All right, you thought Tom spoke fast, I was just giving my time instructions, so here we go, get ready, seatbelt. So one thing I wanted to mention, the talk on the GCS. Just remember it's inversely proportional to the time of day when you're talking with your neurosurgeons. All right? This is how I can tell if you're awake or not, okay. All right, second thing is we're talking about what you must read. You have to look at the four guidelines that are out there, because I'm not going to have time to go over brain death, so you need to look at the brain death guideline, the TBI guideline, the sedation and analgesia and neuromuscular blockade guideline, and the sepsis guideline. Guaranteed, you'll probably get a large number of questions by just going through the four of those. And you have time, I reminded you. So let's talk about brain injury. So when we talk about brain injury, the way to divvy it up is primary versus secondary. The primary injury, it happens in that microsecond. It happened. Trauma, hemorrhage, ischemia, tumor a little more slow-growing, infection, again, some more purulent than others, and we'll come back to that. The secondary injury is things that we can identify early and treat, or perhaps even better, prevent. And you heard some of that in Anna's talk, talking about the ICP management, and we'll come back to that. But elevated ICP, cerebral edema, hypoxemia, hypercarbia, and electrolyte abnormalities, and we'll work those all into the talk. So the engineer that designed the system, he or she did a pretty good job. A head this big has to come through a cervix this big. Something's got to give, right? So thus the fontanel, so that the head can compress, come down, and then sort of re-expand. So I like doing myth busters, so I'm like on volume seven of neurosurgical myth busting. I'm sure you have this in the morning on your rounds as well, so let's talk a little bit about it. So if we take away the scalp, we're looking at the bone, and there's the anterior fontanel. The key thing to remember is under that fontanel is dura, and dura, I don't know if it's Greek or Latin, means tough mother. So the way I used to explain it when I had to go to court for child abuse cases, it's sort of like leather on a couch. You can push it, you can do a lot to it, but it still encases the brain in totality. So we'll come back to that, because the neurosurgeons, a lot of the time, well, the kid's got a fontanel. Well, it's bulging, and it's because the dura won't give. So in the old days when they did the craniotomy, they didn't do to take the dura off, so you had this big, big bulging, another fontanel. So they have to do a duraplasty as well to come back. And that's going to be important when we talk about managing most intracranial problems and pressure. So as we work our way down, so there's the bone, so there's the dura. Anything that happens above it is epidural. Anything that happens below it is subdural. So I'll just go to the next slide. So if we take away the bony calvarium, we're looking, what can happen epidural? So the epidural bleed, the temporal artery is the only artery that's not encased or protected by the bone. So when you see epidural bleeds, they're usually in a temporal sinus, because the artery, you can feel the pulse, is sort of on the outside, not protected. Subdural is just a potential space. There's nothing in there. There's a couple of CCs, it's sort of brain sweat. We'll come back to that, because that's another neurosurgical term that I love, versus brain debris. Nice trying to explain to the mother what he meant after he leaves. My kid's got debris? So we've got the dura above and below. Under that, we have the arachnoid membrane, which when you're looking at the brain and we take things away, is the shiny, glistening part, right? And so that's the happening space. That's where the CSF sits, floats. We'll talk about that later on with shunt capades, but the CF is made and kind of moves around, bathes everything. It's a protector. It's fluid. And that's where the cranial nerves run through. That's where your blood vessels run through. So when bad things happen, pus accumulates. It's in the subarachnoid space, the happening space. I point this out just to show you the central sagittal sinus. We'll talk about that. Largest vein sort of in the body, draining. We'll come back to that a little bit later. And then there we are. We're right down, cortical veins going from the central sagittal sinus. Now those are the veins, the bridging veins that get torn in non-accidental head trauma. So when you're reading the vignette, if you see the word boyfriend or babysitter, you know the diagnosis. It's like general P, you read the exam, breastfeeding is always the answer. There are just certain concepts that are like, you know, God, apple, pie, and mom. So read the vignettes carefully. So Monroe-Kelly hypothesis. So if you want to be a neurologist, neurosurgeon, this is really the only concept you have to understand. And it's the brain is inside. It's under the bone, but then again, you've got the inelastic dura. So 80% in most of us, we all have a relative or a friend where maybe it's not 80%, makes up the brain tissue that's under there. So unless it's coming out on presentation, there's not a lot you can do about it. However, the other two components, 10% is cerebral spinal fluid and 10% is blood volume. So that's the component. So Monroe-Kelly says that if one of these components is increasing, one or both of the other have to decrease to keep the pressure the same. So another way to look at it, and I don't know how I did this, but I flipped it. It's Monroe-Kelly. Kelly will be happy to see this, but it's Monroe-Kelly. So the way to think about it, I was an engineer in college. And so everything was valves and things like that. And somebody said, ICU care is all physics. So here we have the, if you look at the top, so you've got 80% here, 10% here and 10% here. Things are going great. So we have some sort of a mass or a lesion that's getting larger in that space. But yet the pressure is going to stay the same. Well, the only way to do that, if you're going to do something to Peter, is you got to do something else to Paul and Mary here. Get it, Peter, Paul and Mary? I'm old. Jerry gets it. All right. Anyway. We've got CSF getting displaced. So the way I describe this, if you think of the brain like a sponge, and something's getting bigger or tighter in there, you squeeze the sponge, what's going to happen to the CSF? It's going to get displaced. When we look at CAT scans, that's why we see areas where we hear the word effacement. And you don't have to know, we'll go through, I think, the anatomy that you should know, every particular nook and cranny, but they're named by anatomical structures that are sort of near where that fluid would accumulate. Then if we don't recognize it early on, and we allow this lesion, whether it's a hemorrhage, an infection, a stroke, something going on, squashing down the brain there, only a certain amount of CSF can drain. And it's based on your cranial spinal axis. So if you're a newborn, your spinal axis is this long. If you're Shaq O'Neill, it's this long. So although we always say the infant has a fontanelle, the adults tolerate it better because they can displace blood into the venous plexus. And we all know the venous plexus because when you try and do a spinal tap, you get a bloody tap. You know, although it never happens, but, you know, okay. So that's how you can remember where the venous plexus is. But you can see basically what happens, that something's got to give or else the pressure is going to go up. So another way to understand this concept and the way they like to test things is pick your favorite textbook, whichever one is out there and you want to go through. Look at every diagram in there, just kind of slowly flip your way through. Because they're there for a reason and it's easy to test, you know, PFTs, whatever they're going to show you. Cardiac curves. You will see those again. So basically what this shows is that if we look at the volume down here, so 80% brain, 10%, 10% blood volume. So everything's going along here. We've got that lesion growing. And then what happens, you hit a point in time where you've got an exponential increase in pressure. And the patient at that point in time, if they're still awake, GCS is greater than eight and they're talking or they have a bad headache because pressure's starting to build. And then what happens, it exponentially just shoots up. So you can study and learn this one way. This is like the good things here and these are the bad things. Memorize one set and then you know the opposite goes the other way. So basically what it is, is saying that, you know, we have a hemorrhage, this massive hemorrhage or brain contusion. The brain is starting to swell. You've drained as much CSF as you can. Your blood has been displaced. So there's nothing more that the engineer that designed the system can ask it to do. So we have to intervene. So we want to be able to recognize raised intracranial pressure. Two things, if the change in GCS is more than two, even if it goes from 15 to 13, that's a warning sign. If you're measuring pressure, once it hits 25, that's called a plateau wave. That's a harbinger of bad things to come as well. And if you're really into interpreting, they're not going to ask us for that, I don't think. Wave forms, you can tell the compliance based on how tight the measurement looks, but they just want you to recognize increased pressure. So those are two ways you can do it. Or a blown pupil, a change in neuro exam, and we'll come back to that. So status epilepticus. So we were talking about this, like, how do you know what they're going to ask or whatnot. Up until, I guess, five years ago, you used to, from the ABP, you'd go online and you'd get the current contents, like concepts you should know, and there was about 3,000 of them. It was 180 pages. I just logged on the ABP, which is not a very friendly site now, and you got 10 pages of saying how much of this. We designed this course based on what the exam used. This course goes back to 2006. So 20% of the exam was cardiac, 20% was respiratory, 20% neuro, and the rest was the other 40%. So but you can write a question in any one of those and move them back and forth. So don't try and study and figure it out that way. I had 300 and something neuro content specs that I'm trying to get through. So even if you look at the full lectures, they're not all there. But anyway, let's get back to the definition, operational definition. So any generalized tonic-clonic seizure that lasts more than five minutes. Remember, it used to be an hour, 60 minutes, 30 minutes, as you sort of work your way through the history of epilepsy. Spontaneous termination is unlikely in greater than five minutes. Some will stop at six, some will stop at 10, 20. You don't know. There's no good predictors of yet. There's no data out there to help us with that. The longer the seizure continues, the harder it's going to be to stop, and there's a greater degree of neuronal damage. So what do we worry about? So status epilepticus, we'll talk about treatment in a second. But the other definition, there's two others you need to know, refractory status epilepticus. And that's basically, for most of us, after we've gone through two or three medications, the patient still continues to seize. In pediatrics, those are unusual. They're usually related to infections and encephalitis of some sort, as opposed to your common seizure. So again, we talk about maybe 60 minutes, and if you look at the timeline, when you start your drug, you give it over how much time you can infuse the drug, and whatever. Non-convulsive status epilepticus. So even if you do everything perfect in a patient with a seizure, you may have stopped the motor part of the seizure. You don't know electrographically what's going on. So we know the majority of these drugs, the way to think about it is, you look at what most of the medications we give, sort of related, like ethanol-like. So the patient's going to be sleepy, not that anybody here has ever been drunk, but push you away, not want to answer questions. If they're not waking up in 90 minutes or so, you want to consider an EEG, because you want to know what the brain is. The brain's still misfiring. You may have some dysautonomia with a little bit of tachycardia, but you may have a fever, and you're trying to ferret it out. You want to know if the brain is still active and hopping, because then you have to stop it. So non-convulsive is a fair target, I think, for a question. Patient's not waking up. It's got to be 90 to 120 minutes. After that, I'd be worried. And so again, the engineer that built the system, it's like sort of a yin and a yang. So you've got inhibitory neurons, and you've got excitatory neurons. The neurotransmitter for the inhibitory neurons is GABA-aminobutyric acid, GABAergic, GABA inhibits, and I'll come back, versus the glutamate, which is the excitatory. The glutamate, the NADP, and there's all different kinds, the excitatory receptors. And they sit in a balance. Nobody here is flailing and seizing. Everything is sort of a mix where we're balanced. And if you think about the primary recommendation to treat a seizure, it's to give a GABAergic drug. So benzodiazepines are the first drug we give. So when you give the GABAergic, you're telling the negative nervous, the inhibitory system, hey, take over and stop this. And I'll show you the next slide, physiologically, how it works. It hyperpolarizes the next neuron in the line, and it tells that one, go to sleep. Now you've got excitatory neurons that use glutamate. And so the way to think about it is like the old cartoons with the devil. One here saying, yeah, do it, do it, do it. And the good ones over here saying, no, no, no, no. And they're kind of fighting. And so when we give a benzodiazepine, what you're doing is telling the good one to tell everything else to calm down. And again, earlier is better. The longer you let the seizure go on, the harder it's going to be. And we're going to have to get to a second and third drug. And the way it works, so don't forget, we've got a billion neurons coming all different directions. So you've got the excitatory. So you've got your glutamate. You've got your inhibitory. And they're talking to the next cell, which is talking to 10 million other cells. They're going back and forth. So what happens when a neuron depolarizes, it becomes more positive. So from a resting potential of minus 70, you get it up to 40 or so with sodium influx. Then it fires. After it fires, there's a period of hyperpolarization, which is depicted here, where you can't make the neuron seize again. So what the benzodiazepines do is they open a chloride channel and they make the cell more negative. So they bring it down even below minus so it can't fire. So what you're doing is putting out the fire with the benzodiazepine. That's why it's a first-line drug. And you're taking advantage of the inhibitory nervous system, the GABAergic system. As seizures go on and on, we see complications. So again, our job as intensivists is to recognize them, treat them, and if we're lucky enough, prevent them. So this sort of line here defines early versus late. So early, what do you see in the first 30 minutes versus late after 30 minutes? When you think about it, it's a massive sympathetic release when you're seizing. So they're tachycardic, they're hypertensive. Most people don't, but if you ever go in and you watch somebody seizing, put your hand on the diaphragm. It's rock hard because the muscle is contracted so they don't ventilate. So Conway's rule number one is never get a blood gas during a seizure because it's going to be horrible. And then they call me, oh, and I'm like, well, stop the seizure. Then they call me back with another horrible one, oh, did you stop the seizure? Well, why do you keep asking that? So it goes back and forth. But at the end of the day, you've got to stop the seizures to prevent the complications. So if you let them go on and on, not a big surprise, they get hypercarbic, they get acidotic, dysautonomic because now the sympathetic system is going kooky. Early on, their CK is normal, not a big deal in pediatric patients, but you get elderly patients can become a big problem, knock out the kidneys. And you know, just so he's not here, but we can live without kidneys. You can't live without other organs. I wanted to point that out to her. But that's just my feeling. Anyway, potassium is normal. But the key concept here is cerebral blood flow because this is a metabolic storm and the brain needs all the oxygen it can get up there. And the cerebral metabolic rate goes up, you know, if normal is 100, it triples. The downside is after 30 minutes, because by now you've used up a lot of your endogenous catechols, you don't have that epi surge anymore, norepi and the things that you had. Your ICP, the brain is swelling a little bit. So now bad things are starting to happen. You can develop arrhythmias, again, more common in the elderly than the young. They have pretty young, healthy hearts. You can get some renal failure. But what happens is that the cerebral blood flow is coming down because the blood pressure is coming down. However, your metabolic need is still at 300%. So that's why we want to identify, recognize quickly, and sort of use the system the engineer put in, get the inhibitory system to get on board with us. This is just to show you an example that if I really wanted to, I could make my neuro questions for the board into a respiratory question about dead space. So don't feel comfortable when somebody says, well, this was all that was covered. You can do anything with anything. And if the board runs out of questions, they call the pulmonary board and say, we need some pulmonary questions. And so they've got an endless bank of questions that are available. So the perfect anti-epileptic. So it's sort of like the perfect significant other or spouse. They don't exist currently. But you kind of do the best you can. Full disclosure, today's my 46th wedding anniversary. So yeah, how does it work? I'm here. She's back in New York. No, but anyway, just leaving that as an aside. So a lot of times they like to give you a hypothetical. So you're going to make an anti-epileptic drug. So this tells me how well you really understand epilepsy or not. So you want it to be GABAergic because you want it to make the negatives really help you hyperpolarize the cells, put them to sleep. And you want it to be antagonistic NMDA. You'd like it to block the other receptors. Again, as of now, there's no drug that fits this. You want it to be fast acting, obviously, after five minutes. You want it to go across the blood-brain barrier. Anytime you see a question about the BBB, if the word lipophilic is in any of the answers, that's it because the blood-brain barrier is tight endothelial cells. And it's got to be lipophilic to get across, get in there, and put these cells to sleep. You'd like a short half-life. So if something bad happens, it's a short amount of time. You'd like it to be neuroprotective. And you'd like the risk profile to have low or no side effects. All right, stroke. Each one of these could be like a Grand Rounds, you know, or like a two-hour lecture for your fellows. But anyway, two things, two types of stroke. We talk about ischemic, and we talk hemorrhagic. And this is just two examples. They're in younger patients. They're equal etiology. The adult world is probably 80% ischemic, 20% hemorrhagic. Think about congenital heart disease. It's usually a patient that's from another country with uncorrected cardiac disease, right-to-left lesion, and they send something across, gets to the left side, gets up to the brain. And we'll talk about that in a little bit versus a hemorrhage. Again, memorize this. No, I just put this in here. It's a nice flowchart to work up to patient what you need to do for a stroke. And again, if I have to go through it now, I'll have one. So we'll keep going. But so just to talk about one of the concepts is to understand anatomy physiology early on in our careers. And so they'll give you somebody with a deficit, or you'll see an imaging study. And in that area, they'll give you a physical exam, and the patient can or can't do this, that, and the other thing. What they're testing is, do you understand the blood flow to particular major areas of the brain? And if you're not sure, the MCA is the largest artery, has the biggest territory. I would pick middle cerebral artery. They're not going to test you on the anterior carotid artery in the third ventricle. They're going to go big, or go home, I guess. But anyway, they can do this a bunch of different ways. So I'm just, when you're studying conceptually, go back to basic anatomy and physiology, because that will help you through and understand how things happen. You don't have to memorize a gazillion lists. So the five Ps in the management of stroke, we worry about the parenchymus. You want to limit the infarct size. So the area that's unaffected is the penumbra. So that means the cells around wherever the bad thing happened work. They may be dysfunctional, but they're salvageable. The longer we don't recognize bad things going on, the worse it will be. Penumbra means umbrella. The bigger it's going to get, and you're going to have a worse outcome. The pipes, we want to improve compromised flow. Aim for normal vitals for age. That's the easiest way to stabilize a patient. When you have a list of choices, what are you going to do? Always pick the least benign or the one that's not going to hurt the patient. Remember, do no harm when you're looking at the test choices. Perfusion. We don't want to have hypotension. You don't want the patient to be hydrated. So we'll put them on maintenance fluids so we don't get crazed. The penumbra we talked about. And then you want to prevent complications. You don't want the patient's fever is the most important, and I'll show you in a slide or two. Fever's bad. I mentioned in toxicology, you don't want to miss it in the serotonin syndrome. You don't want to miss it in neuroleptic malignant because we get caught up dealing with other things and we kind of forget about that fever is bad for brain. You look at the studies for outcome. If fever wasn't treated, recognized early on, the patients do worse. So you want to think about it. Worry about glycemic control. The studies for tight control, the experts are in the room here, but we had more incidents of hypoglycemia, which is probably the worst thing to do to an injured brain than whatever. We just aim for like normal glycemia. Deep vein thrombosis, you know, again, if it's a trauma patient, you're going to discuss it with your trauma team, your surgeon. I work at a trauma center. They usually wait 48 hours. There's always the asterisk patient that for some reason we wait a little bit longer. But PE is kind of low incidence in PEDs anyway. So it's probably just, you know, grace of God that we get by. We worry about the other things and that'll come with time. Just as a picture of a penumbra. I love this slide. This slide is very old from the New England Journal, 2000, so it's a 24-year-old slide. But basically it's the same thing. So this is a board review course. Everybody's like, oh, they don't teach us anything new. That's because it's a board review. Physiology hasn't changed. Now, whoever's doing this in 100 years is going to be the same thing, but it'll probably be a five-minute TED talk anyway. But so this is just what goes on in the neurons, what happens. And so you hear them talk about sometimes glutaminergic storm. So it's the excitatory neurotransmitters. And basically the underlying pathophysiology of all of this is intracellular calcium, calcium influx, because the pumps that usually keep electroneutrality don't work anymore. So it goes in and it basically knocks out the neurons. But you can see on the side, electrical activity, 15 seconds. It happens quick. Inhibition of synaptic excitation, two to four minutes. So the inhibitory system is whacked, can't help you anymore, breakdown. So anyway, it's intracellular calcium. Arterial venous malformations, just to mention them, because an occasional favorite is a kid in high output failure. And you stethoscope, you hear a murmur on his head, and it's because he's got a vein of galen. And the blood is, because there's no capillaries in between the vein of galen and the artery, the venous system gets arterialized. So they come in and heart failure, and everybody focuses on the heart. You get burned once. You're the first one to run in with the stethoscope and tell everybody around you about that case. But you don't want to miss it. The second thing is AVMs are biphasic, early eight to 10 years of age. And then again, later on in life, you see them. And when they bleed, what we're worried about is the complications of, right? It happened. It's genetic. We're not sure what the cause was. It's a little gazillion-dollar workup. But we want to recognize the problems. So there's a large interparenchymal bleed. And you may notice the area around it has sort of got some edema. And we'll come back to that in a little bit in the controversy with steroids. So the second, what else that's even rare, intercranial aneurysm. So the blood vessels, they run in the subarachnoid space, bathe in fluid. So they're kind of protected when we walk, talk, do things, move around. You can take a certain amount of protection. But so there's a problem with the takeoff or something, vessel, weak neck, and infectious disease, varicella is a known association for whatever reason, that you may see these aneurysms. And there's not very many out there. But when they burst, they release blood into the subarachnoid space, the happening space. So this is a, I had an artist where I used to work. So I had to sign these all over to SCCM. So I like to use them when I can. Anyway, so what happens, that blood causes problems. Because here's the subarachnoid space. And here, the dorsal has been removed and the arachnoid space, and you can see the clot just sitting there around major vessels, cranial nerves, and things of that sort. So just to help you understand it. Also, the blood products and the platelets, release platelet activating, all these different things are going on. So they pretend the good news may be the patient survives. Then we have to wonder what happens next. So one of the things that happens is that we start to get vasoconstriction. You start to see problems, right? So in the old days, there were calcium channel blocker, you put them on something, the motopene, you did something to kind of prevent this a few days out. So again, I'm not a neurosurgeon, I'm not an interventional radiologist, sorry. I'll come back to this. I have a slide about the God's place in the brain, but we'll go back. So the complications, you've got to time things out. So you had the mass of whatever happened. And then you can see, as the days go by, what is the most likely? Which is a good question. Which of the most likely is to explain, you know, day three something happened. So I just put this in here for you. You can see that hydrocephalus, because the blood in the subarachnoid space, goops up the CSF, and it obstructs flow, and it goes through, and you get into trouble with obstructive hydrocephalus. Much like we see it in the preemies with the IVH and things of that sort. And then the vasospasm that I talked about when the blood is up, you see on day six to eight. And what you usually see at the same time is the hyponatremia. And you've heard a bunch of lectures on the hyponatremia. Is it cerebral salt wasting? Is it SIDH? And you definitely want to be able to differentiate the two of those. And you know, vasospasm, reblading. So just think about complications of each thing you're kind of studying. I just mentioned cerebral vein thrombosis, because these kids usually present with seizures. And so those were the major event. It tells you on here, you can see the percentages of what the likelihood of a cerebral vein thrombosing is and whatnot. But what I want to do is cut to, in pediatrics, you're going to see it in a couple places. CNS infections. You worry about it with sinusitis. If you look at, I think it's last week's New England Journal, one of the picture cases of the week, it's like a 25-year-old that has proptosis and whatnot. It's from a cavernous vein thrombosis. Sort of there, interfering with flow, drainage, and you know, it can be lethal or cause blindness if you're not careful. But what you want to do is when you look at it, dehydration in kids is not an uncommon cause for this. You know, we go to aim for the brain, because that's what a thrombosis is. This day and age, neurointerventional people can do a lot for this. And so I appreciate you skipped a slide, and she had like four different. So this is the most unlucky person in the world, so I can demonstrate all four bleeds. So we always talk about the lens shape, opacity of an epidural. Remember the epidural is outside the dura, so it's not protective of blood, it's on the outside of the dura and starts pushing down. So that's why it sort of looks like an eye lens. Then we have the subdural hematoma here, below the dura, and something gave. Here we have a brain contusion, cerebral contusion or bleed. And then up here, the arachnoid membrane goes around the brain, so you got the sulci and the gyri, so the fluid. So subarachnoid blood that's here today, that's small, may be gone tomorrow, because the CSF constantly recirculates. We produce a certain amount, 10, 12 cc's an hour. In an adult, we make a couple hundred cc's, but we turn it over two or three times. So when you think about the choroid epithelial cells, they're like renal cells, which is why sometimes you use Diamox in the NICU to sort of help with this problem. So we'll talk about CSF. So again, we're talking about the 10% that we can do something about. So the CSF pathways, it's made in the lateral and the third ventricles, then it comes down the aqueduct. You've got the fourth ventricle, and then it goes down the spinal cord and bathes, goes back up to the top of the brain. You've got arachnoid granulations running side by side with the superior sagittal sinus. So it goes back in there, and then that drains down into the body, and you sort of get rid of the CSF. So anything that can obstruct CSF flow, like I showed you, the subarachnoid hemorrhage or an AVM that bleeds, sort of anything can do it. So fluid is made, it's got to circulate. If something blocks, you get into trouble. So one of the more common things and one of the concepts used to be recognize pediatric tumor, blah, blah, blah, obstruction. So to put a tumor, it's a slow-growing mass, so you may not, I mean, hopefully you'll pick up that the head circumference is growing, but the fontanelle will slowly split. So in that case, because it's a slow grow, you know, the Monroe-Kelley hypothesis holds up because other things are giving as the head grows. But so if you look at the different tumors, I put this in there, the percentages of where you see most of them, but just to show you what the problem is. So here, so here's the fourth vent, the aqueduct, and you can see this tumor sitting there, and you can see the mass of hydrocephalus. Now, hydrocephalus shows up better on CAT scans than MRIs, but I just want to make the point, and here you've got a large tumor obstructing the fourth ventricle, and you can just see the backflow of CSF there. So these are kids that need shunts. A lot of times, postoperatively, the neurosurgeons may put in an EVD until the blood products are gone and the brain debris clears itself and the shunt won't plug up. So peritumoral edema, this is the only indication that there's data that one should use decadron or a steroid. And it's vasogenic edema, and it's located around sort of the tumor space. And we'll do a question, a similar presentation of it later, and I'll make a few other points there. So if a patient has a shunt, the shunt is always the problem. We've all been on the phone with our neurosurgical colleagues, and they're like, you sure it's not a fever, you sure it's not an infection, you sure? Nope, nope. It's the shunt. Mom tells you it's the shunt. You know, hours, days later, whatever, we get to it. But it's basic plumbing. So the shunt starts here. Usually we place them, they're in the lateral ventricles, and then it comes down and there's a valve. And it's a one-way valve. It's like the NICU. Once you're born in the NICU, you go out, you can't go back, right? So it's the same way. The shunt is like a NICU, and you can only go one way. And if you really look close up at the shunt, what amazes me, there's actually an arrow on it to show you which way it should go. In my shunt-coupé lecture, I have a picture of one that went in the wrong way. And what happened was that, I don't know, they told me it flipped around or something. So anyway, she already mentioned neurogenic shock versus spinal shock. It's important to know it, because they love to give you, they'll show you an MRI. It's one of my favorite questions. It'll have a lesion from severe trauma showing that the cord was transected or badly damaged. And it takes out the sympathetic chain. So you have to think about what the sympathetics control, that norepinephrine is the distal. The other thing is the sympathetic that goes from the preganglionic right to the adrenal gland where it dumps out epinephrine, right there versus norepi. And so you want to be able to differentiate it. So I put this in only because it's a good website. The other thing is, it's worth taking a little bit of time and reviewing the neuroanatomy of the spinal cord. So you've got the great butterfly, which is where the cell bodies are, and then you've got all the myelin. So don't forget, all of those things that go up and down, all those tracks, control different things. So you could theoretically be asked to give you a patient with signs and symptoms and ask you, where is the injury? So the most common is complete, is central cord syndrome. But if you go to this website, they're very well explained there. I'm going to skip that. Can I go right into the next talk? So just for you folks, you've got... If I can go right into it, yeah. So just so you know, there's 18 or 20 teaching slides that follows this. Take your time, go through it. Review how to do a good neuro exam. You want to know the cranial nerves. You may see a picture of a patient with their eyes going in some funky direction, figure out which nerve it is. And if they show you in their testing, like facial, they got to tell you what the patient's doing. Because a lot of times it's like, well, which side is normal or not? So just take your time, but knowing how to do a good neuro exam is going to be very helpful.

neurosurgery

neurocritical care

brain injuries

strokes

seizures

intracranial pressure

neuroanatomy