I guess I can go ahead and get started. I'm Dr. Schmidt. I'm a clinical assistant professor at Thomas Jefferson University. I'm going to be talking about emergent and non-emergent management of elevated intracranial pressure. And I'm the last session here and I'm between you guys and being done with this. So I'll try and make it quick, but also useful. I have no disclosures. So outline, we're going to kind of go through some of the scientific fundamentals of intracranial pressures in turn, including the physiology, as well as monitoring. We're going to talk about acute elevation in ICP. And then we're going to talk about chronic elevation in ICP and how the two are very different disease categories and therefore very different ways of working them up and treating them. So physiology, one basic concept we're going to discuss is the Monroe Kelly doctrine. We're going to talk about herniation and then we're going to talk about different ways of monitoring. The Monroe Kelly doctrine is the fundamental science behind all of this. Essentially, there's only three things in the intracranial space, brain parenchyma, CSF, and blood, and it is a fixed volume. So any change in one results in a compensatory change in the other, or due to the laws of physics, an increase in intracranial pressure. So let's say you have something like a bleed. It slowly starts displacing brain parenchyma and squeezing out blood and CSF. And once we reach a critical threshold when no more mass can be displaced, then you get an elevation of intracranial pressure. So ultimately the main issue with intracranial pressure is that it affects perfusion of blood flow to the brain tissue. So cerebral blood flow, we measure it in mLs per 100 grams of brain tissue, is essentially what keeps the brain cells alive. Anything less than 20 is considered ischemia to the tissue. It's not getting enough oxygen, and anything less than 10 results in cell death. Now, this is difficult to measure directly, but we measure it indirectly based off of what's called cerebral perfusion pressure. So cerebral blood flow, the amount of blood going through the tissue, is essentially the perfusion pressure over the resistance. So the resistance is changing based off of cerebral autoregulation, so the diameter of the vessels inside of the brain. And so that is why, this is a little bit of some math here, some algebra, but if we say cerebral perfusion, or blood flow is perfusion pressure over resistance, and perfusion pressure is the mean arterial pressure minus the ICPs, so blood flow is essentially the mean arterial pressure minus the ICP over the cerebrovascular resistance. So because of that, the cerebral perfusion pressure is an indirect way of establishing cerebral blood flow. And also this kind of indicates the main point is that ICP issues are essentially ischemic issues. And kind of going back up to that CPP is that a physiologic range for cerebral perfusion pressure is between 50 and 150 millimeters of mercury. And so we wanna keep things in that range in order to maintain normal homeostasis in the brain. And the body has its own ways of regulating that, mainly through adjusting cerebrovascular resistance, which is, as we all know, PCO2-mediated, in order to maintain cerebral blood flow, which is the end result, but in pathological states that can not be sufficient. So a normal physiologic ICP is typically below 15 millimeters of mercury. We usually use 20 millimeters, we usually use millimeters of water when we're checking, because that's what we check opening pressures on. But anything greater than 20 millimeters of mercury is pathologic, and that's when we hook it up to an EVD, that's transducing millimeters of mercury. Now we've all been in the neuro ICU, you've seen the drainage receptacles and how they have millimeters of mercury and H2O. Those numbers are slightly different, the importance is that you know which one you're using at the time. But in general, regardless of which one you're using, if it's above 20, that's very bad. What the guidelines suggest is maintaining it less than 22 millimeters of mercury and maintaining perfusion pressure greater than 50 millimeters of mercury. So, going back to the pathological states, when we see elevations in intracranial pressure, we initially see a compensatory change, so you get increased CSF outflow, where the CSF leaves the intracranial space. Obviously in situations when this is obstructed, that cannot occur, and these patients can have more rapid decline. So that's situations with intraventricular hemorrhage or posterior fossa masses or things that are compressing the fourth ventricle or any sort of obstructive hydrocephalus or even post-hemorrhagic non-obstructive hydrocephalus. If we can't get rid of that CSF outflow, then the pressures can increase more dramatically because you can't have that compensatory change. Additionally, you get an increase in venous outflow. And issues where you have obstructed venous outflow can also cause problems with intracranial pressures. Like venous sinus thrombosis, where the main issue there is cerebral edema and the brain can't compensate for that, and it can result in critical increases in pressure. So if the brain can no longer compensate, then you get the decompensatory change. So you get decreased perfusion pressure, global ischemia. And then the last sort of event is this herniation event. And I like to think of this as if we, you know, are at the end of the Monroe Kelly doctrine, we've displaced as much blood and CSF out of the intracranial space as we can. The only thing left to displace out of the intracranial space is the brain parenchyma itself. And this kind of results in a cascade because you not only have injury to the brain itself from the herniation, you get additional ischemic injury from both direct compression. So think of pressure on the brainstem. This is why transcentorial and uncle herniation is so dangerous. It compresses the brainstem resulting in ischemic injury. And you also get compression of the blood vessels. So in uncle or transcentorial herniation, you can pinch off the PCAs, the posterior cerebral arteries, and then that can cause a stroke, which can then cause a further cascade of worsening cerebral edema and intracranial pressure. You know, subfall scene herniation up at the top of the brain there, we typically don't worry about as much because those structures are more well tolerated. But if it's severe enough, you can pinch off the anterior cerebral arteries that are up there, and that can cause ischemia and a further cascade. And again, which sort of herniation event is largely dependent on the pathology that is occurring. Now, the central transcentorial herniation is sort of the classically described when there's diffuse increase in pressure and everything kind of squeezes and pushes down against the brainstem. And that ultimately results in the patient's death. And that is essentially once you lose cerebral blood flow, it can no longer maintain cerebral activity, cell death, and then that is permanent and unfortunately continues to cascade. And eventually when you have brain death, you lack cerebral blood flow entirely. So how do we measure this? You know, there's some non-invasive ways we can do this. It varies off presentation. A common way is ophthalmological findings, right? So we always say the eyes are the windows to the brain. The most common thing we see is papilledema. You can see the pictures on the right there of what a normal optic disc looks like versus one with papilledema. It's not really numerical, but it can be helpful. And then we can assess cranial nerve deficits. So sometimes elevations in intracranial pressure can cause issues with cranial nerves, which we'll get to next. And then we have invasive ways. So direct CSF sampling, parenchymal monitors, and then other types of monitors. So invasive monitoring, we have sampling of CSF. Going back to millimeters of mercury versus millimeters of water, when we're measuring it based off CSF sampling, we're talking about millimeters of water because we are actually measuring the height of a fluid column. So when you do a lumbar puncture, the patient in the lateral decubitus position, first off, make sure they don't have some large mass lesion. This has to be communicating hydrocephalus. And you place the lumbar drain, or you place the lumbar puncture needle into the intrathecal space. And literally the height of the fluid as it comes out of the needle into your column is what the opening pressure is. And that's how many millimeters of water does it rise over the fluid, the plane of the fluid. You can do this with lumbar drains as well, though it's not really as accurate and the needles tend to be larger if you're doing it up front. People who are real sticklers for getting the most accurate measurement will actually do a lumbar puncture with a small needle, get the opening pressure, and then do another puncture in the same trajectory with the lumbar drain needle before inserting lumbar drain. The other way for doing this is an external ventricular drain. This is sort of the gold standard for people with intracranial processes in terms of being able to continuously monitor the intracranial pressure as well as treat elevations in intracranial pressure by draining off fluid. So this is typically if we are very worried about what those numbers are and we're worried about prolonged CSF diversion. So probably the most common procedure that we do in neurosurgery for those reasons. Then we have other ways of invasive ICP monitoring that don't involve fluid. And these essentially are an intraparenchymal monitor, what we would call a bolt. These are very common in trauma, especially if they have diffuse cerebral edema where they maybe don't have good ventricles to get an EVD in, but you need to measure the intracranial pressure. You can just, you're essentially placing a monitor into the parenchyma itself. The downside to these is that you can lose accuracy over time and you're kind of relying on the equipment to calibrate what the actual pressure is because you can't really calibrate it as easily off of itself. Whereas an EVD, we've all been in the ICU and done this where you put the pressure monitor at the level of the tragus, you open everything up to air, clamp off the drain, and you re-zero everything. And essentially that level is what zero is and then you open it up to air and you get a nice new waveform based off of where you've re-zeroed the monitor. So you can continuously recalibrate it and EVDs can stay in essentially until you worry about infection. Whereas ICP monitors after a couple of days, they really start losing accuracy. And then there's other types of monitors that are generally less accurate. There's less evidence in support of them, but some people do it in a pinch or in the post-operative setting. I used to put in subdural monitors after craniotomy, sometimes if I was worried about swelling or epidural, subgaleal, again, not quite as accurate as an interparenchymal monitor and less data, but in a pinch, if you're worried about something, sometimes they can offer some news. So acute and decompensated ICP elevation. So this is what I really want to focus on because this is the more dangerous variety of this. The chronic, which we'll get into, is exactly that. It's chronic. It's something that is typically not worked up or treated emergently and is a completely different entity than what we see with acute decompensated elevations in ICP. And this is, in our minds, a neurosurgical emergency until stabilized. So presentation can vary, can range when it's mild, just some headache, can progress to altered mental status, decreased sensitivity, decreased mental status, decreased responsiveness. I would say that agitation is usually one of the critical signs that we see before someone starts slipping into obtendation and coma. So if you have a patient, you're worried about elevations and intracranial pressure, they have a headache, and next thing you know, they stop complaining about the headache and start acting severely agitated and confused and altered and almost combative, especially if the pathology is in the posterior fossa, that that can actually be a sign that they're starting to decompensate. And if you wait too long, they're gonna progress pretty significantly. Important thing here, always remember ABCs, right? As this progresses, if their mental status continues to decline, if you get a GCS less than or equal to eight, you gotta intubate and monitor the ICPs. You can no longer monitor them clinically. And there's rationale behind that, which I won't get into, but just remember less than eight intubate, that's sort of the mnemonic. Sometimes depending on what the pathology is, if there's a focal problem, like a large expanding tumor or a tumor that bled or a bleed or something along those lines that you may have a lateralizing or focal lesion, and again, there may be associated cranial nerve palsies, which I'll get to next. And then at the very late stages, you may start getting cardiopulmonary changes. And this is where patients can die, not even from brain death, they can have cardiac death before progressing to brain death, because this can be very severe in certain situations. So the Cushing's triad, hypertension, bradycardia, respiratory irregularities. Ideally, if someone is getting to the point when it's severe enough, you're seeing Cushing's, they're already intubated. If you're seeing bradycardia and hypertension and that patient hasn't been intubated, they probably should be, so you're gonna miss the third. But either way, that hypertension bradycardia can represent that that patient is very, very sick. And I've seen one or two patients with rapidly expanding bleeds or issues intraoperatively with CSF diversion or something, and they can go into essentially coding because it becomes so severe. And that is, like I said, imminently life-threatening. And as I mentioned before, only 33% really get the whole triad. So like talking about cranial nerve palsies, we talked about cranial nerve too with papilledema. Third nerve palsy is what people very commonly think of, especially with lateralizing lesions, we call it a blown pupil. And essentially it's from compression of the fibers of the third cranial nerve at the skull base. Usually if you're seeing this, that patient is on the verge of herniation or herniating because the brain tissue is compressing the third nerve. And that essentially you get unopposed sympathetic innervation of the eye causing the blown pupil. And that's an emergency. That patient needs something immediately done or they're going to progress to brain death very quickly. A cranial nerve six palsy. The pathology here is a little more complicated. It's similar what we believe to paranoid syndrome, essentially compression of the dorsal midbrain. So you get compression of the cranial nerve six fibers that kind of cross in the back there, which can affect the patient's lateral gaze. So they'll get a lateral gaze palsy. And paranoid is when it can progress and they also lose their up gaze and this accommodation convergence palsy. And this is something that we can see with patients who have progressive hydrocephalus or if it's a local lesion, it's a pineal tumor, which isn't related necessarily to ICPs. That's just where the pineal gland sits. So someone has paranoid and it's not a pineal tumor. They have probably hydrocephalus. So etiologies for this, cerebral edema from trauma, TBI or diffuse axonal injury, just get hyperemia into the tissues. Liver failure. We see this in patients with Tylenol overdoses and then diffuse ischemia anoxia. So sinus thrombosis, cardiac arrest, again, overdose situations where they have just systemic hypoxia. We see it in status epilepticus and then we see it sometimes in infectious. So these are really when the entire brain is being affected by this pathology and causing a diffuse cerebral edema. And then hydrocephalus, again, we can see that whether it's communicating or non-communicating. I always highlight this point. I know I said obstructive earlier. We really prefer the phrasing communicating and non-communicating because at the end of the day, even communicating hydrocephalus is technically obstructive but it's obstructive at the level of the arachnoid granulation. So sort of the end point of CSF resorption resulting in global increase in CSF and thus elevated intracranial pressures. Just to highlight with the infectious, certain types of meningitis can be very bad. Streptococcal meningitis is one. The body exerts a very robust inflammatory reaction to that which can cause increases in intracranial pressure if they have a diffuse meningitis. And cryptococcus is one that actually can cause, very commonly causes a severe hydrocephalus with it. So those patients oftentimes need CSF diversion. So focal causes, very commonly we see this in the case of hemorrhage, neoplasm. Well, that's the one area that does kind of bounce the line here between chronic and focal and acute elevations in intracranial pressure. Usually if this is causing an elevation of intracranial pressure pathologically in the acute phase, it's cause you're either, there's some abrupt change in edema. Maybe there's some either radiation necrosis or some ischemic events related to the tumor. It's causing hydrocephalus or obstructive hydrocephalus or potentially some sort of hemorrhage within the tumor. And this is obviously worse than the posterior fossa where there's less space. Again, infection can cause this. Things like abscess and empyema, they tend to cause an immense amount of edema in the tissue and infarction, which we're all very familiar with. I'd say that this was something when I started my training, we saw very frequently was patients with malignant MCA strokes going on for, we're all familiar with the phrase hemicranial watch where you're watching their neurological status to see if they develop malignant cerebral edema and thus requiring a hemicraniectomy. And I'd say since the advent and expansion of mechanical thrombectomy, I think one of the major benefits we're seeing and now the latest literature is even suggesting patients with large core infarcts with proximal occlusions to revascularize them anyway. And I suspect one of the benefits we're seeing from that is that these patients are avoiding, you're salvaging enough tissue to prevent the global edema that results in a hemic, or the global hemispheric edema resulting in a hemicraniectomy for these patients. So something that I think we don't see as often as we used to, and I think that's the reason why. So in terms of diagnosis, what we see on imaging, you know, if it's global, you're going to see the sulcal effacement. So if you look over on the right there, you can really see in spots A and B how the sulci are really kind of compressed up against the table, the inner table of the calvarium. You're going to see compression of the basal cisterns. So down there in the bottom right on D, you can see that the basal cisterns there around the brainstem are really being squeezed by the medial temporal lobe. If there's hydrocephalus, you can see ventricular enlargement. Again, if it's a focal or lateralizing lesion, you might see midline shift. So that red arrow pointing to the large hematoma, and you can see that the ventricle has been shifted over. Typically, we measure that at the level of the third ventricle, which by definition should be midline in the brain. And again, it kind of depends on what you're seeing. So those images you're seeing over on the right there, those bleeds don't look bad, but that's somebody with DAI from trauma. And so they actually have a diffuse cerebral edema because of their trauma, sort of a diffuse white matter injury, which radiographically only looks like some small hemorrhages, but at the level of the brain tissue itself is actually quite catastrophic. And enhancement you may see with settings like infection or tumor or inflammation. So a quick case presentation, 45-year-old gentleman, no past medical history, prevents following a motor vehicle collision. Rather, he was hit by a car as a pedestrian, unresponsive in the field, right pupils fixed and dilated, extending on the left, withdrawing on the right, got a large scalp laceration, no other signs of trauma. Now, you look at that scan, you can see that subdural there on the right side. Like, oh, that subdural doesn't look giant, but look at how much midline shift he has. Look at the level of cerebral edema, right? You can't make out any of the sulci. There's significant, the brain appears hypodense, more hypodense, essentially darker than you would expect. And then you see that midline hemorrhage in the posterior corpus callosum, suggestive of a DAI. So this is a situation where this patient has significant brain edema. So what's next? This is where we're going to talk about management of this. So first steps, right back to basics for everything in medicine, ABCs, ABCs, ABCs. You know, when I took my neurosurgery boards, I had a case and the first thing they want to hear is you're assessing the patient's airway, breathing, and circulation. You know, everyone always needs to remember, if you see that patient, they have poor mental status, resuscitate, intubate, even if it's done in the field. You know, one of the things we do know is in cases of head trauma is that hypotension and hypoxia is associated with poor outcomes. That's one of these things that's been shown over and over again. And so we know at a minimum, you need to avoid those things. And it makes sense, right? They are the, if you don't have a good blood pressure, you're not going to perfuse past whatever's going on in the brain. And if you don't have oxygen in your blood, you're not going to get oxygen anywhere in the body, including the brain. So that's absolutely the priority for everyone. Make sure that these patients, if you're worried about trauma, they're getting their appropriate primary and secondary surveys. You know, there's a reason people undergo these screens. You need to assess and rule out other injuries too. You know, that patient with that large hematoma, you know, we get sometimes very myopic and are thinking we got to get this guy to the OR ASAP, but he got hit by a car. What if he has a, you know, a ruptured spleen with a massive retroperitoneal hematoma and he's hemodynamically unstable, he'll code on the table before we can even get the bone off. So that's very important in cases of trauma. Again, remember GCS less than eight intubate. So less than eight with suspicion for elevated ICP intubate, and you put in an ICP monitor and that's because you can no longer reliably follow their clinical exam to monitor their ICPs. Now, ideally, if they don't meet that criteria, you can follow their clinical exam and use that as a surrogate. You know, one of the reasons that that number of eight is sort of the magic number is that by definition, you know, you kind of stop following commands once you get to that point. And so you can't tell whether or not they're actually kind of processing information. So, or sorry, following commands and or, you know, not opening eyes. So it's one or the other and you really, you know, lose your ability to follow their clinical examination. So again, proceed with imaging as appropriate based off what you're treating. An important thing here, obviously, if there is a surgical lesion, so you know, a mass lesion, a lateralizing lesion with an acute decompensated elevation and intracranial pressure, the first approach, you know, you can do your, the medical maneuvers, which we'll get into. But ultimately, that's all on the way to treating the proximal cause, which is this large hematoma with diffuse axonal injury, you need to decompress the brain, get rid of the hematoma. So the patient was taken for a right-sided decompressive hemicraniectomy, we did leave in a subdural ICP monitor, you know, some improvement in their neuro exam, but post-op day two, flap becomes firm and tight, ICP monitor starts showing a 30. Again, this is one of these situations where a subdural monitor, while not in itself necessarily a great device, in this context can be helpful, because you can kind of decide, you know, how you can proceed with aggressive medical measurements. So CT scan doesn't show any neuro abnormalities, just diffuse cerebral edema. Same thing at face cisterns and sulcine, normal ventricles. So here's where we get into management of acute ICP crisis. Now of note, this patient shows up, you're doing some of these maneuvers on your way to the operating room to help decrease that acute bump in intracranial pressure. So again, our goal, ICP less than 22, perfusion pressure greater than 50. So the early kind of simple maneuvers that you do for all patients, whether they have a monitor or not, keep harping on basic resuscitation, avoid hypoxia, avoid hypercarbia. So make sure that their PCO2 doesn't go above 40. I usually say not above 35, treat anything, any fevers that might be going on, volume resuscitation, make sure you're using isotonic solutions. If you're using hypotonic solutions that can exacerbate cerebral edema, control their hypertension. A lot of these patients with intracranial pathology is they lose that ability for auto regulation. And when they lose that capacity, you might be thinking you want to keep the pressure very high to fight against the intracranial pressure, essentially make sure that you're maintaining a good perfusion pressure, but you just need to get it above 50. If you're going too high, that brain which can't auto regulate, all you're going to do is induce hyperemia and that's just going to result in transidative flow, worsening the cerebral edema. Again, make sure basic things, avoid hypo and hyperglycemia that can exacerbate things. You can increase their venous outflow, just elevate the head of bed 30 to 45 degrees, straighten their neck, avoid constriction. Oftentimes in patients who come in with polytrauma, head injury, you're often worried about a neck injury as well. Now this is where you sometimes have to make trade-offs or make decisions about whether or not to keep a cervical collar on. If that patient's in a coma, they're probably not moving anywhere and if they have diffused cerebral edema and it's a not largely unstable fracture, there may be some role for taking the collar off or keeping it loose. Again, some light sedation and analgesia. If that patient is awake and you're following their exam, make sure you're avoiding over sedation because then you're going to lose their exam. So things like codeine, mild analgesics, avoid things like NSAIDs, aspirin because of the bleeding risk. Then as we progress, this is sort of a stepwise progression. If that patient needs a monitor, you lose their exam, GCS less than or equal to 8, or they're intubated, they need an EVD or some sort of monitor in place. If ICPs continue to be elevated off of that, then you introduce heavier sedation, heavier analgesia. So IV opioids, benzodiazepines, you can give midazolam, propofol, essentially try and keep that patient very, very sedated. And then if necessary, paralysis is kind of the next step. So osmotic therapy, this is something that we do pretty routinely. An important factor here is that you need to make sure that they're in an osmotic state where you're actually doing something other than killing their kidneys. So you need to make sure that the serum osm is less than 320. Once it's above that, then they start losing efficacy and you risk hurting their kidneys. And if you hurt their kidneys, then that really cascades things because these medications essentially become useless almost entirely. And that becomes even more dangerous. So mannitol, this is an important point. That's why I put it in bold. This is something that, you know, you will fail a test if asked this. This can cause a very robust diuresis in that patient. So before giving it, they must be uvolemic and normotensive. If they are hypotensive, if they are hypovolemic, you are going to dramatically exacerbate the situation. Again, ABCs, if they're hypotensive, do not give them a medication that's going to diurese them two liters, because that's going to make the problem a lot worse. And you're going to be chasing your tail by giving them fluid. So typically, we do a 0.25 to 1 milligram per kilogram bolus over 20 minutes. You know, I typically in a pinch do a gram per kilo. And you can do, you know, infusions of 0.25 Q6 to try and get to an osm goal, you know, around 300 to 320. And really how this works is, you know, you're increasing the tenacity of the intravascular space, pulling fluid in, decreasing the fluid content in the brain parenchyma. And you're increasing rheology to your optimizing blood flow, or the flow of red blood cells through the tissue in order to optimize oxygenation. Another option, hypertonic saline. Typically, we go for a serum goal of 150 to 155. This can be done in boluses. At Jefferson, we use 23.4% through a central line, or you can do 3% boluses or continuous. A lot of this, what you have available, what the protocols are is very institutional dependent. An important caveat here is make sure that you do not correct essentially more than 12 cc's in 24 hours, or 12 mL equivalents in 24 hours, because that can result in central pontine myelinolysis, can paralyze a patient. It's an extremely rare phenomenon, but something you need to be cognizant of. And commonly, when you see this is in patients who are alcoholics. So that's a very high risk factor for this. So just be cognizant of that. You know, I think I've maybe seen it on the differential as a realistic possibility once or twice. You know, throughout my entire career, it's very rare, but it's sort of a never event with patients. Just always kind of bring it up slowly. And then furosemide, similar to mannitol, they have to be euvolemic normotensive. There's very limited evidence for this. Other additional management, hyperventilation, try and get their pCO2 down to 25 to 30. Again, you're getting that auto regulation, you're constricting the blood flow and the presence of blood within the brain, and essentially decreasing the, you know, the pressures that way. This is not a good long term solution, the brain very quickly adapts to this, it only has a short effect of about eight to 20 minutes. I always think of this as a holdover for other interventions, especially in TBI, because you lose that auto regulation or in pathological states in the brain, you, it might not even change the perfusion, or there is the vascular resistance in the brain, because they've lost auto regulation. But again, this is something that only lasts a couple of minutes. This is patients go into the operating room, or you're thrown an EVD in to control the hydrocephalus, or, you know, you're waiting for that 23% bolus to take effect or the mannitol to come up from pharmacy. These are sort of, that's sort of your bailout move to buy time. And then hypothermia is, you know, there's some evidence out there, it may improve outcomes. People kind of vary on this. You know, it is a potential option, if you're really, you know, at that critical point, when you're having trouble controlling things, it may improve outcomes. There's no good evidence to suggest prophylactic use, this has been studied, essentially, patients come in with TBI and getting put on cooling to see if that prevents swelling down the road. That did that has not panned out. And typically, you know, it's done in more critical scenarios where you're struggling to control ICPs. So this is when we kind of get towards the very controversial steps. So let's say you've done everything else, and the pressures are still going up. This is when we get into these last leg kind of bailout moves. And these are these are highly controversial. The big one being barbiturate therapy, so essentially a pentobarb coma. Major reasons why it's controversial, the benefits only seen in mortality, not necessarily neurological outcomes. So like a lot of the things we do, got to talk with family about this, talk about what our goals of care are, what are we looking at as a reasonable outcome for this patient, knowing that this may help them survive, but it will not make them better. This is very high risk, because it can cause profound hypotension, decrease cerebral blood flow. And the other factor to this is that if that patient is progressing, and this is looking like an ultimately futile situation where you may be approaching brain death, and that that end of the discussion, you're going to prevent the ability to get that examination, you cannot do a brain death exam while they have pentobarb on board, you have to have a low, low level in the system before you can do a brain death examination. So unfortunately, I've seen the situation where this is started, and all it's done is just prolong the pain for the patient and family another two to three days while they wait for it to wash out through their system. It essentially just decreases metabolic demand in the tissue, and it vasoconstricts in normal tissue, so shunts some of the blood to the more ischemic tissue to try and preserve brain function. These are the doses, essentially you try and get them in diverse suppression to get them in a pentobarb coma. And lastly, surgical treatment, kind of the last avenue on the more aggressive surgical front. Again, this is also controversial, the outcomes have only been improved if you see an improvement in ICP. And similarly, what we see is increased survival, but not necessarily neurological outcome. So it increases the rates of vegetative state, it's emergent and life saving, but you need to have realistic conversations with what we're looking at with the family. At a minimum, it has from those who go to the OR, you have to have a 12 centimeter decompression at a minimum to have any effect. And if there is a lesion there, that's sort of the variable, like a hematoma of whether or not you're actually going to chase that. So key takeaways, neuro exam is your best ICP monitor. But once their GCS starts going down, you have to get a monitor in. But until that point, try and avoid things that are going to cause you to lose your exam. If there is a surgical cause, treat it, you can do your medical interventions on the way to the operating room, but treat the proximal surgical cause. And proceed with progressive stepwise interventions. And you can do parallel interventions, right? You can do initiate hyperosmotic therapy, set them up, take off the collar, if they're on a vent, you know, maybe over breathe them for a little bit. And if the ICP spikes, give the mannitol as well. And you can, you know, have progressive aggressiveness of your interventions moving forward. And then just be aware of contraindications and controversies for this. So a big one, like I harped on diuresis when they're hypotensive, and the effects of things like sedation, paralysis, and ultimately pentobarb coma are going to have on your management. All right. I think I'll keep going and see if they take questions at the end. So chronic elevations in ICP, this is a very, very different pathology. And this essentially slow minimal changes with time. And this is because the body enacts robust compensatory mechanisms. And when the longer the time course, it can enact more robust compensatory mechanisms. We see this in slowly progressive lesions, like tumors or chronic subdural hematomas. We can see it in hydrocephalus that, you know, expands more insidiously. I will say normal pressure hydrocephalus, just to get this out of the way, this by definition is not an issue with intracranial pressure. By definition, it is a normal pressure hydrocephalus. So it's neurodegeneration due to fiber stretch from ventricular expansion out of proportion to cerebral atrophy. So this is a totally separate pathology. This is all the lip service I'm going to give it. Just look out for enlarged ventricles, someone who has urinary incontinence, gait dysfunction, and cognitive dysfunction. So wet, wobbly, and wacky. But that is not what is an issue. And then probably the most common thing we see outside of these, you know, prized chronic subdurals and tumors is a pseudotumor. So idiopathic intracranial hypertension. So just to kind of, the differences in presentations between the two, you know, slow growing lesions tend to have a more insidious progression to headaches. And then typically you have this, you know, patient has these chronic headaches, maybe some bouts of confusion or something. And then some, by the time they're seeing you, there have been these brief, decompensatory, more acute type issues. So mental status changes, you can have, you know, focal issue, focal deficits based on where the lesion is, seizures, things like that. One of the big things you're going to see with this is imaging out of proportion to the examination. So, if we go back here, you see that large about three centimeter lesion in the left high parietal lobe with significant mass effect and midline shift, but that patient walks in to see you. You know, if that was an acute subdural hematoma, that patient is going straight to the operating room if they're not dead on the table, but because it's been growing over some time, the body's compensated. So, the imaging kind of looks out of proportion to the examination, and these are the patients where, you know, ED calls you in a panic in the middle of the night, and then, well, what's the patient look like? They're like, oh, they're awake, alert, and oriented, but, you know, is this an emergency? And you say, nope. So, the management for these, it's very clear, just treat the problem. You know, if they are presenting with that acute decompensatory symptomatology, then go back to that management, proceed in a stepwise fashion, and, you know, expedite the operative intervention. And if it is a tumor, you know, this is not an option for hemorrhage, stroke, TBI, the things that we've mentioned in the past, is that steroids dramatically make the situation worse in those pathologies, because all it does is increase the risk of infection, and that is, those situations result in a cytotoxic edema from tissue injury, which does not benefit from steroid treatment. So, all you're doing in TBI, stroke, hemorrhage, is causing systemic risk of steroid therapy without any focal benefit in the brain. So, if, however, it is a tumor, and they have significant vasogenic edema from the tumor, that does benefit from steroids. So, in those specific situations, and this is where you're probably going to see this slow and insidious progression of ICPs in these patients that you can get some benefit. And then on the other side, we have pseudotumor. This is compared, presents very differently. It typically does have a slow and insidious onset. They may or may not have progression of their symptoms. Their primary symptoms are usually headache-related. The hallmark of this is that they're going to have a normal neurological examination, with the exception of, most commonly, issues with their cranial nerves. So, papilledema, vision loss, blurriness, obscured vision, again, from the eyes or the windows to the brain, from the increased pressure in the optic nerve. They may have a gaze palsy. This is a pathology often associated with obesity. We actually believe that may contribute to the pathophysiology of this. And on imaging findings, you're going to see slit ventricles and empty cella. And oftentimes, we see venous sinus stenosis. Now, you do need to make sure it's not thrombosis, which would be more acute presentation, but that is a common finding we see with pseudotumor. And the management here is medical to start, but it can be surgical, and the main thing is you treat the symptoms, and at the end of the day, if we have to treat the problem, that's what we do. So case presentation, 47-year-old obese woman, history of diabetes, hypertension, migraines, presents with months of worsening headaches. It is worse with bending over, coughing, sneezing, and this is associated with blurry vision. It's different from typical migraines, and she gets no relief from usual headache medications. So the pathophysiology of pseudotumor, ultimately, we don't really know for sure. The biggest suspicion is that this is related somehow to venous outflow obstruction. This is why we think obesity plays a role. That increased tissue on the body can reduce jugular venous drainage, which can propagate up into increased intracranial pressure, and then often, we see that transfer sinus stenosis. Now, the question is, you know, chicken or the egg, did the veins get narrowed because of the pressure, or did the narrowing cause the increased pressure in the brain? Another thought is disruption of CSF homeostasis, so either increased production or decreased resorption. We already talked about the imaging findings, and by definition, you know, this is diagnosed typically with a lumbar puncture, and for it to be idiopathic intracranial hypertension, they have to have intracranial hypertension. Now, I'll say a quick caveat. There are some case reports out there, and I've even discussed a patient of mine with a neurologist of someone who had all of the symptoms and findings, but had a relatively normal opening pressure, and the argument I would give is that we're probably dealing with some other pathology, because by definition, it is not idiopathic elevated intracranial hypertension. And these are those imaging findings, so empty cella on the right, and on the left, you see the stenosis of the transverse sigmoid junction there. So management, nonoperative management, typically weight loss, you know, 6% weight loss can result in improved papilledema. Another medication we often give is Diamox to decrease CSF production, you know, furosemide sometimes given to also encourage diuresis, and sometimes that can help symptoms. Steroids typically provide some temporary relief, but not good for long-term use, and obviously if we're dealing with obesity, that can make things a lot worse. Now, surgical, this is, you know, an area of debate and ongoing discussion of what do you do and when, you know, sort of the gold standard is spinal fluid diversion. Historically, this is the standard that's been done surgically. So starting either with serial LPs, you know, see if sometimes patient just needs one LP to get some symptom relief, and then they can go out and lose 40 pounds and symptoms and the issue gets better. Lumboperitoneal shunt, ventricular peritoneal shunt, there's been papers debating which one is better. Either way, 50, half of them need some sort of revision or additional treatment down the road, so maybe not as durable. Optic nerve sheath fenestration, this is for patients typically without headaches and isolated vision loss, but again, 30-35% also need additional treatment. This idea of a temporal window where you essentially just do a temporal craniectomy. We see this more often done in younger children, not as popular today and certainly not with adults. This is kind of the big new popular method of treatment. You know, we do quite a few of these at Jefferson and this is venous sinus stenting. And the idea here is, you know, whether it's the chicken or the egg, the venous sinuses are narrowed and if we can open them up, we increase venous outflow and then can decrease intracranial pressures underneath the symptoms. So it's becoming increasingly popular, there's a lot more data coming out. As of now, about 12% have needed additional stenting or procedures, which compared to the numbers from before is actually quite good. The downside here is that, you know, it does, they have to be on antiplatelet therapy. This has its own risks associated with it and it, you know, that antiplatelet therapy may limit the ability to do additional treatments or make them higher risk. If that stent is fresh, they need to be on dual antiplatelet for at least 3-6 months and if their symptoms get exacerbated and they need a shunt, you're going to be doing a shunt on platelets, which is always dangerous. So pearls here, again, remember generally a normal examination, imaging typically non-pathological except for the findings we discussed, typically a slow chronic history, headaches, some vision changes and typically managed medically first line and surgical options only if those are failing. And the big debate now is CSF diversion versus stenting as upfront treatment. So summary, you know, just to kind of discuss the major differences, acute versus chronic. Acute is an emergency, right? The priority is stabilization, resuscitation. Management initially based off examination. If you have a favorable exam, you can have a more conservative treatment course. But once things progress, ICPs go up, GCS goes down, monitor goes in place, then you have to start being more aggressive with your medical management and surgical management is really a last resort in terms of things like hemicraniectomy unless you're treating a focal contributory lesion like a hemorrhage or a tumor that bled or a hydrocephalus or something like that. Again, going along with this, lesional might be urgent or emergent if the patient's decompensating, but you'll see that on imaging. And lastly, pseudotumor, that chronic ICP elevation is non-emergent. Oftentimes, if the vision loss is acutely getting worse, you may want to expedite things, treat it a little bit more urgently. Typically start with an LP that often gives relief and then go from there. Imaging is typically the nine other than the characteristic findings and always trial medical management first. Okay. Questions? Thank you so much, Dr. Schmidt. There are a few questions in the chat. The first is, what are your thoughts on keeping ICP monitors in status post-craniectomy patients? Yeah. Well, you saw by my case example, I'm not 100% against it. I mean, in general, I'd say I don't do it very often at all. Typically the situations where I think there may be some benefit is in TBI, where TBI or malignant MCA strokes, where they can still have issues after the hemicraniectomy and you may want some sort of targeted therapies, but again, it's only good for a couple of days at most. Now you can always go off of the flap and you can always treat empirically, essentially get them through the swelling window and just empirically treat them as aggressive as possible. But if it's a young patient and we're kind of super critical and diffuse TBI and we're debating, are we going to really throw Hail Marys and do the other side or pentobarb coma and how aggressive are we being with the family? What are we looking at? I might consider it very much case by case. I'd say very rarely would I actually do it, especially in my current practice, I don't treat as much trauma and given that the malignant MCA stroke rate has gone down significantly because of thrombectomy, I mean, I honestly, I can't, I don't remember the last time I did one other than the case I presented. So. And hopeful. Thank you. The next one is for patients with EBD, do you typically drain PRN if the ICP is greater than 20, drain a certain amount per hour or set a level 20, for example, and keep open? That's a great question. And that is a topic of debate even amongst surgeons. There's some, I would say there's some things that make sense to me. And there's very minimal literature. So some of the literature we have suggests specifically in subarachnoid hemorrhage that a closed system draining only with ICP elevations may have some benefit. Now, again, that's like single institution that actually came out of Jefferson. Single institution, you know, we obviously have a practice preference. It's by no means a guideline, but that's kind of how I was trained and it makes, it makes sense to me that you don't need to necessarily be aggressively draining those patients. My concerns with leaving it open is especially if someone has a hemicraniectomy, I would definitely avoid it because you're essentially creating like a siphon for the atmospheric pressure, which I believe is dangerous unless you absolutely have to leave it open. I also think there is some danger in regards to, you know, nursing care, technician care. You know, if it's open, yes, you have warnings everywhere, but you know, that patient needs to be calm. They need to be, you know, relatively still. Everyone needs to be very comfortable and aware of what's going on because if you leave that drain open, patient gets up, stands up and walks 20 steps, they'll drain 5,000 cc's, which is dangerous. So I always have a lot of caution with that. So my general preference, I would say for most situations is keeping it closed and draining it only if the pressure gets elevated. Now caveats to that, I would say someone with very bad hydrocephalus who is requiring a ton of drainage, I might just keep it open just to, you know, not torture everyone and just or do a certain amount an hour just to make sure we're really draining aggressively. And someone with bad IVH, I tend to keep them open or drain them and or drain them aggressively, you know, a set amount an hour. My thinking there is if you stop, if you stop the drainage, because there's so much blood in that CSF, and this is purely anecdotal and based off of what makes sense to me, not necessarily data, is that, you know, you kind of have a higher chance of clotting off the catheter because you get this stagnant blood in the system. Whereas if you keep it open, you know, and the pressure is high, it's going to drain, you're going to get that flow through it, which is going to prevent it from clotting off or, you know, draining it a couple of cc's an hour just to kind of keep some of that flow going through it. And also that if you're aggressive with drainage and aggressive in IVH, you can help clear out the IVH and work towards getting that patient out of the hospital. So again, that's, I hope that makes sense. I've always thought of it that way, too. If you stop the flow, then somehow you're making them more inclined to clot. I agree with you about the signs, too. I think, you know, the signs in the room are great. But after the first day, people just become blind to them anyway. I feel like they're just part of the decorations, like the flower pictures on the wall. Yep, exactly. You know, and, and, and people very, you know, everyone, people are people and people can make mistakes. And, you know, the most highly seasoned, well-trained doctor can walk in the room and patients like, oh man, let me just sit up. And you're like, yeah, sure. Let me help you. And you start raising the head of bed. Next thing you know, they're 20 cc's above where they were. And they just drained 30 cc's of CSF. And you're like, oh, that's a good into our next question is how do you address complications from a shunt or drain that becomes blocked or infected causing ICP? Yeah, yeah. If it's a shunt and it's in fact, I mean, the general answer is interrogate and replace if needed. You know, I would say sort of, let's start with shunts. If it's not working, you need to figure out, interrogate it. And that's a totally separate, that would be a talk in its own right of how to effectively interrogate and work that up and identify the issue and replace that issue. If it's infected, it's got to come out at a minimum to drain the clavicle, but usually take the whole thing out and swap it out for an EVD until the infection clears. And then you can talk about replacing. Um, for EVDs, yeah, I mean, yeah, you can kind of troubleshoot it, try and see if you figure out what the problem is. If there's an issue in the distal tubing, now again, you have your proximal catheter and then it connects to the drainage system. Essentially anything from that connection to the drain or to the drainage system is distal. Anything from that connection to the ventricle is proximal. If it's a distal issue, usually you can just sterilely access it and flush it out. Outside of that, really know what you're dealing with before making your next move. You know, some people proximal flush, I certainly do in certain situations, but you need to be very careful with that and make sure you're scanning and that, you know, your catheter is in great position and, and, and so on and so forth. Someone who has a ruptured ophthalmic aneurysm that was treated with a pipeline and they're sitting there with an EVD on dapt and their drain clogs, that's not someone you want to be flushing. But on the other side too, that's also not someone you necessarily want to swap an EVD out for. So, yeah, I mean, it, it, it kind of depends what you're dealing with when the EVD clogs. In general, if you, if you don't have a reliable ICP in a sick patient without a good exam, you need to fix that situation urgently, meaning swap out the EVD or put another one in. Okay. Then the last question is... If you can't fix it by flushing or whatever, messing with it. Last question is thoughts on routine CSF surveillance with cultures, etc. for patients with EVD as well as antibiotic prophylaxis with EVD. Great question. Good questions. So I, we used to check routinely. I am not a fan of doing that. I find the rate of like just getting some, you know, oh, GPCs, one out of two bottles. Is it a contaminant? I don't know. Now we got to get ID and the catheter stays in another week for, before you can place a shunt. I found that, you know, I run into, I don't know if necessarily it's helped. But that being said, in the, a whiff of infection in these patients sends CSF. A hundred percent sends CSF. The biggest thing you can miss, it's right, like you have it right there. You have access. The biggest thing you can miss is, is an, is a ventriculitis. Because that can be catastrophic for patients. I've seen a couple of cases of that and it's not pretty. So yeah. And also a low threshold to start antibiotics in someone with an EVD and suspicion for infection. I think that the data has kind of pushed against this, but you know, early when I was training, it was almost a rule. If someone with an EVD has a fever, send CSF and start broad spectrum antibiotics with CNS coverage immediately. You know, don't wait to see what cultures result or anything or, you know, you need to prevent it from getting worse up front. But that, that's kind of fallen out of favor, but very low threshold, I would say to start antibiotics. And yeah, antibiotic impregnated catheters, if you can, if you have them. Awesome. I think that's all the questions. Thank you so much for your time. That was very helpful. Absolutely. Thank you guys for having me again and look forward to seeing you next year.

elevated intracranial pressure

Monroe-Kelly Doctrine

cerebral perfusion pressure

acute ICP management

chronic ICP management

CSF diversion

ICP monitoring

mannitol therapy

EVD complications