And part of the question, does it precipitate seizures? First was about seizure precipitation. Second thing was about hypotension related to ketamine in patients that have not been depleted like shock and adrenal insufficiency. I see, yeah, okay. So in terms of seizure exacerbation, it's any anti-epileptics can actually cause seizures depending on dosing and variety of them can actually have a pro-epileptic effect. But personally, I have never seen ketamine precipitate seizures. Yeah, I think that's why we use it for seizure management. I know I've seen it decrease myocardial contractility in patients who have chronic or acute adrenal insufficiency. So that's a valid point for sure. The third question was more of a comment, I guess. Drainage for source control is arguably the most important measure in management of severe closed space infections. Paradoxically, meningitis may be the only infection in which this is not done with the exception of crypto where elevated CSF warrants slumber drainage or post neurosurgical infections where EVDs can be done for CSF drainage. In the pre-antibiotic era, this hasn't been the case and there's a case report. I know Dr. Mainali is on her way to Paris. Dr. Phelan, do you mind commenting on this closed drainage or closed infection and drainage and why we don't drain other infections like we drain crypto? Sure, so I mean, I think source control is still super important. So I think if you have a fluid collection that can be drained in one way or the other, an abscess for example, you know, I think that that still holds true. But I think they were talking about in the setting of like a diffuse meningitis, is that correct? Yeah, I mean, I think it's like any other infection diffused through a large volume of distribution. It wouldn't really be logistically possible to drain the entire system. I don't think in the entire CSF. And as far as like CSF diversion, you know, there certainly is a role for CSF diversion in the setting of hydrocephalus, which is sometimes associated with meningitis. But outside of that, I don't think that there's been any proven benefit. Thank you for that. The next question is kind of on the similar lines. Maybe Dr. Chirula can take this. How do you feel about intrathecal antibiotics for ventriculitis in patients who have an EVD for hydro anyways? The question probably is indication of intrathecal antibiotics, I guess. Sure, I can take that one. Well, our practices, if they have a severe ventriculitis, we tend to be very aggressive, depending on which organism is involved and treating with intrathecal antibiotics. And actually, we've actually moved into more, even aggressive measures actually going in there endoscopically and clearing out any septations or anything else specifically if we see those on imaging. So I think intrathecal antibiotics do have a role. Obviously, that's not the first thing we jumped to, but we go close monitoring with serial imaging and then taking it from that route. I guess the role probably is limited to antibiotics that don't have good CNS penetrance. And you have a bug that is only susceptible to that particular antibiotics and the intrathecal administration doesn't cause toxicity. I was in the intrathecal Tobra and Azocin at one point, which actually lowers your threshold pretty dramatically, but that's a great question. Another question, if any of you guys wanna take it, or I don't know if Dr. Kadena is here. How would you treat thrombocytopenia and ICH with sequestration and inability to keep your numbers more than 100K? Maybe I can take that question if Dr. Kadena is not there. So I think my understanding is, so for people who paid attention to the hematology lecture, sequestration is where the spleen pool basically takes off the platelets and they're taken away from the circulation. My understanding is in the terms of stress, the pool of platelets still gets into the circulation and these patients actually don't present with bleeding as often as we would suspect to. That's number one. But if you do end up having a bleeding patient that just happens to have a sequestering disease, underlying the treatment of choice in sequestration is splenectomy. So I guess you probably will have to do a splenectomy, but I've never encountered a case myself, to be very honest. In the 11 years I've been practicing. But my hope is that ICH is a stress enough. So when a sequestered patient does have an ICH, the pool of platelets come in the circulation enough that it kind of allows you to keep the platelet count up. But great question. Another question is maybe for Dr. Malayandi, when sodium is over-corrected in a short time period, do we need to bring it down to D5? I'm assuming that they said when the sodium is like, maybe patient has been hyponatremic in a short period, do we need to give D5? Sure, so ideally if the sodium is rapidly over-corrected or significantly over-corrected, so particularly patients who might be in an SIADH phase or who are developing concomitant DI in the setting of hypertonic therapy. So you're already giving hypertonic saline and then they go into DI. So sometimes the sodiums will jump very dramatically, 170s, 180s, well above 160, or the gradient that you've generated is well above what you need to manage your cerebral edema, then yes, we do need to correct that. As opposed to jumping to D5 right off the bat, if possible, if the patient can tolerate enteral free water replacement, that would be preferred. But if there's absolutely no other route for free water replacement, then it was unique to me at my institution because I had never seen it before I came here, but our nephrologists use a lot of D2.5, which I actually was not accustomed to previously and initially was concerned about hemolysis, but we haven't really seen it and they've been doing it for a long time. So that's something else if you're worried about the dextrose content specifically and these patients tend to be hyperglycemic as well and that certainly can contribute to injury. So if need be, you can certainly give IV fluids to replace that, but if possible, enteral would be preferred. I think I haven't had such a case in a while but I had to kind of revisit the correction. But in my fellowship, one of our indoor attendings used to say that it's not the actual number that matters, it's the back and forth fluctuations. So sometimes the rebound that you do to correct it, what happened, it's okay to let it just slide down and kind of decay away by itself rather than trying to correct it. You never know which one is the one that caused the problem, whether it was over-correction or trying to fix the over-correction. And I think if I understand the latest research in aquaporin channels also shows that it's actually at the sodium levels, it's the aquaporin dysfunction of these patients that predisposes them to myelin lysis. That's why we don't see much myelin lysis in our neuro-ICU population. That's actually a great point, Aarthi. We had one case of a patient who was a severe, like a grade four subarachnoid, a young woman who went into severe DI. Her sodium went from 155 to 182 in a matter of four hours, trying to replace volume and all these things. And so we did try to slowly correct her, very slowly and gingerly, and she did develop some amount of rebound cerebral edema that we then had to manage, but she settled out over a couple of days. How much injury did that cause? Who knows, but it can be very tricky once they get that high. And the last question is, we are about on the hour. When do we consider T3 administration over T4 and myxedema, or is it usually a combination of both? I can take that one as well. So essentially, most recent recommendations are to use combination therapy, just because of the onset of action, particularly given the severity of the symptomatology and the mortality with that presentation. So what would be combination therapy is recommended for most patients, except potentially in the elderly, people who have underlying tachyarrhythmias or severe coronary artery disease. Those would be cases where you would consider T4 monotherapy. Thank you. And the last comment or question is, what are the good sources for sample death questions? You will get a set of, I think, 25 questions as a part of this review course as well. Again, they're not much, but it's kind of the start. Our hope is to build that question back pretty robustly over the next year or two. The SDCM website also has certain other resources for critical care questions, the MK-SAP series, and that's a really good question back for critical care questions, not specifically neurocritical care. Beyond that, I'm not aware of any single resource that I can kind of recommend within the CME guidelines. So thank you, everybody, for another afternoon, and we'll see you next Tuesday. Keep studying, and good luck with the boards for people who won't attend it next Tuesday, but please make sure to catch up on all the recordings. Have a good day, guys. And thank you for the faculty.

ketamine

seizures

drainage

intrathecal antibiotics

myxedema