like stroke syndromes all right so the last thing that i want to talk about with clinical features is a thing called the hunt and hes score so the hunted headscore are really important because what it tells us is mortality you know a subarachnoid hemorrhage is a pretty serious condition and so we utilize the hunt hess score not to prognosticate initially but to get a good idea of what's their risk of dying so if someone comes in and they're completely asymptomatic that could be a potential score of one but it also could still be a score of one if they have like a very mild headache and maybe even some some nuchal rigidity or some neck stiffness okay so these are things to be thinking about they can get a score of two if their headache is a little bit more moderate to severe and not only do they still have nuclear rigidity but they also have cranial nerve deficits so maybe one of their pupils is unequal okay three is they're coming in and you know they're a little bit like lethargic okay they're a little lethargic maybe they're even a little confused so maybe a little lethargic maybe a little confused on their mental status exam but they also have focal deficits so maybe they have weakness in one of their arms or one of their legs okay and the next one here is that they're stuporous or maybe they're obtunded so you're having to give them repeated repeated repeated stimulation having to maybe say hey john doe wake up wake up wake up or apply painful stimulus hey wake up wake up wake up they do wake up but it just takes a lot of stimulation to get them up and if they are showing early signs of posturing maybe they're decorticate posturing maybe they're having early signs of d cerebral posturing so this could be a bad sign and a score of four all right the last last part of the hunt has score is going to be a score of five which is the worst case scenario very high mortality rate if you're applying painful stimuli lots of painful stimuli and they're not arousable or alert whatsoever they're in a comatose state right and then the next thing is if they're posturing apply painful stimulating they start having this abnormal kind of extension posturing and they start coming in like this adduction extension posturing that's called a d cerebral posturing okay and again this would be the worst case scenario so high mortality rate at this level okay so that covers the basic clinical features let's now move on to the diagnostics all right so we have the basic idea of the clinical features right headache meningeal signs increase icp we also have those focal deficits and we went through the hunting test score to determine the rate of mortality now we have to diagnose these conditions right we've got to figure out do they have a subarachnoid hemorrhage how do we do that the first things you're going to obtain is a non-contrast ct scan of the head and what are we looking for well subarachnoid hemorrhage pattern is very kind of classic generally you would see blood white on the non-contrast ct scan that would show up in a couple different areas one is they could show up in the sulci so in the little ridges between the gyri they could also show up in the cisterns there's different types of cisterns where it can become very evident it also could show up where else it could also show up in the ventricles sometimes you can get extension of that bleed into the ventricles causing ivh another thing to be looking for is if there is blood in the ventricles is it enough that it actually is causing the ventricles to puff up in other words are those ventricles dilated and do they have hydrocephalus and what are the different types of hydrocephalus the acute one would be an obstructive hydrocephalus the chronic one would be a communicating hydrocephalus so that's the big thing that you want to look for with the non-contrast ct now if you see a subarachnoid hemorrhage type of pattern on the non-contrast ct what you can do is you can start actually giving a score based upon that non-contrast ct called a modified fischer score and what a modified fischer score does is it determines the risk or the rate of developing what's called vasospasm which can lead to what's called delayed cerebral ischemia so it's indicative of their risk of developing vasospasm we'll talk about that there's it's one of the second most common causes of mortality um in patients with subarachnoid hemorrhages so how do we kind of grade um like the modified fischer score based upon the ct scan we have a couple different grades you have one two three four and it's really actually pretty simple it's if you have a thin subarachnoid hemorrhage and we classify that by less than five millimeters and no ivh so you have the subarachnoid hemorrhage in the sulci and the cisterns but it's less than five millimeters there's no ivh or hydro the next thing is two so a thin subarachnoid hemorrhage still less than five millimeters within the sulci and the cisterns but you have ivh maybe with some hydrocephalus three is you have a thick subarachnoid hemorrhage within the cisterns and the sulci greater than five millimeters and you have no ivh and then in this case four would be you have a thick subarachnoid hemorrhage greater than five millimeters within the cisterns or the sulci and you have ivh present okay that is the modified fissure score it determines the risk of vasospasm or delayed cerebral ischemia based upon the non-contrast ct now let's say you get the non-contrast ct you see subarachnoid hemorrhage blood pattern as we described above what's the next test that you would do a good test is a ct angiogram of the head and neck because it gives us a look at the vessels to see is there a part where there's an aneurysm that actually ruptured because maybe we can find the aneurysm so that's where a ct angiogram can come in nice and handy is we're looking at so this actually helps us to identify the actual vessel aneurysm okay so that's one reason we can do this it can help to identify the vessel aneurysm now there's one problem with this is that sometimes it can be missed if the aneurysm is less than like three millimeters sometimes they even say potentially four millimeters if it's smaller than that the cta might not be able to pick it up another thing with the cta besides identifying the vessel aneurysm is it can help to distinguish a very particular type of presentation that's very similar to subarachnoid what's called rcvs reversible cerebral vasoconstriction syndrome also known as call flaming syndrome in reversible cerebral vasoconstriction syndrome they can present with kind of a subarachnoid hemorrhage pattern on their non-contrast ct and their clinical features but in rcvs they actually have whenever you get the cta it shows areas of kind of like stenotic areas so it would show stenotic or narrow areas for rcvs whereas you would see the actual aneurysm that ruptured in a subarachnoid hemorrhage the other thing to be thinking about with the ct angiogram is just remember consider the risk of what's called contrast induced nephropathy whenever you give contrast if a person has a very low gfr glomerular filtration rate they have a high creatinine you can actually injure their kidneys and cause an acute kidney injury from the contrast so again something to think about when you're doing a ct angiogram okay so we got a non-contrast c ct found the subarachnoid hemorrhage pattern used it to determine their risk of vasospasm within the future use the cta to find the vessel that actually did rupture or distinguish it from our cvs what's another test that we can do if we want to go straight to the gold standard baby the best test that you can do is what's called a angiogram a digital subtraction angiogram this is the gold standard test this will give you direct visualization so visualization of vessels in a three-dimensional image so this is a real-time kind of look at the vessels it's kind of the gold standard you get a very good look at those vessels and see if you can find any aneurysms any dissections any avm so on and so forth so it's definitely the gold standard but again with this it's kind of invasive you're actually threading catheters up through the veins and filling them with contrast so that you can visualize them on these studies and so there is risk of puncturing an artery causing like a retroperitoneal bleed if they come up through the femoral structure or kind of dissecting cerebral vessels so there is complications the other nice thing about this is that it can also be utilized as therapeutic if you're in there finding the vessel that has a aneurysm you can then just go ahead and coil it which we'll talk about a little bit later okay the next thing that you can do let's say that you get a patient with a ct they don't show that classic subarachnoid hemorrhage pattern but you have a high suspicion you get a cta it doesn't really show it then you still have this high suspicion i still think that they have a subarachnoid hemorrhage and you just didn't get the angiogram yet because you don't want to risk it you can do a lumbar puncture so a lumbar puncture remember the subarachnoid space isn't just within kind of the brain and brainstem area it also extends all the way down that spinal cord right and so what we can do is we can take and tap into the subarachnoid space near the lumbar area l3l4 enter space take some of the csf and guess what's going to be in that subarachnoid space blood if you have a subarachnoid hemorrhage so if you do a lumbar puncture one of what are some of the things that you may pick up in this one is that the test tubes will fill with blood and what's important to remember to distinguish this is it a traumatic tap or is it actually a true subarachnoid hemorrhages as you fill these vials up they'll stay pretty bloody and the same kind of blood is huge throughout every single kind of test tube the second thing that you can do is after you take and accumulate these actual test dudes and send them to the lab they'll do what's called a centrifuge and after you centrifuge these it actually causes some of the heme within the red blood cells to break down and give off this yellowish hue to the actual test tube which is called xanthochromia which is very highly sensitive and somewhat diagnostic of a subarachnoid hemorrhage okay so these are the quick little things that you can do now that you've diagnosed a subarachnoid hemorrhage based upon any of these measures if you want to figure out the underlying etiology you have to think about those causes so hypertension they come in hypertensive or is there trauma were they on drugs get a tox screen do they have genetic causes test for underlying genetic conditions if you suspect it do they have fibromuscular dysplasia angiography can show that also get like a renal ultrasound so thinking about the particular cause is other things that you can add into your diagnostic steps but at this point we've diagnosed a subarachnoid hemorrhage let's now start talking about how to treat it all right we're at the last part here in engineers of subarachnoid hemorrhage and probably one of the most important parts treating these patients so this is a very significant condition when someone comes in with a subarachnoid hemorrhage it's considered to be kind of a neurological emergency and so in that kind of situation what is the most important thing to do in an emergency airway breathing circulation that is the most important thing right away and then we'll talk about some of the other interventions so airway why would the airway become a problem think about this ninja nerds if you guys have someone who has a pretty decent sized bleed what does that do to the intracranial pressure it increases the intracranial pressure right and so you start putting injury and compression onto the brain stem where does the what does the brain stem do especially in the pons and medulla area it controls your respiratory center and the respiratory center is what helps to drive the muscles that are involved in breathing if you have high intracranial pressure and you're pushing down on that brain stem it can decrease your respiratory activity that's one thing to think about we often use this kind of mnemonic of saying if their mental status is declining because of a large bleed increasing the intracranial pressure so high icp and decreasing the level of consciousness we kind of use this thing say gcs less than eight into bait so it's because they're worried about them not being able to protect their airway from that large bleed in high intracranial pressure so that's one thing to be thinking about in these scenarios the other thing to be thinking about is what if they're just generally hypoxic so maybe if they're hypoxia you can try particular types of measures like putting them on a nasal cannula oh it's not working put them on a rebreather still not working putting them on high flow or cpap bypass still not working into bait so again if they're acutely hypoxic or refractory so we put refractory hypoxia for whatever reason to all kind of non-invasive invasive measures you intubate them as well okay now once we intubate them and we protect their airway there is uh particular ways that we should ventilate them that neural neuro patients usually benefit well from relatively two modes of ventilation one is cmv continuous mechanical ventilation and what you do with this one is you hook them up and you actually control particular parameters one of the common ones is volume control and so you can set a title volume and you can set a respiratory rate which affects their co2 and their ph you also can control their oxygen status by controlling their fio2 their percentage of oxygen and their peep how much you want to keep those alveoli stented open and the last thing you can also control is how fast you want that air to run into their lungs which is the flow rate okay so these are the things that you'll do with cmv once you set all these parameters you modify things a little bit so tidal volume and respiratory rate alters the co2 and ph fio2 and peep alters your oxygenation and those are things that you have to think about how do we kind of monitor how well we're ventilating these patients well you kind of monitor based upon their spo2 okay so their percentage of oxygen as well as their abg if you're getting chest x-rays as well that can also determine how well you're ventilating the patient okay another mode that's really cool and it's becoming a very hot one in neurological patients is called asv adaptive support ventilation and with this one you pick the percent minute ventilation you pick the fio2 and you pick the peep and then the machine figures out based upon the lung mechanics of the patient how well what the patient wants and what the patient's able to do it determines how much pressure you're going to push into their lungs how much volume you're going to give them how fast their respiratory rate is it's all dependent upon the patient it's called closed loop ventilation that's a very interesting way one of the nice things about asv is this allows for spontaneous breathing okay so this allows for the patient to be able to take their own breasts and get what they need cmv you can do that but it's preferable that you give them a very targeted amount of volume or very targeted amount of pressure and really you're trying to not have as much spontaneous breaths on those modes and again we'll have another lecture on that in the future but big thing for airway can protecting their airway if they have decreased level of consciousness refractory hypoxia due to the high intracranial pressure two modes cmv asv asv is a little bit more preferred next thing we've sterilized their airway and their breathing circulation that's what probably got them in this mess in the first place is this high blood pressure that acute rise in blood pressure we gotta lower that blood pressure baby so let's lower it how do we lower the blood pressure and what's our goal i guess is the big question right so blood pressure control is very very important it's going to prevent that bleed from continuing to occur in that subarachnoid space so what we like to titrate to is a systolic blood pressure pre coiling or clipping systolic blood pressure less than 160 millimeters of mercury okay it's the desire goal after you secure them with a coil or clip it's a little bit more liberal and you can kind of change based upon what the patient needs but the best things that you can do for this is very tight iv control medications and i want you to remember nicardipine as a big one this is a calcium channel blocker it's going to vasodilate those vessels that's an infusion you have le beta law la beta law is an alpha and beta blocker so it'll help with decreasing inotropic chronotropic and dilating vessels hydralazine is primarily a vasodilator so it's going to reduce that afterload as well hydraulizing would be the more preferred option if someone has a very low heart rate and you don't want to give them libado law and the other option is you can give them something called enalopril an enalopril is basically a ace inhibitor and so it's going to allow for vasodilation as well as reduced preload and so that will be helpful as long as they have a normal kidney function and a normal potassium okay so these are things to think about with blood pressure control all right abcs taken care of here's the next thing there's a textbook on the neuro icu stuff and this guy named lee said you should always think especially with subarachnoid hemorrhages abc evd so we've taken care of the abcs the next thing we should assess is do we need an evd an external ventricular drain well how do i know whether or not i need an evd if a patient comes in and their hunting head score is really bad so maybe they're you know they're like a three four five hunting head score that's already kind of an indication of getting an evd so what are some of the indications so indications primarily are dependent upon a couple things one is a high hunt has score so if they have a high hunt head score they're they're kind of like they have a high mortality rate so they probably need an evd most definitely that's a big thing the second thing is do they have intraventricular hemorrhage if they have blood in their ventricles that's a problem why is that a problem what can ivh lead to remember i told you if the blood gets stuck in the ventricles can the csf continue to flow no and so what's an issue with that obstructive hydrocephalus and so these are potential indications for someone needing an evd ok what are the benefits though why would i want to put an evd into someone and what the heck is an evd i actually should explain that right an evd is a catheter that you kind of thread through the skull into the third ventricle generally and it pulls off csf and pulls off blood so the benefit to that is that if someone has an ivh so let's actually put here in a nice little different color here let's put pink if someone has an ivh what the actual ev do evd will do is it'll take the ivh and it'll drain the blood from the ventricles and that'll help to relieve the hydrocephalus the other thing here is that it can actually decrease the ventricle size and why is that a problem again think about this guys whenever you have inside the skull increase in blood csf or brain tissue that's increasing intracranial pressures if i pull blood out of the ventricles that's going to decrease intracranial pressure if i decrease some of the if i pull off some of the csf inside of the ventricles that's also going to decrease the intracranial pressure so i'm trying to do these things and by decreasing the ventricle size and pulling blood out that's going to help with reducing intracranial pressure here's another thing to think about though very very important sometimes when people get an ivh if they get an ivh that really clots so now that blood that's sitting in the ventricles has been sitting there for a while and now it's not actually allowing for any blood to be drained through the evd holy crap if i can't drain the blood from the evd through the ebd what's going to happen to their intracranial pressures it's going to shoot up so here's where you guys might have like an aneurysm thinking about this but guess what we can do in these patients we can actually put tpa into the ventricles to break up the clot and if you break up the clot you may be able to break it up enough to reestablish drainage through that evd and so sometimes whenever you have these you utilize magic medications called intra fecal tpa that you will push through their evd into the ventricles breaking up the clots that you can drain that clot very very important and it's only small doses and very localized another benefit to the evd is it helps you to monitor their icps which we can talk about here in a second so it actually gives you real-time monitoring of their icps and when we look at this it's kind of a graphic form here you get this kind of like form here where you look at a pressure wave form a p1 a p2 and a p3 and it helps you to determine their overall intracranial pressure usually icps are desirable to be less than 20 millimeters of mercury if it's greater than 20 millimeters of mercury and it's sustained that can be an icp crisis and that's what we'll talk about over here in a second okay so big things to think about indications for an evd high hunt has score ivh hydrocephalus why drains the blood if the blood's clotting give them eternal tpa to help to break up that clot reestablish the drainage pull off csf so that you can decrease the ventricle size decreasing the hydrocephalus and monitor their icps because if their icps are rising acutely above this number and staying sustained we can give medications to treat that the last thing that i want you guys to think about is remember that last type of hydrocephalus that i told you guys about so in someone who has kind of a communicating hydrocephalus because that blood gets stuck in those arachnoid granulations what can happen with that well sometimes it can cause a hydra that stays around for a while and so sometimes what may need to happen with these is that you do it you do an evd but guess what may happen in the long term you may need to actually have kind of a long-term shunt between the ventricles to the peritoneum because it's just taking so long from those arachnoid granulations or they're kind of like destroyed in some way from trying to drain that blood from the subarachnoid space and sometimes they may need what's called a ventricular peritoneal shunt or a vp shunt okay and so that's something to think about as well so we got abc evd what else well here really quickly since we're already at this point now where we're monitoring the icps with the evd we already said that if the icps are saying sustain they're greater than 20 millimeters mercury for a long period of time why am i stressing on the sustained if you cough your icps go up if you are in pain your icps go up if you have a fever your icp goes up if you're having a bowel movement your icps go up so after those kinds of events let them calm down treat their pain let them calm down and stop having bowel movements let them stop coughing or treat the coughing in some way shape or form that will reduce their icps if the icps are sustained despite those measures what do you do big thing to think about here first one make sure that the neck is midline this may sound so stupid but it's very important if the neck is midline you're allowing nice venous drainage keep the head of the bed elevated at 30 degrees if your head of the bed is elevated that allows for gravity to pull the blood down from that venous system the next thing some people will say hyperventilation you have to be very careful with that because you increase the risk of stroke but sometimes we do allow for permissive hypercapnia but you just have to be careful remember this is only a temporary measure you don't want to do this for very long the next thing that you would do is is you could give things like mannitol mannitol is basically an osmotic agent yanks water from healthy cells and helps to dehydrate the brain shrinking the brain size if you shrink the brain it's one of the three components that can decrease your icp the other one is you can give hypertonic saline and there's different types of hypertonic saline if you want to give something that you really want to acutely change you give something called 23.4 percent if you want to do it over a longer period of time you give three percent hypertonic saline same concept as mannitol makes the blood really salty and pulls water from the healthy cells of the brain tissue dehydrating it shrinking the brain size okay but these are the measures that you will take whenever there is elevated intracranial pressures along with the evd hopefully draining some of the blood in the csf from those ventricles all right we talked about that let's move up into the next part of our treatment process all right ninja so we did abc evd controlled their icps next thing is coiling clipping very very important this has to be done within the first 24 hours of these patients arriving to the hospital very important to get this done if you don't coil or clip or just basically secure that aneurysm they can continue to keep bleeding or they have a high risk of a rebleed which is almost a 70 mortality rate so very significant there now question that comes here is what the heck which one do i do coil or clip i don't want you to get too bogged down in the details this is where the interventionalist will actually be more involved but coiling is a little bit more particular so it kind of depends upon a couple factors so one is we say age the other one is we say the neck of the aneurysm so the neck of the aneurysm the third thing is if they have uh are they they're hemodynamics and then the last thing is the location of the aneurysm these are kind of the ways that we determine them so for coiling it's been seen studies have shown that it's better for older clipping is better for younger now coiling is you're literally taking kind of like these coils endovascular you go to ir they go in there and they stuff all these coils into the vessel and basically prevent that vessel from being able to bleed clipping is they actually open up the skull and then kind of go around wherever the vessel is and put a clip at the base of it or that neck of where the aneurysm is okay so we got older younger for coiling versus clipping the neck for this one you've got to stick coils into this area that neck is really big the coils could just fall out right so we want this we prefer a smaller neck so small neck this one it doesn't matter because you're clipping it at the neck so if they have any size a big or small it's preferred but let's just make it easier here and let's say a large neck so that's easy for us to remember the next thing hemodynamically coiling is actually better when they're hemodynamically stable in this kind of city are hemodynamically unstable so hemodynamically unstable they have cardiopulmonary complications of some kind coiling is actually preferred clipping is better when they are not hemodynamically unstable we prefer that they be as hemodynamically stable as possible to get clipping done okay and then last but not least location coiling can occur ever anywhere it doesn't matter it could really we can put any vessel but it's most preferred when it's the vertebral basilar vessels so the vertebral basilar system okay clipping is best whenever it's the mca the aca and the ica terminus okay those are the best of preferred points for that one so coiling clipping big thing has to get done with the first 24 hours what do we pick it depends upon age neck hemodynamics and location boom let's move on we've secured them with a coil or clip what is the next biggest complication that we have to watch out for with these patients it's re-bleeding re-bleeding has a 70 percent mortality rate and this can occur really at any time when the patient's in the icu uh it's the most high risk usually within the first 24 to 48 hours but it can extend up to two weeks now let's say that a patient is either secured or not secured doesn't really matter and they re-bleed if they re-bleed what do you do to try to stabilize that until you can get them back in and recoil or clip or revise that coiling clipping so we need to talk about the treatment that's temporary so sometimes what you will do is you'll give medications that will stabilize the fibrin mesh okay so whenever you have this rupture of the vessel your platelets are going to try to come to this area and clawed off that injured area and then fibrin is going to try to come and stabilize that actual platelet plug well what we want to do is try to keep that platelet plug as firm as possible and stabilize the fiber and within that structure and we can utilize drugs to help with that one of them is called amino caproic acid and the other one is called tran examic acid also known as txa okay so you can give these medications to help to stabilize the fiber and mesh what is important to remember though is that these have high risk whenever you give these medications it'll try to stop them from bleeding but it's going to increase their risk of clots so if someone has a history of coronary artery disease or peripheral artery disease you better be very careful because you could cause them to have an mi or an acute limb ischemia that happens so think about that as well it has to be taken into consideration the other thing is you can also replace the fibrinogen so if i want to replace some of the fibrinogen to help make more fibrin mesh i can give a drug that will help to kind of replace the fibrinogen and that is called cryo precipitate okay and then lastly sometimes if you're consuming a lot of these platelets within that you can also potentially have risk of low platelets and so if there is low platelets what do you do you give them platelets so you transfuse them to a particular goal usually a goal sometimes it depends upon the patient but preferably greater than 100 000 okay so re-bleed high mortality rate what do we do we have to go back in what's the ultimate goal the ultimate goal this is the temporary but the ultimate goal is revise coil clip but in the interim to stabilize that fiber mesh until they can go and do that amino caproic acid tranexamic acid to stabilize the fiber mesh replace the fibrinogen to help to form fibrin strands by cryoprecipitate and if they're low in platelets because you're consuming them you give them platelets okay we talked about coiling clipping re-bleeding the next thing that i want to talk about is vasospasm all right vasospasm delayed cerebral ischemia is a very important complication to remember with subarachnoid hemorrhage so with vasospasm what happens is you have this vessel that actually ruptures right so there's your your aneurysm that ruptures when it ruptures what happens is you release a lot of inflammatory because there's a lot of inflammation that occurs a lot of inflammatory mediators are released and these inflammatory mediators or vasoactive substances can cause vessels within the circle of willis to start clamping down and squeezing and as you clamp down and squeeze on this vessel it's going to narrow if you narrow that vessel what can that do as you clamp down on it because of causing it to spasm well what happens is you may decrease the blood flow to a particular area of the brain if you decrease the blood flow to a particular area of the brain for a long period of time this can lead to ischemia and if that ischemia occurs and it's prolonged and you haven't been able to reverse it what can be the problem with that well ischemia that is untreated can then progress to infarction and so they can actually stroke okay that's a big thing to remember here so vasospasm delayed cerebral ischemia is vessel ruptures inflammatory chemicals are released vasoactive substances are released causing those vessels in the circulators to kind of like squeeze and squeeze and squeeze causing spasming narrowing those vessels decreasing the blood flow to particular areas of the brain of whatever vessel it is leading to ischemia to the area and then have not treated infarction where they actually develop an acute ischemic stroke it's important to remember that vasospasm occurs most commonly on days 4 to 14 after the subarachnoid hemorrhage now this is a serious one so this one has a very rebleeding high mortality rate this is the second one for mortality so how do we basically monitor for but we do it through two ways one is you can do what's called daily tcds which are called transcranial dopplers and what these do is they determine the velocity of blood flow that are moving through these vessels remember your physics what is what does physics say physics says that as you decrease the kind of the diameter of the vessel what would that do to the velocity of that vessel it would increase the velocity so if you make kind of a little pipe smaller it's going to flow faster through it so it's going to increase the velocity so what we would expect is as we measure their transcranial dopplers the velocity of the blood flow through those vessels if they're having spasm what would the velocities look like higher or lower it'd be higher and so what we're looking for is how high really we want this to be greater than 120 centimeters per hour up to greater than 200 centimeters per hour that is indicative of vasospasm now the vessel that this actually looks like through research is this actually utilizes the mca but this can somewhat apply to all the other vessels the other thing that we look at is what's called the lindegaard ratio which takes the mca over the ica and gives you a ratio which helps to support if this is truly vasospasm if it is greater than 3 to greater than 6 this is also suggestive of vasospasm and again this is called the lindegaard ratio which takes the mca velocity over the ica velocity and gives you a particular number if it's greater than three to greater than six it's indicative of vasospasm the other ways that we can monitor that's one way one way that we can monitor is through daily tcds the second way that we can monitor that is what's called a cta where you literally take and go and visualize push contrast through the vessels and look to see if the vessels are narrow at certain points within the circulation that could be another way regardless though what is the treatment for these situations so when someone has vasospasm it's kind of may seem a little odd but we treat them by first trying to reduce vasospasm by relaxing the vessels and so what we can try to do is to relax those vessels or dilate those vessels we can give something called pneumotapine and so nimotipine is a calcium channel blocker that will try to dilate or relax those vessels it's been shown to reduce some of the you know severe outcomes associated with vasospasm and like immortality the second thing that we can do is we can cause induced hypertension so we already have very little blood flow let's increase their blood pressure so that we can push as much blood through those narrow vessels so induced hypertension is another thing and what we do is we aim for a systolic blood pressure of like 160 to 200 millimeters of mercury so we can really push as much blood in those vessels as possible and so sometimes you may have to use things like vasopressors like norepinephrine or phenylephrine or you may even have to use inotropes pure inotropic agents like dobutamine and milranone the third thing that you'll want to do here besides trying to relax the vessels induce hypertension is intra arterial dilators so you actually take them to interventional radiology they thread a little catheter and they spray little types of arterial dilators into the area things like verapamil things like milrinone things like nephetipine and so on and so forth trying to really dilate those vessels and stop them from spasming that is the way that we try to monitor and treat vasospasm to reduce the risk of strokes which can worsen their already terrible prognosis if they have high hunt head scores okay oh and real quick to see if you guys remember what was the score that can determine their risk of developing vasospasm or delayed cerebral ischemia it was called the modified fissure score which we used from our ct let's see if you guys remembered that all right the next thing to think about with subarachnoid hemorrhages they also have high risk of seizures and it's very simple as you have blood in that subarachnoid space what is that doing that's touching the cerebral cortex that's where your upper motor neurons are located right that's where the cell bodies of those neurons are located if they become agitated by the blood they can start firing and triggering this abnormal excessive kind of synchronous electrical activity leading to seizures and this can present a bunch of different ways this can present as a focal seizure depending upon the area where the maybe the blood is most concentrated or maybe it can cause a generalized seizure where like they have a tonic chronic seizure and sometimes they may not even present with any visible signs of a seizure and they present what's what's called non-convulsive status epilepticus where they just have declining mental status and other abnormalities that you only can really pick up their seizure activity on a continuous eeg so sometimes you may need a eeg to determine if the patient is truly kind of seizing but either way the best thing to do is to treat these patients with anti-epileptic medications okay the next thing is pyrexia believe it or not this is a very common scenario very common situation that arises with subarachnoid hemorrhage it's very simple blood within that subarachnoid space can irritate the hypothalamus and what happens is as you agitate that hypothalamus and tick it off real good it's going to try to increase your body's temperature and lead to these really nasty fevers pyrexia so what do we do to try to treat this and the other question is why do i need to treat this because fevers guess what this can do it increases the risk of vasospasm you know what else fevers can also do they can also increase intracranial pressure so these can become really problematic whenever you're febrile we don't want that so we want to try to get rid of these fevers or this pyrexia and so the ways that we do this is we use cooling measures we're not going to go through all of them the ones that i want you guys to remember is it's very simple what can i do put a cooling blanket on them i could do what's called an arctic sun that's a common one that is utilized in arctic sun another one that's a commonly utilized one is what's called a zoll catheter you actually take a catheter thread it into a subclavian vein or an ij and what happens is it has cold water running through the catheter and through this coil that cools the blood so that's ways that you can do that you can also just give cold infusions so cold normal saline infusions now here's the problem when you try to cool them down through these measures guess what happens their natural reaction to you trying to cool them down with these measures is shivering and when and when they shiva guess what they're going to try to do they're going to try to compensate for that and they're going to basically counteract everything that you're trying to do if they're shivering they're basically creating an adaptive homeostatic mechanism to bring their body temperature back up which is a problem because we want to bring it down so what we have to do is is we have to decrease the shivers and how do we do that there's so many medications i'm only going to list a couple you can give things like magnesium you can give things like boost boron you can give things like a bromocriptine you can give things like propofol you can give opioids like maperidine or fentanyl and worse case scenario you may have to just shut down their muscles and all and paralyze them so that they stop trying to compensate and shiver so these are very important things to think about the next complication is if there wasn't a million already with subarachnoid hemorrhage is cerebral salt wasting whenever they have that hemorrhage it triggers a release of epinephrine norepinephrine and what happens is that epinephrine and norepinephrine so here we'll say like epinephrine and norepinephrine what that does is that triggers your heart to release what's called atrial natural peptide and that atrial natural peptide acts on the kidneys and what it does is it inhibits aldosterone and adh what does aldosterone do reabsorb sodium and water if you inhibit that what happens to the sodium in water ends up dumping into the urine it also inhibits adh what does adh do reabsorbs water if you inhibit adh what are you going to do dump water into the urine so what happens is is they cause hyponatremia in the blood and it also causes low water volume in the blood okay and so that's called hypovolemia so you can develop hyponatremia and hypovolemia why is hyponatremia bad hyponatremia is bad because guess what it can worsen cerebral edema because if the the actual blood is really less salty now what happens is water will actually move from the blood into the brain tissue worsening cerebral edema worsening intracranial pressures why is hypovolemia bad if the person's in vasospasm and you have hypovolemia what do you do to the cerebral blood flow you decrease blood flow and that can also worsen vasospasm so how do i treat cerebral salt wasting i inhibit the atrial naturatic peptide so i treat them by giving them a drug that will oppose atrial natural peptide i give them aldosterone but we give this in the form of what's called flu dro cortisone which is basically aldosterone so it's going to reabsorb sodium and water that amp is trying to cause you to get rid of i also can give them back sodium and water how do i give them back sodium and water i can give them back sodium and water so give sodium back with the water i can give them normal saline infusions i can give them three percent hypertonic saline infusions or i can just give them salt tablets and either way i'm going to try to get that salt back up and try to get that volume back up and that's the big thing to think about here engineers are at the last part of the complications stress cardiomyopathy and neurogenic pulmonary edema this usually happens in like you know day one or two okay of subarachnoid hemorrhage upon day one day two when there is that hemorrhage it causes a massive surge of norepinephrine and epinephrine and what that does is that puts lots of stress on the heart muscle causes the heart muscle to become so stressed guess what happens it can become slightly ischemic okay it can also decrease the ejection fraction so now they develop low cardiac outputs which can lead to hypotension and it also causes apex ballooning okay very weird kind of situation there so with stress cardiomyopathy what happens is hemorrhage occurs massive amount of catecholamines like epinephrine norepinephrine are released whenever that happens it puts a lot of stress on the heart which leads to ischemia it can lead to the heart becoming stressed and having a decreased ejection fraction cardiac output hypotension and it also can cause the apex to balloon you know what they call that stress cardiomyopathy another name for it takatsubo cardiomyopathy you know what's interesting is they can present with ischemia so if you look at their actual ekg their ekg will show st segment elevation they'll have a troponin leak so their troponins will be positive you'll look at their uh their uh echo and it'll show decreased kind of like a global hypokinesis of the muscle but what's big big big kind of identifier here is that there's ballooning of the apex okay so that can happen in this scenario how do i treat that well i treat this by giving medications that'll decrea that'll actually increase the cardiac output because the problem is i can become hypotensive so how do i do that i give them things that will actually increase their map or their cardiac output so i can give them things like vasopressors or inotropes so things like norepinephrine dobutamine mill renault and so on and so forth what's the other complication again the other complication is from that massive catecholamine storm you release lots of norepinephrine and lots of epinephrine and what that can do is that can act on the vessels and cause these vessels to become kind of permeable and leaky within the pulmonary system if they become leaky guess what happens some of that fluid the plasma leaks out into the interstitial spaces and into the alveoli leading to pulmonary edema and that fluid that accumulates around the lungs can cause hypoxia so now they can have difficulty breathing as well as hypoxia so what can they have hypoxia and dyspnea and then if you look at their chest x-ray it's going to look all pulmonary edema-like so that could be one reason is because of the catecholamine surge causing the leaky leaky capillaries but what else could do it if someone has takatsubo cardiomyopathy or stress cardiomyopathy and their left ventricle isn't pushing as much blood out where can that blood kind of backflow from that left ventricle to the left atrium left atrium to the pulmonary capillaries from the pulmonary capillaries it can leak out into the interstitial spaces so not only could the neurogenic pulmonary edema be due to the catecholamine surge but it could also be from takatsubos and so how do we treat these well you have to address the hypoxia there's a lot of fluid there so the way that we treat this is increase the peep because people help to get rid of a lot of that edema or and increase fio2 oxygen percentage so that you can get as much oxygen into the alveoli to push across the lungs and the other thing is give them things that will increase the left ventricular cardiac output so giving them things like vasopressors and giving them things like inotropes will address the problem if it's the stress cardiomyopathy that's related to this edema okay ninja nerds that covers subarachnoid hemorrhage all right ninja nerds in this full-length feature film on subarachnoid hemorrhage we cover so much information that i hope it helped i hope it made sense as always ninja nerds until next time [Music] you

Channel: Ninja Nerd

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Keywords: Ninja Nerd Lectures, Ninja Nerd, Ninja Nerd Science, education, whiteboard lectures, medicine, science, subarachnoid hemorrhage, SAH, hemorrhage, brain, neurology, brain bleed

Id: 7giq9aD79Ew

Length: 81min 10sec (4870 seconds)

Published: Tue Jul 27 2021