All right, guys. So this is no relevant disclosure. So our case continues. So the patient is intubated. He's loaded with 60 mg of levotiracetam. So again, we suspect that he's having seizures. We appropriately treat him with an appropriate loading dose. His gaze deviation resolves, and you kind of see some of these sort of static, not really evolving patterns on EEG. But clinically, he looks terrible. He's no longer withdrawing. He's flexure posturing. The MPI is in there well below three. And he's got some anisocoria. So this is just not a really great sign for our patient. And so knowing that this has been such a difference in his exam, you send him back to the scanner. And what you find is you still see some of those subarachnoid hemorrhages that Neha had pointed out to you. You still see that there is a little bit of contusions here. But really, you know, when Dr. Dengayesh was talking to you about the cisternal space around the midbrain, we see that there's just a few swelling, and that space is really starting to be obliterated, right? And that clinically matches what we're seeing on exam, that this is a tight and swollen brain. So our objectives here are to talk about the ways that we use invasive neuromonitoring. We'll review where we place it and what data we're getting back from invasive neuromonitoring. And then some of the complications and pitfalls of specifically external ventricular drains, which are the most common approach. So how is invasive neuromonitoring accomplished? Well, there's two main forms. There are these parenchymal probes, which are going directly into the brain parenchyma. And then there are external ventricular drains, which are advanced all the way into the CSF spaces. There are different advantages and disadvantages. I'd really like to highlight that the advantage of these parenchymal probes is you can put a lot of other types of neuromonitoring in with that pressure probe. So the Camino probe may tell you what the ICP is, but you can pair that with a Lycox monitor at PbO2. You can look for cerebral microdialysis. You can put in a depth electrode. So these become sort of multimodal monitors. The advantages of external ventricular drains are that they are the gold standard for doing ICP management, and they are both therapeutic and diagnostic, right? So we are able to relieve some ICP by taking off CSF. The disadvantages for these parenchymal probes are that you can't use them for treatment. They're less widely available, and there's more of a regional pressure that you are getting back. And we're going to talk at the end about external ventricular drain complications. So who needs an EVD? Well, I think we have at least more guidance in the brain trauma population than in sort of other patient populations. So when we think about the American Brain Trauma Foundation guidelines, patients who are in a coma, so a GCS less than 8 or equal to 8, with an abnormal head CT, or patients with a GCS less than or equal to 8 that has a normal head CT if two of these are true, age greater than 40, motor posturing, systolic blood pressure less than 90. The other patients who get EVDs are for treatment of obstructive hydrocephalus or for the need for clearance. So a patient who comes in with intraventricular hemorrhage, that's going to use an EVD for therapeutic clearance of that blood and to relieve hydrocephalus. And then sometimes our surgeons will use this actually to promote dural hearing, to give the CSF a path of least resistance so that the dura can heal in some of these dependent brain tissues. So just to kind of go over the setup here, it's actually a very simple system. It works by gravity. And so the way that we are determining how much is drained into the chamber is how low or how high that drain chamber is. So when you raise the EVD, meaning you take that collection chamber up to a higher number on the scale, you're basically saying it's going to drain less because the brain's pressure has to be higher than the pressure you've set the EVD at. So lower settings facilitate drainage. Higher settings are allowing sort of a pop-off valve. So if the patient gets into a crisis, they can drip a little bit of CSF out, but they're not facilitating drainage. And these need to be leveled at the tragus. That's really important because if you are moving the bed up and down when the EVD is open, you are basically changing the system in relationship to your CSF collection site. So again, lower settings facilitate drainage. It's important to know at your hospital which numbers you are talking in. Centimeters of water are not the same as millimeters of mercury. The Brain Trauma Foundation uses ICP values in millimeters of mercury to convey elevated ICP of greater than 20 to 22. That's millimeters of mercury. That is not the same as centimeters of water. It's just important to be consistent about the units you're using. We talked about it. Don't adjust the bed with an open drain. And for most EVDs, open is drainage. Clamping measures the ICP. So for a large point of the time, the number that's being generated on your monitor is just sort of a random number generator. It's only accurate if you've actually clamped the drain to actually measure the ICP. That's not true of all EVDs. There are ones that are sort of higher that can continually measure the ICP. But for most of them, it's a random number generator unless you are actively clamping the drain. All right. So we not only get the absolute number of what is the ICP, we get a lot of data from what is the waveform? So a normal waveform is going to show you that there's three sort of peaks. So P1, the percussion wave, that's just our systolic blood pressure. P2, that pressure reverberating through the CSF in the ventricles. P3, the dichroic notch. Most of the time, it kind of looks like your A-line tracing with a little extra notch in there. If compliance is compromised, meaning that system is tight, there's not a lot of room and little changes in volume are going to equal big changes in pressure, what you start to see is there is this signature of poor compliance. P1 is now less than P2. And so the way I describe it to students is it kind of looks like the ICP waveform is giving you the middle finger. It's not really happy with you. Again, that's just looking at compliance. And so again, we're looking, we're trying to understand where are we on the scale of how much pressure, how much volume variations the brain can handle. Really what we're interested in is can the brain still get enough cerebral blood flow? And the way that we think about this is knowing that there is a direct relationship between cerebral perfusion pressure, our MAP, and our ICP. I mean, this is a foundation formula that I think we all recognize from medical school. It's important, though, because for most of the time, the brain is able to keep cerebral blood flow constant over many pressures, and the way it does that is by cerebral autoregulation. So when we start to have higher cerebral perfusion pressures, maybe because the MAP goes up, then the brain is able to constrict, letting the same amount of cerebral blood flow into the brain space. And again, this is really elegantly regulated. However, because that cerebral vascular resistance is ATP dependent, in brain tissue that is injured, there is a loss of that ability to tightly regulate how much blood flow is coming into the brain system. And what that means is that the brain flow, or the cerebral blood flow becomes really directly reliant on the perfusion pressure, which means that changes in our cerebral perfusion pressure, whether due to MAP increases or decreases, or ICP increases or decreases, can lead to either hyperemia, which then imagine you're putting more blood in a tight space that can increase your ICP, or it can lead to ischemia, where the brain is not seeing the blood flow that it needs, and that tissue suffers secondary injury. So I think a theme of all of this has been that neuromonitoring should be used to prevent that secondary brain injury, and this is how we're doing that, is because we're calculating the CPP so that we know that the brain is getting the adequate amount of blood flow it needs. This is not the same for all patients. This was a beautiful discussion by Dr. Parks in the session earlier. There's probably ways to make this more individualized for our patients using CPP optimization, but that's kind of a window into the future. Does it help? I think when we think about invasive neuromonitoring, we're thinking about putting something in a patient's skull. Should it help? And I think best trip is I'm just going to leave you as a window that in this trial, it did not show a difference in outcome at six months, but I think we should think about this trial as a clinical and radiographic exam cohort versus invasive ICP monitoring. I think a lot depends on who's randomized, what happens before they're randomized. I think this left us with a lot of questions and probably just emphasizes that one value might not predict outcomes, but that this can be integrated into a lot more that's going on to help us, you know, get the best possible outcomes for our patient. Finally, some complications to go through. Hemorrhages are actually very common, but significant ones are actually less than or about a percentile. So we scan everybody after we put in an EVD just to make sure we're not missing this. If they're flushing the EVD, if the EVD gets caught, that's going to put your patient at risk of having one of these hemorrhages. And so, you know, we try to, not in this case, but in most cases, we put them in the right frontal lobe so that, you know, the damage done to the brain is minimized. Ventriculitis. This is a big one if our patients have their EVDs in place a long time. The longer you leave these in, just like any other invasive line, the more complications you're going to have. The issue with our patients is that it can be really hard to interpret their CSF, right? These are patients that are going to have blood in their CSF. They're going to have protein in their CSF. Their glucose and their systemic glucose are varying. And so, you have to have a much heightened level of suspicion for this, really keeping a close eye on, you know, altered mental status and sampling that CSF of the patients developing fevers and you don't have a source. They're becoming more altered and you don't have a source why. Routine sampling doesn't seem to help us pick these up. You just have to have a heightened clinical suspicion. Again, remember that BioFire, although very helpful for community acquired meningitis, that's not going to pick up the bugs that are in this patient population. Finally, just like two seconds about how to wean. Rapid weans associated with fewer ICU days, it's fewer non-functioning EVDs, and, you know, this is probably a way to get the drain out sooner, but again, this is a lot of per protocol and hospital policy. So with that, thank you so much, so we stay on time.

invasive neuromonitoring

parenchymal probes

external ventricular drains

intracranial pressure

cerebral perfusion pressure