0:01 [snorts] 0:08 What's up ninja nerds? In this video today, we're going to be talking about CNS infections. That's primarily going to focus on things like menitis, encphilitis, and brain abscesses. We'll talk about a couple other things along the way, but that's going to be the primary focus. Again, if you guys are really enjoying these videos, you feel like you feel a little bit more confident about these topics, you feel like when you come to the exam, you feel like you can just crush it, then support us. You can do that in a couple different ways. Hit the like button, comment down in the comment section, you can subscribe. Also, highly, highly urge you to kind of consider this. Go down in the description box below. There's a link to our website. On our website, we have a lot of different things to offer, notes, illustrations, quiz questions. We're also developing other things like flashcards and QBangs. So, go check it out. I don't think that you'll be disappointed. All right, let's get right into it and talk about CNS infection. So, again, when we talk about these, it comes down to menitis, encphilitis, and brain abscess. So in simplest definition and if I asked you okay how would you 1:00 define meningitis it's the inflammation of the meningis right and so the meningis consist of a couple different components you have the pomater the arachnoid mater and the dura mater so it's inflammation of those meningis usually due to an underlying infectious ethology which is why we're talking about this an infectious disease and sephilitis is inflammation of the brain parankma usually due to an underlying infection right now we'll talk about this a little bit later when we get into more of the eeologies a lot of times s patients can have a combination of menitis and encphilitis and that is called meningo ensephilitis. It's the inflammation of the meninges and the associated probably localized nearby brain parankma. And the last one is a brain abscess. That's kind of a walled off infection containing just usually pus material or non-perulent material that's in a walledoff capsule and this is usually occurring in the brain parankma. What I want you to think about is these are all usually infectious in eeteology. Let's talk about how do these pathogens actually gain access into the central nervous 2:00 system. And there's a couple different routes. By [clears throat] far, probably the most common are going to be these two. So hematogenous means the pathogen kind of gets into the bloodstream. It crosses a mucosal barrier of some sort or it gains access to our circulation. From there it moves through the circulation and it then can seed into the meninges into the brain parankma and lead to its unfortunate damage. So let's talk a little bit about hematogynous spread. So let's imagine here for a second that we have a pathogen and it's kind of gained access into the circle of willis circle of Willis. We have the anterior circulation via the internal corateed arteries here. So here we're going to have the internal corateed arteries which are going to be giving the blood flow to the anterior portion of the circle of Willis. And then over here we'll have the vertebral arteries which are going to be supplying the posterior circulation. That's what we know about this kind of flow. What I want you to think about here is what are ways that we can get pathogens into the cerebral circulation and then from there they kind of float out into the meningis and infect the meningis or they get into 3:00 the brain parankma and cause encphilitis or they get into the brain parankma and cause like a focal area of inflammation infection and then a pus like material that gets formed a capsule around it. Well, I think what's really really interesting is one of the most common ways is usually what's called naso fingial invasion. Now when we talk about this most of the time there's a couple different pathogens that I would be concerned about especially bacterial. So there is one called streptococcus pneumonia and there's other ones like hmophilus influenza there's other ones um for example things like neria meningitis these are pathogens that they can kind of be within the nasop ferrenx and they may colonize they may build up there and for whatever reason maybe the person develops kind of a breakdown and their overall immune system and their ability to kind of prevent that from getting past the mucosa once this let's 4:02 say that we have these small little vessels back here in the nasop ferinx right over here. Let's say here's kind of some vessels, right? If this gains an opportunity to just kind of invade past this mucosa and get into the bloodstream, that's where we kind of get these problems. And again, I think it's important to remember that there is a couple different species that we should really really consider is really common here. One is called strepcockus pneumonia. So I'm going to abbreviate that one as this. All right, that's probably one of the most common mechanisms by which streptococcus pneumonia gets its way into the bloodstream is it seeds its way past the nasoper mucosa into the bloodstream. There's other ones other ones that I would actually think are worth remembering are going to be things like niceria menitus and another one is called hmophilus influenza type B. So we'll put here niceria menenjitus and the other one is called homophus and we're going to put h flu type B. These 5:04 usually can colonize around that kind of nasopringial mucosa. Usually streptocckus is going to be one and then here maybe you have a diplocus for niceria and then maybe you'll have some type of gram neg for the homophus influenza but either way they're colonizing you get kind of a breakdown and the barrier there maybe a weaker immune system for whatever reason and boom these things fly right into the actual bloodstream. Now imagine here for a second these pathogens gain access. So let's say here's some pathogens they get into the bloodstream. If they get into the bloodstream, they can move their way up via these vessels, right? And then from here, if they get into the circulation, that's one way, right? Same thing here. They can move their way up from the poster circulation and gain access into this kind of circle of Willis. Or you can have these pathogens moving up via the anterior portion, the A, and they can get access. Either way, these things 6:06 are now in the vascular system. Once they're in the vascular system, the thing that we get concerned about is let's say that these make their way into the MCA territory. Makes its way into the MCA territory. Well, now these pathogens can do a couple different things. One is maybe they could just move their way right across that bloodb brain barrier and they kind of start causing maybe like a focal area of inflammation. And then that focal area of inflammation gets a little bit worse. And eventually it starts to become necrotic. And then as it becomes necrotic, it starts to form this walled off thing called an abscess. And let's kind of represent the abscess as having some perilent material inside of it. So this is one thing that I would definitely consider. So this right here is what we would refer to as a brain abscess. And it usually starts off as cerebritis. So often times this is more of a progression where you have something 7:06 called cerebritis which usually starts off early days 1 to four and then it kind of starts to get liquefive around days 4 to 10 and then usually walls off and makes this nice capsule at days 14 plus and that's usually where you eventually get this thing called a brain abscess. So brain abscesses can form pretty simply from pathogens getting into the bloodstream and crossing the bloodb brain barrier. Another thing here is same thing let's imagine this cane's access into the circulation. It moves through here and sometimes some of these pathogens cause a significant amount of inflammation. They cause a really really nasty amount of diffuse inflammation throughout this actual lobe or this portion of the brain. Sometimes if it's really really diffuse inflammation we can call this encphylitis. So we can call this encphylitis. Now this can happen due to hematogenous spread but we'll talk about this a 8:06 little bit later. Often times the most common eeteology is usually something called retrograde axonal transport because it's a way by viruses getting access into the CNS. The last thing I want you to think about is what if these pathogens get here and right they cross over they cross. So here's the bloodb brain barrier. This could go into the CSF. So they can get into what's called the blood CSF barrier. They can cross and get into that corate plexus. Maybe they get into your ventricle systems right which are in here or they get access eventually into that subacoid space. If that happens and these pathogens get into the area of the meninges, that's when we start experiencing some inflammation of these meninges and that's when we see these patients developing something called menitis. All right. Out of all of these, I would say the most common ones to usually have these conditions occur due to hematogenous spread is usually going to be menitis and brain abscesses. And 9:09 what's a very common way by which this occurs? It's usually things like streptococcus pneumonia or nicer menitis or mopus influenza type B [snorts] via nasoparingial invasion. They cross that area. Another route is let's say that I have a person IV drug abuser. They got some kind of device that was placed. Maybe they got a pacemaker. They had a cardiac surgery whatever. But they have maybe some underlying, you know, heart valve disease. And what happens is they form vegetations on their mitro valve or maybe they form vegetations on their aortic valve. And these are infective little what we call infective vegetations. They contain bacteria pathogens. And oftent times there's a bunch of ones that we could consider. I'd say the ones that you definitely want to think about is your strepccus verans species. And another one is going to be like your stafloccus arius. These are probably going to be and we get really worried about MRSA for this one, but these are usually going to be something concerning for these types of pathogens. What's problematic with this condition is that 10:11 in this condition when you have these like nasty infective vegetations, if they kind of break off of the valve, if they break off the valve, I now have these freely circulating things called septic emblei. And now these septic emblei can just move along. This thing can move right up the left ventricle into the aorta or they can break off of the aortic valve into the aortic circulation and then they can go right up into your systemic circulation. And now I got septic emblei causing this. What's the condition that lead to septic emblei that can then spray this thing up and showered into your actual brain tissue? That's called infective endocarditis. So infective endocarditis is a very very common way by which we can actually seed and spread these pathogens. All right. All right. Now the next one now these can come from anywhere. So when I take hematogenous seeding this tends to be the one that we kind of really want to think about is the nasoperinx. It's just 11:12 probably colonization probably exposure and again they can stay there. They act like commensal bacteria a lot of the time or commensal kind of organisms and if you have some kind of like breakdown in the actual overall immune system or barrier they can invade that's just how these kind of things work but this one is usually an underlying infective condition and there's another scenario what if I have a really nasty infection in the lungs really nasty infection of lungs or maybe it's not just an infection maybe this thing is a true abscess right these are also very very common reasons that these pathogens can kind of seed into the bloodstream. They have the pulmonary circulation nearby. And so all these have to do is just get access to the pulmonary circulation. And if they get into the pulmonary circulation, baboom skis, here they come on their way here to get into the bloodstream, right? And so this is usually something that we would see in really nasty pulmonary infections. Usually conditions, for example, things like pneumonia or maybe even a lung abscess. 12:16 And these things can definitely gain access to our pulmonary circulation. Now, there's so many different pathogens, but I'd say probably the ones that I'd really want you to consider for this scenario is going to be streptocockus pneumonia. And another one which we can actually talk about a little bit later, especially in people who are like maybe more of the immuno compromised states. Maybe they had a transplant, maybe they have HIV, maybe they're on imunosuppressive medications. But there's another one called nocardia. So I think about streptococcus pneumonia as a very prevalent type of pathogen here and another one in certain cases I would think about no cardia especially in the imuno compromised patients but either way we're seeing here how these pathogens are all gaining access to your circulation and there's other conditions it doesn't just have to be these it's just these probably tend to be the most common ways uh of infective sources gaining access or a person who's colonized and then they invade past that area You can see this with urinary tract infections like pyo. You can see this with intraabdominal GI infections or 13:17 abscesses as well. [snorts] It's just they're going to be a little bit less common. These are going to be the ones that I really want you to consider. All right. So that's hematogenous spread. What about contiguous spread? So what do I mean by this? But it's not that this is gaining access per se into the the arterial circulation, the circle of wills by which it can then throw these infective materials into the meningis into the CSF into the brain matter. This stuff, it can actually get in there, but it's going to spread via bone or like small little veins that are on the actual near these kinds of structures. So, a couple things I want you guys to think about. Let's say that a patient has rip roaring mastoidis, right? So, let's say that this patient, we'll actually do this right here. Let's say this patient has what's called mastoiditis. So it's a really one of their mastoid sinuses becomes infected with a pathogenic material. So we'll say there's some pathogenic material that's actually going to be in this particular area. All right? Or let's say that they have what's called acute otitis media. So acute 14:19 otitis media which is an infection of the middle ear. So here we're going to have the external ear and let's say here we kind of we'll represent it with this like blue. We'll say this is the tempanic membrane and then here is going to be the middle ear and there's going to be some infection that's actually residing in that area. If this kind of happens what can occur is that these can then easily spread their way right into the actual brain tissue. So from here what you get worried about is if these spread through the bone right to the meningis or they spread where right into the actual brain parankma. And so that's what we get kind of concerned about is this infected material getting here and getting here and then eventually forming a abscess or triggering something like menitis. Yeah, exactly right. I know you guys were saying it, but you can start off with cerebritis and eventually that cerebritis can then progress unfortunately to a brain abscess which 15:20 is kind of like a capsule that gets walled off and you have all of that perent material there. All right. Usually what we get concerned about with auditis media, right, is it definitely can cause menitis and it can cause brain abscesses. I'd say it's much more common for you to see things like brain abscesses though and so we'll talk a little bit about this for a second. So you definitely can see this condition here which is going to be menitis and you're definitely going to see things like brain abscesses as a result. This deserves just a quick little discussion on something though. So when we talk about brain absesses, I'd say that's the more common way by which you probably experience these kinds of infections, these CNS infections is probably contiguous spread from a source nearby where they just spread through the bone or they gain access to a mystery veins. But I want to talk about this for for a second. [snorts] When the brain abscesses occur due to these two conditions, it's usually going to be in 16:22 two locations. So the most common is think about the actual location of where the middle ear and where the mastoid sinus is with respect to the parts of the brain. It's close to the posterior fossa and it's close to the actual middle cranial fossa which is where the temporal lobe sits and where the cerebellum sits in the posterior fossa. So the most common locations that I get worried about with these is going to be the temporal lobe and the cerebellum. So whenever you have these conditions where you have an abscess where you have an abscess in the actual temporal lobe or the cerebellum think about these as the two potential sources to that. Now pathogens that we usually associated with these is more often than not usually it's going to be something you can have streptococcus pneumonia for shorskis you can also have streptococcus verans and sometimes we don't see them a lot usually more dental you may see some anorro but it's not too common usually 17:24 most of the time with these infections it's usually going to be things like again streptococcus pneumonia maybe some type of like streptoccus viran species with acutitis media you can see pseudamonus I've seen pseudamonus with like very chronic ear infections patients who have diabetes or have an imunocmpromised state all right but that's something to think about for these let's come over to the other aspect let's say that I talk about a patient who has maybe frontal sinusitis right so let's say frontal sinocitis or they have ethmoid sppheninoid oid sinusitis or they have some type of pererryo dental disease. Perryo dontal disease um usually these are like nasty abscesses. When we think about these, what I want you to consider is when patients have some type of let's say really nasty 18:26 infection here in the frontal sinus, really nasty one maybe in the ethmoid or the sppheninoid sinuses. If these spread, they typically can again spread where they can spread to the meninges or they can spread to the actual brain matter itself. Same thing can spread to the meningis or they can spread to the brain matter itself. If they do that and they infect these areas, you can get menitis or you can get what? Think about this. Let's kind of put this one right here or put this one right here. What would be the potential things that could happen? You could start off with a little bit of cerebritis that then could progress to a abscess. Again, cerebritis that could then progress to a abscess. And that's what we get worried about is primarily these abscesses, these nasty little sons of guns, right? Where you get cerebritis progressing to an abscess 19:28 is the things that I want you to definitely consider. All right. So with this, if a patient has frontal sinusitis, you can spread pathogens easily there. If you have ethmoid or sppheninoid sinusitis, you can spread infections here. And if you have some type of periodontal disease, uh, usually, for example, if you have like a really nasty dental abscess, these can seed that way as well. All right. And we'll kind of just bring this one here where we'll show this same kind of event here. There or there. This is the key thing here. These will trigger the formation of brain abscesses. That's one thing that you can definitely expect. You can also expect something like menitis. But I really want you to more likely associate this with the brain abscesses. When we think about brain abscess with these, the problem with these kinds of brain abscesses is the location and often times the pathogen that we get kind of concerned about. Usually with brain absesses from a frontal sinusitis, 20:29 an ethmoid or sphino sinusitis or a periodontal disease is more likely to involve the frontal lobe. So that's what we kind of get concerned about with these is some type of frontal or maybe even parietal lobe abscess. All right, but I'd say definitely consider this in a frontal lobe abscess. The reason why is when patients develop symptoms, headache, fever, maybe a focal neural deficit, you get a CT scan, you see this ring enhancing lesion in the frontal lobe, you should start looking on the CT scan. Hey, is there any kind of like really like poor like involvement of the orac a pacification of the actual sinuses like the frontal, the sppheninoid, the ethmoid sinuses? Is there any kind of like dental processes that are going on that could explain this? And then correlate that with your physical exam. If I see an abscess that's actually a ring enhancing lesion in the temporal lobe or the cerebellum, I should be looking is there anything going on with that middle ear? Is there anything going on with the mastoid sinus that could explain these processes? Same thing with a patient who experiences menitis. often times it's more likely hematogenous seeding. It's not as often 21:30 that you'll experience it from a contiguous spread, but you can. All right, so we got that down. I think pretty good. Let's move now to the next way that these pathogens can kind of get their way into the cena. So they can get in via the blood. They can get in by spreading through bone or maybe getting access to small like little veins that are nearby in the face. And you know why? It's because if you have like small little facial veins like little opthalmic veins or mystery veins, they can actually really kind of get their way into the actual brain tissue. They can kind of access our cerebral venus sinuses. And so often times it's actually quite interesting. Patients who experience things like maybe frontal or ethmoid or sppheninoid sinusitis, not only do they have a high risk of brain abscesses, they pro probably also increase the risk of a cerebral venous sinus kind of condition. One of those we call cavernous sinus syndrome. We'll talk about it maybe when we get into the complication section, but they often times kind of go hand in hand where brain abscesses and cerebravenous sinus thrombosis can kind of occur simultaneously due to the same kind of 22:30 like shared source. All right, cool. So, we talked about pathogens gaining access via blood. Pathogens spreading through the bone or through small little kind of emissary veins. What if they use the neurons to their advantage? What if we have pathogens that can do this? So, what's kind of interesting is let's say here I have a I have some nerves. We're going to kind of call this here. We'll say this is our allactory nerve, right? The old factory nerve. All right. Now, when we talk about the oldactory nerve, it's one of those that actually it runs through the little space here called the cribopform plate. Let's say that you actually took and this is a weird one. This is why it's an odd one. Let's say that you actually you went into an area where I don't know you had maybe you had a sinus infection and you're using a nutty pot. Netti pots are kind of those old school things that you use to kind of like help to move out some of the mucus from those nasal cavities. Sometimes what you're always told to do is to use the proper water source. Usually some type of like cleaned water like a distilled water of some sort. You don't want to use water 23:31 from like the tap or something that could potentially contain pathogens. So sometimes you increase that risk when you you increase this potential amoeba or parasite that can actually get into your you know right into this area. Another one we also consider this in the clinical vignettes is when a person was out near a river or kind of a freshwater source and they dived in and that water rushed up their nose. The reason why is there's a nasty little amieba um parasite if you will that can gain access via this process. So what it can do is it can rush right up through the nose and then what it'll do is it'll travel along the olfactory nerve up through the cribopform plate where it can then cause and wreak absolute havoc to the actual brain tissue and these patients can often times experience things like meningo and sephilitis oftentimes. So oftentimes they're going to get a combination something called maningo [snorts] and sephilitis. Now, this is a pretty rough one. This 24:32 one, most of the patients, I'd say die. There's a high high mortality rate with this one. That's why it's actually super important to remember it. But I want you to think about this again with what kind of like trigger with a fresh water right up the actual nostril hole. So, fresh water. I'm not kidding. I want you to remember it went up the nose. Somewhere in the clinical vignette, they're going to present this. Usually this is associated with neglaria fowlery. So this is a really nasty type of amieba that can actually cause this type of infection. But again what it does is it uses these nerves as a way of being able to kind of transport itself up through the cribopform plate and gain access into the central nervous system. So that's one. [snorts] The reason why I really want to stress on the retrograde axonal transport here because this is technically technically if we're being really really particular um is this is this this kind of doesn't actually gain access and get use the actual transport proteins along the axon to transport its way up. It just moves along the 25:34 olfactory nerve up through the cribopform plate. These ones that I'm going to talk about truly do utilize retrograde axonal transport. Let's kind of pick a color here. Let's go with purple. And let's say here I have some nasty viruses. And these viruses are present. And what they're going to do is they're going to gain access. They're going to hop on to these axon terminals. And when they hop onto the axon terminals, they then can utilize these specific transport proteins to move them along the axon where they go and they kind of live in the cell body which can be again these dorsal root ganglons. They can be inside of the cell bodies of the spinal cord. They can even move their way up into the ganglion of like cranial nerves as well. So what happens is they'll go here into the cell body and they may kind of go into this period of where they cause damage and you can experience some kind of symptoms. Usually, for example, um if a patient got infected with some type of nasty lesion, maybe it was something 26:36 like HSV1 or HSV2, they could exhibit certain types of cutaneous lesions, maybe some type of herpetic lesions that would actually take place or genital lesions that would take place around the actual genital mucosa. Or if it was the vericella zaster virus, this could then actually cause potential dermatal rashes or lesions, vicular lesions that can appear. and that's going to appear on a dermatal pattern. Sometimes they're going to occur along the facial nerve where they get that Ramsay Hunt syndrome. Either way, they can go and they can reap their kind of like overall damage. What happens is sometimes these viruses go into a period of kind of latency. So in other words, you kind of go where you have this process where you have the infection like the actual onset, then it moves into a period of a latency. So latency and then from there it gets reactivated and usually that reactivation of the virus is where we see these potential problems and it's usually in an amunosuppressed state. So usually you'll 27:37 have this hop on it'll gain access to your neurons move along the axons gain access now it's in the spinal cord or it can be near the cranial nerves and then from here this thing can move up and it can then start to wreak havoc on your actual brain tissue. And usually this could be I'd say most often it's the the actual brain parankma but it could be the meningis but I'd say most often more than not you see these patients experience things like encphylitis every now and then you may see a little bit of menitis but more often than not these are going to cause encphilitis. When this kind of process happens usually they cause the infection of that particular skin area. They then access the nerve. They move in. They remain kind of latent in the cell bodies and then an imunosuppressed state. Something happens to them. That virus reactivates and then from there it can then kind of travel along these areas to your actual central nervous system and really reap these kinds of damages that we can experience with these patients. The reason why I tell you this is because these are going to be the pathogens that we oftent times most see do this. You 28:39 can see other ones like rabies can do this as well, but we're not going to talk a lot about rabies. All right. So this covers another mechanism by which these pathogens can gain access to our central nervous system. Let's cover the last one. And it may seem weird like the reason why I'm doing this, but I promise it actually is going to help when it comes to us taking the foundation of how we're kind of explaining this, which is the pathogen can gain access to the central nervous system through seeding of a pathogen into the blood or spreading um via the bone or via the nearby facial or emissary veins to gain access to the CNS or they had a retrograde axonal transport where it kind of traveled along a nerve. And then last scenario is direct inoculation. The reason why I tell you these is when we start thinking about these patients who comes in with a fever and a headache and maybe they have other symptoms like meningial signs and cortical signs. And you're going to start going through you're going to get your lumbar puncture. Maybe you get a CT scan. You find out if they have menitis, if they have encphilitis, if they have some type of process like a brain abscess. Then 29:41 your job is to potentially think about where could this have come from because it may guide your particular antibiotic of choice. And that's why it's important to think about this. All right, so let's come to the next component here, direct inoculation. This one's actually pretty simple. I'm not kidding. Imagine you got nailed with a tomahawk to the head. [snorts] So you have some type of penetrating trauma. The concept behind this is if you have penetrating trauma, if that, let's just say you dip this tomahawk in like, I don't know, poo poo, and it's got some kind of like fecal matter along it, you're a weirdo, right? And you're doing something like that. If this is dirty, it's got nasty pathogens on it, it can easily seed over here and it's can just directly infect the actual brain tissue. And this is where you can definitely get things that we get concerned about like menitis, cerebritis that can progress to a brain abscess. Right? So that's one thing that I would definitely consider as a penetrating head trauma. And the reason why we consider this is that there's specific bacteria and I'll talk about what those 30:42 specific bacteria are in a second. So that's one. All right. The next thing I would also consider is any kind of neurosurgical procedure. If I'm popping this person's top, right? Right? If I'm if I'm if I'm popping that top, if I'm cracking a piece of the skull off, I'm doing a cranottomy, a craniactomy, I'm going in, I'm doing a bur hole, anytime I open up the brain matter and the actual brain itself to exposed pathogens everywhere in the world, that stuff can just get its way right in. So, I like to think about this with any kind of like neurosurgical procedure. So any kind of neurosurgical I should say neurosurgery of some sort any kind of neurosurgical procedure where I'm removing a piece of the skull I'm using some kind of like burr hole cranottomy craniactomy I'm accessing their actual duramater or their brain it's a direct route any kind of bacteria that's in the vicinity anything that's on any pot it should be always sterile but if there's some chance that there's a non-sterile instrument that pathogen 31:44 it just gains direct access and so If it can travel along this area, right into the brain or into the meninges, I mean, come on. We know what's going to happen here. I've said it about 3,000 times, right? You can get some cerebritis and that could progress to potentially a what? An abscess, right? Or it can get into the meninges and you can get menitis. So, that's what I want you to think about here. All right. The last thing is what if I put a device where maybe I have to have a small little burr hole, but I'm running a device into a ventricle like an EVD or I'm rerouting that down into the parthenium with a VP shunt or I'm accessing an actual reservoir for me to inject like intratheal therapies like chemotherapy like methtoresate. Those are all kinds of scenarios where I increase the risk of pathogens traveling along this tunnel source, right? and then into the ventricles and I can get ventriculitis into the vent meninges 32:47 into the brain matter where you increase the risk of abscesses. I think you get the point. This is a tunnel by which all of these things can potentially lead to infections. So this is where we get worried about like any kind of device and I think like cranial devices, spinal devices. Let's just say for now, maybe in this scenario, we're going to use some cranial devices. This is where I would think about maybe a couple different things. If you see it in the vignette or you're on the wards, I would think about things like an EVD, a VP shunt, and maybe an Omia reservoir. They're not too common, but you may see it on the encology ward. But EVDs, these are usually more acute in scenarios of acute hydrophilis or intraventricular hemorrhages. a VP shunt which is going to be more of a long-term scenario for things like communicating hydrophilis or congenital abnormalities. And then lastly could be a oma reservoir. Usually these are going to be things more for the intratheal therapies like chemotherapy of sorts. All right. [snorts] So reason why I tell you all of these 33:49 things is that in these potential scenarios where you have a cranial device, you have a neurosurgical procedure or you have a penetrating trauma, these increase the risk of very specific types of pathogens that I get concerned about. Those pathogens usually are going to be as such I would get worried about uh we call these uh coagulase negative staflloccus epidermis. Right? Another one is called staflacccus arius but the more specific component of this is merca. And the last one I get concerned about is sudamonus origigosa. These are the particular pathogens that you want to think about in the scenarios of direct inoculation because the reason why that's important is it guides your antibiotics of choice. Usually these are things like venkcomy and some type of thing like sephopm or marrapenum or septacadm whereas things that are usually due to contiguous spread you're covering more particularly things that 34:49 are like you get concerned about with like usually streptococcus species and anorobes so maybe more your grand positives and anorobes things that are usually hematogynous you're covering primarily probably your gram positives and you're covering some gram negatives as well so that's what I want you to think about in these scenarios and I promise this will come and make more sense as we move into the next sections like causes. It also make a lot more sense when we get into the treatment. The whole point of infectious disease is you want to do your best to tie what is the true underlying pathogen that's causing this disease. There's a lot of times that we use empiric therapies. Your goal is to then narrow those things down or at least what's the most likely pathogen for me to cover this empirically. Let's move on now. All right. So, let's talk about the eeologies now. So again I think this ties a little bit of this together to think about when patients have acute bacterial menitis right because a menitis can be acute bacterial it can be aseptic or sometimes we call that more particularly viral menitis and and why 35:50 we say aseptic and you know viral is because again the most common eeology usually oftic menitis is viral menitis. It could be due to drugs and there's other eeologies along the way but we're going to stick with viral for right now. And then there's these rare rare types of menitis that you may be tested on, but we'll probably talk about these more individually in their own lectures. Um, and usually these are things like TB menitis, things like cryptocal menitis. Um, you may see lime, rocky mountain spotted fever related related menitis, neurosyphilis, that guy's always in there somewhere. Triponymopitum's always jacking up people. So those are the ways I want you to think about is usually acute bacterial menitis, aseptic viral menitis and then kind of like your rare ones that really we only think about if they have specific host risk factors or exposures per se. All right. So the reason why I want you to think about menitis is menitis is again it's inflammation of the meninges usually due to an underlying infection. So if we think about the areas by which these patients will have this the meninges the problem with these is that it's so 36:51 diffuse. So it's kind of really widespread. Um and that's what we get kind of concerned about with menitis here is this can be pretty widespread. So that's what we're going to think about with menitis is usually there's an inflammation of the meninges. It can be pretty diffuse. It can be pretty widespread. What I want to then kind of say is okay let's talk about menitis in the forms of acute bacterial aseptic viral or the rarities those zebras that we don't often think about. Then what we're going to do is we're going to take acute bacterial menitis and we're going to break it into community acquired pathogens and hospitalacquired pathogens. And the reason why is we'll talk about a little high yield factor that you're going to be tested on which is the type of antibiotics. So in acute bacterial menitis there is a couple different pathogens that I want you guys to think about. First one and by far the most common is going to be streptococcus pneumonia. Sometimes we call this like numoccoal menitis. This is by far the most common. And again let's kind of link it back to the route which is the most common way by which you can get this type. It's usually the hematogenous 37:52 seeding. It's the nasopering mucosa by which it can actually get into the bloodstream. There is other ways. You can definitely get this from you know pneumonia as well. And you can definitely even get this from contiguous spread. It's just more likely more often than not we're going to see this from hematogenous kind of seeding from a nasoparangial mucosal source maybe some type of acutotis media maybe from pneumonia but more often than not the nasoparangial mucosal invasion. All right, with this the thing I want you guys to understand is that this pathogen it's going to be in the nasop fairing. So what pretty much increases your risk for this particular pathogen. And there's a lot of different things that I really think is important. So when we think about this one, if you if they presented a patient with menitis, acute bacterial menitis, you could pretty much like have no other kind of like risk factors mentioned. You'd probably suspect it's streptococcus pneumonia. You'd be pretty close and you'd be pretty good if you made that guess. But any kind of preceding I'd say pneumonia, acutotitis media, 38:55 sinocitis or any kind of like upper respiratory tract infection per se really suggest it's a high incidence of strepicus pneumonia that's causing this type of menitis. Another one that I definitely want you guys to think about here is if a patient has coclar implants. Klear implants really increase the risk of these particular pathogens kind of getting their way in. All right, so that's another one that I want you to think about. Other things that I would consider for streptococcus pneumonia is usually going to be a person who doesn't have a spleen. They aren't up to date with their vaccination. They haven't kind of kept up to date with their vaccination. So those are other kind of things that I would consider is maybe a patient with a could be due to cickle cell. That's usually often times the things that they can think about or they had a splinctomy for whatever reason. Um and another one that I would also consider as we talked about here is maybe um undervaccinated maybe they weren't sticking up with their their vaccination status. I'd say out of all of these the ones 39:56 that they're probably going to try and like you know test you on is going to be related to this. A patient who had a proceding pneumonia, acutitis media, sinocitis really puts this kind of pathogen on the top of the list for the most likely trigger for this patient's acute bacterial menagitis. All right, the next one that we also want to think about is niceria menitis. So this is again a strepcockus species. This is a gram negative diplocus. So this is going to be my niceria menitus. This one I think is really important to remember as well when we talk about nar menitis. The thing about this one is that it'll present in a couple different ways. We'll talk about it a little bit more in kind of the complication section. But this one we think about it usually in those who are going to be in more c so this is spread via these respiratory droplets and so those who have very very close contact with very large populations. You're in very close with other individuals. So any kind of crowded environment um and so these crowded environments I would say you 40:57 know let's say dorms it's probably less common though now in dorms because we require vaccinations um any kind of military barracks right um you can even think about nursing homes homes those are things I would think about particularly for this kind of like risk factor so think about a crowding kind of environment where they were in a dormatory they were in a military barrack they were in a nursing home of some sort and they had a close kind of contact exposure with an individual with nicer menitis. Another one is we think about this in patients who have some type of compliment deficiencies. So this one's a little odd but compliment proteins are really really important for being able to kill nicer menagitis. Right? So compliment proteins is basically you have your you know whenever you have an antibbody that binds to a pathogen like niceria it activates your C3 compliments and usually your C5 compliments which are really important for membrane attack complexes they help to optinize the pathogen and make it easier for the fagosytes to eat them. So these are 41:59 really really important. So a patient who has some type of compliment deficiency of some sort is really really important. Now going with that a lot of the times they may ask this and that is that they're on a drug called echalysisab and echolymab is a drug that we give to patients who have something called peroxismal nocturnal hemoglobinura basically in the vignette you'll have a person who wakes up in the morning when they wake up in the morning they have very very dark urine if you were to get maybe a spot CBC at that point in time you would find that they maybe had kind of a hemolytic anemia and usually this is due to a mutation in what's called the pig a gene and they have this kind of compliment activity that's causing the licis of these red blood cells. Well, you give echkymab to inhibit things like the C3 and C5 proteins particularly C5 and that basically inhibits the membrane attack complexes. It puts them more susceptible to infections from nicer menitis. So that's what you want to think about. And then the last thing we think about with this particular pathogen is again the same thing is those who don't have a spleen. 43:00 Why? Okay, actually I didn't explain that before. Why does not having a spleen or whether your cickle cell actually caused a loss of the spleen or you had to get a splinctomy for whatever reason why does that put you at very high risk for infections from streptoccus pneumonia nicer menitis and we'll talk about another one hemophilus influenza type B it's because the spleen is crucial to getting rid of encapsulated bacteria so if you don't have the dang spleen you can't get rid of those encapsulated bacteria so it puts you at risk right that's what's important here so we think about this Again, same thing. Those who ain't got no dang spleen or if they were not vaccinated. But again, one of these things that usually is important is that we require these vaccinations to be up to date to go to these particular kinds of institutions or you know uh whatever kind of process that you're going through. All right, next one is hmophilus influenza type B. So H flu type B. This one again I think it's kind of the same thing where a lot 44:00 of the times we think about aplenia we think about the undervaccinated population that are the most particularly at risk for this one. I say this is a less than 10% eeology for acute uh bacterial menitis but it is something to think about. So again we'll write down this one really really high risk in those who have a splenia or a splinctomy or they're undervaccinated. All right, let's come to the last one here. The next one that I want you guys to think about here is going to be Lysteria. So, Lysteria is a nasty son of a gun, man. Lysteria monocytogens. Let's write this one down. Lysteria mono cytoines. This one here is really something that we only consider in those patients who have a couple particular risk factors. The way that you get usually streptocockus pneumonia, niceria and hlflu is most often via respiratory droplets. All right. So respiratory 45:01 droplets they kind of get into those nasal fingial kind of airways and that's why they colonize and if there's a particular problems where you have any of these conditions put you at risk they can invade they can get past that mucosal barrier get into the bloodstream or even when they get into the bloodstream they're supposed to be broken down they're not broken down and that's when they can wreak havoc on the body. Same thing here. Liststeria has very specific risk factors. This one's not really via respiratory droplets. This is actually spread through it's it's weird. It's through kind of like uh particular deli meats. And so deli meats, if you're going out there, you eating lemon baloney sandwiches for lunch, hey, maybe back off if you have these particular risk factors. Other things is like unpasteurized cheeses and things of that nature. It puts you at risk. Now, you can eat these things and there's going to be lesseria in it, but if you have the immune system and none of these risk factors, you shouldn't really have to worry about it. But these are the patients that we do get concerned about that I'll mention. So the particular risk factors that you 45:52 should definitely think about is age. So any age particularly greater than 50 years of age, right? Another one is alcoholism and those conditions that usually go along with alcoholism that usually is a result of alcoholism is cerosis. So we think about those who are you know suffering from alcoholism but also suffer from the undesirable complication of that such as cerosis. Another thing is AIDS. And I really like to add this because you're kind of noticing maybe a trend here. Oo, that was loud. Age, alcoholism. And then we'll add another A, which is going to be for AIDS. But really, this is more just to help you remember that it's any amunompromised state. So that doesn't just have to be a patient with AIDS. That could be a patient who has a transplant. They had a solid organ transplant reason. They're on some type of imunosuppressant. Maybe they're on a steroid of some sort, a high dose. That's something else to think about. And the last one is this 46:52 one's really a stretch, but man, they they a a pregnant I don't I don't know why it doesn't really work, but we're going to I don't know. We're just going to go with it. They they is pregnant. So a pregnant woman in this particular scenario the reason why is because in pregnant individuals if they do have this potential scenario they may have some TH cell kind of like changes like immunity related changes but if that pathogen gets into their bloodstream the worry is that it can be transmitted via the placenta to the fetus. That's why we really get concerned about that. We really really urge pregnant women to stay away from things like unpasteurized cheeses and deli meats and things of that nature. But these are the particular pathogens. And so the real kind of thing that I want you to take away is streptocox pneumonia by far the most common. Really think about it in these potential scenarios. For nicer menitis, you're probably going to more likely see it in this particular kind of like scenario. And there's some other things that we'll add on here. Usually with nicer menitis, 47:53 this presents in a very very classic clinical scenario. I'll talk about it later, but usually they present with what's called a peticial papuric rash. And they can also cause things like DIC and they can cause things like septic shock and they can cause things called this waterhouse Frederickson syndrome. We'll talk about them more as like the worst case scenario to correlate and think about with menitis. But usually that's one thing that'll just tee you off is you have a person who was in a crowded area. Now they have particular paparic lesions. They have symptoms of menitis. They're bleeding or they're clotting abnormalities that are present on their labs and then on top of that they are very very sick hypotensive and they have a lot of electrolyte abnormalities. is in sodium and potassium and glucose. All right, age flu really the undervaccinated population and then thinking about these particular triggers makes you consider lististeria. I'm I promise we're going to wrap this up and think about this clinically in a second. But before we do that, we got to wrap it up with this concept with acute bacterial menitis. It can be you know hospital acquired. It's 48:50 just like just like pneumonia. If a patient develops bacterial pneumonia, acute bacterial pneumonia, we have to think about this. Is this a community acquired one? These are often times the triggers or is it hospitalacquired? Is it from a potential ventilator tube? Is it because they were exposed to something in the hospital that put them at risk? Same thing here. Is there a hospital acquired pathogen at risk here? Because often times patients will come to the hospital with menitis. It's not often it's rare, really rare that they're in the hospital for something else and they develop menitis unless they've had specific types of procedures. So the thing I want you to think about and we already talked about earlier with direct inoculation is think about this with coagulase negative stafloccus. Another name just so you know is called staflacccus epidermis. Write that down. Staflacccus epidermis is a coagulase negative staff. Another one is staflacccus arius. But which one do we care about? Msa or msa methasylan resistant is what we we we really care about. And the other one to think about 49:51 is sudamonus originosa. These are the particular pathogens that you have to be considering. And again the whole point here is that a lot of these are being spread by what process? Hematogenous seeding or contiguous spread by which these can get access to our CNS and cause menitis. This is via direct inoculation. Right? And this is going to be things where they had some type of trauma. I like to think about these in CSF leaks as well. Like if you have like a basler skull fracture with a CSF leak that can cause this potentially process for these pathogens to gain access any kind of neurosurgery or procedure that they've had or any kind of devices that they have placed are dwelling in which can create a tunnel or a tract for these to get in EVDs VP shom reservoirs. The reason why I want you guys to think about it like this is if a patient comes into the hospital, they're presenting with a severe headache, acute onset. They're also presenting with, you know, a fever. They're also presenting with 50:52 some menial signs, which we will talk about. And you suspect acute bacterial menitis. The most common pathogens are going to be these. And in the very very rare select scenarios, you may have these. they got in either through hematogenous seeding or they got in via contiguous spread. You'll have to figure that part after you diagnose their condition and you say, "Oh, the LP came back when the Graham stain culture came back. It came back with streptocockus pneumonia. Where did it come from?" We have an idea of where it came from and we can think about that. But here's what I want you to think about. The reason why this is important is when we think about patients who have let's say for example the community acquired cases oftent times the one that we're trying to cover for streptoccus pneumonia hmophilus influenza type B and neria all right so niceria menenitus these are the three most common pathogens and so with this we want to 51:52 cover for these particular pathogens. Listeria is only common in a select few scenarios. And so for this, you know what we go with? We often times go with something called venkcomy plus sept trioxone. All right, sept trioxone. So that's often times going to be our go-to. And this is usually pretty excessive to be honest with you because a lot of the times you could probably get away with sept trioxone because that would cover all of these. But in some scenarios we've seen some potential resistance to cetraxone by streptoccus pneumonia and that's why we add on the venkcomy but septra will probably cover all of these properly. The next thing that we think about is is there lysteria. So if there is liststeria and we have one of the A's which I know I know this is like it's a little bit of a stretch but you have any of these potential risk factors they're greater than 50 alcoholic serotic they're immunosuppressed or they they a is pregnant then you add on a particular agent you add ampeoin to the mix so what 52:57 does that mean I'm on venkcomy plus sept trioxone and I add on the ampeoin so that's why we think about this is because then if there is the particular ular risk factors. We're adding that one on. The only other scenario is does the patient have a hospitalacquired risk. So maybe that you're worried about that coagulase negative staff, you're worried about MRSA, you're worried about sudamonus origigosa. In these scenarios, you have to be able to cover for these and the concern is usually MRSA and quagalas negative staff would respond pretty well to venkcomy, but sept trioxone won't cover sudamonus. So what would you need instead? Some type of anti-seudonal coverage. And again, we'll get into this more in the treatment section. I just want to tie the eeteology to the treatment for you. And that is when we go for something oftent times more than not, venkcomy plus sephopene. Another really good option that we'll get into a little bit 53:58 later is another one. I'll actually write it down. So it's or marapenum. Maro penum but these are the goals cuz Veno is going to cover the coagulates negative staff the MRSA sudamonos and originos would be covered by the sephopime or the maripenum. [snorts] So this is why I want you guys to understand the eeologies and to understand how these things get accessed because it helps you to think about your treatment appropriately. All right we covered the really really feared one acute bacterial menitis. This is the scary one. You have to recognize this one. And the reason why is this, if not treated properly, carries a high risk of mortality. All right? If you continue to go untreated and you don't recognize this one, this carries a high rate of mortality. Even if you treat it, it still can carry a high rate of mortality. This one's going to present very acutely. They're going to be sick as sh. All right? So, you have to be able to recognize this one. This one, it's not as bad. It's still they're still going to present with symptoms of 55:00 headache and they're going to present with symptoms maybe of a low-grade fever and they may present with some menial signs but it's usually not going to be as severe with these. We don't often do anything about these unless it's the rare eeology that can be possible like HSV2 or VZV. So let's okay let's actually think about these. If it's HSV2 or maybe even VZV, these are things that we actually consider. The only time you would even consider these is if the patient had particular risk factors for that. And the reason why we actually consider this one is this is the only one that you can do something about. Do you guys know what that is that you can do something about with this one? You can give this person a cycllovere. All the rest of them that we'll talk about, you don't do anything. You just it's supportive care. you treat them as you treat their fever, treat their headaches, treat any other kind of like, you know, neurological complications that they have, but you're not giving a specific agent for that condition. So these are the ones that you have to 56:01 worry about and really it should kind of go hand inand look for particular lesions. So for example, if I think about these genital lesions or dermatal like vesicles, right? So maybe some genital lesions, they got some some some bumps on their on the dingdong. Uh, so genital lesions you could be concerned about or some type of um vesicles. So maybe like the dermatal kind of pattern. So a dermatal rash. We'll get rid of this one. A dermatal rash or vesicles. Dermatomal pain and maybe some vesicles that are popping out that kind of make you concerned. That would signal more of the VZV. This would consider can signal more of that HSV2. Funny enough, the more common ethiology for these is usually what we call our interero viruses. So interero viruses are usually going to be two particular ones. One is called the echo virus and the other one is called uh the 57:02 coxsaki virus. I know it sounds like a really weird like a madeup virus. I know but echo virus and the coxsaki virus these are kind of nasty ones and usually they're seasonal. So probably like summer, early fall, you may see some outbreaks. So what we usually think about for these ones is usually a summer fall outbreak of viruses and they'll present kind of interestingly where they'll have two things. One is they'll either have an upper respiratory tract infection or some type of GI infection plus a rash. So usually these would signal that a patient may have some type of viral eeology going on as an upper respiratory tract infection or maybe a GI infection uh maybe like a interocolitis of some sort [snorts] uh plus an underlying kind of maculopapular rash that may make you think about a potential viral ethology. And if that is the case and you end up getting a whole CSF panel, you find out that they have maybe more of a viral menitis and sephilitis type of picture 58:03 and it's you do a PCR and you find out it's due to the entire guess what you do you do nothing. And that's why it's important to remember that. But funny enough, these tend to be the most common ethology. So whenever a patient has, if you were to kind of say, hey, if I told you what was the most common ethiology of aseptic viral menitis, you would say this. And so what would you do for it? nothing and that's why it's really important to remember that. So often times if we think about this being probably somewhere around 70 to 80% of the cases is this that means very little of it is HSV2 probably VZV and the last ones are kind of the random ones things like um probably MS maybe even like measles rebella things like that we just don't think about these really you think about this maybe MS they would try to test you on the exam and the only reason they would do that is you'd have a person who maybe was like undervaccinated for their MMR so maybe they had undervaccinated status and this is for their MMR their measles 59:03 ms rebella. But the only reason I would say that they would consider mentioning mumps is because this presents with very specific clinical features that kind of like scream it and they could kind of like maybe let you lead into thinking about that before you get the results of the PCR. And that's if they had like orchitis. So they got a swollen nut um in a male or you got a swollen parotta gland a parotitis that's something I would think about. All right so paratitis or oritis would make you think potentially about this condition like measel mumps rebella but primarily mumps. So the reason why I tell you this is that for these when you have a patient who presents with menitis you're going to be treating them with those drugs to cover well all of these pathogens if they have the risk factors aseptic viral menitis you're really only going to consider the ascycllovere as an add-on when if they have particular risk factors and usually these kinds of 1:00:03 conditions don't commonly occur if they're not amunosuppressed and so this would be something I would maybe consider in an immune immunosuppressed patient or if they have these types of risk factors I may add on the asycllic but often times if it's aseptic viral menitis we don't do anything and so we don't really need a specific treatment for that all right what about those rare pathogens so when we talk about rare pathogens there's there's not a lot that I want you to go crazy on here because we're going to talk about these individual pathogens in separate lectures but for right now I want you to think about potentially something like TB B right maybe cryptocal menitis. So TB menitis cryptoco menitis maybe lime maybe rocky mountain spotted fever. Another one could be neurosyphilis. And then the last one we talked about is um actually I know I spelled this wrong and the only reason I know this is because you guys can't see this but this 1:01:04 guy Rob he's he's on the other side of the screen. He looked at me with the the beady eyes. All right. So, I know I butchered that one, but anyway, we fixed it up. Neurosyphilis. And the last one is the Nigelia. All right. So, the Nigelia, and we actually talked about this one a little bit, so we'll kind of maybe breeze past this one because I don't I don't want to bog you guys down with stuff like this that you're probably not going to be tested on too much in this scenario. TB is something that I would think about if the patient had specific history. Maybe they'd have a positive tuberculin skin test. Maybe they have a chest X-ray or CT scan that shows some weird kind of like calcified nodules in the lungs. Maybe they have HIV co- infections or they have an HIV or they have an immigration status. So they were from an endemic area. They were in a prison something to that effect. All right. Cryptocal menitis is one that I actually would want you to consider. So TB, I would think about it, but again we're going to talk about this more when we get into lectures that talking about tuberculosis. Cryptocal is one that I want you to consider. And the 1:02:04 reason why is they they may consider this we'll talk about this more in the HIV lecture but AIDS AIDS with a CD4 count less than 100 you really want to consider a fungus like cryptoakaco menitis lime again we see this more particularly with there being a tick exposure so they're probably somewhere in the northeastern United States and so with both of these lime and rocky mountain spotted fever I would think about you know any kind of tick exposure So tick exposure is a pretty common one, but they may not present that on the exam. What they may present that makes you even think about these is there was some recent travel to these particular areas, northeastern United States, the Rocky Mountains, and then what happens is they present with clinical manifestations that maybe make you consider it. And the only reason I tell you that is because all of these have different treatment methods. We don't treat these with this. We treat this one with like rafampen is purizenomide, ethbutol. We treat this with a very 1:03:04 specific antifungal amphotarin B which is you know amphoterrible. It really jacks up the kidneys. And we also give something like fluocytosine. For this one we give doxycycline doxycycline. For this one we give penicellin. And for this one we throw the kitchen sink at them and hope that they survive. The whole point is that if you did this for this you're not going to get that true coverage of these. And if you added all of this on, you will have so many drug reactions, you won't know what the heck is going on with your patient. So that's why we only think about these if they have very specific risk factors. So for here, they'll probably say on the exam a bilateral facial nerve pausy and maybe a ridiculopathy that can kind of scream a lime and if they had their migraines rash present somewhere in there, makes you think about it. But the more particular one is this maculopapular rash and usually it's on the hands, the wrists and sometimes the trunk and it's very characteristic rash that makes 1:04:04 you think about this one. Neurosyphilis the obviously if they had you know a sexual history HIV is another common risk factor for this one as well but there's probably two things that'll make you think about it and scream it out loud. Um and that is usually if they present with something called tabies dorsales and it's kind of within the name but it affects your dorsal white column. Um so tabies dorsales is it can damage the dorsal white column. And so what does the dorsal white column control? Propception, vibration, fine discriminative touch. And so if you have damage to that, you're going to lose some of those potential sensations. So they may have some atexia. They may have difficulty with particularly their fine and discriminative touch, maybe their propriceptive kind of uh understandings, their vibration. So that's something to think about. And the other one is called an Argal Robertson pupil. And the only reason they would kind of mention that one is that um 1:05:07 neurosyphilis has a very high affinity for the Edinger Wes, sorry, the pretectal nucleus, which is in the midbrain, the posterior midbrain. And so when it hits that, that controls your third nerve, the Edinger Westfall nucleus, which controls your pupil kind of response. And so what would happen is you would kind of do their pupil response and you would notice that they would not have their constrictive response to light because you're nailing the pre-tactyl nucleus, which then you can't send signals to the third nerve to allow for that pupilary light reflex. So they lose that. But then if you have them follow their finger inwards, they can accommodate. And so they have that type of process which we can kind of sometimes call like a lightener disassociation. Um and that's an Argal Robertson pupil. All right, that would scream a neurosyphilis. All right, nigaria is that water rushing through the nose from a freshwater source. TB again with this one, they're probably going to present some type of history like any endemic history. So probably some type of immigration from a particular area. Um and then the other 1:06:08 thing is other risk factors. they may have HIV. That's another really positive one. And then the other thing is to think about like a maybe a positive TB test. So maybe a positive TB test or their chest X-ray. They have an abnormal. So they have some type of like positive chest X-ray for like maybe like a nodule of some sort. These may make you think and consider something like tuberculosis. All right? But again, the only reason I'm mentioning these is because these have very specific therapeutics that we target. We don't we won't cover them with these. You're only going to think about these in the proper clinical scenario. So to kind of recap, menitis when a patient comes in with menitis, it's either this or this. Usually rarely is it this. You're going to cover them with these antibiotics. Rarely will you need to add on a cycllovere unless it's this. And then again with these patients, if they have these particular risk factors, you can consider adding these. But often times you're going to add on the specific test. I'm going to check for a P corology and I'll do a CSF antibbody 1:07:09 test for these. I'll check my FTA. I'll check the VDRL. For this one, I'll check the microacterium culture and the acid fast. For this one, I'll check the crypto antigen. You get the point. I'll send the specific test to identify it and then treat accordingly. All right, let's move on now. Let's talk about the other eeologies. All right, so let's move on to the next thing which is encphilitis. So, we talked about menitis. The really important one to remember is the acute bacterial menitis with encphilitis. This one is actually due to a couple different kinds of viruses that you really want to consider. And so [snorts] what are some of these? I think the most important ones to really consider is going to be again your HSV. But this is usually going to be HSV1 um or some type of vericella zaster virus. Right now with these it is really really important to remember uh something kind of nasty about encphilitis. Encphilitis is inflammation of the actual brain parankma [snorts] but there's oh wow that's a lot. There's very specific loes 1:08:11 that tend to be affected and I really want to kind of go ham on this one. When a patient has headache and fever and maybe they have some meningial signs that could suggest menitis but you can have patients who have encphilitis and sometimes if they have a little meningial irritation they can also have menial signs and so that's why sometimes when a patient comes in with a a fever a headache maybe an altered mentation or personality cognitive behavioral changes we have to have a high degree of suspicion of encphilitis and the reason why is [snorts] encphilitis especially this is this is going to be the one that I need you to remember here. So HSV1 actually just for just for simplicity sake let's I'm going to actually I'm going to put VZV down here just just to be more specific. I'm going to put VZV right here. HSV1 is going to be really really important. And there's a couple things I want you to think about this one. With HSV1 the most common location 1:09:12 of encphilitis. So this is first off it's the most common. So it's the most common. So let's actually write that down. the most common cause of encphilitis. And the second thing is the area of the brain that it has a predilction for. Do you guys know the temporal loes? The temporal loes. I know you guys were screaming that out through the through the camera. The temporal lobe, baby. So, this is going to be a very, very particular thing. And the reason why is often times this will cause maybe a bilateral asymmetric temporal lobe inflammation. And sometimes it can even be hemorrhagic. this stuff can be really really nasty. So HSV1 is really really really important and the reason why it's really important is that this is the one that since it's the most common and oftentimes with encphilitis it'll present with altered mentation seizures personality cognitive behavioral changes. So they have memory, they're irritable, they're restless, they're not their normal self. That's the ones that we want to add on a cycllovere. So a cyclloe would cover this kind of 1:10:12 consideration if there was varicelazer virus or HSV2 causing aseptic menitis. But what's the most common one? It's most often going to be the echo viruses or the coxs virus. For this one, the most common is HSV1. And the reason why this is important because this carries a super high risk of mortality if you don't treat in encphylitis properly especially HSV1. So this one we treat with a cycllo verir. So again it's really really important to remember that HSV and sephilitis carries a very high risk of mortality. That's extremely important. Now if a patient does have VZV guess what you can do the same thing. you can treat them with a cycllovere, right? So, that is something definitely to consider. But another one that I think that sometimes they can try to test you on for the exam is certain types of arbo viruses. Uh, and these are usually spread by certain types of insects, especially 1:11:12 things like mosquitoes. And there's one particular one that I think that they may try to get you on with the exam every now and then, and this is called the West Nile virus. Now the important thing here is that if you have West Nile, you're not going to treat them with anything specific. It's just important because they may ask you what is the most likely pathogen. And the reason why this is important is with West Nile virus, this also tends to cause an acute flaccid paralysis. So this tends to cause myelitis as well. So you may see the patients exhibiting what's called acute flaccid paralysis. That thing is limp, right? So acute flaccid paralysis that's the important thing to remember. So if you hear acute flaccid paralysis and encphilitis symptoms in other words they're presenting with fever, headache, altermentation, seizures, cognitive behavioral changes and they have acute flaccid paralysis with some type of recent travel to the areas that this is a high-risisk disease and they've had those mosquitoes that are nearby that could be the potential eeology. But either way, the important one that 1:12:14 really really matters is HSV1 because if you don't treat HSV1 and sephilitis, the patients has a super I'm talking like untreated. I think it's like 55 to 70% chance of mortality if you don't treat it. So that's why it's really really important to remember. All right. Now, really quickly, it is possible to have both of these. So you can have menitis and you can have encphilitis. So all that is is let's say that a patient has some type of encphylitis here and then they develop some kind of associated inflammation of the meningis or the pathogen infects both of them. That is an important terminology to understand. A lot of the time there is a significant degree of overlap. So this is called meningo and sephilitis and this is very common. I'm not kidding. A lot of pathogens tend to cause both. So this is extremely common. So that's why sometimes when we think about these patients who come in with fever and headaches, right? And maybe 1:13:16 some phototohobia and maybe phonophobia, it's really important to then start kind of thinking about what really screams the encphilitis picture. And we'll get into that. That's usually those altered mentation, seizures, cognitive behavioral changes, aphasia, focal deficits. that screams more of an encphylitis than it does scream more of a menitis type of picture. But often times they can have a degree of overlap and this is pretty common with viruses. This is pretty common even in pathogens like bacterial menitis as well where you can get this kind of degree of overlap. All right. So that's the last thing I wanted to finish with with the menitis and encphilitis is that you can have a degree of overlap. The last CNS infection that I want to talk about ethologies with is brain abscess. So we think about this patient comes in fever, headache and then you start thinking okay could they have menitis? Could they have encphilitis? We'll talk about the clinical signs. You say all right I think that they could have menitis they could have encphilitis. I don't really know. I got to get an LP. I'll get my blood cultures right now. I'll prepare for the LP. I'll get my LP and I'll 1:14:15 start them on these therapies and I'll start them on things to cover the bacteria and if they have any focal neural deficits if they have any seizures altermentation and I have a thought any kind of like small thought that they could have HSV and sephilitis I got to add on a cycllovere what about brain abscesses brain abscesses again they can present with headache fevers the fever doesn't have to always be there but the headache is usually the case and it's not usually sudden onset it's progressive but the focal neuro deficits is what's really key so that's When I like to think about this, let's say that we get a CT scan because a patient has focal neural deficits. I got to be concerned. Do they have a stroke or a bleed, right? I want to know if it's a piogenic looking abscess or a non-piogenic. Does it have a perent material in it or not? So piogenic ones. Usually with these, there's a couple ways I want you guys to think about this again. So a piogenic is usually it starts off with some type of cerebritis. Then that cerebritis becomes has a liquefactive necrosis and then eventually that liqueifactive necrosis. So you have early cerebritis, late cerebritis and 1:15:18 then an abscess. And this guy's throwing markers in the air [laughter] and then we'll kind of do this. So you start off with early cerebritis, then you start causing liquefosis, late cerebritis, and then a brain abscess. So there's a perlent material there. Where this one, maybe it doesn't actually have some type of perulent material. There's no pus. Maybe there is some type of pathogen in there or maybe there's a parasite in there or maybe there's other kinds of things like fungus in there, but it's no pergolent material. That's what we call non-piogenic. Piogenic is pretty scary. And these are the ones that we're going to treat with very specific antibiotics. Non-piogenic, we have specific therapies for that we'll kind of talk about, but this is the one that you're probably going to have most of the time considering. I'd say you'd probably be lucky enough to say this is 90% of the cases and that's going to be the other like small 10% of cases. All right, with piogenic, the next thing I want to say is let's say I get the CT scan, right? And I see this kind of like I see this ring enhancing lesion and that's what you'll have in both of these, a ring enhancing kind of lesion. 1:16:17 I want to know does it look like it's perent? Usually that's where I can kind of get into what's called MRIs. So I'll for right now I just want you to trust me. I want you to trust me that if it's a piogenic one, it's usually going to have some type of positive MRI finding. All right, we will go over this in the diagnostic section, but for right now, just trust me. And the non-piogenics are not going to have a very specific MRI finding. From there, I want to know how many abscesses do I have? Do I have one or multiple? This is not always perfect, but it's pretty darn close and at least good enough for your exam. That if you have a solitary abscess, it's important to know where it's at. Right? This goes back to talking about routes. If I say that I have an abscess, a solitary abscess and it's located at the frontal lobe or I have an abscess and it's located around the temporal loes. Then what am I thinking about? I'm 1:17:18 thinking about very specific kinds of sources. So, for example, if I said I had a frontal lobe abscess, which types of uh sources would I be kind of thinking about? Come on. Come on. Scream it out, guys. Yell it. I'm thinking about my sinusitis and my dental, right? Dental infections. So, this is usually going to be your frontal ethmoid. We got to make some room here. frontal ethmoid and maybe we can squeeze this in here your sppheninoid sinocitis and then what's the other one that we're thinking about the dental infections right so periodontal disease of some sort so then I'm thinking about dental infections this can be covered with the same antibiotics unless it's maybe from this next step over here so here we're going to say this is a frontal lobe abscess right 1:18:19 here Then we're gonna say this could be a temporal lobe abscess. And sometimes these can occur in the cerebellum as well. So let's say here we have a temporal lobe. Temporal lobe abscess. Where then would you want to start investigating a little bit further on the MRI or the CT scan? So I want to look here at the ethmoid sinuses, frontal sinuses, and I want to look at the teeth. For the temporal lobe, I'm going to want to take a look where? At the middle ear, and I'm going to want to take a look at the mastoid sinus on the the CT scan. So I want to get some temporal facial bone kind of like windows. So I'm going to want to look at the mastoid sinitis. I want to look for some mastoiditis. And I also want to look for any kind of evidence of acute otitis media or aom. This is why it's important because at these levels it guides what type of antibiotic you most likely can stick with. A lot of the times with empiric brain abscesses we oftentimes will start them on things like venkcomy sept trioxone and metroniditool because it's going to cover any kind of strep species staff 1:19:21 species and also any kind of anorob. But if we have a pretty good inclination of what's the most likely ethology especially if it's from frontal lobe or temporal lobe abscesses from these you probably don't need that venkcomy coverage. you could probably get away with sept trioxone and metroniditool. If they have the ma the acutitis media with some chronic ear disease, you may want to consider things like sudamonus, maybe bump it up to sephop. But either way, I could probably get away with metroniditool and I could probably get away with sept trioxone to cover most of these infections. And maybe for that chronic ear diabetic HIV infection where the sudamonis becomes a risk for acutitis media, I would consider instead of sept trioxone, I'd consider things something like sephop. But that's the reason why I want you to think about these. These are piogenic abscesses that are locationspecific that may point to the underlying ethiology and source which then may narrow down your antibiotics. Whereas if I also think about another location, what's another location for these? Another location that I want to 1:20:24 be concerned about is the cerebellum. So cerebellum is another one as well. So you definitely can get these as well. And usually when it's the cerebellum as a potential source. So a cerebellar abscess. So we'll put here cerebellar abscess. Guess where you want to be looking? It's the same kind of concept. I'd want to be looking at these. So again, I want to be looking at some kind of issue here. Let me take a look at their middle ear. Let me take a look at that mastoid sinus and see if there's anything going on there. But this is the concept I want you to think about. If it's solitary, think about these particular ethologies. If it's multiple, okay, then it kind of gets a little bit more challenging with multiple. What I want to know is where is the location in general to the gray white junction? If I see abscess here, if I see abscess here, if I see abscess here, abscess here, and they're 1:21:24 along that gray white junction, this almost likely screams to me hematogenous seating. This here screens contiguous spread from a nearby source, right? This screams hematogenous because it got access to the cerebral circulation. So if I accessed my MCA, if I accessed the PCA, if I accessed the ACA, I could spread these infected material to multiple vascular territories. Do you get what I'm saying? So that's where it's important to remember is if I see multiple abscesses along that gray white junction, that watershed area, that is what screams to me potentially from a hematogenous source. So these are usually going to be along that gray white junction. So along gray white junction and the other important thing is that they may be involving 1:22:25 multiple vascular territories. So, okay, multiple vascular territories and that more than anything screams a hematogenous source. And that's important because what are the two main hematogenous sources that I talked to you about? Yes, it could it come from the nasoparangial mucosa? Yes. But what was the most common thing for the nasoparangial mucosa? What was the particular pathogens that we got worried about that caused which CNS infection? It's usually strep numo, hmophus, influenza, niceria. they cause menitis. It's not as common for those to get in and cause something like multiple brain abscesses. Usually with these we get worried about two particular things. I get worried most often about things like infective endocarditis. And the reason why this is important is with infective endocarditis I actually have to go and figure this out. So afterwards I got to do with this usually the CT scan, the MRI can give me an idea if one of these kinds of areas are infected or inflamed and I can do a good 1:23:27 physical exam. I can take my probably something you don't use a lot, right? I use my otoscope, take a look, take a look, I'm going to look up through the nose. I'm going to look in the mouth. I'm going to see if I can find any kind of lesions and do a good ENT and dental exam. For infective endocritis, I'd have to do an echo and I'd have to have my blood cultures to tell me what kind of pathogens in the blood. Another one is something like pneumonia or really nasty lung abscess. And the reason why I'm telling you about these as the potential source of flinging off these pathogens into the bloodstream causing hematogenous spread and that then leading to all of these infections that you kind of see here bop bop bop bop is the type of pathogen associated with this one. We already talked about these. It's usually going to be streptococcus virans maybe also what else your anorobes so with the solitary ones I want you to often times associate these with two things strepus verirans which there's different types of groups 1:24:29 but uh strepcus anguinous is usually going to be one and then the other one is going to be your anorobes and usually their most important one here is going to be bactaroides fragilus and if you have these you can get away with sept trioxone and metroniditool. You may need to add on again either swap out the septraum for sephopm or merapenum if you got that uh pseudamonus for the acutitis media but with multiple I got to worry about specific things the most important one is I want to worry about staflacus arius right from MRSA I mean MRSA for this particular thing that's what I definitely get concerned about and another one is strepccus verans For pneumonia, I want to worry about things like streptocous pneumonia, but I also want to consider a really nasty one. You guys know what that one would be? The really scary one that you want to consider is something called nocardia. 1:25:30 And again, we're kind of tying these together back to the stuff that we talked about before. So this is the things I want you to think about because the reason why this is important is in patients who have multiple brain abscesses I want to be able to cover things like streptococcus virardans and staflacccusaorius. So I could probably get away with something like venkcomy and probably seph trioxone. Same thing for this one. I could probably get away with venkcomy of seph trioxone. If it's nocardia that's a little bit different. We'll talk about that later in the treatment section. But this is really going to be in those imunosuppressed patients. I'll have to have very specific clinical guidelines that make me determine this one. It's a little bit more challenging. But often times with a hematogenous source, you can probably get away with something like venkcomy and you can probably get away with something like sept triacone because you're covering those species. This is why you have to tie the eeteology, the specific pathogen to the antibiotic choice of that regimen. Now, let's take a second and say, okay, brain abscess, they're presenting with specific symptoms. I get 1:26:26 an MRI. It shows findings that scream more piogenic. I need to know is it this whereas if it's multiple lesions the ones I want to think about more often than not is going to be streptococcus virans for sure skis but I also want to think about know I put the period there I want to think about staflacus arius and that's that ma one every now and then if we have the specific risk factor and we will talk about this I promise more in the treatment section no cardia usually imunosuppressed people all right usually immunosuppressed people we'll talk about a very specific diagnostic test that screams this one, but most often this is going to be the case. So you can put this patient on again what kind of therapies usually sept trioxone metroniditool sometimes you may have to consider switching up switching up the sept trioxone for sephopm if they have sudamonus this one venkcomy sept trioxone and I'm pretty much good if you have not a clue of where this could be you can put them on sept trioxone venkcomy and metroniditool 1:27:27 and it covers everything all right let's say you have the non-piogenic source in other birds. There's no specific MRI findings, which I will I I promise I'm going to I'm going to tell you guys about it's looking at the DWI and the ADC sequence, but these don't really scream that piogenic source. Maybe they also don't have any kind of features that screams it from a hematogenous or contiguous spread as well. With these, there's a couple, all right, that I would want you guys to consider. with these. The first one I want you to think about is toxopplasmosis. So toxopplasmosis, this is a nasty one. All right, so it's a weird type of parasite that usually you can get and those who p those patients who are usually pregnant are very susceptible, but a really susceptible population, we kind of almost call this like an AIDS defining illness, is those patients with AIDS. So if a patient has AIDS 1:28:27 and they have a CD4 count, AIDS with a CD4 count less than 100, you really want this to be on your your actual kind of radar. There's specific locations that scream toxo. So what toxo really makes me want to think about here, so I'm going to put toxo here, is let's say that I have this kind of what appears like a ring enhancing lesion. And it's like it looks like a brain abscess. And actually I want to be very specific. I want to put it where it often most occurs. So here in the deep subcortical area we'll have a structure called the basil ganglia. That's often times where you'll see these. Usually you're going to see these most often where in the basil ganglia. So toxopplasmosis oftent times occurs where? In the basil ganglia. So let's write that down. If you see multiple lesions in the basil ganglia and they have AIDS CD4 counts less than 100 or you don't 1:29:28 even have that but you suspect it you want to definitely consider could this be toxopplasmosis and in those scenarios you would have to send off a cerological study like a toxopplasma Gandhi Ig antibbody and then you may have to put them on a specific therapy this is why it's important to think about these because guess what I'm not going to put everybody body who has a brain leion on kind of stuff for toxopplasmosis because that's a lot of medications. They get three different meds, right? I need to have specific risk factors and specific findings that make me think one over the other. All right, the next one is called neuroysteric. Oh man, I'm so bad at spelling. This is called neuroscystericosis. Right. This one is actually due to um so you want to think about this I'd say most likely as a person who traveled and it's an endemic areas. So probably the things I would think about is like were they in Africa um or South America and I'm not kidding where like were they trying like weird 1:30:29 types of foods usually like a pork kind of related meal that can contain a tapeworm and that tapeworm is called teniaolium. All right. Now, tenosolium is a nasty little son of a gun. And when this thing gets into the bloodstream, so it's actually due to a parasite. Um, and again, this one is going to be tenia tenia. This here is actually going to get into the bloodstream. It works its way up into the brain tissue. And this is a really, really unfortunate one. It can produce, I'm not kidding, sometimes you can have a couple, sometimes you can have hundreds of these little what look like cysts all over the brain. And what we see with this condition with the neuro cysticosis is you're going to see these lesions but what you're going to notice and again we'll get into this more into the 1:31:30 diagnostics is you're going to see the mouth. It's so they have the skulllex the little portions they latch on to tissue. This is called a hole in dot sign. the hole and dot sign and the hole and dot sign really signals to you potentially nurosceryosis especially if they had some type of recent travel they were sampling foods from areas of Africa South America I would definitely be thinking about this kind of condition right so what what do we call this again it's called a hole in dot sign that is usually somewhat pathonmonic screaming something like neurosysterosis all right the last ones I'm not going to go super crazy about, but I want you to think about any kind of fungal kind of pathogen. So, any kind of fungal pathogen, you really want to think about these. Um, I'm not going to go through all of them, but usually it's going to be things like aspergillis. Um, actually, I should mention one. One of them that I do think is really worth mentioning because they may try to test 1:32:30 you on it is called mucor micosis. So, let's actually write this one down. [snorts] It's called mucor mucor micosis. So this is a nasty fungal pathogen. Um and it's usually due to like a risopus uh kind of species mucoralis. And with this one usually what happens is these patients they usually often times present with a couple different symptoms. One is they can have sinusitis. So they often times have a pretty nasty sinusitis. And then another thing with this is that with these infections they can spread to the bone. So they can get orbital involvement and they can spread to the brain. And so you may get these patients with abscesses, these kind of like non-piogenic kind of lesions here and they can get orbital lesions as well. But here's the nasty thing is that sometimes with this they have this chronic sinusitis. It can literally become necrotic tissue and it can produce things called escars. So when I want you to think about mucor mucor micosis is a patient who probably has some type 1:33:32 of I'd say oftent times yeah probably most most often they're going to present this on the exam with a patient who has diabetic ketoacidosis. So some type of DKA patient, maybe a neutropenic patient, they're going to have chronic sinocitis. They may have some chronic orbital pain, but the big thing that's also associated with this is these necrotic escars that they have usually over the sinuses and the face. [snorts] That is going to scream something on the range of mugor micosis. All right? And these can cause potentially these nonpiogenic brain lesions as well. So here taking away from the eeteologies here the big things to remember acute bacterial menitis I want you to think about strep numo I want you to think about neria I want you to think about homophus influenza and lististeria that's going to give you empiric coverage right with that add-on of ail for lististeria then you think about hospitalacquired scenarios and only those select cases because that guides whether or not you add on a pseudamonal coverage the only time you worry about the antiviral asycllovere is in 1:34:34 primarily the situation if it's HSV1 and sephilitis that's going to present with very specific clinical signs and symptoms. All right? But you have to get that one on there because they have a high rate of mortality if you don't. For the brain abscess, you want to know does it suggest a piogenic or non-piogenic? If it's piogenic, you want to know, okay, is it solitary one? So, is it in one location, frontal lobe, temporal lobe, cerebellar lobe? I may have the source on the image and I can kind of treat my specific antibiotics appropriately to cover those. If it's multiple, then you're thinking about more of a hematogenous site and I got to go looking for that hematogenous site. I probably have to get a CT scan of the chest and pelvis. I'll probably have to do an echo and blood cultures and figure out where this is coming from. But at least until then, I can cover where I think it is. And then for those non-piogenic sources, we're thinking about the rarities, but I'd say out of all of these, the one that I really want you to consider is going to be that toxopplasmosis because that's the one that they may present again with these ring enhancing lesions in the basil ganglia that AIDS 1:35:29 patient and that's when you're going to want to know that one. send off some specific corology studies and start them empirically on specific therapies. All right, at this point we've built a pretty good foundation I think on the eeologies, the risk factors, the pathogenesis behind menitis and encphilitis and brain abscesses. Now what I want to do is I want to talk about how does that actually present clinically so that we can think about that and then worst case scenario what if these patients don't present with fever and headache and meningial or cortical signs but they present with very specific complications I should be able to identify that and also if I diagnose them with this condition I need to know what kind of course do they have that I need to watch out for. All right my friends so now we're going to move on to the clinical findings especially those things that are classically representative of CNS infection. So when I I have a patient who comes in often times it is really important to know that they will have kind of a similar presentation. It may be different slightly in the onset or the aggressive 1:36:30 nature of the symptoms but for the most part if I see a fa a patient coming in with some type of fever and headache I want to start thinking about some type of intraraanial process that could be going on. Right? That's the first thing. The next thing that I want to add on that maybe adds some specificity to menitis or encphilitis or to brain abscesses can [snorts] come with this component here. So let's say here down on this side we're going to have menitis and sephilitis in the brain abscess and then we have menial signs and cortical signs for the most part and pure menitis pure menitis they will have the presence of positive menial signs and for the most part as long as it's pure menitis they should not have any cortical signs for encphilitis and brain abscess they shouldn't really have any menial signs but they should have some type of cortical signs I'm potentially present. All right. So, all of them can present with fever. All of them can present with headache. Usually for 1:37:31 menitis, it's a very severe acute onset, especially if it's acute bacterial, fever, headache. This one definitely can have a fever. More likely the headache is concerning, but we're really going to talk about the cortical signs and why that's important. Brain abscess, it's more of a progressive headache. They don't have to have a fever, but they will have some very concerning cortical signs. We know that menitis can have fever, headache, and meningial signs. And so sometimes we actually call this menismas and there's very specific things that can help you to think about this. Now the problem is is that you know when we think about meningial signs usually what happens is when you have menitis it changes the degree of the stiffness and the rigidity of the neck and so we can call this I like to prefer I preferably like to call it nucal rigidity and so that's generally there is this this stiffness of the neck that's really it's hard with neck flexion right and so it usually can precipitate a lot of pain with some type degree of neck flexion so they're oftent times can have a degree of neck stiffness and some, you know, difficulty and 1:38:33 rigidity whenever they actually want to flex the neck. And so we call that nucal rigidity. So that's one of the potential menial signs, right? So definitely think about this. Again, this is the back of the head of the patient. This is Rob. He's definitely got that that kind of like bald spot there going on. But this right here is going to be the thing I want you to think about is some type of like stiffness of the neck. That's usually going to be a result here of the actual meningial inflammation. and it's going to be really really difficult for them to be able to flex their neck. So, a lot of pain there and stiffness. The other thing that we also can consider is specific tests. The problem is is that these tests that I'm going to tell you about do not exclude menitis if they're negative. There is one that is actually I I um during during the research I found actually did have like a pretty good sensitivity. We'll mention that one as well, but these are two tests that you always are going to see on the exam. So one of them is called the Bradzinskis. So it's called the Brezinski 1:39:34 sign and the other one is called the Kernig sign. Now if they have a positive Bzinski sign and a positive Kernig sign, it does bring about the suggestion of menismas or the potential for menio signs which does potentially suggest menitis. The problem with these two is if you have a negative Brazinski. So if there's a negative, I just want you guys to really really understand why this is important. A negative Brazinski and Kernig does not exclude menitis. These are literally probably only about 5% sensitive. So that's not a great test at ruling out things. It may help you to rule in this consideration with Brazinski sign. All you're trying to do is you're going to have the patient lay flat on their back and you're going to gently bend their neck or flex their [snorts] neck. So that's 1:40:35 what you're going to do. You're going have lay down and you're going to try to gently kind of bend or flex the neck. When you do that, this will precipitate pain and a response of their actual knees and hips. They're going to want to flex their hips and they're going to want to flex their knees. And so the way I like to think about this is a couple different things. Whenever you bend the neck, so bend the neck, this will produce pain, but it also will precipitate hip and knee flexion. All right? So hip flexion and knee flexion. So again, essentially what you're doing is you're bending the patient's neck. As you do that, it'll precipitate pain. And one of the responses to that is that they will flex their hips and flex their knees. Here's a short little video clip to kind of show you what that is. >> To test for the Brazinski sign, place a hand behind the neck and gently flex the patient's head toward the chest. A positive exam is marked by involuntary 1:41:36 flexion of the hips and knees, as you see here. With a positive kerning sign, what you want to think about here is that they're still laying flat, but then what you're going to do is you're going to get their hips and like you're going to get their hips flexed to about 90°. And then what you're going to try and do is you're going to try to extend the knee out completely. But it's actually going to be really difficult to do that. So what's going to happen is you're going to try and extend out this knee. But that process is going to be really difficult to do. It's going to precipitate a lot of pain. So that's usually the key thing is that this will precipitate a degree of pain and there'll be the inability the inability to be able to fully extend the knee. So pain and inability to extend the knee. All right. So again knee extension is becoming the difficult aspect in the kerning sign. And whenever you bend their neck, it causes hip and knee flexion as a result and pain in both these situations. Now again, the 1:42:36 negative aspect of this test, if they don't precipitate these findings, it doesn't necessarily exclude menitis. With the patient lying flat, bring the hip and knee to 90°. Support the knee and ankle. Now, gently extend the knee. [music] Stop when you feel resistance or the patient reports pain in the hamstrings or lower back. What I will say is there is another test that is I'd say almost about 100% sensitive. And so the other one that I would want you to consider is you can actually have the patient on their own go ahead and rotate their head from left to right and do this a couple times. All right? So you're going to have them go left, right, left, right, left, right, left, right. It's called the jolt accentuation maneuver. If this worsens their headache, that pain that they have, that could be concerning. And again, it's about 100% sensitive for menitis. So again, you could look for something called a jolt accentuation maneuver. So it's called a positive jolt 1:43:37 accentuation maneuver. And all you're having them do is essentially just rotate their head at least two to three times per second from left to right. And if it worsens their headache or precipitates a worsening of their headache. So again we'll say with this rotation they get a increase in their headache that is a positive sign and that could be indicative of menitis. And again if this is positive it's about 100% sensitive. So if it's negative, you can at least with pretty good degree of certainty say it's unlikely menitis. And so this one I think is an important one to remember because it does have approximately somewhere around 100% sensitivity. So approximately 100% sensitivity. These ones might be about 5% sensitive. And so that's why they're not great tests. But for the exam, you're going to see these. You're probably not going to see this one. So okay menitis will have 1:44:38 fever headache and they can have some meningial signs nucal rigidity positive berszenskis positive kernigs or positive jolt situation maneuver can they have cortical signs they can it's just not something that I want you guys to think about right away and so with cortical signs I want you to associate this more with brain abscesses and encphilitis but you can see this with menitis so menial signs this screams which one this is going to scream more of that patient patient who has menitis. All right? It's going to scream more likely than not menitis. All right? Whereas the patient who has cortical signs, this could scream any of them. Right? It's just more often than not that you want to think about this one with encphilitis and brain abscess. So, I want you to think about this more with encphilitis and a brain abscess. And the reason why this is important is because if you 1:45:40 think about patients who experience encphilitis, it's inflammation of the brain parankma, right? And which is the most common location for what's called HSV1 encphilitis. I told you that if there is any particular type of encphilitis, this is the one to remember. And what is the most common location that is affected or inflicted by this condition? It is the temporal lobe. So this whole area here is under fire. [snorts] This area here is potentially getting just completely gas lit, right? You then want to think about what are the potential things that could manifest in that scenario. Well, think about this in the temporal lobe. All right? You're going to have structures like for example the hippocampus. So if the hippocampus is affected, what could you potentially have? you could have some degree of memory impairment that could be potentially visible in these patients. So memory impairment is something I would consider. The other one is the amygdala 1:46:42 or any kind of like limbic nuclei. So hippocampus technically has a libic nuclei but let's really like dig deep into this and say let's think more particularly things like the amydala. This is going to cause behavioral changes. So if you see some type of cognitive behavioral changes, this really should make you think potentially about HSV and sephilitis. The other thing is that this is where speech is controlled, right? So this is going to be important for speech because there's very close areas nearby. So you have your warnicks area and then you have the archopiculus that's actually going to be between these two as well. So this is going to be very very critical for a lot of speech. So you're going to have association fibers in your speech centers there. So speech and understanding. So I'd say speech and a lot of the aspects of speech is really important. And so let's say in this scenario, what could you potentially experience? These patients may have aphasia. Um and so that is another 1:47:42 potential thing that I would want to watch out for. So a patient who experiences things like aphasia, memory impairment, cognitive behavioral therapy changes or cognitive behavioral changes makes me really want to think about something going on with the temporal lobe. So some type of again temporal lobe involvement may scream this potential picture here. All right. So if I had a patient who came in, they had headache, they had fever, they had cognitive changes, so they have a lot of memory impairment, they have behavioral changes, so they're having psychiatric changes that are inappropriate, or they're having difficulty with their speech, I then can't fully rule out encphilitis. Another really important thing and we'll talk about it over there but this carries a very very very high risk of seizures and so that's another one we will talk about it more but it is very high risk for seizures and so these patients have a very high incidence of seizures so that's what I want you to think about for HSV and sephilitis. All right. So, 1:48:42 we're talking about here menitis. We're most likely focusing on acute bacterial menitis. Here, when we talk about encphilitis, we're most likely talking about HSV1 and sephilitis. All right. The next thing I want you to think about with brain abscesses, they can experience a lot of focal neuro deficits. And those focal neuro deficits depends upon where the abscess is actually occurring. So for example, if I have an abscess that's occurring here in the frontal parietal lobe or if I have an abscess that's occurring here in the cerebellum or if I have an abscess occurring here in the um let's say in the brain stem or here in the temporal lobe depending upon that location obviously you're going to have mass effect and on top of that you may have destruction of the neurons in this area because of the infective process and so just think about that. I think the biggest thing is think about mass effect and then also the destruction of the appropriate neurons. But if I have nearby structures that I'm compressing down or I'm losing function of, you can make sense of it 1:49:43 that of what they kind of, you know, what kind of focal deficits they may experience. So for example, if I were to write out here some focal deficits, well actually let's write this out. Let's say brain abscess is the really big thing that we're thinking about here. What are some concerning features that may scream this over HSV one and sephilitis or menitis? Well, the big thing here is if I think about these focal deficits, let's say that I had one in like that frontal parietal lobe. What would be a concerning feature here? I would definitely be concerned about maybe some type of hemiparesis. So maybe they would have some type of weakness or paralysis of the affected limb on the contrlateral side. If I had it affecting the temporal lobe, well, what kind of things could be happening with the temporal lobe? Again, I could experience aphasia. I could experience a lot of these potential activities as well, but I think aphasia is a really, really important one. Let's say that I have this occurring in the brain stem. What kind of problems would happen if I have it occurring in the brain stem? What's really, really important? That's in the brain stem. 1:50:42 Cranial nerves. So, cranial nerves could be affected. So, they could exhibit potentially cranial nerve palsies. And then lastly, if it's in the brain stem, I'm sorry, in the cerebellum, we could experience atexia, maybe vertigo. And so those are other important features to also consider is potentially something like atexia, vertigo. So these are going to be potentially some focal neuro deficits that's dependent upon where the actual brain abscess is. And so if I were to kind of just like maybe uh coordinate these, this is one, right? Two, three, four. So one, two, three, four. So that's what I want you to take away from this. When we talk about a patient experiencing something types of symptoms of menitis, we think about fever, headache, and we think about meninj menismas. Do they have nucal rigidity? Do they have a jolt accentuation maneuver? Do they have a positive brazinskis? Do they have a positive kerning sign? If that's the case, that could suggest more of a 1:51:43 menitis picture. For those who experience fever, headache and they have cognitive behavioral changes. So they have memory impairment, they have new kind of onset irritability, uh anxiety, um maybe kind of like personality shifts and changes, they have increased incidence of seizures or they have a fasia that's new onset, think about HSV1 and sephilitis. And if the patient has more of a progressive headache, maybe they have a fever, but they have new onset focal deficits, depending upon where that abscess is, may be explaining their underlying symptomatology. So this is the big thing I want you to think about with these patients is again menitis, fever, headache, meningial signs. For those with encphilitis, it's fever, headache, and usually these specific cortical signs here. And then another thing I want you guys to also associate with cortical signs is one other thing. Usually with cortical signs is not just the effect of these but also altered mental status. Altered mentation really screams more of a cortical 1:52:45 involvement. Some type of involvement of the higher level cortex [snorts] or maybe even the reticular formation. So don't forget that a lot of these patients who have encphilitis and brain absess can also present with altered mentation. All right. Now that we've discussed the classic findings, let's now move into the potential complications that we can see associated with each individual CNS infection. All right. So now let's move on to the complications. Menitis. We know that this is a patient who comes in. We get concerned about fever. We get concerned about headache. We get concerned about nuclear rigidity. Maybe the positive brzensky, the kernig, the jolt accentuation maneuver. Those are the things that are going to scream more of that menitis picture. Now it is important to remember menitis can cause cortical signs. It can cause alter mental status. It can cause focal deficits. it's just less common. So what I want you to also associate with menitis is a couple other potential clinical complications when I think about menitis and it's again inflammation of the meninges right there's a couple other things that you want to really really associate this one 1:53:44 with. So numacco menitis carries a really [clears throat] high risk of sensory neural deafness. So what happens is and I don't want to go too crazy but the infection that occurs in the meninges it usually also infects the CSF and the CSF can be continuous with the coclear duct which is inside of the actual what the inner ear and so this can lead to potentially damage to the cookia so there could be damage so coia damage so what can happen is some of the infected material that's actually inside of the CSF can spread to to the cookia and lead to a cytoine response and an inflammatory reaction that can cause damage to the respective cookia. So they can have damage to their colear area and that hair cells could die and if the hair cells die you could lose the function again whenever those fluid fil movements occur that it affects the actual normal depolarization of the vestibular cclear nerve. The other thing 1:54:45 is that there could be damage of the respective nerve itself. What is this nerve that carries information from the actual cookia? This is going to be the cranial nerve 8 which is the vestibular cclear nerve. So there could be damage of the vestibular cclear nerve. And if there is damage of the vestibular cclear nerve even if you have the hair cells responding to these fluid fil movements they're still not going to be able to send the signal down the vestibular cclear nerve to your actual medulla and pawns junction. And so you're going to lose that signal which controls a lot of your hearing. So usually with sensory neural deafness there is going to be thus the term deafness but there also can be associated features with this things like tonitis and things like vertigo that can also be accompanied with this. What I really want you to remember is that there is a very specific pathogen that is most often associated with sensory neural deafness. What is the most common bacterial cause of acute bacterial menagitis? It is strepccus pneumonia. So streptocous 1:55:45 pneumonia is going to be a very high incidence of leading to coclear damage and cranial nerve aid damage. And if you damage the cookia or you damage the cranial nerve 8 that is what precipitates the sensory neural deafness. One of the things that we try to be able to reduce this incidence is whenever you get strep numo it's going to cause an inflammatory reaction. that inflammatory reaction can be potentially mitigated by giving um antibiotics by giving something prior to the antibiotics. And that's what we're going to talk about later in the treatment section. But you may you may be able to pre prevent this this theoretically could be prevented with dexamethasone. All right. And the concept behind this and then also just early identification too. So early identification of the actual condition is going to be really really important. But the concept behind this is that if you actually give this patient dexamethasone and you give that prior to the antibiotics, you may be able to reduce a lot of the inflammatory reactions that are causing some of these potential complications. And so that's 1:56:47 really really important. The other thing I actually get really worried about with this condition is when patients get menitis, not only can it cause damage, can cause cranial nerve eight damage, but imagine here you get some of this infected material and the meninges. And a part of the meningis, if you guys go back, we have what is this structure here called? Here's the bone. Then the orange is the perryostial layer of the dura matter. The green is the meningial layer of the duraater. Then you have your subur subdural space, your arachnoid mater, your subactoid space, and the pink is the pomater. Well, here in that subacoid space is the cerebral spinal fluid. And what happens if you get some of these pathogens that get into this subacoid space. What happens is is the subacoid space is supposed to carry CSF to the arachnoid kind of like val these little val valves and then push them off into these little venus structures the cerebravenous sinuses. These pathogens can alter that process. 1:57:47 They kind of imagine it gets kind of it clogs up the arachnoid villi. If it clogs up the arachnoid villi, you then can't push any of this CSF into that vein. What happens then is you end up with cerebral spinal fluid building up. So there is a CSF buildup. And now this occurs primarily where in the beginning the subacoid space. So it's going to build up in the subacoid space. When this starts to build up in the subacoid space you have to remember what the subactoid space connects with. So here's going to be the the actual arachnoid matter here in blue with all these like little lines these little tacula and it connects to your fammen luchka and then your fammeni which is going to be connecting to the fourth ventricle. Then you have your cerebral aqueduct, the third ventricle, and the lateral ventricles. So what's going to happen is this stuff is going to start backing up. And when it starts backing up, it's 1:58:48 going to make it harder. So the pressure, it's going to be harder for things to move down in this direction. So things always want to flow from the lateral ventricles to the third ventricle to the cerebral aqueduct to the fourth ventricle. But now you have this back pressure from the subacoid space. And what that's going to do is it's going to make it harder to drain. And if it's harder to move this stuff in that normal direction, what's going to happen to all of these beautiful ventricles? They're going to start ballooning up. And then you're going to start seeing some enlargement of the ventricles. And what is this condition called when you have an enlargement of the ventricles? Well, we call that ventricular megley, right? But specifically the enlargement of the ventricles to the point where it's due to some kind of obstruction is really referred to as hydrophilis. All right. So this is called hydrophilis. So hydrophilis in this potential scenario is due to infected material in the subacoid space clogging off the arachnoid villi leading to a CSF 1:59:50 buildup. That CSF buildup then leads to a decrease in CSF flow. So now you're going to have decreased CSF flow via ventricles. And then what that is going to do is is that is going to lead to this potential condition called hydrophilis. Now there's a very specific type of hydrophilis in this scenario. Do you guys know what it's called? So there's one where you can obstruct it with something inside or outside. something's inside the actual ventricle or the cerebrum that's obstructing the normal flow or you have something outside that's compressing it and a facing it and making that little area smaller. That's called obstructive hydrophilis. In this case, there's not something that's compressing it or obstructing it inside. It's something that's communicating with the subactoid space. It's causing this back pressure making it harder for things to move forward. That's called communicating hydrophilis. So, this is specifically called a 2:00:52 communicating. So this is called communicating hydrophilis. Now in patients who have hydrophilis, what would be their potential clinical picture? Do you guys know? Often times with this one, it's pretty straightforward, right? Tonitis, vertigo or deafness. For hydrophilis, the symptoms kind of depend on the degree of the severity. So the problem with hydrophilis is is whenever you have an a decreased amount of CSF flow, it's going to cause the ventricles to get bigger. So it's going to lead to ventricular enlargement, right? So your ventricles are going to get enlarged. The problem with that is that whenever you cause the ventricles to enlarge, it kind of increases the amount of overall CSF inside of the skull. And what that can do is that can increase your intraraanial pressure, which we'll kind of get into in a little bit. And so that's one really concerning feature here is an increased intraanial pressure. So what we look for with 2:01:54 elevation of ICP due to hydrophilis is a couple different things. One is they're going to have headache. That's obviously something that they priority had prior to this with the underlying diagnosis of menitis. But the other thing that we get concerned about with high ICP is things like nausea and vomiting. that can be due to the activation of the creek chemo trigger zone. The other thing that we can have is if we do a fundoscopic exam and we look all the way at their optic disc, we can notice some swelling of the optic nerve sheath and around that particular area called papal edema. All right, papadeema on fondoscopy. So if we notice papadma on fondoscopy that is also concerning and that could be an indication of high ICP due to this hydrophilis. And the last thing that we actually get worried about is when we think about it I don't have a structure here but you have what's called your anterior cranial fossa your middle cranial fossa and you go posterior cranial fossa. The sixth nerve is probably one of the most 2:02:55 sensitive to increased ICP. So whenever the sixth nerve is moving up, it runs across a structure called the clus. And whenever the pressure is high, it smashes it down on that. And the sixth nerve is supposed to cause what? Extra ocular movement supposed to control the lateral rectus. And so what happens is it alters that movement and it can lead to dipopia or double vision. And so you want to watch out for dipopia. So these are usually due to the potential things that I want you guys to think about in association with a patient having hydrophilis or this in and that hydrophilis is going to explain their increased ICP and maybe associated with nausea, vomiting, papalma and dipopia. The next thing that I want you guys to think about associated with menitis and this one is actually kind of interesting. I don't want to go super crazy, but it's actually been seen with it is cerebral, venus, sinus thrombosis. And we see this with both menitis and we actually can see this in brain abscesses 2:03:57 too. But one of the things here is it's actually pretty kind of simple to think about it. So when a patient has menitis they have you know these pathogens that are along the meninges well think about this again orange is the perostial layer of the dermater green is the meninja layer of the dermater then what is this part here this blue one that's the arachnoid m and then the pink one is the pomater well if you guys remember the meningial layer of the dura mater breaks away from the perryio and creates this thing called a faulk this case let's say it's the faulk cerebri and that's where a cerebral sinus sits That's usually and for this example the false cerebra it's the superior sagittal sinus. If you have all of this infected material of the meningis and it's pretty diffuse right we talked about it can be really really diffuse that inflammation is going to cause a localized kind of phabitis. So there's going to be all of this inflammation here. That inflammation is going to be localized and it can cause phabitis. And that 2:04:57 phabitis, inflammation of that vesicle, that vessel can increase the risk of thrombosis. And if I clot off this vein, I impede the cerebral venus drainage. And that's what we get worried about is we get worried about a basically a phabitis which is going to increase clot formation in that area and this is usually more of like what we call separative uh thromboflabitis and this is basically going to be due to an underlying infection like menitis and that is going to cause inflammation of the vessel. That inflammation is going to increase the risk of clot formation and that clot formation is what we're going to see some problems with. All right. So now if we have some type of like let's say again menitis and it's affecting the nearby veins that are in that kind of location of that meningial irritation and inflammation yeah we could definitely develop thrombosis and so you have to think about the potential veins that are actually located here. So for example, let's say that you have this top one here. This is called your superior 2:05:59 sagittal sinus. Here you're going to have another one which is called the inferior sagittal sinus. All right. So here we have the superior sagittal sinus. Here we have the inferior sagittal sinus. You also have another one here called the great cerebral veins. But I don't want you guys to go too crazy with that one. And then another thing is that the inferior sagittal sinus usually empties into this confluence via something called the straight sinus. Then you're going to have this one over here after the confluence. And this is going to be called your transverse sinus. And then lastly, you're going to kind of bend it and move it downwards. And that's going to be called your sigmoid sinus. All right, that's going to be this one right here. And then after that, you also have something called the cavernous sinus and the superior and inferior petroal sinus, which is 2:06:59 supposed to eventually empty down. The whole point is that the sigmoid sinus eventually will empty downwards into something called the internal jugular vein, which drains that out of the actual skull and into the internal jugular system, which will then take that back down to the right atrium. Right? Whenever you have any kind of like condition like menitis, it can actually cause pretty diffuse inflammation of the meningis where you can definitely get superior sagittal sinus thrombosis, inferior sagittal sinus thrombosis, transverse sinus thrombosis, sigmoid sinus thrombosis. The important thing to remember is that brain abscesses oftentimes go with these as well. I won't go crazy, but I want you guys to think about this for a second. If a patient has a frontal lobe abscess, let's say that they had a frontal sinusitis, maybe they had a sppheninoid or ethmoid sinusitis or something like that and the infection spread via the actual bone or via the small veins, it can cause a frontal abscess. But what also could it gain access to the superior sagittal sinus? So they could get superior sagittal sinus thrombosis. If a patient had let's 2:07:59 say auditis media or they have mastoidisitis and it lead to a temporal lobe abscess what structures are really close to that temporal lobe the transverse sinus and the sigmoid sinus. So these tend to be the most three affected. So these are the ones that are most affected often by conditions such as brain abscesses and menitis. All right. Now the symptoms of these are kind of depending. Superior sagittal sinus thrombosis is pretty nasty. It can definitely cause increased ICP. It increases the risk of having what's called venus infar where there's so much back pressure because you can't get blood out of the vein. The blood backs up and it actually it halts or impedes the normal cerebral artery profusion and so you don't get as much oxygen to that actual brain tissue and it can infarct or it can cause enough back pressure that the veins start to rupture and you bleed into the brain. So you can get Venus hemorrhagic kind of changes as well. So that's really really important with these. These usually are going to potentially cause some kind of 2:08:59 change particularly you may have pain within like the ear area uh and also just the other nearby structures that we want to talk about. So here's the last thing I want to think about with cerebrus thrombosis that we talked about this one very very briefly. This is called the cavernous sinus. We'll talk about this a lot in the um infections particularly for the ENT infections but the cavernous sinus is important because it's very very highly associated with again CNS infections as well. So let's say for example here I have what's called the sppheninoid sinus right so here's your sppheninoid sinus and that's why if you get some type of sppheninoid sinusitis that infection can spread where right to the cavernous sinuses right and so that's one important thing you also have these kind of like small little emissary veins that come from parts of the face as well so if you get an infection somewhere again frontal ethmoid sinuses that can also spread there as well but if an infection spreads here to these structures Again, what are these called here? These are called your cavernous sinus. So, this is 2:10:01 called your cavernous sinus. The cavernous sinus is really important because there's a couple different structures that run through it. All right. One is you have the internal corateed artery. So, the internal corateed artery actually runs up through this puppy right here. All right. So you have an internal corateed artery that runs up through here. That's one thing. But the other thing here, let's actually do this in orange, is you have some nerves. You have cranial nerve three, cranial nerve four, cranial nerve six, and then you also have cranial nerves particularly five. Two different divisions V1 and V2. So again, which are the actual cranial nerves here? This is going to be cranial nerve three, cranial nerve four. cranial nerve six and then you have the V1 division of the actual trigeminal nerve and then over here you'll have the V2 division of the actual trigeminal nerve. So we have V2 of cranial nerve five and then V1 of 2:11:07 cranial nerve five. So these are going to be the different kinds of cranial nerves that we can have here. And the reason why this is so important is that when actually a patient develops some type of infection, let's say of their sphenoid sinus. So say here we have an infection and this infection occurs at the sppheninoid sinuses. So you get a sphenoid sinusitis. That infection can then spread here to the cavernous sinus. And when it spreads to the cavernous sinus, this can cause enough inflammation in this area where [clears throat] it actually can start to compress on these cranial nerves and that can increase the risk of something called cavernous sinus syndrome. So cavernous sinus syndrome and this is oftent times associated with menitis and brain abscesses. And usually what happens is because you're compressing things like 3, four, six. And also the other thing is that this is literally directly behind the eyes. It can actually cause 2:12:08 so much bulging of the eye. So we call that proptosis. It can also cause swelling of the actual conjunctable. We call that chemosis. And it can cause a lot of orbital pain. But also on top of that, it affects the actual extraocular movements. And that's called opthalmoplasia. So usually the things that we see with this is we see the patient will have severe pain behind the eye. So they'll have orbital pain but they'll also have associated proptosis which is kind of bulging of the eye. They'll have chemosis which is a really really significant swelling and redness of the conjunctiva. And the next component here is opalmo plasia which is basically you have this this difficulty or this weakness of the extra ocular muscles due to 3 four and six being altered and you can't move the eye in the appropriate directions that you need to and so this is what we can see potentially with cavern cavernous sinus syndrome and again we'll we'll talk about this a lot in the ENT infections but we definitely can see this commonly associated with potentially brain 2:13:10 abscesses and we can see is often times associated with menitis. So that's what I want you to know is that these can be these kinds of problems here can be associated associated with brain abscess and menitis. It's not to say that they are a common cause of cavernous sinus syndrome or cerebrous sinus thrombosis. they oftent times just happen to go hand in hand. The reason why I'm mentioning this is that oftentimes when a patient is diagnosed with menitis, we'll do like a CT scan, a non-contrast, we'll find that they have kind of this ring enhancing lesion. Often times we'll do other studies like CTVs, which is a CTV or sometimes if we do an MRI, we'll do an MRVOG and the purpose of that is to help to kind of really see if there is any of those cerebravenous sinuses that are thrombosed and kind of affected. All right. So the next thing that I want to kind of finish off with is again we know 2:14:11 that patients who have menagitis have an increased risk of sensory neuro deficits. It's actually probably the most common complication. It can be transient oftentimes can be permanent as well. Communicating hydrophilis is a really big one because it contributes to an ICP crisis and cerebravenous sinus thrombosis especially with that little one that we talked about called cavernous sinus syndrome. They're oftent times associated with things like menitis and associated with things like brain abscesses. It's not all the time and it's not often that the condition itself such as menitis and brain absesses cause on its own things like cerebravenous sinus thrombosis. There's something that you're actually going to see probably most often kind of correlating with one another. The whole purpose of that is that again that when we're doing CT scans, finding these things like brain abscesses, we're probably also going to be adding on CT venogs or MR venogs to really see, hey, here's the abscess, but also is there any other kind of associated nearby venus sinuses that are afflicted because they came from a shared source, a frontal ethmoid sinusitis, a dental 2:15:07 abscess, otitis media, etc. All right. The last thing I want to talk about here with menitis and I told you I was going to talk about this when we talked about the ethologies is niceria. So niceria menitus so I'll write this guy out niceria meneniditus is a gram negative diplocus right so gram negative diplocus and this thing is super nasty man it releases lots of like different types of endotoxins like lipopolysaccharides and these endotoxins they lead to a bunch of different issues. One of the big problems here is that they can increase the production of things like tissue factor and other kind of coagulation enzymes but also it can trigger a increased production of things like interlucan 1, interlucan 6, tuminccratic factor alpha from a lot of our endothelial cells and our immune system cells. So this is going to be a really really problematic thing is that these things are pumping out the endotoxins and again these endotoxins are sunzaguns because they can increase the activity of things like tissue 2:16:07 factor which is an important part of our coagulation cascade and our pro-inflammatory cytoines like interlucan one interlucan 6 TNF alpha. Now why is that important? Well, if you increase tissue factor and maybe other coagulation enzymes, what's going to happen is you're going to increase the activity of the extrinsic pathway, push them down to the common pathway, and lead to clot formation. Now, let's say that you do that and you cause a bunch of clots to form all over the place. Now, you have tons of these things called micro thrombi. All right, that's one potential issue here is that you have tons of these micro throi all over the place because you're activating the coagulation cascade. The other problem here is that if you cause so much coagulation activity, you consume so many of your clotting proteins. And so that's the other issue is that you make so many clots that eventually you run out of clotting proteins and you run out of platelets. And I'll explain another 2:17:08 reason why you run out of platelets. And that basically increases the risk of bleeding. All right? So they also will have not only clots but they'll also have bleeding. All right? And that bleeding is again due to the consumption of our clotting proteins. So they're going to have a lot of bleeding due to the consumption of clotting proteins. So you're going to see clots and you're going to see bleeding which seems paradoxical, right? The reason why this is important is because this kind of combination causes the presentation of something that we get concerned about called DIC. So I know you guys have heard of DIC. We talked about I think like a million times in hematology. But with DIC, it's some kind of process that increases the risk of widespread clots that consume your clotting proteins that precipitate bleeding. So what would we think about with DIC? Well, if I consume clotting proteins, we look at clotting proteins and we measure their activity via the PT, the PTT or the PT INR and the PTT. [snorts] That's one thing, 2:18:09 right? Now, when we think about PT INR and we think about PTT, these are measuring the activity of the extrinsic pathway and the intrins I'm sorry, exttrinsic pathway, intrinsic pathway. These will be elevated. it's going to take a longer time now for these patients to clot because we're consuming all of their clotting proteins. The other thing is we look at something which is kind of a measure of clot burden which is called D-dimer and that's going to be through the roof because you're forming tons and tons and tons of clots and so I should also expect a bump in the patient's dimer. The other thing is whenever we are actually kind of doing this kind of process where we're really really making a lot of clots and we're consuming a lot of the clotting proteins. The other thing is is that you run out of very specific proteins that you need to help with the clots and that's called fibbrinogen. That's one of those really really important clotting proteins and you're consuming so much of it to make 2:19:09 clots that you run out of it. So the fibbrinogen levels tend to be pretty low as well. And then one other thing that's often times associated with this condition is that whenever you have these micro throi, you're supposed to have things like red blood cells and platelets that are running through here. And what happens is you shred up the red blood cells, right? And these are called chistocytes. That's one thing. But the other thing is that you're consuming a lot of the platelets. And so that's one thing that happens is as red blood cells are moving through here, you're shredding them up and you get things called shistytes. But to make these micro throi, what do you need a lot of? You need a lot of platelets. And so platelets get consumed like a son of a gun. I actually need my maroon marker here. So the platelets are going to be consumed to make a lot of these micro throi. So we need those platelets there to help us to make these micro throi. So what would I expect to happen to my platelet levels? I expect that to go down because I'm consuming them puppies, right? So my platelets will go down. 2:20:12 And if I'm ripping up red blood cells, what do I expect to go down? My hemoglobin and the hemoglobin. And usually this is why we would see anemia. Usually this is a type of hemolytic anemia. So I would see thrombocytoenia, maybe a hemolytic anemia, and I would see all of these kind of abnormalities in my coagulation parameters. So this is what we get concerned about with niceria. And I think that's a very good reason to be concerned. The other thing here is that these endotoxins also are problematic because they cause a lot of these cytoines to be pumped up. And what these do is they work on our blood vessels and they cause our blood vessels to undergo vasoddilation and increase capillary permeability. So whenever you cause vasoddilation, so we're going to really blow these puppies up. We're going to increase the actual diameter and we're going to increase the capillary leakage. What's that going to do to your overall blood pressure? It's going to drop that son of a gun like a bad habit, right? So we're going to see two things here. Vasod dilation 2:21:13 and increased capillary leak. The combination of this the vasoddilation will drop your systemic vascular resistance and that's going to drop your blood pressure and the capillary leak is going to cause you to lose fluid. It's going to cause third spacing. It may cause a little bit of a hypoalmia or decreased effective arterial volume and that blood volume drop will drop the appropriate blood pressure. And this is where we see patients going into shock. And usually this is a type of septic shock, right? So that's something I want you guys to think about is usually with these patients who have nerium men anditis, we may see shock, we may see DIC. And here's one other thing to kind of go with this. This is kind of interesting. Um, so for right now, I'm just going to move the hemoglobin out of the way. Whenever you kind of consume your platelets and you cause all of these kinds of bleeding processes, we may see some associated especially with the DIC, we may see some rashes. And this is one of the key things that we see associated with this condition is they may see what's called a peticial 2:22:14 or peruric rash. And that is almost always going to be present on your exam and it's going to scream niceria menitis. So if you see a patient has a particular rash, maybe they have some coagulation abnormalities, maybe they're really really septic appearing, you want to think about niceria. Another way that they will do this, I won't go too far, but this also can get in your joints and it can also cause septic arthritis. And so sometimes one of the ways that they'll actually present is that they're having difficulty ambulating. So don't think about don't don't forget about that one as well. The last thing I want to talk about is whenever a patient has this severe hypotension and they have this DIC both of these things kind of really just piss off the adrenal gland really really bad. And so what happens is I'd say more likely often than not is this bleeding and kind of like uh processes of clotting and bleeding inside of the adrenal gland and probably even a combination of hypoprofusion. It just really really jacks up the adrenal 2:23:15 gland. And what happens is they undergo this bilateral kind of hemorrhaging inside the adrenal gland and this just it's it's so bad. It really knocks off their cortisol levels and it knocks off their eldoststerone levels. All right? So they experience kind of like an adrenal insufficiency essentially. So they have low cortisol and they have low eldoststerone. Now I want you to think about this for a second. If your adrenal gland sucks in this scenario and it can't pump these bad boys out, what could I expect and a couple of things if we can mash these in here? Right. Well, aldoststerone is supposed to reabsorb sodium. Are you going to be able to do that? No. So, I see a drop in the sodium. It's also supposed to secrete potassium. Can you secrete potassium? No. So, the potassium goes up. And what's cortisol do to your glucose levels? Increase it. If you don't got cortisol, what happens to your glucose levels? Drops. And so we're going to see a drop in the glucose. And so oftent times you may see these 2:24:16 electrolyte and min nutrient abnormalities such as hyponetriia, hypercalemia and hypoglycemia. This in a combination with also cortisol is also important for being able to control your blood pressure. Aldoststerone is supposed to control your al overall sodium and water reabsorption. So your blood volume can drop. This patient could also worsen their blood pressure. So, we would experience a rapid worsening of their blood pressure. This here, I'm gonna give it my best go here, guys. This is called Waterhouse Frederickson syndrome. And this is essentially whenever there is bilateral adrenal hemorrhage. And that bilateral adrenal hemorrhage leads to a loss of cortisol, a loss of eldoststerone. They experience electrolyte abnormalities, glucose abnormalities and rapid worsening of their blood pressure oftentimes associated with meningoia. All right. So that's what I want you to take away from 2:25:17 this with neria menitis is nari menitis can be associated with a particular papiric rash. It can be associated with severe hypotension. It can be associated with dic and it can be associated with an adrenal crisis. Overall with menitis the big complications I want you to associate this with is sensory neural deafness and communicating hydrophilis. This here is more often a result of a shared source of infection between menitis in this condition rather than a sole result of menitis and brain abscesses. Let's now move on to the next complication associated usually with encphilitis. All right. So encphilitis is one of those things where again you think about a patient with fever, you think about headache, you think about an altered mentation, you think about some type of change in their memory, behavior, speech such as aphasia, um and high incidence of seizures and sephilitis. I'd say again menitis can increase the risk of seizures. Brain abscesses can also cause seizures, but the one that carries the highest incidence of seizures is going to be 2:26:19 encphilitis. Right? So that's the one that I want you to think about. So again there's some type of inflammation of the brain parankma. Most often it is the temporal lobe and the temporal lobe is just a very very sensitive area for some type of seizures to occur. Now with these seizures, if you develop seizures, oftentimes what we get worried about is, you know, if they become focal or if it gets to the point where they start to become generalized, right? So that's what we get worried about is focal versus generalized seizures. All right? So could this be focal depending upon the area that will determine the actual type of presentation they have or is it going to be generalized? So focal mean that you may have a focal you know tonic clonic movement of one extremity right whereas if you have a generalized seizure this may precipitate a fullbody tonicclonic convulsive seizure. Now the 2:27:20 other thing I want you guys to think about with seizures is you know with these you run the risk of something called statusep epilepticus and status epilepticus is this you have seizures for more than or equal to 5 minutes or you have a seizure that you don't return back to your baseline if you have seizure and seizure seizure in succession that's what we get concerned about with is status epilepticus with another concept here of seizures is again I really need you to remember that if I talk about them in order of like commonality so order of let's say um commonality. We'll just use that term order of commonality here. You would start off saying that encphilitis is going to be the most likely to cause seizures. Then you would go to something like a brain abscess. And then after that you may kind of move forward into something like menitis. So all of these definitely carry a risk 2:28:22 of seizures. It's just most often you're going to be thinking about this one with encphilitis. All right. Again, that is going to be encphilitis. Encphilitis definitely can cause other potential complications. It's just the thing I want you to associate it with is seizures. Menitis I want you to associate with sensory neural deafness communicating hydrophilis. And think about that DIC shock and waterhouse Frederickson syndrome with neria or meningo coakal menitis. I gotta be careful with the way I say meningo coakle. All right let's move on to the next part brain abscess. All right so let's now move on to brain abscess. So when we talk about brain abscesses again menitis you worry about that particularly the communicating hydrophilis the sensory neural deafness that's the big things and sephilitis you really worry about seizures but again remember menitis can cause seizures brain abscesses can cause seizures as well. That's all. As long as you have cortical irritation, you can get a seizure. It does not matter. Now, if that that brain abscess is a little bit more subcortical or it's cerebellar, you may not see any kind of like seizure activity. But if that brain abscess is 2:29:24 near the frontal lobe, the temporal loes u near those gray white junctions and they're scattered, but they're near the cortex, you can 100% have an increased seizure risk. But menitis and sephilitis and brain abscesses, cortical brain abscesses increase the risk of seizures. with brain abscesses in general. A couple of things I want you guys to think about and I think it's important to think about this because it it really carries a high risk of mortality is a abscess rupture. All right. So what I mean by this is it can increase the risk called a ventricle um let's say ventricle rupture. So let's say here you have an abscess and it's very very close to an associated ventricle and what happens is that abscess kind of starts getting close and close to the wall of that ventricle and then all it does is is it literally empties its contents into the ventricles. What that's going to do is is that's going to cause a couple different issues. One is if the infected material gets bad enough it can cause maybe an obstruction. maybe can go 2:30:26 clog up the arachnoid villi and that can increase the risk of things like hydrophilis, right? But the concerning feature here is you run the risk of something called ventriculitis and ventriculitis is pretty terrible. It's one of these things where these patients oftent times don't do very good. You often times have to put them on things like intratheal antibiotics to really help to clear this stuff out. Sometimes they need VP shunts because it can cause communicating hydrophilis. Usually if an abscess does rupture into a ventricle, it can really produce a prolonged kind of course for them such as ventriculitis and that ventriculitis definitely can increase the risk of things like uh communicating hydrophilis. So I would write down that this does carry a high risk higher risk of something called communicating hydrophilis. High risk of communicating hydrophilis. oftentimes with these kinds of conditions, you may need those long-term things like VP shunts to help them out. 2:31:26 All right, but that's something I want you guys to understand here. The other concept is that these brain abscesses, they can have mass effect. And when you have mass effect, imagine that I'm kind of pushing on this ventricle here. Imagine I'm squeezing on it. By doing that, when you compress at a particular area, you impede flow. So, let's actually kind of pretend here for an example here. Let's say here I have the ventricle and then this abscess is going to squeeze let's say right here [snorts] right at this point. If it squeezes right here and it compresses in this area it can then narrow the ventricle. So let's then say here as an example it's going to narrow this ventricle. If you narrow that ventricle, it's going to impede the normal kind of downward CSF flow. So CSF is going to want to try to be able to move down this way, 2:32:28 but we're going to inhibit that process because we're going to exhibit some mass effect. By doing [snorts] that, when you inhibit this, you build up the pressure inside of the ventricles. And what happens to this ventricle? It gets larger. And that's when they start to experience some enlargement of the ventricles. What's that called? Hydrophilis. Right. So usually these patients exhibit something called hydro sephilis but it is due to not a communicating process. It's an obstructive process something that is blocking the flow of CSF downwards because this brain abscess is mashing there. Maybe it's mashing on the third ventricle. Maybe it's mashing on the cerebra duct. Maybe it's mashing on [snorts] the fourth ventricle. All of these things that hydrophilis we know does what? increases things like nausea, vomiting, papadeema, and dipopia. And so those are all potential symptoms of hydrophilis. The last thing that's probably the most concerning with a brain abscess is the risk of herniation. Usually when you 2:33:28 have these types of processes where you have a brain abscess, if they're large enough, they're going to exhibit mass effect. And that mass effect can start kind of pushing things in opposite directions. So let's imagine you have an abscess here and it's pushing brain structures this way. It can herniate parts of the actual brain matter underneath the faulks. Or let's say that you have a brain abscess here and it's pushing the enkus over this way. Or maybe you have one somewhere within the basil ganglia and it's pushing things down in the brain stem. Or maybe you have one here in the cerebellum and it's trying to squeeze pieces of the cerebellum out through the fam and magnum. Well, these are called herniation syndromes. And so you have one, two, three, four. So one is referred to as a subfalene herniation. Right? So we call this sub falsine [snorts] herniation. Two is called uncle herniation. Three is called some call a 2:34:28 dianalic shift or a trans and this is a downward transtorial herniation. And then four is called tonsular herniation. The problem with this is that these all produce specific neurologic deficits. Usually subfausalian herniation compresses the ACA territory. They develop contrlateral hemiparesis. With uncle herniation, they develop a third nerve pausy where they have a dilated and non-reactive pupil and sometimes contrlateral hemiparesis. Transenter is you're pushing down in the brain stem. So they have a declining level of consciousness and sometimes they can have some changes in their pupils where it's more midline position and fixed and then tonsular herniation is you're kind of compressing and pushing the tonsils out from the frame and magnum and then get kind of cardopulmonary arrest and Cushing triad types of presentation. So that's what we get worried about is this type of herniation and that's why sometimes in the exam what you'll see is it's harder to pick this out. So the 2:35:29 whole concept is if I have a patient who has a brain abscess, I get a CT scan, I find the brain absess, what else should I be looking for? Hydrophilis. What else should I be looking for? Is the abscess very very close to the ventricle? Is it opening up into the ventricle? With herniation, do I see any evidence of herniation syndromes? And then lastly, clinically, I want you to always coordinate this with specifically something called the Cushings Triad. So this is all herniation but correlate this with the Cushings triad. Do you guys know what the Cushings triad is? I know you do. Come on, let's write it out. What's the Cushings triad? So the Cushings triad is a couple different things. One is with that triad we get worried about. One component is heart rate. The other one is blood pressure. And the other one is respirations. So this is heart rate, blood pressure, respirations. What I want you to do is I want you to remember the heart rate will drop. They'll become brada cardartic. 2:36:29 The blood pressure will go up. They'll develop a reflex hypertension or actually they'll cause hypertension to try to peruse the brain. And sometimes it develops a reflex brada cardia or sometimes that brada cardia is due to a loss of the cardiac accelatory center activity. And then usually the last thing is irregular respirations. So irregular respirations. All right. So the Cushings triad is again a low heart rate and increased blood pressure and irregular respirations. That is what we refer to as the Cushings triad. So if I have a patient coming in, they have maybe headache, fever, they have some focal deficits, and then they also are presenting with a declining level of consciousness. Maybe they're presenting with a high blood pressure, a low heart rate, irregular respirations, level of consciousness is really, really, really kind of declining. What should I be concerned about? I'm worried about herniation type of presentation and that CT scan will really help me to identify that. The last thing that I want to kind of talk about is again it's kind of going along with the herniation is the 2:37:31 most common feared complication among all of these three menitis and sephilitis and brain abscess is an ICP crisis. So whenever the patient's ICP goes up whether that's due to hydrophilis or whether that's due to diffuse edema whether that's due to blood whatever it is the ICP increases the risk of brain herniation and that brain herniation is what increases the risk of death and that's what we get concerned about right so let me kind of explain here something we've probably talked about this a lot and again I don't want to go crazy on the neural ological complications. I know it probably seems like it like I'm doing that right now, but I promise we're going to talk more about these in neurology because I wanted to make more sense there. Infectious disease should be kind of maybe thinking, hey, what are the potential complications? And the reason why I talk about these complications is because we actually treat these kind of alongside the underlying menitis, the 2:38:32 underlying encphilitis, the underlying brain abscess. But I don't want to go through crazy crazy mechanisms and pathophysiological processes. I want to briefly talk about something called the Monroe Kelly doctrine. So it says that the the skull controls a fixed space which occupies the brain, the blood and the CSF. So we're going to represent the black here as the brain matter. We'll represent the blue here as the CSF and we'll represent the red here as the blood. All of this is what sits inside of the skull. If you increase one of these or multiple of these more than what they're supposed to be, it's going to increase the ICP. That's what I want you to think about. So if a patient has menitis, how does that increase the ICP? Well, one thing it does is it increases your brain edema. So it causes something called vasogenic edema. So it basically kind of you lose the capillary foot process kind of a connection at the 2:39:33 bloodb brain barrier and fluid can leak from the actual capillaries or vessels there into the brain tissue and cause associated edema. So that's one mechanism. The other one is it can cause hydrophilis. So it's going to cause edema. So brain edema and that's going to increase ICP and it also can cause hydrophilis. Which type of hydrophilis? most often communicating hydrophilis but the combination of these is going to increase ICP because edema is going to do what it's going to increase the amount of brain matter your swelling of the brain matter hydrophilis is increasing the CSF inside of the skull that's a fixed space that's going to increase the ICP if the ICP goes up enough you can present with herniation syndromes and [snorts] Cushing triad presentation what about encphilitis it primarily acts by causing diffuse cerebral edema especially in the temporal loes it doesn't often times have any kind of effect on the patient's what ventricle size and so because of 2:40:34 that that would be the primary way of the patient increasing their ICP the last one here runs that really scary risk with brain abscesses they can definitely cause mass effect you're having a a big lesion inside of the brain tissue that's occupying more space and exhibiting mass effect. And so one of the things that we'll see here is we'll see an increase in mass effect. And that mass effect is just due to the underlying brain tissue in this case the infected tissue and that's going to exert an increase in the ICP. [snorts] The other one is hydrophilis. What kind of hydrophilis? most common is obstructive and so it's going to compress on a ventricle and impede the flow increase the CSF and that is going to cause a problem with the ICP so mass effect is going to be one problem hydrophilis is another one and the combination of these will increase the patient's ICP you increase the patient's ICP you run the risk 2:41:36 depending upon where that lesion is the underlying process of herniation syndromes and Cushing's triad Right. So my friends that really leaves us kind of like talking about CNS infections with respect to how do these pathogens get into the brain. How do we then think about the underlying eeologies? What is the most likely pathogen causing bacterial menitis, viral menitis, encphylitis? What is the most common causes of brain abscesses depending upon if there's piogenic, non-piogenic, solitary, multiple? And then from there, how do we think about CNS infections clinically? Do they present with fever and headache? Yeah, all of them. Well, which ones present more with the menial signs and which ones present with more of the cortical signs? That helps us to kind of think about that and diff kind of develop a nice differential diagnosis. And often times you may get those presentations, but sometimes the patient may come in with a new onset seizure. Sometimes they'll come in with features of increased intraraanial pressure due to hydrophilis or due to 2:42:37 mass effect. And those are the things I need you to think about. Also, sometimes as a result of their underlying disease, even though you treat them appropriately, they may develop complications such as cerebravenous sinus thrombosis, sensory neural deafness, and seizures. And that's what I really want you guys to kind of start putting all of this together. So now, what I want to do is let's take a step back. We've really built our foundation. Let's say if I needed to know as a clinician the bare minimum to say, here's how the patient's presenting. How do I figure out if it's a sephilphylitis? How do I figure out if it's a brain absess? How do I figure out if it's menitis? And how do I figure out what the most likely pathogen is that can guide my empiric and then narrow treatment? Let's do that now. All right, my friends. Let's now think like clinicians. Let's talk about the diagnostic approach. One of the most common classic findings probably across the board of CNS infections is fever and headache. A lot of them are going to present with a fever and headache. Menitis, brain abscess, encphilitis. You know, I think that's kind of one thing to start off with. The next thing I 2:43:35 think that adds to the utility that makes you even more suspicious of an intraraanial process or at least a CNS infection is the presence or absence of meningial signs and cortical signs. So menitis will present with fever, headache, that's a very common presentation and often menial signs whereas you know conditions like encphylitis it usually doesn't have menial signs and brain abscess doesn't often have menial signs. That's one thing to think about. Now what are meningial signs? We talked about this on the whiteboard, right? Usually this is referred to as like nucal rigidity. So neck stiffness, that's one thing. So neck stiffness kind of limited range of motion with the neck. And going with that, if you try to have them do specific maneuvers, the negative presence of those maneuvers doesn't completely exclude the possibility of menitis, but the presence of them does make you a little bit more suspicious of them. What do I mean by that? Well, there's two tests. One's called the 2:44:36 Brazinskis, and we talked about the Brazinski. When you're kind of flexing the patient's neck, it puts a lot of stress and tension on those meningis. And one of the responses to that is that they start to kind of flex up their hips and their knees. Another one is called the Kernig sign where you're having them lay flat. You're bringing their hip into kind of a flexion point. And then what you're going to do is their knee is kind of like at a 90 degree angle and you're going to start trying to extend that leg. And when you do that, it's going to precipitate pain and resistance to that type of movement. So the again the absence of the positive signs here does not exclude menitis. That's really important to remember. There is a newer test. This goes a little bit beyond the likes of being tested on. for clinical uh kind of discussion there's called a jolt accentuation maneuver where you're quickly moving their head from side to side that may precipitate a lot of pain and stiffness and resistance to that movement and the presence of that does scream a high likelihood of menitis and 2:45:37 you know if it's no if it's negative that almost almost completely rules out the possibility of menitis either way as clinicians fever headache menial signs screams menitis on the textbook All right, for the cortical signs, that's going to scream more of the possibility of encphilitis and brain abscess. Menitis may or may not have cortical signs. It depends if it's actually led to what's called meningo encphylitis. So menitis doesn't often cause cortical signs. It can, it's just not as common. and encphilitis 100% there's inflammation usually of the temporal lobe where you're going to see a lot of these processes occur especially things like seizures cognitive behavioral changes and brain abscess is usually an infection that's usually more encapsulated and it's involving an actual brain tissue a particular lobe that will cause associated cortical signs like focal neuro deficits so fever headache meningial signs screams menitis fever headache cortical signs screams 2:46:38 encphilitis what are those cortical signs that should make you think about these. That would often be an altered mentation. So, if a patient's confused, if they're difficult to arouse and wake up, if they're kind of having difficulty being able to answer particular questions, knowing where they're at, right? Knowing what their name is, knowing what the year is, knowing who the president is. Those kinds of things kind of help us to understand if they're alert, if they're awake, if they're oriented to person, to place, to time. And so, that's really important. Focal neuro deficits are dependent upon the area that the actual encphilitis and brain abscess is. They may present with hemiparesis. They may present with a cranial nerve pausy. They may present with potentially aphasia. And so that's dependent upon the location of where the infection is. And then seizures especially with encphilitis if it's near the temporal lobe and it's involving the outer gray white you know the outer gray matter the cortical region that's a high increased incidence of seizures right and then cognitive behavioral changes 2:47:40 often we see with encphilitis because it's involving the temporal lobe where we have structures like the amygdala where we have structures like the um the hippocampus things that are part of your limbic nuclei that control not just your behavior but also your memory and so that's really really critical to think of these things. So for example, if I said a patient had fever, headache, menial signs, you think menitis. If I said fever, headache, altered mentation, cognitive behavioral changes and seizures, you really want to think incphilitis. And if I said fever, headache and and a focal neural deficit, that often times more than not points to a brain abscess. Now these aren't always perfect. So what I want you to always remember is when a patient has a fever, they present with maybe cortical signs, meningial signs, you have a high degree of suspicion for a CNS infection, you need to get them on the proper antibiotics if it's a bacterial infection. The reason why is mortality can increase if you're not treating them. Before you put a patient on an antibiotic, you should always obtain blood cultures because if you give them antibiotics and then you obtain blood 2:48:42 cultures, you may sterilize those potential cultures. And so that's one of the things that you should always try to do unless you just don't have an option. But try to get blood cultures first. That's why I kind of talked about this here because in maybe 25% of cases it may come up positive blood cultures especially in the patient who has things like menitis or abscesses of the brain. All right? So get those cultures before you start the antibiotics. The next thing you should do is okay I have a patient with a fever, headache, they have some cortical or meninjial signs. I think that they have a CNS infection. get the blood cultures. Depending upon their presentation, I may start them on some antibiotics. I may add on some steroids right off the get-go, depending upon which one I think it is, right? But the next question that you have to ask is I need to be working in tandem. So, a lot of the times you're diagnosing and treating in the same parallel pathway. So, in other words, I'm kind of thinking, okay, this could be menitis, right? That that let's say that I have fever, headache, menial signs. First thing I'm going to do is I'm going to get some blood cultures. I'm going to 2:49:39 start them on empiric therapy and then I'm trying to also at the same time do I need to get imaging? Do I need to get an LP and move through that process? How do I determine if a patient who I think has menitis or has a CNS infection needs a scan a non-contrast CT scan? We look at something called the fail signs. Do they have it or not? So what are the fail signs? The fail signs is do they have focal neuro deficits? Do they have hemoperesis that's present? That's kind of one thing that's going to be possibly concerning. Do they have a fasia? Do they have sensory changes, cranial nerve pausies? I' I'd probably get a CT scan, right? The next thing is do they have an altered mentation? We can be concerned about that, right? Because focal neuro deficits sometimes scream a potentially a brain abscess. Altered mentation scream maybe in sephilitis. Are they immuno compromised? So meaning HIV, did they have a recent transplant? The reason why is these patients are super high risk for brain abscesses. They're 2:50:40 also super high risk for very scary types of menitis that can quickly progress and become very very very sick. All right, the next one is a lesion. Do they have a known CNS disease or do they have evidence of increased intraraanial pressure? Usually on the exam, this is presented on some way, shape or form where you've evaluated the eyes and you've somehow been able to see the papula or the optic disc and you see the papa edema. That would be an indication to not stick a needle into their cerebral spinal fluid. All right? And then the last one is going to be the S, a new onset seizure. I want you guys to think about this for a second. The reason why you ask these questions is that if I don't do these things and I go ahead and I stick a needle into the cerebral spinal fluid and they have a brain abscess, they have a lesion that's actually present that's increasing their intraanial pressure or they have a structural focus that's increasing their ICP that any of these things could explain and I stick a needle into their CSF and I drop the pressure of their 2:51:42 spinal canal that could theoretically cause herniation. So a lot of these things are trying to reduce the risk of herniation and also identify if there is a brain mass in the process. All right. If they have these signs, you need to not do an LP right away and instead you have to get a CT scan because you want to find any possible structural lesions that could explain their presentation and also avoid herniating them if you're going to get an LP. All right. If you do not have fail signs and they present with a CNS infection that concerns you for menitis or encphilitis, you definitely want to get an LP. And so I would go right to an LP if they don't have fail signs. All right. Now, another reason I would do an LP is if I had fail signs, I got the non-contrast head CT, but it showed no brain abscess, no kind of lesion that was present. and I have a high degree of suspicion that they got menitis or encphilitis, I'm going to get an LP. LPS are great for menitis and 2:52:43 sephilitis. Non-contrast or CT scans, MRIs, those are better for brain abscesses. You don't want to do an LP for a brain abscess. It's not going to help you. All right. Now, when we do an LP, all it's trying to do is test the cerebral spinal fluid. Because if you think about it, dude, what's in what's a part of the meningis? You have your dura mater, you have your arachnoid m and you have your pom mater. What's the space in between the pomater and the sub the um arachnoid m the subacoid space. So if you have inflammation infection of the meningi that's including the subacoid space. So what I want to do is is I want to tap into that and test the CSF for bacteria, viruses or fungi if the particular exposure risk factor exists. So I'm going to do that. I'm going to access their cerebral spinal fluid by going and tapping in around that probably L3 L4 region. Stick a needle in there and then once I've done that, always a part of your process, especially if you're concerned um for 2:53:44 these patients, you should always do what's called an opening pressure. So, what you'll do is you'll stick a needle in. You'll kind of pull the stylet out. Am I getting any fluid? Nope. Stick the needle further. Pull the stylet out. Nope. No fluid. Stick the needle in. Oh, I got some fluid. All right. Take your next apparatus here. Put it on. And what that's going to do is is it's going to give you your monometry, your pressure, what's the pressure upon opening and accessing into their cerebral spinal fluid or their subactoid space. And that's important to determine because the higher the pressure is, the more it concerns you for possibly an abnormal infectious process. Usually anything kind of less than 15 is relatively normal. And as you go above that, it's obviously abnormal. Now, another thing is you have stopcocks on this that control the way that you want to then collect fluid. usually have tubes that you're going to collect in sequence one to four and you're just going to keep collecting that CSF, taking a look at the color, taking a look to see if it looks perent. Does it look clear? Does it look bloody? Those are key things. Usually bacterial is going to appear 2:54:40 more cloudy. Usually HSV and sephilitis appears bloody. And so that's something that you really want to consider. All right. Now, after we've done this, we're then going to take these samples, these four tubes. We're going to send it off to the lab and we're going to test it. When we test the actual fluid, we're testing it for a couple different things. Now, opening pressure, we already talked about that. That's something that you can do at the bedside. Opening pressure is oftentimes high in any type of pathology like bacterial menitis, right? You're going to see it in viral menitis and encphilitis. Sometimes it can be a little high, but another one that's really important is TB menitis. This one can have a pretty high opening pressure. And the last one is cryptocal menitis. Can also have a high opening pressure. So this is something that may help you if you tap in you see a high opening pressure that may make you think about bacterial and if the exposure and risk factors are right you could think about TB you could think about cryptocal if the opening pressure is kind of normal or just on the verge of being a little bit elevated you can think about viral 2:55:42 menitis or HSV and sephilitis right the next thing is to actually send it off to the lab and the lab will give you what's called a cell count with a differential in other words they'll tell you do you have a lot of white blood cells that are present in the CSS That means inflammation, right? And the type of white cells also can help to guide you to which type of pathogen to suspect. With polymorphonuclear lucasites, which are just neutrfils, dude, that's going to be the predominant one and it's going to be in the thousands. It's going to be pretty high for bacterial. Whereas usually with like viral menitis and sephilitis, TB, cryptocal, it's more often high white cells, but it's primary lymphocy predominant. And that's what I want you to think about for these. All right. The next thing that you also want to get is you want to check what's called the glucose. The glucose tells you about the metabolic activity that's going on in there. If there's tons of bacteria, if there's lots of mcoacteria, if there's lots of fungus like cryptocus, these things are going to chew through the glucose for their metabolic processes to 2:56:43 divide and to grow. And so the glucose levels will probably be low for bacterial TB and cryptocal, but they're going to be likely normal for your viral processes because they're not going to be dependent upon glucose. All right, so that should be normal, whereas these should be low. All right, we got the opening pressure down. Almost all of them are high except viral cell count. Bacterial is going to scream neutrfils in the thousands. Viral, TB, cryptocoyl, they're lymphoy predominant. And obviously with TB they tend to have a like probably in the hundreds to thousands. Cryptocal hundreds to thousands. Viral is not super high. The next thing here is protein. Protein is really important as well. It's an again a marker of kind of inflammatory processes. It's not specific. And guess what? All of them have high protein. So it's not really going to be super helpful. Okay. [laughter] So with that being said, you kind of start stratifying at least for the most part bacterial and viral. That's really the big goal here is you can easily distinguish between these two. All 2:57:45 right. What you need to then tell you what is the likely pathogen is the Grahamstain, the cultures, the PCRs, any other miscellaneous test that you add that's dependent upon the patient's exposure, their risk factors. For example, for bacterial menitis, the cultures, the PCR, that's going to give me the things that I really am concerned about. What are the most common pathogens? Go back to it. Ask yourself what was the most common streptococcus pneumonia. That'll come up on this test. What was the other ones? Well, I told you to think about niceria menitis and think about hmophilus influenza type B. Right? Then I said, what if you have a person who's an alcoholic, they're have cerosis, they're pregnant, they're old, greater than 50, they're immunosuppressed, lyisteria, right? And then the other ones that I told you to think about is this more particularly probably in the hospitalacquired realm. if they had a vent an EVD an Ommya reservoir, they had a neurosurgical procedure and you tested it, you start thinking about things like staflacccus, especially the MRSA um and 2:58:48 then sudamonus originosa, right? Those are for the hospitalacquired ones. And so this is where again we're kind of adding in what we talked about on the whiteboard and bringing it to place and life in the clinical world. The viral ones I often you can send off a bunch of them. So when you do a PCR, you can do a viral panel and it's going to give you a bunch of them. But the only ones that we really want to know is the ones that we need to give them an antiviral. All of these are once we find out the type, they're already on empiric antibiotics by now, right? So I had a patient come in fever, headache, menial signs, they didn't have fail signs, they got the LP already in this time frame, they're on antibiotics. Once they get the cultures and it comes back with the specific one, we narrow the antibiotics down. So not only is it diagnostic, but it guides the particular antibiotic that you have to choose. That's why we're doing this in tandem. Right? For viral, we only add on the asycllovere if I have concerns of HSV. Do they have cortical signs? In other words, if I can't confidently say 2:59:48 that I don't think that they have HSV and sephilitis, they need to be on a cycllovere. That's important to remember. If they have altered mentation, if they have seizures that are new onset, if they have cognitive behavioral changes that I'm putting them on a cycle until I get the PCR back and if the PCR comes back negative, sometimes it could potentially been drawn too early and you may have to repeat it. But again, you can discontin it based upon your level of suspicion. All right. So again, viral. What do I only care about? There's only two. HSV and VZV. Those are the only ones I care about. All the other ones I'm not going to do anything with. It's going to be supportive care. TB menitis, we don't often get this unless I have the particular concerns. But you'll get what's called, you know, the miccoacterial cultures and you'll even get on like acid fast, you know, staining to look to see if these things are present, right? Cryptocal, again, I'm not doing this one all the time. I'm doing it if they have specific risk factors. And you'll do something called a cryptocal antigen test. And sometimes 3:00:50 they do an Indian ink smear. But if you ever had to pick between those two, always pick this one first. You get the point. When you're getting an LP, you're already having them covered for the most common antibiotics for bacterial and only adding viral coverage for the viral encphilitis like HSV or VZV. If you have the concerns there, once you get the cultures, the PCR testing back, you narrow it down. All right, I'm only going to cover these if I have the risk factors and I'm going to test them for it if I have the degree of suspicion. That brings in the next question. When do I actually have suspicion to test for other things? It really depends on what they present to you in the vignette. The things that they would present with TB is they probably had some kind of recent travel to an endemic area. They're immunosuppressed, especially HIV patients or they were in areas where there's high risk of exposure. Probably prisons, those are a big one that they'll talk about. homeless individuals, drug abusers. Those are people that you'd have that high degree of suspicion and you would get the acid 3:01:50 fasting, you'd get the mcoacterial culture, and you'd probably put them on a ripe regimen of some sort. All right, the cryptocol, I'm only going to do that if I have a patient who has AIDS, and they probably say somewhere in there that the CD4 counts less than 100. That means that that's an opportunistic infection for them, and I need to consider that. and then I'll put them on the proper therapy if I have that comeback positive because once you put someone on amphoterasin you you know it's a pretty nasty drug and you want to be sure of it. Neurosphilis is kind of a random one, but if I have I hear anything on the vignette of Tabies dorsales and Argal Robertson pupil, you get the VDRL, you get that kind of antibbody, the fluorescent antibbody testing to see if it comes back positive. Lime menitis, you're looking for, you know, an arythemma, migraines, rash, you're looking for again that bullseye rash presentation, but another thing that you're looking for is do they have any neuro kind of presentations like, you know, for example, bilateral facial nerve pausy is a giveaway. All right, bilateral facial nerve paly, neuropathies, uh those are things to 3:02:51 think about and then potentially test them for lime, especially if they talk in the vignette about they travel to the northeastern part of the United States and they were hiking, right? That's something to think about. With that being said, niggleria, this one, the patients are sick as crap. I mean, they they look horrible. Um, usually what they'll say in the vignette is there was a person who jumped into still water, whether it was a, you know, a pool, they jumped into a pond, a river, and a lot of that freshwater source rushed up their nose that contained the amoeba, the neglia fallery, and you'll test that. You'll actually look at it on a wet mount and you can do a PCR for it. But you're putting them on so many therapies that these patients are on, I'm not kidding, antibiotics, antivirals, they're on um anti-cancer me. It's so insane what you have to put them on. And usually they have a high rate of mortality. One thing again to add on, I kind of talked about it. You have a patient come in fever, headache, meningial signs, maybe they have some cortical signs. They have no fail signs. You get the LP. You're kind of like waiting for that to give you 3:03:46 back at least the first things. Usually the first thing that comes back is your glucose, your cell count, uh the differential, and then your protein. You're going to have to wait a little bit for the culture and the PCR. All right? That takes maybe about a day or two for you to get something like that back. and sometimes depending upon what else you're testing for even longer. So in those time frames you're treating them for what you suspect. When you're treating them for what you suspect, let's say that they're on an antibiotic, they're on an antiviral because you think that they may have HSV and sephilitis. If that PCR comes back negative, but you still have a high degree of suspicion, one thing I think that's always helpful to do that aids to this the actual diagnosis and helps you to have a little bit more confidence is to get an MRI. The reason why I say get the MRI is because sometimes the temporal loes they tend to be the most om um like often affected. And so for example, if I look at the MRI here, here's my right temporal lobe. Here's my left tote temporal lobe. Do you see all this hyperintensity? All of this on that kind of that T2 flare has all of this 3:04:40 kind of like hyperintensity vasogenic edema classic of HSV and sephilitis. usually can be bilateral and it's usually asymmetric, but it's almost always the medial temporal loes that light up on T2 flare, especially with the clinical presentation of fever, headache, and some cortical signs. In that scenario, I would keep treating them and I would also reorder the PCR to do it about like 3 to seven days. Keep treating them until that PCR comes back. But if you have a high degree suspicion, definitely get the MRI. It adds to the utility of the diagnosis. It's not a guaranteed one. It's not like oh they have it but it definitely helps you in those those kinds of moments of uncertainty if that makes sense. All right we've gone through the processes of really determining if they have encphilitis to determine if they have menitis. Boom. What about that person who does have a mass lesion? So I get a CT scan. I see something like this. When I see something like this I could think brain cancer. I could think about a brain mass. But I could also think about a brain abscess especially if they have fevers and headaches and cortical signs. So, always in these situations, get a 3:05:43 better look. MRI with and without contrast is going to be the best way to go. It's going to look to see if it enhances. It's going to look to tell you if it's piogenic or not, if it's non-piogenic. And then you're going to have to assess the risk factors. Let's do this step by step. It's kind of taking it a little extra. And so, you may not need to know this, but I think it helps you as you become a clinician. The first thing that you want to ask is, does it look piogenic on MRI? What does that mean? A couple things that you look for. or it's not always the case but it definitely helps you is looking at the clinical context but also when I look at these images I have to go through a step by step the first one is I want to look at the T2- weighted image I can see kind of a mass here but I see a lot of vasogenic edema so we call this hyperintensity on the T2- weighted image the next thing is I also want to look at the uh the ring enhancing lesion this is usually on the postcontrast contrast will show ring enhancement and that is usually indicative of some kind kind of like you know breakdown in the bloodb brain barrier that we can see in situations like abscesses and so I want 3:06:45 to see that kind of ring enhancement you can also see this in cancers though too right so I want to see that ring enhancing so ring enhancing lesion T2 weighted image is going to show basogenic edema both of this can happen in cancer and abscess what may help is that whenever you have a piogenic lesion that that actual kind of perent material may come up bright on DWI so you see how it's bright here bright here that's the DWI and then ADC should be the opposite. It should be dark. And so we can have a dark lesion on ADC. If you have these particular findings, it suggests a higher likelihood of a brain absis, especially a piogenic one, than it does a non-piogenic lesion of some sort. So that's what I want you to think about. Flare, I have hyperintensity contrast imaging. I see ring enhancement. DWI bright ADC dark. If that's the case, the next question that you have to ask is, is there multiple or solitary brain lesions? Why do I ask that question? The reason why is because the location is then going to be the next thing. If I have a solitary lesion, I want to know 3:07:46 is it in the frontal lobe? Because if it's the frontal lobe, what's the area that I should what are the possible eeologies to suspect here? Because look, I got a I got a nasty abscess here, right? What should I then say? I should probably go and look for what type of causes that led to this. What are the big things to think about? I'd probably start thinking about things like a frontal ethmoids, phenoid, sinusitis. I'd be thinking about maybe a dental abscess or infection that spread there. That's what I'm starting to think about. Temporal abscesses, on the other hand, here I have an abscess. I have concerning features of what seems to be a temporal abscess. I've confirmed its findings that it's piogenic on the MRI. What am I then going to start looking for? Looking at the mastid, looking at the middle ear, right? So, that's why I want you guys to think about that. So again, the source evaluation is critical because sometimes it guides how you're going to manage these patients. So for example, again, frontal, I do a really good ENT and dental exam to look to see if I find any sinus infections. Do I see any kind of opacification of the frontal, the ethmoid, the sppheninoid 3:08:46 sinuses? Do I see some bone erosion there? Do I look at the mastoid sinus and see that there's some bone erosion, opacification? Do I look at the middle ear and see that it's opacified and there's bone erosion and that's the way it accessed itself into the brain? Those are important. So CT scan is also going to be super critical along with just examining them first. Okay. Now multiple lesions I ask the question because when you have multiple the first thing I ask is where is those multiple lesions? Is it in the gray white junction or is it deeper in the brain or somewhere else? If I see a lot of them are on the gray white junction that means it was occurring along vascular territories. That means it was probably spread through the blood. So that means that this was a hematogenous spread and that means I think infective endocarditis and I think about a lung abscess. So here I can appreciate look at all of these like ring enhancing lesions and they're multiple along multiple vascular territories. That would make me think right off the get-go of infective endocarditis. I'm going to get an echo 3:09:46 right away. That's a question that you may be asked. The other one a little bit less likely to be asked and kind of rare especially in certain patients. They probably have to have a certain degree of immunosuppression as you think about no cardiois. We'll talk about that in just a second. But with echo cardiograms, you're going to be getting the blood cultures. We already ordered that. That's cooking in the meantime. But the echo cardiogram will find if you have any vegetations. As we can see here, they have a vegetation for shores skis right there. All right. So that's the benefit of also ordering the uh blood cultures up front because it may tell you the particular cause of their overall CNS infection. Oh, it's stafarius or it's streptococcus virans and the source of it is from the echo because we're going to follow that due criteria going back to infective endocritis. All right, cool. The other one I told you no cardiois did get a chest CT. That's the one to also did do a particular image for. They'll present with some features that concern you that are coming from the lungs. The chess CT will show you that they're probably going to have a lot of like areas of 3:10:41 pneumonia with some lockated abscesses that are concerning for no cardia. All right, especially in patients who are immunosuppressed. All right, that's the piogenic ones. What about the person who doesn't present with a piogenic leion? It doesn't show that T2 flare and it doesn't it doesn't show a T2- weighted imaging with hyperintensity. It doesn't show the ring enhancement. It doesn't show the DWI um that's bright in the uh ADC that's dark. It just kind of presents in a different way that doesn't support a brain abscess that is pervolent in origin. It supports something else. In those scenarios, I then urge you to assess the MRI a little bit more to get an idea of where these are, what they look like, and then take into consideration their history along with do I need to get HIV and specific cerological testing. So history, do I need HIV test? Do I need P corology test? And take a good look at their MRI and characterize it. Let me explain. If I get an MRI and I see lesions in the basil ganglia bilaterally like this or maybe even you know unilaterally if I 3:11:43 see again ringen enhancing kind of lesions here that present in the basil ganglia that is highly concerning for toxopplasmosis. So what do I do? I get an HIV testing unless I know that they have an HIV uh positive. I would check the HIV. I would check their CD4 counts. All right, that's what I'm doing. If they have HIV, their CD4 is less than 100, I'm super concerned for toxopplasmosis. So what do I do? I get the corology test to test for the IGG antibodies of toxopplasma Gandhi. And if that comes back positive, there's a high chance I got cerebral toxopplasmosis. Right? [snorts] For the other scenario, if the MRI shows these lesions that are I'm not kidding, it looks like Swiss cheese and and you have a hole everywhere with a small little dot in the center of it. This makes me concerned about a tapeworm like teenolium. And this is usually the skollex of it. So there's just holes all over the place with dots in the middle of them all over the place. This is super concerning for neuroscystericosis. The thing I'm looking for here in the history in some way, shape, or form is they're probably not HIV positive, but 3:12:44 they've traveled to areas and they've kind of like that are more concerning like Africa, you know, South America. They tried some food that was a little funky in those areas. They got a tapeworm. It reached its way up to the brain and just wre havoc. That's what I'm looking for. All right. And in those scenarios, I would order the anti-cystic antibodies from their serum because their immune system should have had a reaction to it. And if those come back positive, it does add a degree of concern for neuroscystericosis. All right. So really, really critical that we do that. Now, the last thing I want to add is that we really don't always have to tap into these abscesses. Um, or even in this case, the nonpiogenic brain abscess. You don't always have to do that. The reason why is you incur risk when you stick a needle, when you do anything into the brain tissue, especially depending upon location. So you should only do it if you have the particular indications to do that. And what are those? If the lesion is big and 3:13:45 it's a very arbitrary number, but anything greater than 2.5 cm, I prefer enough that the lesion is big enough that it's causing problems. Like for example, if I have an absess in the posterior fossa, that's already a small area. The problem with having a posterior fossal abscess is it can cause hydrophilis. It can cause maybe some cranial nerve palsies. So [clears throat] with a posterior fossa absess, I worry about herniation. I worry about hydrophilis. I worry about cranial nerve pausy. So in those scenarios, I'm probably going to want to reduce the risk of that happening and test it. And also probably while I'm there drain it because it's going to cause complications. Another one is if the if the actual abscess is causing like herniation symptoms. In other words, they're developing subfalene, uncle herniation, they're having neurological deficits that are truly not getting better with antibiotics. And that's another one. They're not getting it better with antibiotics. That's probably the most likely one that you'll see on the exam. That would be a very strong indication to tap into it. The reason why is if I tap into it, I can test it for a particular pathogen that I'm not 3:14:41 treating with accordingly. And sometimes I can even aspirate and drain it to just have source control. And so that's why it's really important to remember this one if you forget all the the rest of them. The last one I also like to add on is if it's close to a ventricle. If an abscess is kind of close to a ventricle, it has a high risk of kind of fisializing with that v that ventricle, if you want to think about that, and opening up into the ventricle and dumping that pus into the ventricle, and that can lead to communicating hydrophilis, a lot of nasty stuff like ventriculitis. So really critical that we identify that as well. If that's the case, you better go ahead tap into it, pull off that, send the cultures, send off all the tests to the lab. And then again by doing some of that draining of it you also may provide some therapeutic benefit of mass effect um and associated complications from that like a ventricular rupture like mass effect like posterior fossa leading to hydrophilis and maybe even some nerve pauses as well. All right wee man that was a lot for CNS infections but I hope at the end of this that you get the whole point is that you need to first 3:15:40 concern yourself with is this a CNS infection? This is the way that you do it. You then need to say, I'm going to give them antibiotics, maybe antivirals if they have the concern for HSV and sephilitis, but I want to make sure I get my culture so I don't sterilize those cultures. I then need to ask, do they have a risk of herniation or do they have a structural lesion? If they do, get the CT. If they don't, get the LP. If I get the CT and it doesn't show me any brain mass, but I still have concern that they have menitis, you better get the LP. The LP is going to help you to determine if you have menitis or encphilitis, especially HSV, VZV. And if you have those particular exposures and risk factors, you can go down the line to more rare eeologies. If you got that mass lesion, then you then got to figure out is it piogenic or not? If it's piogenic, you then got to figure out where's the location, where' it come from. And if it's multiple, you then got to think about again where would I be concerned about it coming from? Infective endocritis is probably the biggest one. And then if it's non-piogenic, you always want to think about toxo and you always want to think about your 3:16:37 neuroscysterosis. All right, my friends, let's now move on to the treatment. So when we talk about treatment, we're going to focus a little bit on bacterial menitis. So we got some nasty bugs in the meninges and it's causing some unfortunate infection, inflammation there. We just got to kind of remind ourselves, okay, when we're talking about this, what is the therapies that I'm going to institute? Well, antibiotics are going to be the key. But before I initiate antibiotics, it's kind of crucial especially with um streptococcus pneumonia. So we call this pneumacco menitis. It is extremely beneficial to give dexamethasone prior to the antibiotics. And so a lot of the times we can say with a lot of degree of certainty that when we talk about community acquired menitis, it's usually either strep numo, nicer menitis or homophus influenza type B. And so we can start them off with dexamethasone. benefit to potentially providing it before the antibiotics is that you may reduce the inflammatory reaction for whenever the antibiotics cause their bacteria or bacterial static effects which may lead to toxins and cytoine releases etc. you may be 3:17:37 dampening that response prior. Um so that's one benefit but again the primary reason that we initiate this is to reduce neuro disability maybe even potentially mortality especially with numacco menitis. Again, we usually only continue this for about four days, especially if the cultures prove that it is streptococcus pneumonia. All right? Oftent times by the time you actually get the cultures back, you're almost at the end of the dexamethasone anyway. So again, that's why we usually give it empirically. Prior to the antibiotics, they're going to be placed on antibiotics. You'll get your cultures. By the time your cultures actually probably come back, you already have almost 3 days, two days of dexamethasone that you usually just finish it out or discontinue it. Now with the antibiotics that we're talking about, it's critical to know your empiric coverage. So the most common coverage for a community acquired type of you know menitis is you're covering strep numo niceria menitis and you're covering homophus influenza. That's going to be your venkcomy and sept trioxone. The vank is going to cover any kind of like 3:18:37 numoccoal resistant uh type of bacteria to septrioxone. So venkcomy will cover like resistant uh pumacus the septrain and the septrain will cover n pumacus and it'll also cover nicerium men and it'll cover homophus influenza. Now kind of go back to a little bit of your step one your basic sciences here that we have a cell wall we have your cell membrane you have your cytoplasm you got a bunch of other structures here this is a pathway that makes tetrahydropholate that's incorporated into the DNA DNA is obviously crucial for replication of cells you have a lot of enzymes that are critical to that especially topo isomeases and DNA polymerases from DNA you make RNA and RNA is then translated to make proteins which utilize ribosomes like the 50S and the 30S and there's obviously so many different proteins that are crucial to the structure of a lot of our cells. So when I talk about this, the reason why I tell you this is that it's a good reminder to think about how venkcomy and sept trioxone really work. And what they do is they work against cell wall synthesis. They're going to break down the cell wall and 3:19:37 that's going to make it easier for these cells unfortunately to die. And that's one of the benefits of these drugs. Now you can do that in two ways. If you're a member, you can decrease the synthesis of the pepidoglycans that make up your cell wall or you can also do it by decreasing the cross-linking of the pepidoglycans, which is the benefit of sept trioxone. All right, so just a quick little reminder for those of you who are thinking about that step one stuff. Either way, this is empiric coverage for those individuals less than 50 years of age. All right, the next therapy is your venkcomy plus sept trioxone adding on ampecylin. Ampecylin again is just going to act similar to sept trioxone. It's going to break down the cell walls. But the important question to ask is when do I use it and we use it for those individuals who are greater than 50 or they have other particular risk factors for lysteria greater than 50 amunosuppressed pre-existing conditions like alcoholism or cerosis or pregnancy. Those are the things that make you highly suspicious 3:20:38 of lysteria. So you add on the ampecylan all right next one venkcomy sephopime or meapenum. When do I do this one? Again, if a patient comes in, they're getting dexamethasone. The empiric coverage is this. The only time I add on the ampeo is if I have indications for lististeria. The other scenario where I may not even use a may not use sept trioxone is when I have a patient who is concerned that they may have an infection due to hospitalacquired pathogens. And that's when I may use something like sephopene which again it's going to inhibit the cell wall synthesis and marapinum is going to inhibit the cell wall synthesis. It's a beautiful thing that almost all of these inhibit the cell wall synthesis. What I want you to remember here is when do I use them? [clears throat] I use them in a hospitalacquired infection scenario where I need to cover a patient who had neurosurgical procedure. They had a cranial device like a EVD, a VP shunt, an Omaya reservoir, something where there was access to their central 3:21:39 nervous system and in that scenario they had an increased risk of MRSA and sudamonus and so I need to consider that or they have a penetrating trauma whether this was unfortunately due to getting hit in the head by a machete they got cracked in the skull whatever it may be those are opportunities for pathogens like MRSA and also sudamonus to get their way And that's why we add on sephopm um or we can do marrapenum because marrapenum covers sudamonus and it also can cover a lot of your your gram negs um and even anorobes as well. So venko covers your mRSA sephopenum can get you some of that sudamonus coverage and even anorobes and other gram neg coverage. All right. So again way I want you to think about it is patient comes in they get dexamethasone if they have a concern of bacterial menitis. Then after that you add on vank and sept trioxone if they're less than 50. If they're greater than 50, they have predisposing risk factors like amunosuppressed or they're alcoholic, serotics, am um pregnant, you add on a to the vank and sept trioxone. If they have a concern 3:22:42 for MRSA or sudamonus from these potential scenarios, you still give vank to cover the MRSA, but instead of giving septrixone and ampeill, you switch it to sephopim or merapinum to cover the sudamonus. That's the difference. I hope that makes sense. All right. The last thing I want to tell you guys is that we have to remember when a patient has menitis especially bacterial menitis it is critical critical critical to know if a patient has niceria menitis right now again we're going to cover niceria with the sept trioxone right and they're going to be on these antibiotics for a decent amount of time one of the important things is to have that kind of like overall contact exposure for those that are going into the hospital to visit this patient but it's also critical for those who had close contact. So a loved one, a family member, someone who was around this person a lot, they need to be treated prophylactically with the proper antibiotics. And so what may happen is in the exam they're going to say, okay, you have a patient, you 3:23:43 end up confirming they have nicer menagitis. You then narrow your antibiotics down to sept trioxone. But then you're asked, what type of antibiotic do you prescribe the family member who lives at home and was exposed all the time to this patient? What is it? You have three options. One is rafampen. Two cyproloxisin. Three sept trioxone. So that is what I want you guys to remember. This is a really high yield point that'll likely come up is that we want to give close contact antibiotic prophylaxis to those who have nicer menitis. Again, if they have been diagnosed with it, the live loved ones who live with them, anybody who had close contact exposure should be treated with one of these three agents. HSV or even VZV and sephilitis is treated with a cycllovere. All right, a cycllovere is a beautiful kind of drug but it can cause some nephrotoxicity and so we always have to be aware of that. But how viruses really work especially in a neuron is they bind to a receptor. They get endocytosed. They then get taken into the cell where they release their 3:24:44 kind of viron, their virus particles, their nuclear material, their enzymes. And then what happens is they oftentimes can get reassembled, incorporated into the DNA, and they kind of reassemble their own viruses, which then unfortunately can then get pushed out and go to another cell. And in that process, they can cause licis and destruction of this cell. What I want to do is I want to prevent this virus from going on and infecting other cells. I want to reduce neuron damage and the progression. How do I do that? I need to inhibit a particular point in the cycle and that is where I'm going to inhibit them from synthesizing new nucleic acids for new viral particles and usually how a um a cycllover will work is it'll act as a nucleotide analog so guanosine analoges where they try to get incorporated into the DNA and terminate DNA formation synthesis replication and that's the benefit of ascycllovere which is really good in HSV good in vzv and you also have gans and cyclloe can also act in this way and that's good particularly more uh with CMV 3:25:44 infections. All right. Again, when do we give h when do we cover uh HSV with a cycllovere? We do it in a patient who's already on empiric antibiotic coverage for menitis and they are on dexamethasone but you cannot rule out encphilitis. In other words, they present with seizures, they present with cognitive behavioral changes, altered mental status, and I'm waiting on the LP to give me my PCR results. Until that comes back and I have a high degree of suspicion, I keep them on a cycllovere. If it comes back positive, get rid of the antibiotics, get rid of the steroids, and keep them only on a cycl. That's the concept. So, it's usually given in combination with empiric antibiotics and dexamethasone. But again, once you actually get that PCR to prove that they have HSV or VZV, get rid of the other ones and only keep them on a cyclare. All right, that is the primary indication. So it's a part of empiric coverage, but it's going to be definitive therapy if it's confirmed HSV or VZV and sephilitis primarily. You 3:26:47 can consider a menitis. It's just less common. All right, brain abscesses. These are some nasty infections, man. And I you know when you give antibiotics you're trying to cover a plethora of pathogens. Venkcomy again it's inhibiting the cell wall synthesis. Seph trioxone inhibiting the cell wall synthesis. Metronitool a little bit different. This one doesn't actually work against the cell wall synthesis. It actually creates like these kind of like reactive oxygen species and causes essentially it damages the DNA. So again your bacteria is not going to be able to properly replicate. All right. This is your empiric coverage. You give this to patients who you have no idea what the source is of their brain abscess. So you find an abscess. All right. Start them on vank. Start them on sept triacone. Start them on metroniditool. Why? Because the vank is going to cover any kind of pathogen like staflacccus orius right especially merca related. Sept trioxone is going to cover a lot of your other pathogens like streptocoal species. Um, and then metroniditool is 3:27:48 going to cover any chance of anorobes, especially if this came from a dental source like bactaroides, faggillis or fuso bacterium. Those are some really nasty ones. And so you want your MRSA coverage, you want your Graham um you want your streptocockal coverage and any other kind of gram neg. But this one's going to really get your potential for anorobes. All right. Now, if you know the source, it makes it a little bit easier. So for example, metroniditool and sept trioxone that means you're covering your anorobes and you're covering probably most likely your streptocous species like the veridans and pneumonia. So that's going to be potentially more of that dental and syogenic source and otogenic source. So it's coming from the ear, it's coming from the the actual teeth or it's coming from the sinuses. Venkcomy and sept trioxone, you're dropping the anorob coverage. So if I don't have anorobes, that's probably screaming to me more likely this is coming from a hematogenous source. So I'm really trying to cover things like strep and and MRSA which is infective endocarditis. That's where you'd be 3:28:50 thinking about that one. Ah so if I had a patient essentially if they came in the vignette and they had a MRI that showed multiple ring enhancing lesions along in the gray white junction they have a nuance of heart murmur or fever they have other features of infective endocarditis echoes positive and they say what's the proper therapy to treat this abscess you would say venkcomy or septrioxone because it's going to cover the most likely pathogens for that scenario now the only time where we'll really amp up our game and cover it with venkcomy and sephop is if I have a concern for MRSA but here's the other one pseudamonus and this can actually cover your sudamonus as well. Um, so when we think about that, we got to really be concerned. What would be a scenario where I would be exposed to things like, you know, strep species and staff species and pseudamonus. What would I be thinking about? I'd be thinking about some type of direct inoculation, a neurosurgical procedure of some sort, um, a cranial device that was inserted in a penetrating trauma. But really, that's that is the thing I 3:29:50 want you to think about here. Just as a reminder, menitis that is bacterial, dexamethasone. If it's usually those less than 50, ven and sept trioxone and you'll be safe. If you have the lististeria concern, add ampecylan. If you have a patient who probably presents with a hospitalacquired or penetrating related trauma, you need to cover MRSA and you need to cover sudamonus. That's ven. And then instead of doing septraone or ampillin, you switch it over to sephop or you use something what else? Maripenum for the HSV encphilitis. If you have a concern of encphilitis and you can't prove that they don't have it as you get the LP as you get the PCR and you're waiting give them a cycllover part of that empiric coverage that you covered with the bacteria. Add on the ascycllovere once it comes back positive for HSV or BCV continue and get rid of the rest of them. That is the goal. Now for brain abscess if you have no idea of the source cover them for anything possible. Cover them for things where you have anorobes and you have strep. 3:30:52 Cover them for things where it could be a hematogenous source. Right? But for those who you are very concerned for sudamonus, you cover them with the sephopene. You consider things like the MRSA coverage or you can do monotherapy meipenum. All right, that is what I want you guys to take away from this. All right. What about treatment of complications that can come from CNS infections? Seizures are really really common especially with encphilitis. You can see with brain abscesses and probably the also possibly with menitis because all of them can lead to cortical irritation. So the big thing to remember for this is when you think about the way seizures really work, you have a presinaptic neuron, you have a post synaptic neuron. This is an area that generally what's happening is is you have a neuron that can release something called GABA. And what GABA does on that post synaptic neuron and it binds onto a GABA receptor and it controls chloride ion influx which can then kind of inhibit that neuron. Right? Well, if I want to kind of enhance that mechanism, what would I do? I would give a benzoazipene. And the benefit to giving 3:31:53 a benzo is that it's going to help to stimulate, it's act as an agonist and binds on to that receptor and enhances chloride ion influx. Now, I got a crap ton of chloride in this neuron. It's going to then inhibit that neuron's post synaptic action potentials. That's what we give for the first line of a patient presents with status epileptic. In other words, they seize for greater than or equal to 5 minutes. They seize consistently without returning to baseline. That would be an indication. And then from there, you want to prevent the recurrence of those seizures. And so that's where another concept comes in. You know, neurons not only do they have this GABA pathway, they have a glutamate pathway. And that's controlled via these voltage gated sodium channels. They cause sodium to rush in, depolarizes, opens up these calcium channels to rush in. Calcium is crucial because what it really helps with is it helps these vesicles that contain glutamate to then fuse with the actual membrane and release the glutamate. What glutamate does is it binds to these AMA receptors and other receptors and flushes in sodium can flush in calcium as well and 3:32:54 that's going to activate the neuron. Right? Another thing is that glutamate gets recycled and it gets brought back into the neuron where it can be put back into these vesicles and this can be helped with this SV2A process. This is a molecule this cinaptic vesicle protein. What I can do is I can give a drug called levatorazzitam which is called keera. And what it does is it inhibits that SV2A. It inhibits it from then allowing for this to fuse with the cell membrane drops the glutamate drops the sodium and drops that post synaptic neuron action potential. Essentially it's the same thing as a benzo but these are better for what? Preventing recurrence. And that is the thing I want you guys to remember. So this is more of that prophylaxis if you will. So if a patient presents with a seizure and they continue to seize benzo but then preventing them from seizing in the future the answer is an anti-epileptic and the most commonly utilized one is going to be levator just due to its overall reduction in adverse effects and side effects. All right, hydrophilis we 3:33:57 talked about this as a complication can occur in menitis can occur a lot in brain abscesses whether it's obstructive whether it's communicating whenever a patient has another condition called cryptocal menenitis we can do serial LPS it's better than putting in an EVD it's better than kind of actually um sometimes putting in VP shunts because they get clogged up a lot from the heavy amounts of protein and so we prefer to do LPS pretty frequently to really reduce that pressure and some of that hyd hydrophilis. So it's like just like you would do an LP. You're just accessing it instead of actually kind of in this case, you know, measuring. You can still measure the opening pressure. You can still accumulate all of these intest tubes, but you're just trying to drain CSF in these scenarios because of the communicating hydrophilis process to reduce the hydrophilis and the associated increase in the ICP. All right. Now, EVDs are really going to be more in the acute scenario. So if I have a patient with cryptocinitis and they say which one would you do to reduce the hydrophilis, you'll say serial LPS. If I had a patient who had not cryptocanitis 3:34:57 but they had menitis, they had obstructive hydrophilis from a brain abscess and they're having severe hydrophilis, their ICP starting to rise, what do you do? It's always an EVD. It's the acute management of hydrophilis. That's what you're going to use it for. All right. The concept behind this is that if you have your ventricles, right? What you want to do is is you want to use a catheter threaded into the actual ventricles and if there's let's say that there's um hydrophilis that's all the way up at the arachnoid villi, right? All this pressure builds up kind of all proximal to it or if you have an obstruction somewhere let's say here in like the cerebra duct of the fourth ventricle, you want to pull all the fluid off that's accumulating proximal to that. And so that's where we use this catheter to drain some of that CSF. And if we drain the CSF, we can actually reduce the hydrophilis and the associated increased intracraanial pressure. Now long-term, if a patient continues to suffer from hydrophilis and we just can't wean them to get them the EVD out permanently, we may need to bridge them to something called a VP 3:35:58 shunt. And that's just a little bit more of a long-term option where we're just running the catheter from the ventricles instead of to a a thing where it can drain into a bag. We're going to just drain this right into the peritineal cavity. And that's an alternative, but that's going to be more of the long-term approach. That's what I want you guys to think about there. All right, that's hydrophilis. So, we talked about seizures, we talked about hydrophilis. Now, hydrophilis can cause a bump in the patient's ICP. When a patient experiences a high SCP, that's common with menitis. It can be common with encphilitis, especially if they're seizing like crazy. That increases the ICP. But brain abscesses can cause a pretty significant increase in ICP because there's a mass effect. They also increase the risk of obstructive hydrophilis. So this is common with all of them. What you always want to do when a patient presents with an ICP crisis, their ICP is really, really high, greater than equal to 20, they're presenting with neurological signs of herniation. First thing you do is you temporize them. These things aren't going to fix the problem. They're going 3:36:49 to keep them from dying. What is those things? You're going to get the head of the bed greater than 30 degrees. That's going to it's going to help the jugular venus drainage, get the blood out of the brain to reduce the actual overall that monitor, get some of the blood to decrease the actual all the structures that are components that are making up that that [snorts] fixed space. Again, if I drop the blood and get some of the blood out, that reduces the blood inside of the actual skull and that reduces the ICP. Another one is hyperventilating. That reduces blood flow to the brain. Reduces blood, reduces the ICP. Uh analesian sedation that actually reduces the basil metabolic rate. So the neurons aren't as hungry. They're not requiring as much blood flow. They're not requiring as much metabolism. And so that reduces again the theory of bringing more blood flow and demand to those actual angry and you know irritated areas of the brain. Hyperosmolar therapy is really trying to reduce the size and so it's actually pulling fluid. This is things like manitol and hypertonic saline. That's going to pull some of the fluid out of those actual brain cells and to make 3:37:47 space inside of the skull. All right? So it's going to reduce some of the edema. These are just temporary. If you don't fix the underlying issue, they will they will herniate regardless. And so it's important to remember to do this for whenever the ICP reading on the EVD shows up greater than 20 or you have clinical evidence. In other words, they have papadema, nausea, vomiting, dipopia, they have signs of subfalene, uncle herniation, transenterial herniation, anything like that or they have radiographic evidence in combination with that. So in other words, they have clinical signs and their CT shows that they're subfausalian herniation. It shows that they're having uncle herniation. It shows that they're having transctoral herniation. give them the temporizing measures. All of this is useless if you actually don't treat the underlying issue, right? And so you have to think about this. You're trying to do these things to kind of keep their ICP at bay while you're trying to figure out what's the ultimate reason that their ICP is high. And it goes back to the Monroe Kelly doctrine. Is it an abscess that's increasing the amount of like brain tissue and overall substrate? Is 3:38:45 it a problem with um overall CSF? Is it a problem with blood that shouldn't be there or more blood that's there than normal? And so in none of these situations is it really a blood problem. It's it's usually just brain substrate in this case an abscess or you have a lot of hydro you know hydrophilis that's causing an increase in the amount of CSF. So what are the two ways that we deal with that? I already talked to you about the CSF one. It's an EVD. That's acute management. You may need a VP shunt longterm but at least acutely it's an EVD for that hydrophilis. The brain abscess you're trying to treat that with antibiotics but if it's causing things like herniation right then you got to go ahead and drain these puppies. And that's when doing like a surgical abscess removal or a drain, reaching out to neurosurgery is is going to be strong uh indication. And so one of the neurosurgery team is probably going to ask you, okay, why do they need it? Well, having an ICP crisis is a pretty good indication as long as you have traded other areas of issues. But at least tell them, well, the abscess is greater than equal to 2.5 cmters. But more importantly, it's in the posterior 3:39:45 faucet, so it's causing a lot of mass effect on my on the patient's ventricles. is causing some other kind of neurological signs of herniation. Another one is they have visible mass effect causing things like subfausaline, uncle herniation because of the location of where that abscess is. Another one is if they aren't getting better with antibiotics. So you put them on antibiotics and the abscess continues to not change or not get better or gets worse somehow, you need to definitely go ahead and drain that and then send that off to figure out what the heck is going on. But another one is if it's really close to a ventricle because if those ventricles if that if that abscess ruptures into that ventricle they're going to get ventriculitis. They're going to get worsening hydrophilis and they're not going to do well. So you need to always be quick to try to drain those abscesses and remove them if they fit the criteria for ultimate you know treatment issues that are going to if you don't fix it are going to continue to cause ICP crisis to persist. So again how do we do this? You can do this sometimes. You can do it stereotactically where you kind of 3:40:46 really hone in and you try to suck out all the pus in that area or you'd go through this in a surgical kind of like drain way or removal where I'm going to literally drill through into the area of location where it's the the prominent area. Obviously, subcortical ones are a little bit more difficult and you probably reach for more in these areas of doing an alternative therapy, but generally in this one, I'm going to go ahead and just maybe create like a area where I can drill through the skull, open it up and expose the area of interest and then help to remove and you know, generally you're going to help to remove a lot of that abscess material in that scenario. But again, I think that gives you the point. So patient comes in they seize benzo to get them to stop seizing if they fit status epilepticus criteria prevent them from seizing with levatorazzam hydrophilis if it's problems where they're having hydro due to cryptocal serial LPS are better than an EVD any other indication of hydrophilis besides that EVD long-term they need it because they can't get off the EVD VP shunt and then lastly if the ICP crisis temporizing measure but then 3:41:47 fix the issue if it's a CSF problem EVD if it's an abscess that's causing mass effect problem surgical drain or removal. I'm sorry, surgical abscess removal or drainage of that kind of abscess. Another complication comes especially for menitis and brain abscess. They often times kind of coalign with one another especially an infection started somewhere in the nasal like you know a sinusitis of sorts or a dental infection or even sometimes even in the um otogenic ones. They can spread and they can cause abscesses and they also can cause associated like septic thromboplabitis where they can cause cerebral venous sinus thrombosis. You're going to treat these patients with antibiotics if it's an infectious eeology. But anti-coagulation is critical so that the clot doesn't propagate and get any worse. So you have to put them on things like low molecular weight hepin. It's more preferred than unfractionated heperin. If they continue to have that clock get bigger or they start to have ICP crises, then we actually make the risk of going in and reaching out to the IR team and going up 3:42:48 endovvascularly and trying to remove the clot out of the veins, which is a risky kind of procedure. So, it's only if they're not getting better with anti-coagulation that clot continues to propagate and get worse or they're like severe. They have an ICP crisis and there's the only option. You can do things where you go in there and you aspirate it. You can sometimes even use like a mechanical throctomy and retrieve it that way. Um, sometimes you can even go in and kind of release thrombolytic materials like tpa to break it down. Um, and then sometimes you can actually just use an angiojet and kind of pull that sucker right back that way. Um, and then we have even seen that, you know, balloon stabilized aspirations as well. Either way, these are getting more into the details of ways that the interventional kind of like radiologist will go about this. The whole point is is I'll consider throbectomy if they're not getting better with anticoagulation or they're experiencing an ICP crisis and I have no other option because anti-coagulation isn't going to get rid of the clot right away. I need more endovvascular therapies. All right. Woo. We did it my friends. We went 3:43:45 through CNS infections. We dug deep. I think we got through it. And I really hope that at the end of the day you understand it. I hope that you know when you have a patient who presents with concerning features of a fever and a headache and maybe some menial and cortical signs, you know the steps to take. you know how to cover these patients empirically for the most likely pathogen. How do you utilize these kind of cultures to guide which antibiotic to narrow down to when do I add antiviral coverage? When do I add the fungal coverage, etc. These are all critical things to know and understand. But man, I hope that you guys like this video. Hope that you learned a lot. I hope it made sense and ninjers, I love you guys. I thank you guys. And as always, till next time.
