like so bright and early. So I'm a neurointensivist by training. I spend most of my time in the neuro ICU seeing patients with mostly cerebral vascular disease. But I have the luxury in that position to get to do a lot of ICU consults as well. And I think this is a frustrating and common occurrence that we get called for all the time of, you know, the patient was sick, and now, you know, we kind of made them better, and they're still not waking up. And how do you approach that patient? There's no disclosures, nothing relevant. So delirium, as we know, is incredibly common in the ICU population. You know, maybe a third of patients who are not on the ventilators, up to 80% of vented patients if they are formally screened. Common problem. However, 10 to 15% of non-neurologically admitted patients, so patients who did not come in with meningitis or stroke or something else, will develop a neurologic problem during the course of their ICU admission. That's actually kind of a lot of patients, right? And so I think when we think about reducing a problem to a syndromic diagnosis, they are delirious. They have toxic metabolic encephalopathy. We have the potential to really miss reversible causes that could be treated. And so today we're gonna talk about, you know, this is a very broad topic, but a little bit of an approach that I use when I'm seeing these patients, that I get called from other ICUs to kind of think about, why is the patient not waking up? So first, who does this apply to and who does it not apply to? So this is not the patient population that was specifically admitted with a neurologic problem, right? This is not a patient with meningitis. This is not a patient who came in with a stroke or interstitial hemorrhage. This is not a patient that's at high risk for a neurologic infectious complication. Not someone who's had a recent neurosurgical procedure. Not someone who's got an open skull. This is a patient who is altered beyond what you think would be appropriate for whatever systemic illness they came into the ICU, right? They came in with liver failure and that's kind of been corrected. They came in with sepsis. You treated that. They came in with some other syndromic diagnosis that's very common in critical care and they still just aren't waking up. And so you've also done the base work. You know, by the time I'm getting consulted, people have already checked the ammonia level. People have already looked to make sure that their BUN is not 150. They're not hypoglycemic. They're not hyperglycemic, right? You've done the basic work here. So how do you approach those patients where it's not clear just from your typical metabolic screening what is going on? You have to be really thorough in these patients and so you have to cross your eyes and dot your, sorry, dot your I's and cross your T's. So we're gonna use this nice mnemonic dots, okay? So starting from the beginning, D for drugs. I know you're all thinking, duh, I looked to make sure the patient wasn't on fentanyl and they're not on a sedative anymore. But I think there are a ton of things that we can do from the medication list and I see the pharmacist shaking their heads here, yes. This, I have to tell you, is at least half of the consults we get. We dig through the medical record. We look at what drugs they were exposed to or not exposed to. And that's a really clear, a really important thing to do is to go back to the patient's home medication list and think, did you not restart their levodopa, right? Like this Parkinson's patient is gonna look terrible without their support. Are they off their antidepressants? Are they off their baclofen? Are they off their anti-seizure medications? I think a lot of time we think about what patients are exposed to and forget to think, what have we left off? I think for all the pharmacists in the room, I know that you know this, half-lives really matter. I think we as clinicians sort of say we stopped the drug and now it's gone. This has really been drilled into me in doing brain death testing. When you think about the five half-lives that you need before you can clinically clear someone, it is a long time for a lot of the sedatives that we are giving. So just be mindful that just because you stop something doesn't mean it's not on board. And then reviewing their kidney function, their PRNs. You know, this is like bread and butter, but it's good practice to do this. And then antibiotics, right? I think we have sunk in more and more to cefepime neurotoxicity, but it is not just cefepime. In fact, when you think about antibiotics, basically any class of antibiotics has a potential for neurotoxicity. This is particularly true of metronidazole and izionazid. The cephalosporins are chief offenders of which cefepime is a major culprit, but it is not the only one. And so, you know, the mechanism here is probably inhibition of synaptic transmission that leads to excitotoxicity and delirium and then potentially seizures. But this is just something, you know, to be very mindful of. And if nothing else, this is sort of like, you know, drug fever type thing, where you're like, if the patient's still altered and they're on a class of antibiotics, think about, is that a class of antibiotics that we could switch to and give them a different exposure? It is more common in the elderly and is more common in patients who have impaired renal function. So really, antenna up for those patients. All right, this is not common, but I think it gets missed. And the reason I'm bringing it up is because it's not gonna be seen on a head CT and you're gonna have to potentially go back. So osmotic demyelination causes the syndrome of central pontine myelinolysis or extra pontine myelinolysis. This is something that we see, I would say, once every maybe two years. This is a very unfortunate case of a liver transplant patient, where you can see that trident sign in the pons, which is the classic finding in this disease. It is specifically thought of or traditionally thought of in patients who have rapid correction of their sodium. But it can occur from a lot of different other things. It's been reported in hypokalemia, in DKA. It's incredibly, or our patients who are peritransplant are at higher risk of this condition. The reason I bring it up is because specifically with sodium, usually the team that is aware when this rapid correction of sodium happens is horrified. They know that this happened. Central pontine myelinolysis presents in a delayed fashion. So the team that was really worried about it is probably rotated off service. And now it's a second team that's like, why is this patient not waking up? It has a sort of biphasic appearance. So the patients first come in with seizures, encephalopathy, they get a little bit better. And then all of a sudden they have dysarthria. They have gaze restriction. They become locked in, right? So this is something that is not, fortunately, very fortunately, not that common, but I always think about it. And I go back and I look at the sodiums. I go back and think about, was this DKA patient? In stage renal disease patients, it can be observed in patients who have rapid sodium and rapid concentrations of urea shifts. So this is one of those things to keep in mind and go back because the team that is gonna diagnose this is not necessarily the team that saw the insult happen. And it's not gonna be seen well on your head CT. T for thiamine deficiency. I love thiamine. I just give thiamine like DVT prophylaxis. And the reason is, is that thiamine repletion is pretty much harmless. So thiamine deficiency results in increased dopamine, which causes delirium. In extremes of this, you actually see Korsakoff psychosis, which is just a really incredible neurologic diagnosis of confabulation. It decreases acetylcholine, which causes this cognitive impairment. And the triad, this Wernicke's encephalopathy of ophthalmoplegia, ataxia, and confusion, not often seen. What we're mostly seeing is confusion, plus minus, maybe a little bit of impaired lateral and upward gaze. MRI is actually pretty sensitive for this and is specific for it as well. You see this T2 hyper-intense signal around the cerebral aqueduct in the periaqueductal gray, as well as in the mammalian body, as in sometimes in the thalamus. What's really important to know is sending a thiamine level is not going to be helpful, right? So patients with, or the blood and plasma concentration of thiamine does not reflect your tissue, or your tissue concentration of thiamine. Your blood level can be rapidly normalized if, say, you get a banana bag in the ED. That does not reflect the true tissue concentration of thiamine. You can send a blood thiamine diphosphate level, which is a little bit more sensitive. But again, this to me is a clinical diagnosis and one that has a very low risk of repletion. You might expect it in patients who've been adequately resuscitated, but still have a high lactate and an elevated anion gap. I like this study of end-stage renal disease patients who were in the ICU with encephalopathy. They gave them high-dose thiamine and 90% improved. Now, do I think it's confounded by other things? Could they have gotten better by other things? Sure, but is this harmful? No, and I think that this is one of those things that when I consult for patients who've been in the ICU for a long time, one of the first things I do is high-dose thiamine replacement. I love the first part of this algorithm because it has involved no testing. All you've had to do is sit down and go back through the drug list, go back through their home medication list, think about what they have and have not had in terms of metabolic fluctuations, and give them some thiamine. At the end, we're now gonna get into two tests that are gonna be helpful, right? So the next thing we have to think about is structure. Most ICU patients are complicated. It's harder to get them to an MRI. So what you're going to do to evaluate the structure is the classic head CT. And I think it's important when we're thinking about this to know that the diagnosis of this is actually fairly good. When we send patients down, I hear complaints of like, what are we gonna see with a head CT? But actually, you can see a lot. And in 10 to 15% of patients in the ICU, this actually has the potential to change management. So again, it's a humble test, but one that I think is a good one. So what are you gonna see? When we think about sort of this non-focal, what looks like toxic metabolic encephalopathy, it can be that they've had a vascular event, specifically in the PCA territories or in the right parietal, sort of posterior MCA territory on the right. Those and the thalamus. So those syndromes don't present with like a lot of weakness, gaze deviation, language deficits that are easy for us to pick up on a screening neurologic exam, but can make a patient very encephalopathy. Press and vascular dysregulation makes patients look very confused, seen on a head CT. Subdurals, global cerebral edema and hydrocephalus, all picked up by the humble CT scan. So actually, I think this is a really helpful test and I think we can get a lot of information. It's really important to know what you are going to miss, which is acute stroke. So if there is focality or it is an abrupt change in consciousness, you must, you must, you must think about, is this a basilar thrombosis? Please, if you have any, if this is an abrupt onset change, or you have any lateralized symptoms, send the patient for CT angiogram the first time around. Nothing is more annoying to everyone involved than getting a head CT and then sending them right back down. Neurons over nephrons, I don't care what their kidney function is. If you think that this is an intervenable lesion, please just get the contrast. All right. Finally, seizures. All right. So non-convulsive seizures and non-convulsive status epilepticus is probably very under-recognized in critical care patient populations that are outside of the neuro ICU. This is a simple test. Even a routine EEG, if you can get two to three hours, you're probably going to pick up at least a whiff of that something is abnormal. Longer is better. If you have the ability to do continuous EEG, 24 hours are going to catch 95% of things. If you do not, still getting a couple hours of routine will give you at least sort of a, is this a high risk or does this just look like a little bit of triphasics, a little bit of attenuation? This is really important to diagnose because this is treatable, right? We can intervene. It's important though, that not every spike needs to be treated. I think when you get the reports back from our encephalographers, sometimes they can make it sound like it's a really active EEG and there is a delicate balance of not over sedating patients with anti-seizure medication while taking this seriously and treating seizures. Again, maybe depends on the series used, but somewhere between three to 17% of patients who are screened from a non-neuro ICU, so in a MICU or in a SICU. All right, so takeaways here. Kidney functions, medication list. Honestly, this is like basic stuff, but this is really where the most of our solving comes. Head CT and EEG. There's a reasonable diagnostic. You're gonna get bang for your buck in those two tests and they're simple to do and they're pretty cheap. Always consider vascular imaging for abrupt onset changes and think about thiamine. Just give them thiamine. I don't think you're gonna hurt them. So with that, I will turn it over to our next speaker. So thank you. Thank you.

neurointensivist

ICU patients

reversible causes

DOTS mnemonic

thiamine deficiency