Hi, everybody. Welcome back to the second portion of our POCUS Stump the Intensivist session. During this half of the lecture, you will hear from your faculty that just gave you didactics, Christopher, Enyo, and Artie, and we will present case-based discussions and kind of have a little bit of a pro-con debate. Christopher, why don't you go ahead and start us off with your topics on shock? All right. Thank you, Andrew. Again, my name is Christopher Schott from the University of Pittsburgh and VA Pittsburgh Healthcare System. We'll go ahead and get started on a few cases to show both the pro and con sides of using ultrasound for all patients presenting in shock. So the first case I want to go over with you guys is a 20-year-old patient who presented three weeks after being diagnosed with pericarditis, coming in with generalized weakness, chest pain, and shortness of breath. On arrival to the emergency department, he was afebrile, tachycardic, had an adequate blood pressure, and otherwise normal vital signs. Here is his EKG, and then here is his chest x-ray. Radiology read it as that there was, compared to three weeks ago, marked global cardiomegaly with congestion, bilateral effusions, left greater than right, and bibasilar atelectasis left worse than right. So after he comes back from his chest x-ray, he is noted to become acutely hypotensive, now more tachycardic into the 130s, 140s, blood pressure down to the 80s or 90s over 60s. So turning to the group, what is your differential diagnosis for this patient? Do we think he's now in congestive heart failure? Does he have a pulmonary embolism? Is there cardiac tamponade? Is this due to COVID? And you know, really at this point, it could be many things on the differential. This is kind of in the category of undifferentiated shock. So asking our very biased panel, do you guys want to perform an ultrasound exam? If you do, what do you want to look at? Do you think we can get away with just doing a basic B-mode image? Do we need to do any advanced imaging? I think it would definitely be helpful to perform a focused bedside ultrasound assessment, and then kind of based on what we would see may determine whether we can get away with just using a basic kind of quick look versus if we need to get into some more advanced measurements. Okay. So here are the first views that we were able to obtain on this patient. On the left is the peristernal long axis and on the right is the peristernal short. What do you think you see when you look at this? First thing that jumps out at me is a, you know, a large effusion, you kind of see the heart dancing within the fluid around the pericardium. You know, it's hard to really identify any chamber collapse in this peristernal long and peristernal short view, but the effusion is, you know, circumferential and significant. Okay. Let's go ahead and I'm going to add in, here's another view that I obtained for the group. What view is this that I'm showing? I'm just a neurologist, but I can tell you this is a apical foreshamer view. Excellent. Does this change any of the information in terms of how you're processing about the patient, Arti? No, I think it's a dancing heart syndrome. I'm basically looking for signs of tamponade physiology to differentiate between a pericardial effusion and versus a patient having tamponade and trying to correlate it clinically. Okay. Well, let's go ahead and I'm going to toss in a few more images. On the left side of the screen is the patient's subxiphoid view, and on the right side of the screen is a view of the inferior vena cava. I'll just let you guys look at those for a moment, and then I've got a follow-up question. It looks bad. Looks bad. Why do you say that? Well, to go back, I mean, I think you said the blood pressure was low, right? Yeah. Systolic was in the 80s to 90s over 60s in the diastolic. Yeah. Yeah, so I'm already feeling like, all right, so the problem, all right, and then I'm feeling like this is still bad because the effusion is still there, the heart's still dancing, the IVC still looks pretty large to me. I think I know what's going on here. Okay. So you mentioned the IVC, so that's my next question. So how would you, and I apologize, I didn't have an M-mode image to actually look at the diameter and the percent change, but based on the qualitative assessment, do we think that this patient has a low or normal central venous radiational pressure, an indeterminate, a high, or I can't really tell, I need a CVC or SWAN for that. So I would assume it's pretty high. It looks pretty plethoric. It doesn't really seem to be collapsing more than 50% without, as you mentioned, having the M-mode through it where I could really measure to see if that's greater than 2.1 centimeters and then look at it both in its largest and smallest point. And I can't say that for sure, but the eye test makes it look pretty plump and plethoric to me. Okay. So you're saying that this is a higher CVP, either B or C. Correct. Okay. So I went ahead and I did apply some more advanced measurements. So this is using the pulse Doppler, pulse Doppler spectral mode with the spectral gate right over the mitral valve inflow. And I slowed down the sweep speed to look for the variation during the patient's respiratory cycle. So measuring between the maximum and minimum velocities, I found that there was a 26.88% change. And I did the same measurement over the tricuspid valve and found that there is a 66% change between inspiration and exhalation. So now that we have some more information, what do you think is going on with this patient? So this, this looks like tamponade to me, and you would definitely have echocardiographic evidence of tamponade, those inflow measurements over the, especially the tricuspid valve being a greater than 50% variation with the respiratory cycle is one of the classic findings for tamponade is kind of the echo finding that's similar to pulses paradoxes over the mitral valve. Classically you would expect greater than 30%, but you're right around there. So you definitely have signs of some like increased interpericardial pressure that's causing chamber basically increased pressure differences within your chamber and some chamber interdependence. Good. So if we go ahead and summarize this case, and I'll tell you that the patient did have concerns for tamponade and was taken to the cath lab immediately. And they had 1.8 liters of fluid in the pericardium that was removed. And the cardiology team said that there was an immediate improvement in hemodynamics once they had a needle in a drain in there. So I brought this up as a potentially easy save by point of ultrasound. The key things being, as Enyo noted, really correlating this clinically to the patient, you have somebody who has shock physiology with hypotension, tachycardia, and concerns for tamponade just based on the large effusion that you see. What Andrew brought up was that he wasn't able to clearly see if there was right atrial, right ventricular collapse, but that there appeared to be pulses paradoxes seen on the Doppler. And then Artie mentioned that she called it dancing heart, swinging back and forth, which is kind of that classic teaching of the electrical alternans we see on EKG. So all of those kind of put together, whether it was just with the basics and the physical exam or then really confirmed with the Doppler, showed ultrasound helped out in making this diagnosis. So let's go ahead and do another case. This is a patient who came into our liver transplant ICU, 50s patient with end-stage liver disease, a history of known esophageal varices that had not been banded, diabetes and COPD, comes in vomiting blood, admitted to the ICU with concerns of a variceal bleed. So it was tachycardic to the 140s, blood pressure 70s over 50s, breathing quickly. When he comes in, you notice that there is pallor of the skin, delayed capillary refill, and was having active massive hematemesis. So same questions. Do you guys want to perform an ultrasound exam? If so, what do you want to look at? Do you think we can get by with a basic or an advanced exam? So while I always do like putting the probe on somebody, I think I would not delay treatment in order to do the exam if this guy is actively vomiting blood and hypotensive. I'd want to kind of start my resuscitation and then consider using ultrasound later to help guide it. I like that. When I walked into the room and just saw the active bleeding covering the floor, I think I had a pretty good idea of why the patient was hypotensive. So I agree. I think that this is an example where sometimes a thing is just what it is, and that in this instance, I didn't want to delay securing the airway, starting resuscitation, getting an introducer, massive volume, or the massive transfusion protocol. And then again, we can always come to ultrasound later, but at this point, sticking to the basics, that's what the patient needs. All right. Let's move on to the next case. So this is a patient in their 60s that's just underwent a CABG. Comes out to the ICU after their four-vessel CABG. Still intubated. Has a PA catheter, an A-line, three chest tubes coming out. Kind of the routine care that we see as they come out of the operating room. Initially doing well, but then about an hour after arrival, you notice the patient is becoming more hypotensive. Heart rate is now 120s, blood pressure is over 60s, respiratory rate 22, setting 98% on the ventilator. CVP is 4, PA pressures are 21 over 8, the pulmonary capillary pressure is 7, your stroke index is 18, the SVRI is 3248, cardiac index is 1.4. So same questions to the panel. What do you guys think? Do you want to perform a POCUS exam? What do you want to look at? Basic or advanced? I think this is not a classical neuro-ICU patient, but it seems like the patient needs more volume. CVP is low, VEG pressure is low, index is low, but being a POCUS enthusiast, I would always look. All right. So we'll go ahead and we'll take a look here for Arti. And honestly, this is the best and only view I can get. So because of the patient having had their chest just open and where the surgical dressing is, I can't really get a parasternal view. Where the chest tubes are coming out, the mediastinal tubes and the pacing wires, I can't get a subxiphoid view. So this is really all I can get is an attempted apical 4. What do you guys think? Well, I think I agree with Arti. I mean, you really can't get a ton of information out of this, which is kind of classic on a fresh sternotomy. You can kind of see maybe one or two seconds in there where you can see all chambers are open. So there's not a huge effusion, but that doesn't rule out a focal tamponade. But in the setting of low filling pressures, you know, a high SVR, a low index, I think volume is the first place to look at before, you know, in the back of your mind also keeping in things like kink graft or other reasons for cardiogenic shock post-cardiac surgery in mind. Cool. I really like that discussion. So that's what I wanted to highlight here is that sometimes we get really limited views and that can be due to where patients, especially in surgical units, have tubes and drains and dressings. And sometimes patients' body habitus, you know, that can make it really challenging to get views. Sometimes we don't always get the ones that we classically see when we're teaching those model appearances. And the other thing is using the data that we have available too, right? I mean, especially in the scenario where you have a PA catheter arterial line, I mean, you already have some other data to help correlate clinically. So again, maybe if I really needed to, again, if I was truly concerned about more of, as Andrew said, a focal fluid collection that might be causing tamponade physiology, I would want to go to a TEE at that point. I know I'm not certified or credentialed for it, but I'd have to recognize the limitation that ultrasound isn't really going to help me in this particular instance. All right. Last case to discuss with you guys. So this was a patient who was in their 70s, came down to the ICU overnight for hypotension and shock. By the time we come into the morning, the patient had already received four liters of fluid and had been started on norepinephrine currently at 0.18 mics per kilogram per minute. Through tachycardic hypotensive tachypneic and on six liters of oxygen. All right. So questions for the group. Does this patient warrant a POCUS exam? If so, what do you want to look at? Can we get away with basic? Do we need more advanced? Definitely want to take a look at this point. It seems like they've kind of had beginnings of appropriate fluid bolus. They're on, you know, a good amount of norepinephrine and they don't seem to be responding. So I'd want to take a look to see what else is going on. All right. So here is the parasternal long axis view we were able to get. What are your guys' thoughts, initial interpretation? It's squeezing, you know, maybe thick, but probably kind of try to look at other views. I can't say from this alone, I have the full picture, especially considering they've already had a good amount of crystalloid. Okay. We'll add in the apical four. Does that change your management at all? Does it help clarify? I think that's my favorite view. It seems to be squeezing really well. The right heart is not much bigger than the left heart. I don't see any pericardial effusion here. Okay. It kind of looks okay. Okay. Yeah, I mean, I think based on what you can see when you can see it, that sounds pretty good. So do you guys have any thoughts right now based on this and the clinical scenario? Are we able to just give, should we give more IV fluids? Do we need to go up on pressers? Do we need to start steroids? Do we need to look for more echo information? Probably try to get more information. Speaking again to a very biased panel, of course. So let's go ahead and get more echo information. So in that peristalne along, I went ahead and I put the M mode across the mitral valve and I have this tracing. Oh, that's an impressive EPSS. Okay. So that's one thing we can use this to look for is to see when the mitral valve opens and then looking at that distance between the E point and the septum, the amount of separation. It's actually the distance from there. Anya? Yeah, Chris, I love this picture. Anybody who has worked with me before knows that I'm obsessed with trying to find this, and I've never found it. So congratulations for finding it. But yeah, I see M mode over the mitral valve. I see that you're looking to see how close the mitral valve is to the septum, the EPSS. But interestingly, in the middle there, between the portion to the mitral valve is up during diastole, which it should be, I'm noticing that during systole, though, the mitral valve is still up. And that is not normal, and that's same physiology. It's easy to see, because you can catch it very easily. It has a cool name. But that systolic anterior motion should be causing some LVOT dynamic obstruction, would be my suspicion. And this is a really important finding, because it'll change, I think, my management. So what would you look at next, then, to help maybe confirm that? You mentioned the dynamic LVOT obstruction. Ideally, in a four-chamber view, if possible, you'd want to put color flow Doppler over the aortic valve and look for high velocities. You would then interrogate those velocities, and you expect to see these really high, peaked, dagger shaped accelerations of blood as it's trying to squeeze through the aortic valve. We can't, because the mitral valve is in the way. All right, well, ask and you shall receive. And so here is the LVOT. So is that that classic dagger shape where it's slow and then accelerates at the end and comes up? Is that what you were looking for? Yeah, it's kind of that early peaking. And I see really, really high velocities. Normal should be about 100, maybe 200 here, like 400, 450. So yeah, that feels pretty high. With a pressure greater than 30 as well. Yeah, exactly, exactly. Yeah, that looks like SAM with alpha obstruction. And then just to kind of help with this patient, we did put color flow on across the tricuspid valve. We saw that there was some tricuspid regurg, and when we estimated the PA pressure based on that regurg jet, we noted the PA pressure was around 80. And I think that had a lot to do with how much fluid this patient got already. So yeah, that's exactly right. So this is an instance where we were concerned for that SAM physiology. I'll go back, that due to a dynamic LVOT obstruction. So this patient, interestingly, does not need to be on norepinephrine. That's going to make it worse. We stopped that, weaned that off, put her on the neosynephrine phenylephrine instead of beta blockers to slow down, give more appropriate filling, let the heart have flow through the mitral valve and out the LVOT a little bit easier. We didn't give more fluids only because we felt the patient was already volume up based on her clinical picture, lung exam, that high PA systolic pressure. And then with this treatment, the patient actually really improved. So I added this one as a case to show that this is really a completely echo-dependent diagnosis that really requires its use with more advanced measurements. And that completely shifts away from giving fluids and more of our traditional inotropes to actually trying to slow the heart down, fluids, and just peripheral vasoponstrictors. So that's what I have for you guys. Any overall questions, comments? Thank you, Christopher. That was fantastic. I think we're here. We're all biased. We are all champions of POCUS and using it at the bedside and want to stick it on all the time. And it can definitely aid in our diagnosis, as showed in case one and four. I think your cases overall, though, really kind of demonstrate how this is another tool in our arsenal that should be additive to the kind of physical exam skills and our other skills we have used as an intensivist to diagnose and treat our patients in the ICU for decades now. And that we can't forget about those other monitors, such as the post-cardiac surgery patient, or just looking at the blood on the floor. Just like you wouldn't stop CPR to put the probe on the chest, we got to continue to manage our patients while using this tool to help us. Cool. Thank you, Andrew. Thank you, Christopher. That was great. We're going to switch gears now and have Anyo give us some case-based discussions on lung ultrasound and using it to help us guide our de-resuscitation and diuresis. All right. Thank you. I'm going to go ahead and share my screen. All right. So let's start with case one. I have a 45-year-old male who presents with acute shortness of breath after getting some Narcan. He got Narcan because of an accidental fentanyl overdose. He had a few episodes of bloody emesis prior to arrival to the ED. In the ED, he has vital signs that show a heart rate of 140, his respiratory rate 45, blood pressure 160, systolic, saturated 85% on a non-rebreather. There are some labs sent upon initial presentation. There's his X-ray. They've already called that he's going to need an ICU bed for the time being. So going over sort of our algorithm, ABCDE, as we look at the lung, the heart, and the diaphragm, we'll go ahead and take a look at these images and get your impressions as you're looking at them. And then I'll show them again during the actual questions. So there's our lung ultrasound, looking at zone three. And then here's our peristernal or, excuse me, apical four-chamber view. There's some advanced measurements. And then those are his diaphragm images acquired at the bottom. All right, so let's start with question one. You know his vital signs. He's tachycardic tachypneic hypoxic, but he's talking to you. What would you like to do next based on those images and this additional image here? You know, based off those kind of images here, it definitely looked like he had some tidal recruitment when we were looking at the bottom of the screen. I would be, if he was protecting his airway and no longer having this hematemesis and was talking to us and mentating, I would be OK probably with maybe starting with a little bit of BiPAP to help open him up. Obviously, if he was vomiting blood, I would be more concerned that he may need to have his airway secured and need the increased PEEP to help open him up. So it'd be a little bit of clinical judgment, but I'd be between B and C. Yeah, OK. So clearly, he has lung ultrasound findings of having increased lung water. He's got B lines. He has a few effusions. So we're going to support him, however, that best with our clinical exam. So then question two, his SATs are now 93%. Let's say we chose to do a bit of BiPAP or let's say we just did OptiFlow, but SATs go up. His respiratory rate has come down to 37. Has some mild diaphoresis on exam. Heart rate has slowed down to the 1 teens. And now we're going to look at the heart. Here's that apical forward taver again. Your thoughts? There's an assessment of his feeling pressure. And the question is, based on the echo, do we need to give him fluids or do we need to diuresis him? I think his heart looks like it's pumping away. The E to E prime isn't crazy high. You know, I might not do either. I might just kind of more hold Pat in this kind of situation and see which way we trend. Yeah, I think that, you know, in general, it's easy for us to want to pick one or the other. Sometimes we just have to hold back and say that there's not clear data that we should do fluids because our chambers look pretty plump. Our E to E prime is normal. And a low E to E prime does not mean you need to give fluids but it's not any over evidence of needing diuresis either. Again, his function is normal. His E to E prime is low. And so the fluid in his lung is not from his heart. It's, you know, perhaps non-cardiogenic palmar edema from the Narcan dosing, that sort of thing. So just a few things that I mentioned in the didactics, just remember to utilize these values in the appropriate context with heart rate, regional emotional abnormalities that you need to make sure the mitral valve is working before these numbers, that E to E prime means something about the filling pressure of the LV. Okay, so now it's day four, he's admitted to your ICU. Let's say you have him on, you've transitioned him to OptiFlow, he doesn't have COVID and he's doing great on his OptiFlow, but then on day four, he's reporting some dyspnea. His oxidation status is unchanged. His basic labs have been sent to her pending. And then you decide to add diaphragm ultrasound because you looked at his lungs, you looked at his heart, now you're looking at his diaphragm and here are your images there, both in M mode and B mode, as well as looking at zone three. What are your thoughts and what would you like to do based on the diaphragm ultrasound? So I think being the neurologist in the biased ultrasound panel, I can safely rule out ordering electromyogram. I don't think that's a patient that I would do a needle EMG in. In the zone three view, I'm seeing lots of pleural effusion. I'm seeing the diaphragm move pretty decently. And if I look at the B mode images with the M mode measurements, I'm seeing a decent amount of excursion. And then the thickness is almost changing by 50% between the two cycles. So the diaphragm seems to be working fine. I think again, in this particular case, just based on the diaphragm ultrasound, I don't see any indications for intubation. I don't see any indications for EMG. So again, depending on the patient if the patient's protecting their airway well, I would probably initiate BiPAP. If they're already on BiPAP, I think if he needs a diuresis, that's something I would do to optimize the patient. I'm kind of stuck between A and B, but not based on just diaphragm ultrasound, based on the overall lung status. The diaphragm doesn't seem to be contributing here. Yeah. No, I like what you said about also the sequence, right? Because it just depends on what's happening. Ultrasound is a supplement to what we're seeing when we walk in the room to monitor the patient. And so he's been in your ICU perhaps for days, even though we didn't diurese him initially in the ED, he is fluid positive, has likely a positive fluid balance. He's got these pleural effusions and he's reporting symptoms now. I agree the diaphragm does not seem to be a part of that. It's got good movement by M mode and the fractional thickening is quite good. We're thinking that certainly greater than 30% is reassuring. So yeah, I think exactly what you said, either A or B, depending on the clinical situation. But good to know that I should never order an electromigrant. That's never the answer on the test, right? Or maybe in life. I would say that, you know, consult a neurologist. After you perform the ultrasound. Okay. Good to know. Okay. Let's go to the next case. See if point of care ultrasound can help us with ventilator management and de-resuscitation or diuresis. So 63-year-old female presents with shortness of breath for about four days. A history of hypertension, GERD. In the ED, she's intubated for respiratory failure. So she has to come to your ICU. She's got vital signs that you can see there. Heart rate's in the 90s. Respiratory rate is 35. Blood pressure, systolic's in the 70s. O2 stats are 92%. You can see her ventilator settings there. Of note, her PEEP is 7.5 and she's on 70% FiO2. Some additional labs to help you. Here's her initial radiograph on the top and then a subsequent CT scan that was obtained at the bottom. So back again to the full summary of ABCDE where we'll look at the lungs, the heart, and the diaphragm to guide our evaluation of pulmonary mechanics and de-resuscitation or diuresis. So we look at the lungs. We're at the anterior zones. Then we're again, next picture here, looking at zone three, looking at the base of the lungs. We'll again, look at those pictures in the questions. We'll look at the heart. Another attempted apical four chamber view. We'll get some additional measurements of the filling pressure listed here for you, 18.3. And then the diaphragm is evaluated again in just beam mode here. So thoughts about the lung ultrasound, perhaps this one here, because I don't show it again. The one at zone three. I mean, you definitely can see there's fluid. You see the diaphragm there with, you know, and then fluid above it with some consolidated lung and then some hyperechoic spots in it, which could symbolize some very consolidated lung or even like a pathologic process going on. Yeah, I think as you're looking at each of these images, you're regarding and putting all together, like you're stacking, right? So you're looking at the lungs, the anterior field, you're looking at the base, you're looking at the heart, you're looking at the diaphragm, you're sort of stacking all this all together to again, think about what it takes to keep good lung mechanics, both from the lung pulmonary itself, the diaphragm for support, as well as the heart, which I call the supporting cast. So question number one, based on those images. So your pre-ventilation ABG on that patient is listed there, 72856, PO2 of 60. And the FIO2, remember, was at 70%. Sats are about 90. And you initially started at the PEEP of seven, five, but let's look at the lung ultrasound and see if it can help us adjust our PEEP or not. So I'll play each of these separately. So options are, do I do A, B, C, or D? So in A, here's what our lung ultrasound looks like at that PEEP of five, and I've got plateau pressures there listed for you. Give you a chance to look at that, see what your thoughts are on that image. Okay, then I'm gonna go to picture number two. So now I'm increasing my PEEP to eight. My plateau is 27. And then here's picture three, I've increased my PEEP further to 10, noted plateau. And then finally, option D, my PEEP is now at 12, and noted plateau. So based on these sequences, these images, what PEEP is ideal for this patient? So based off these ones, I would go towards C. I mean, I think you see a transition from like a B-line pattern in image A and B to more of an A-line pattern in C and D. However, at the same time, your driving pressure is the lowest in C with a driving pressure of 18 there. And, you know, you are under that magic plateau pressure of 30 that we all like to aim for. But really, for me, it's the driving pressure being lower. Maybe you're limiting some over distension there. You know, this is probably a dynamic thing where if you're, as you're re-recruiting and diuresing this patient, if you're PEEP trials, this might change throughout your management. But based off these images, I would go with C if this was an exam. Yeah, I agree with that. And, you know, I'd also factor in how the blood pressure is doing too. You know, I mean, are they tolerating the pressure? Are you starting to see the systolic come down, narrowing the pulse pressure from too much into the thoracic pressure? But I think that's a really great sequence to show increasing ultrasound and how that can dynamically change the recruitment going from B's to A lines. Yeah, that's exactly right. It does require now just not, not just doing POCUS one time, but a serial evolution of that to see where exactly the sweet spot is. All right, let's go on to the next question. All right, question two. So she was mechanically ventilated. Here's your initial creatinine. It was 1.2. Based on those, some initial profiles, the patient was given some LASIKs, good urine output, 1.5 liters over 24 hours. A repeat lab show creatinine today of 1.55. So there's been some delta increase in creatinine. And now we're going to look at the ultrasound images again to see if we should redose the LASIKs because the team during rounds has brought up the fact that the creatinine is elevated. So first picture here. We're looking at the anterior zones. And it's a little hard to see, but there's diffuse B lines that are present there. Then the next picture here as we regard the IVC. And then finally, that apical four chamber view again where we look at the blood versus tissue movement in early diastole with an EDE prime of 18. So based on that information, based on that information, what should we do? The creatinine is up. We gave LASIKs yesterday. Do we give more LASIKs or do we not? I'd probably be advocating for like a LASIK strip. You know, I think they did have a good response to LASIKs with some good urine output, but we still don't know the overall fluid balance. You know, a lot of times, at least my patients in the ICU, one and a half liters might not even be enough to get them net negative. So we don't have that. But these images, it still looks like we have a B profile in the anterior zones. The IVC based off just an eyeball test looks like it's pretty plethoric. And then our E to E prime ratio is also up. So on this, I would be kind of advocating for further diuresis. Yeah, I also second that. I mean, I'm not really sure how much utility there is in the IVC in a mechanically ventilated patient as an estimate of the right atrial pressure. But that E to E prime still being, you know, pretty acutely elevated correlating with higher filling pressures and the B profile that I would suggest the same thing that this patient needs further assistance with diuresis. Yeah. And, you know, I think we're summarizing exactly right. It's all putting it together. These are not always easy cases. There's no slam dunk here. Unfortunately, it requires serial assessments, especially once you're mechanically ventilated, to think it through about, again, getting optimizing things as much as possible while understanding that all those optimizations can affect hemodynamics, can affect other systems of the body that are equally important. I think I've got one last question for the group here. So now it's day four, you're still mechanically ventilated, you've optimized, you've diuresed, all those things like that. And so you perform your spontaneous breathing trial. And finally, today, she sort of passes, technically passes. So you're at diaphragm ultrasound as well. You're going to perform bilateral diaphragm ultrasound. And I'm showing you images. The first one here was how she was day one, when she initially arrived to you, what her diaphragm ultrasound values look like, that fractional thickening. And now what her diaphragm ultrasound looks like. So based on that, what are your thoughts? What would you like to do? Yeah, diaphragm ultrasound has been a little tricky there, where there's early literature to suggest correlations with weaning outcomes. So what I'm seeing here is 48% change in thickening fraction on one side, or before, and now it's 20%. So there's definitely been a linear drop. But I think we haven't found that golden cutoff where we can say this patient definitely is, can be extubated or not extubated based on this. So if they're passing the RSV, this itself will not preclude me from extubating the patient. I think it will have to be a very dramatic, either no change in diaphragm thickening or paradoxical motion for me to worry about using diaphragm ultrasound to not extubate a patient. And I think what you, your comment about, I think when I have used it, it's maybe more looking at like either paradoxical or like differences between both sides. So that there's like clear, like one diaphragm is working and one may not be, perhaps. I get nervous about ultrasound that is at the millimeter level. So if you just look at the numbers here, if I change this to, you know, instead of 0.15, if I change it to like 0.14, or I change it to 0.13, now you're at 30%. And it's already pretty hard to see it. I just, you know, at least at my place, oftentimes we may, if we're really worried, we'll get a, we will actually order a comprehensive study. Because at our place, they do diaphragm ultrasound imaging. But for point of care, I think this is tough. And I totally agree with you. I think the clinical exam, putting it all again together is what I would do. Not one thing should tell, you know, like not one thing tells me exactly what to do all the time. And I think you raise a good point. That's been the biggest challenge behind translating diaphragm ultrasound to clinical outcomes. The coefficient of variance of the measurements has been pretty, the bottleneck behind translating, finding the cutoff that predicts extubation failure. Yeah, absolutely. Well, that's all I've got. Thank you, guys. I think that's a great segue into the next cases. Because I mean, looking at, as you said, that scale of change, that's something I usually encounter looking at optic nerve sheath diameters as well. So I'm glad we'll be talking about that in the next section too. Yeah, thank you, Anyo. That was fantastic. All right, we're going to turn it over to Artie, who's going to give us some cases using ultrasound in the neurocritical care unit and for helping us with our ICP assessments. Let's see if I can take my shot at stumping Andrew and Chris and Anyo this time. So thank you for this opportunity. So I'll basically give you two perspectives of whether we should be using ultrasound for every patient with suspected cerebral edema or not. So the first case I'm going to talk about is a 19-year-old kid that is a urea cycle disorder, ornithine transcarbamylase deficiency, non-compliant with medications, and unfortunately comes with acute encephalopathy, dropping GCS, ammonia is in high 300s, and he's unresponsive, not protecting his airway, gets intubated because he's having these cerebrate posturing episodes that are very suspicious for seizures. And the patient gets loaded with benzos, and by the time the EEG started, the seizures have been ruled out. It's a pretty suppressed EEG. So now we are more concerned about hepatic encephalopathy from the hyperammonia itself and the inherent risk of cerebral edema. And the initial CT scan I will show you in the next slide. And as we are doing imaging and planning his management, we've obviously engaged our nephrology folks to start on hemodialysis. Essentially, IHT, because his ammonia really needs to be dropped to reduce the risk of cerebral edema with the plans to transition to CRRT. And then nutrition and genetics has been consulted for a low-protein diet. And then we actually transitioned to TPN, start nitrogen scavengers, and a lipid-rich diet. And his exam continues to be poor. He's pretty suppressed with the Wurzat drip that now we are continuing because of risk of cerebral edema. And then once we get imaging of this patient, on the left side, you can see the coronal and the axial view of the CT scan. And on the left lower corner, you can see the corresponding MRIs that we were able to do as soon as we got him stable. And considering these findings, I know that you guys are not neurologists, but what is your perspective on this CT scan? What are you worried about? Well, I don't see a big bleed, which is often what I'm looking for when I'm getting a stat scan. But I also think it looks like maybe the ventricles are pretty small in there. It's kind of what I'm seeing. Good point. Thankfully, no bleed. One thing that I would point out for a 19-year-old kid that has a pretty full brain, sometimes it almost looks like cerebral edema compared to an older person that has lots of cracks around. But in this particular case, what stands out is although the ventricles are small, they're actually bigger than what you would expect them to be. So here, as a neurologist, what I would say is that for the degree of cerebral edema I'm suspecting from all this gray matter involvement, the ventricles are actually pretty supple and the cisterns are also pretty open. But obviously, I'm very concerned about cerebral edema. So as you can see on the right side, we put a bolt in this patient. The EVD could not be placed because of the ventricular refacement, couldn't get good CSF out. So once the bolt is placed, we start measuring the patient's ICP. And initially, they were normal, but then he has occasional ICP crisis to about 50s, as you can see. And you can see how his blood pressure is changing as these ICP crisis are happening. So over the next few days, the patient gets maximum medical therapy from an osmotic therapy perspective. He gets full sedation to birth suppression with a BISOF like barely 10 and 20, 90 degrees up to optimize venous drainage. And he continues to have these ICP crisis, sometimes in 60s and 70s. So, you know, 14 days into this scenario, it's come to the point that we can't even get a CT scan on this patient because we touch him and he gets into an ICP crisis. So what do you guys think, two weeks of this going, of what this patient's outcome is going to be? I'm very concerned that he's going to have a poor outcome. It's hard. He's only 19 years old. But I would be very concerned with him having ICP spikes with that and being, you can't even touch him without like him having this sympathetic surge that's, you know, causing like a really dangerous situation that could lead to herniation. So duly so. So this patient definitely initially has auto-regulation, as you can see in these epic flow sheets where the ICP goes up and the patient's corresponding blood pressure actually goes up. And over the later half of the course, he actually becomes dysautoregulated where the blood pressure does not correspondingly go up when the ICPs go up. And when I take on service, the patient's actually now two weeks into this, family's wanting full aggressive care. We don't even have a CT scan on this patient. And he goes into a pretty refractory ICP crisis in 90s and I have nothing more to give. And as you can see, despite maintaining maps of about 90s, which we were trying to maintain CPPs with LevoFed, he's not showing any spontaneous increase in ICP. So in this particular case, what's your next step in management? Are you going to continue current osmotic therapy, which is already maximized with maximized sedation? Are you going to consult neurosurgery disorderly on board for a bucket handle hemicraniectomy or being an ultrasound panel? You're going to do an ultrasound or you continue to engage ethics and palliative care and encourage withdrawal of care. I think I'm going to consult you to do an ultrasound for this one. I was going to say the same thing, Andrew. Call you, do ultrasound. Well, obviously I'm on service, ultrasound is going to happen. So say if I do an ultrasound, and I give you two choices, pattern A on the left and pattern B on the right, what pattern do you think this patient is going to have based on what you know about him? ICPs of 99 at this point. A or B? So high ICP is bad, right? I got, I got that. Okay. I'm doing neuro ICU a lot, but I think that's bad. And, um, normal, normal brain perfusion should look like, it feels like, you know, at least translating that to vascular ultrasound, which I'm more used to, um, it should look more like B-ish. Um, so if something's wrong with him, then he should maybe look like A? Yep. That's remember, and I want to go, we talked about how high ICPs will eventually, um, decrease your perfusion. And, um, the, when the ICP goes above your diastolic pressure, the diastolic can actually be reversed. So that's the pattern that you see when the ICP is a higher than diastolic pressure, which in this case they are. But let me give you another perspective. In this particular patient, this is what his TCDs showed. Now, what do you guys think? Does this patient's ICP monitor is wrong or there's something else going on that we need to consider? Uh, yeah, it doesn't really fit the clinical picture that was, uh, being billed because those look much more like image B, which is, I think, more what we were hoping it would look like. Awesome. So we insulate all his blood vessels. They actually have, um, pretty normal waveforms for a patient with an ICP of 90. So if you remember when we talked about high resistance versus low resistance waveforms, this particular patient, we were expecting perfusion to be limited, CPPs to be low because the ICPs are pretty high compared to the diastolic pressure. But in this particular case, the patient was demonstrating very normal low resistance circulation. So the caveat to that is, remember mineralocaine hypothesis that we talked about an hour ago? Just, um, uh, three components of the skull modulate your ICPs. It's brain, CSF, or blood. Now, traditionally we always think of brain swelling, cerebral edema, and when the edema expands and affects the intracranial pressures, uh, your CSF, um, gets out of the brain to go into the spine to make room and your blood gets compromised. That's the typical model of how we think of brain edema as perfusion limiting ICP crisis, or what we call as oligemic intracranial hypertension. But people have demonstrated that there's another possibility where instead of the brain, the blood might be driving patient's intracranial pressures. So hypercarbia causing vasodilatation, excessive nitroglycerin causing vasodilatation, reperfusion injury in a disorder regulated brain where excess blood compartment may be driving the ICPs. And that is something that is being demonstrated here. Although the patient's waveform looked normal, but it was a disorder regulated brain, uh, where the blood pressure was actually driving the patient's intracranial pressure. So what we did in this particular case was we dropped the patient's pressures instead of maps of 90, we started aiming them at 85, then 80, then 75. And we ignored this calculated CPPs. And we actually looked at measured CPPs with TCDs and did serial TCDs and eventually took out the bolt, took the patient off sedation. And the patient surprisingly got extubated, um, um, uh, at the end of another week and was discharged home with, um, uh, some disability. He obviously wasn't normal, but at six month visit, this guy was actually ambulating, um, uh, uh, to some, not ambulating, but using wheelchair and being very interactive and kind of being present in his, um, family's life. So very different outcome that you would expect it. But in this particular case, actually calculating CPPs, uh, was counterintuitive to his management and measuring it, uh, in real world with, uh, TCDs actually changed the management. That's, that's pretty incredible. How often were you guys, um, like doing these serial, uh, transcranial Dopplers? So I think the first day when I did this and kind of changed the whole management to where we're going to stop doing osmotic therapy and backing off drugs, I was literally doing this every four hours because my worry was, what if he truly gets rebound cerebral edema and the perfusion actually gets limited then. And so I was looking for those waveforms, but by day two, the end of day two, I think we backed off doing a point of no return. A point of KTC is often. And then we started actually doing daily diagnostic TCDs by the sonographers and kept on doing that for at least a week and a half before we backed them off. How often are you doing these in general? Like where, cause the numbers in the exam, I mean, obviously are pushing in one direction and that's very surprising to see how much ultrasound completely changes the management. You know, is this something that you're doing fairly routinely to catch when the numbers you're seeing on the monitor don't correlate or what should be the threshold to say I need to order this test? Because again, I don't do as much neuro ICU, so I'm curious how often you're doing it. So honestly, I do it as often as I can because you never find something until you look. I think our traditional paradigms have rested so comfortably on a calculated CPP that we always assume that if ICPs are going up, they're being driven by cerebral edema caused by the brain compartment. And I think we really need more champions and more information of doing these studies by bedside so we can start distinguishing oligemic hypertension, intracranial hypertension from hypodemic hypertension. So I would encourage everybody to learn point of care TCDs and actually do them as often as you can. So let me bring you another case here. So this particular case is the unfortunate case with these bilateral cerebral hemorrhages. A patient is in alcohol rehab for a pretty protracted history of alcohol abuse. And she was actually found altered walking around GCS of 15. And there was a suspicion that she might have ingested hand sanitizer. This is just prior to COVID era. And when she was brought to the community ER altered but GCS of 15 protecting her airway, very high osmolar gap kind of made us suspect that. And at the time of the CT scan, she was awake, she was alert. She was not interactive, basically confused. And when a decision was made to transfer to higher level of care that is our new ICU, she was sedated, paralyzed and intubated only for the transport. So when we bring her in, we have a CT scan that looks bad, you know, the bad bleeds, but not malignant cerebral edema. And the last exam we have is a lady with moving all four extremities, but communicative. So, you know, being a neuroultrasound enthusiast, we perform optic nerve sheath ultrasound as a non-invasive marker. She's paralyzed. So, but she has significant coagulopathy from alcohol. So I don't really want to put ICP monitor in her case. And at this point, we're kind of thinking whether we should wait for another head CT to see if it has progressed, whether we should maximize osmotic therapy. So I need some guidance on how urgent I should escalate osmotic therapy. And at this point, family just wants to withdraw care, which unsettles us a little bit that we have a GCS of 15 person who just got intubated for transport. So we're trying to find more information in the optic nerve sheath diameter, no matter how we measure it, three to four millimeters behind the retina gives us cut off of 3.81 time. And then we measure it again. It's like 4.91 time. And we measure it further backwards to see if you see any thickness, and it's 5.9. So what do you guys think of this ultrasound guiding your management? Based on this, are you going to maximize current osmotic therapy? Are you going to call neurosurgery for a bilateral bucket-handled hemiparectomy? Are you going to measure neuroultrasound at transcranial dopplers? Or you have plenty information, and you will go with the family and actually engage palliative care to withdraw care? So I'm going to be honest, after that last case, I'm going to be really leaning towards number three now. Would have been what I said 15 minutes ago. Well, I'm glad that you became a neuroultrasound enthusiast. From the perspective of optic nerve sheath, obviously, that was a pitfall that I would definitely discuss. So we did end up doing transcranial doppler on this patient. And in this particular case, we did the BMOD ultrasound that showed the bleeds were pretty decent on both sides. People have shown correlations between ultrasound measurements of volume with CT scans. But the therapeutic intervention-changing diagnostic modality was obviously TCDs, in which case you can see very profound oscillating patterns that we talked about, where the ICP crisis is causing no net forward flow. The systole and the diastolic flow are equilibrating now. And this pattern was only found in two vessels, couldn't find any other blood vessel that had any positive waveforms. And this particular pattern, when sustained over 30 minutes and not responding to interventions, can actually progress to cerebral circulatory arrest. So in this particular patient, we obviously, the optic nerve sheath diameter would have misled us if we had not gained extra information. And we've learned about the pitfalls of popular ultrasound where, you know, anatomy of the optic nerve sheath has been pretty variable. We always imagined this to be a nice longitudinal axis, but we've seen it all over the place. And then the studies have also been challenging to replicate in clinical world because people measure optic nerve sheaths very differently. Some people prefer to get a transverse axis. Some people prefer to get a longitudinal axis and then get transverse measurements. Some people like to standardize three millimeters behind on both sides of the optic nerve sheath, some just one way. So that has been a pretty big challenge about translating optic nerve sheath cutoffs as reported in literature, at least in my practice. And I've seen way too many patients with ICPs of 60s that don't have the optic nerve sheath cutoff that predict high ICPs. So I hope that I convinced you that ultrasound, at least in the neuro world, can be a good diagnostic modality, especially when CT scan is inaccessible or is not visible. But it is a tool that you have to use in conjunction with your clinical exam and multimodality guided. You can use it for prognostication. You can use it for goal-directed therapy. And I would encourage you to learn a point-of-care neuroultrasound from perspective of distinguishing your ICP crisis into perfusion limiting versus perfusion driven. I do think that's a place where a focus in neuroultrasound can really impact our future studies, future research and future clinical paradigms, but understand the limitation of the technique and the data that supports these techniques. Got stumped? Yeah, no, thank you, Arti. That was fantastic. I think, you know, as someone who, I can't say I use these transcranial Dopplers and optic sheath things regularly in my practice, but something I need to work on to add to my arsenal, because no matter what unit you're in, I think you're going to run across patients that have increased intracranial pressure and concern with that. I know, you know, with my liver transplant patients in the surgical ICU, and several of our cardiac surgical patients, where there is definitely times where we're concerned about increased intracranial pressure. So this is like a great skill. And I think the cases you highlighted really showed how this can can alter management and help with prognostication, which can be so hard when you can't really get a narrow exam. It's one of the things I find most challenging in the ICU. I don't, I don't have great monitors to tell me exactly what the brain is doing if the patient's not not talking to me. I really appreciate acknowledging the limitations of the optic nerve sheath diameter too, because I think that's something that people want to jump on as like, it's relatively easy to get the view, right? I mean, patient closes their eyes, it's right there. But I like that you appreciate that you noted that it's not always that perfect view that you can just measure three millimeters back. And I think that goes to what we talked about before with Enyo about how a few millimeters can make a huge difference. One other thing that I can elaborate on the pathophysiology is that when you have a sudden increase in ICP crisis, sometimes it can block the egress of CSF at the base of the brain, and the transgression of the, the egress of the CSF into the anterior part of the optic nerve sheath where you actually measure the thickness may not happen, because the CSF is blocked at the base of the brain. And that's a pretty important reason why multiple studies have not shown correlation between high ICPs as much as we would expect with optic nerve sheath. Oh, yes. Thank you all you guys. And I want to just take this opportunity to thank Christopher Enyo and Artie, once again, for your terrific didactic sessions and being champions of POCUS here, here at the SCCM Congress. And thank you guys for leading these case-based discussions. Thank you.

POCUS

Stump the Intensivist

case-based discussions

ultrasound

shock

pericarditis

cardiac tamponade

liver transplant

variceal bleed