All right, my job is so easy because I am going to present you with a couple of cases and because of the background you've already gotten, I'm hoping that you will interpret the shaky videos from my residents and fellows and try to solve these cases with me. I think, you know, one of what you're hearing is certainly the background of what neuroultrasound can be. I think it's going to take a lot of work and effort from us to sort of push the field forward and I'm hoping that through these three cases I'm about to show you, we can really start to see how neuroultrasound can kind of help us dynamically in taking care of patients. So, this is me. I have no disclosures and so hopefully we're going to review novel ways of using point of care ultrasound for complex patient care. You're going to see not just neuroultrasound, but also general ultrasound in these cases and then we're going to try to explore the future of ultrasound use. So we'll start with a case and these are all real cases, so forgive any videos that don't look so great. I certainly don't have videos like my colleagues. So this 44-year-old man was brought to the emergency room. He had stroke-like symptoms. He was within the timeframe for TPA, which he received, and he was identified as having a left MCA syndrome, but CTA was negative for a large vessel occlusion. So he was admitted to our neuro ICU and unfortunately on arrival we identified that he was febrile to 40.2 and rigoring and he started to look septic. And so we performed point of care ultrasound to evaluate his volume status and this is what we found. So what do we see? Anyone want to shout it out? A giant vegetation. We all got very nervous because this guy had just gotten thrombolytic, right? And so the question was, are we going to be able to risk stratify this patient's chances of recurrent stroke and also how can we make sure that this patient does not hemorrhage? Because if this patient has a mycotic aneurysm, that's a very high risk of hemorrhage. So to kind of remind you of the expert consensus guidelines from the American Academy of Thoracic Surgery, what is the effect of neurologic complications and the indication for and timing of surgery? And so you can see that there are a lot of vague comments about getting neurologic and neurosurgery expertise. Now as a neurologist, I can tell you there's no really good evidence for anything that we suggest when the surgeons consult us, right? And so careful evaluation, screening patients, I mean, this is really very vague language that ends up being quite unhelpful when we are talking about a particular patient. So this is what we did, which was transcranial Doppler. And what we're looking for here is microembolic signals. So this is unlike with the types of ultrasound that Dr. Sarwa was showing, this is a blind TCD. So you're just seeing the waveforms on the left of the left MCA and on the right of the right MCA. And I'm just going to be quiet for a second to see if the volume works. Is it possible to get the volume up any higher? Okay. Do you hear those little chirps? Those are little bits of this man's vegetation traveling through the MCAs. Terrifying, right? Okay, we can turn the volume down now. So, you know, doing a microembolic signal study is 30 minutes of looking at the MCAs, looking for any evidence of microembolism. Now, we know that in infective endocarditis, ischemic stroke can occur in anywhere from a quarter to 50% of patients. And strokes are asymptomatic in up to 80%, right? So when we say careful neurologic evaluation, that's not just an examination of the patient right by a neurologist. Oftentimes you'll see neurologists get MRIs looking for silent strokes. While we know that appropriate antimicrobial therapy decreases the incidence of new stroke, we don't actually know who is going to respond well and who is going to be at a higher risk of stroke. Like I just showed you, TCD monitoring can provide evidence of emboli. And there was a study in 2009 looking at all patients with infective endocarditis. And in patients who had evidence of microembolic signals, or MES, neurological complications occurred in 83% of those patients versus 33% of the patients that did not have MES. And this was over a 30-minute study. Some places will do up to an hour of studying looking for microembolic signals. And so I think one of the sort of frontiers, and certainly something that Dr. Sarwal has been working on at Wake Forest, is looking to see if we can use microembolic signal monitoring to either monitor an antimicrobial response, or potentially even triage high-risk patients to earlier surgery. So for example, in my patient who now has a normal exam post-thrombolytics, assuming he doesn't hemorrhage in the 24 hours post-TPA, someone who is actively having emboli despite appropriate antimicrobials might be someone where we want to intervene a little bit earlier before he develops a large stroke, and then suffers the consequences of needing large heparin boluses in an open surgery. So I think this is something where it really does matter if you can get your thoracic and cardiothoracic surgeons on board with you. But certainly this is a little bit of extra information that might be able to help you tailor your therapies. Separately from infective endocarditis, there is data on looking at your therapy for carotid dissection, to see if just antiplatelet is adequate, or whether you need to escalate to heparin, and even escalating to a particular PTT goal based on the presence of microembolic signals. So I think this is really a unique type of transcranial Doppler that can be used for all sorts of different evaluations of patients who have some sort of cardioembolic phenomenon. All right, that was the easy one. We'll move on to a harder one. So case two is a 50-year-old woman. She had had a tracheostomy as a result of severe COVID-19 pneumonia. She had recently been decannulated two weeks earlier. She also, during that hospitalization for COVID, had DVTs in both her legs. She had also recently come off anticoagulation. And so one day prior to admission, she had complained of chest pain and right leg pain to her family, and then she became very short of breath the day of admission. She collapsed at home and was found in V-fib arrest. She underwent 20 minutes of CPR and was intubated before arriving to the emergency room. And after a brief episode of stabilization in the emergency room, she came right up to our ICU. So on admission to the ICU, she has frequent myoclonic jerks. They were very happy to send her to a neuro-ICU for this myoclonus. An unreactive right pupil. She then has a bloody bowel movement while we were assessing her. And you can see a picture of her legs. The left leg, you can see by the presence of a Doppler, did not have any Dopplerable pulse. And the right one is modeled. Shortly after her arrival, she starts to have a worsening presser requirement and worsening oxygenation. So, of course, we're sitting here wondering, what is going on and why did she arrest? So, you know, common things being common, especially in this particular patient. Did she have a massive PE? Did she have an MI? Did she have an aspiration event because maybe she shouldn't have been decannulated? Is she hypovolemic from a GI bleed that wasn't identified in the field? Or has she had a massive neurological event, right? She has an unreactive pupil. She wasn't scanned in the emergency room. And right now she's too unstable to go to the scanner. So, what can we ultrasound? And, you know, certainly to the general intensivists and surgical intensivists in this room, I don't think I need to tell you what we can ultrasound to work up an undifferentiated arrest. But what I would sort of want to point out to you is that if there was a massive catastrophic neurological event that was the reason for this, we can start to use brain ultrasound and transcranial Doppler to get a sense, right? So, even if our body ultrasound is negative and she's too unstable, we might be able to understand a little bit about her neurological status. So, this is her lung ultrasound. Whoopsie. Let's go back and see if we can fix this. Let's try again. All right. So, we see a lot of B lines. We see an effusion. That's the lung ultrasound for us. Definitely there's lung sliding on both sides, though. We get a DVT study at the bedside. And this is what we see both in the left popliteal and femoral veins, non-compressibility in a clot. We do cranial ultrasound now to sort of, let's see, to help understand what we're looking at again. For those of you who have now been taught by Dr. Sarwal, this is our beautiful butterfly midbrain. And then you can see this is the midline. We don't see any large abnormalities. We don't see compression of the peduncles of the midbrain that would explain an unreactive pupil. And then when we do our Doppler, you can see pretty normal waveforms. We see nice, robust diastolic flow. And so there's nothing really super concerning on this to suggest that there is a catastrophic neurological event. So now we start ultrasounding the heart and the IVC. Does anyone want to just shout out what they see or what they don't see? They see RV expansion or they don't? Oh, they don't see RV expansion, yes. RV is very small. And what can we say about the IVC in that last one? Very full. And there's some sort of effusion. Is it pulmonary or is it pericardial? It's a little hard to tell on these ones, but pericardial is right. Yeah, so perfect candidate for the neuro ICU here, right? So in the meantime, while one person is ultrasounding, the other person is putting in an arterial line. And these two things happened pretty simultaneously. And so we were like, that can't be tamponade. And then we got this arterial line and we said, oh, that's tamponade. Not to worry. Cardiology came, did an emergent pericardiocentesis. About 500 cc's of bloody fluid came out. Her blood pressures got, they normalized. She was off pressers within 15 minutes of the pericardiocentesis. Now, we did not do this in our panic. But to remind you that you can look for ultrasound evidence of pulsus paradoxus, either across the mitral valve, looking at the E velocities, or across the tricuspid valve. And just as a reminder, you're going to see a change of greater than 25% along the mitral and greater than 40% along the tricuspid. So you don't need an arterial line. But believe you me, this woman needed an arterial line. So, you know, undifferentiated arrest. It's not uncommon for the emergency room to have done this, right, even before they come to you. And certainly you all are going to do this on your way, on arrival of the patient. Right. You know, ultrasound screening can be super helpful instead of sending you to the ring of truth, which is what our emergency physicians call the CT scanner. And so, you know, you can look for acute MI, PE, tamponade, tension pneumo, severe, evidence of severe hypoxemia either because of severe pulmonary edema, because of, you know, massive effusions, because of pneumonia. You know, if you look really hard, you may even see an aortic dissection or two. But what I want to sort of add to this that I want you to think about the next time you see a patient is trying the brain ultrasound. And if you don't try it enough, you're not going to see anything fun. So I would encourage you to try. Even if you're not sure what you're looking for, just look for that butterfly, and you know that that's your midbrain. Okay. All right. Now to the complicated case. So this is a 62-year-old woman. She'd had chronic thrombocytopenia of unclear etiology. It had been worked up at an outside hospital, and being in New York City, we had no access to any other records, and so no one really knew what it was from. And she had presented to us with a high-grade subarachnoid hemorrhage. She had coiling of right PCOM aneurysm. I'm going to walk you through her head CT. I know this is not a neuro CAT scan session, but just a couple of things. So we'll start at the bottom, which is where everyone should start. And you see coil artifact. You see some subarachnoid hemorrhage. You see two external ventricular drains. Unfortunately, the right one is surrounded by a large tract hemorrhage, probably because of her thrombocytopenia. And over the first couple of days, she had issues with elevated intracranial pressure, despite her bilateral EBDs. They would clot frequently. But despite this, by post-bleed day 5, she was actually awake and following commands. So we were very happy about this until we got a check-in CTA, just to check in while we were looking at the placement of the EBDs, and we found that she had diffuse moderate vasospasm. Unfortunately, that same day, she also had developed melanoma, and her hemoglobin had dropped by two points. And so GI elected to perform an endoscopy at the bedside. And this is so rare where I am, that if GI elects to perform an endoscopy, they have a high suspicion that something's really bad. So this is what they found on the EGD, some small minor varices, a large amount of blood, of course, and then a deal of poi lesion in the fundus of the stomach. And they attempted to clip it. And this is what happened. So, yes, that's a video on the left. We had a total of four liters of blood in coffee grounds come out within about the first ten minutes, as GI was saying expletives, as were we. We initiated a massive transfusion protocol. We actually gave systemic TXA because she was so unstable as we were pushing, you know, code dose epi on her. And after the second round of MTP, she developed elevated peak pressures to 45, plateau pressure was 34, and this was on 6 cc's per kilo and a peep of 10. And now she starts to develop abdominal distension as well. She was dyssynchronous, so we paralyzed her. And we measured her bladder pressure, which was 30. And at this point, the nurse says, not to make your lives even more miserable, but the EVDs are clotted and they're not draining anymore. And we don't have really good wave forms, so I'm not really sure what her ICP is. This is unfortunately something that does happen, right? So what are her current issues? Well, she had started before the EGD with poor intracranial compliance and active vasospasm. And now, thanks to our GI colleagues, we have a couple more medical problems to add, right? So we've got an ARDS-type lung physiology. We've got abdominal compartment syndrome. She quickly becomes oliguric and then anuric over the course of the next two hours. She's acidotic. She is grossly total body overloaded. And we don't know if she's continuing to bleed. So they have injected some epi. They have placed some blind clips, but they really couldn't see what they were doing. And they say, we think she's no longer bleeding, but she may need to go to the IR suite just to see if there's still any extrave. We were not pleased. So the medical management for this patient is fairly straightforward, right? We need to keep her blood pressure up. We're going to, because of our difficulty with ventilation, we're going to allow her to be hypercapnic, high PEEP strategy. We're going to try to diurese her. And when that doesn't work because she's anuric, we're probably going to need to initiate hemodialysis. We're going to sedate and paralyze her, and we're going to transfuse as needed. However, the pesky brain does not really like a lot of this, right? So a MAP of greater than 65 may not be adequate because we don't know what the perfusion is in this person's brain, especially since she had cerebral vasospasm, and now we've given her many pushes of epinephrine, and we don't know what her cerebral blood vessels look like now. Permissive hypercapnia is not going to be acceptable in a patient who has poor intracranial compliance, and in fact may actually have elevated ICP. We just don't really know. High PEEP strategy is going to impair venous outflow from the brain and may put her at higher risk of having elevated ICP. If we were able to get a lot of fluid off, that would not be good for her vasospasm. Hemodialysis is going to cause fluid shifts that may worsen any intracranial pressure issues. And while heavy sedation and paralysis are going to be great for her ICP, we're not going to really know if she is having symptomatic ischemia in her brain because we can't examine her anymore. And there is some data that in very severe cerebral vasospasm, you may not want just a hemoglobin goal of greater than 7, but that patients may be better at a hemoglobin of closer to 9 or 10 because you can increase the oxygen-carrying capacity for those patients. So what can we assess in this patient? Well, certainly volume status, cardiac function. But now you guys know that we can also try to assess intracranial pressure and cerebral blood flow as well. So we're going to do that. So this is her echo. She looks a little hyperdynamic. She's got a big RV relative to her LV, but that might be because of her acute pulmonary issues. And she's got B lines, right? This was her IVC. Now, my fellow wanted to give more fluid. What do people know about IVC collapsibility in the presence of abdominal compartment syndrome? We don't really know that much, right? And it's not just you guys or me. It's really all of us. Certainly, it's been shown that IVC collapsibility is not as accurate in patients who have very high abdominal pressures. This may also mean that the patient's starting to wake up and is starting to buck the vent. So there are a couple of different things that we're going to want to look out for clinically. This is not just something that we're going to look at one image and we're going to proceed with fluid management. At this point, her oxygenation is now 86% on an FiO2 of 70 and a PEEP of 10. And the question is, should we go up on her FiO2 or should we go up on her PEEP? Who would want to go up on her FiO2? Who would want to go up on her PEEP? Who has no idea and wants more ultrasound information? Okay, yeah. It's always the right answer in an ultrasound talk, right? All right. Now, the question that was posed was, well, maybe this patient would actually benefit from higher PEEP, right? Because maybe she's derecruited for some reason or maybe she has areas of atelectasis. But in the absence of being able to monitor the brain because we don't have this ICP monitor, we had to get a little creative. So Dr. Sarwal touched briefly on optic nerve sheath diameter. I'm just going to show you again. So this is the globe. This is the optic nerve right down here. This is the optic disc. And then you can see these two hypoechoic structures on either side of the optic nerve and that's the optic nerve sheath, right? So recall that if your ICP goes up, your optic nerve should not change at all, right? That's a nerve. It shouldn't matter. But the sheath that is surrounding it is contiguous with the dura. And so any elevated pressures are going to be transmitted forward and you're going to see an elevation in the diameter across the optic nerve sheath. And so two signs of high intracranial pressure here. Does anyone want to shout out anything? Papilledema, that's right. So this is a raised optic disc. So this is the sonographic equivalent of papilledema. And the other one that may be true depending on what number you use, the sheath diameter. So depending on the study that you look at and the pathophysiology behind what was going on in those studies, either a cutoff of five millimeters or six millimeters has been shown to be associated with elevated ICP. It very much helps to have a baseline, which we unfortunately did not have in this patient because obviously there are other reasons why your optic nerve sheath diameter may be elevated. So what we did was we did an optic nerve sheath diameter before the PEEP trial and after the PEEP trial. And so what you can see is before the PEEP trial we have this optic nerve sheath diameter of 5.8 millimeters. And afterwards we do it again and you can see it's gotten raised to 6.9. This happens within seconds to minutes. This is a really nice dynamic way of reassessing what you've done and what the effect of it is. So this was kind of concerning and we said, well, I don't know, maybe it's just the angle, maybe it's the person who's doing the ultrasound. And so we also decided to do some transcranial Dopplers. So you can see before we have this nice pulsatility index of less than 1.2. You can see this nice robust diastolic flow. We've got a mean flow velocity of 63. And afterwards, after the PEEP trial, you can see the mean flow velocities have dropped because this is now perfusion limiting and the pulsatility index has gone up. Now we have this very peaky systolic upswing and then you've got quite low diastolic flows. So this was extra information that sort of supported our optic nerve sheath diameter that this patient can't really tolerate having a high PEEP. And so certainly we decided we were going to go up on the FiO2 because the increase in PEEP is resulting in worsening ICP. And so this is also something that we don't know what happens in patients who have, for example, severe hypercarbia due to respiratory failure. They may have mild cerebral edema, especially young patients that can cause problems. And we sort of just blindly do permissive hypercapnia and we don't worry so much about that in patients who don't have neurological injury. But I would kind of pose to you, how do we know that patients don't have cerebral edema and flow limitations in acute hypercarbia and acute acidosis? So I think this is a really nice example of how we can dynamically intervene and then check out what the sequelae of our intervention is. And so Karate and colleagues showed this really nice algorithm that I'm going to sort of break down for you and simplify a little bit. So their step one was do some lung ultrasound. If you think that a patient has ARDS and you think they also have brain injury, do a lung ultrasound. Now, they described two sort of lung ultrasound patterns. One is you have this prevailing anterior A pattern and there's patchy areas that seem abnormal. And then there's a second sort of diffuse pattern that they describe. And so the idea is maybe the diffuse pattern patients may need higher PEEP, whereas the ones who have focal areas may not necessarily benefit from very high PEEP because you're going to have areas of normal lung that get over distended. So once you've looked at your lung ultrasound and identified is it focal or diffuse, now you're going to look at your brain ultrasound and you're going to say, is it safe to do a recruitment maneuver? And they use a couple of different things. We've talked about pulsatility index and optic nerve sheath diameter. They also look at other velocities, both in the arterial and venous system of the brain. And so if you don't think it's safe to recruit, you better try to fix it, right? Because this is suggestive of possible elevated ICP. So do whatever it is you're going to do. Do your MAP escalation trial, you're going to do your hypertonic saline or increased sedation, and then you're going to look again. If it is safe to recruit, then you're going to do a PEEP trial. And after your PEEP trial, you're going to repeat the brain ultrasound. And so you're going to go up stepwise, two at a time. You can be a little bit more aggressive if your brain is totally normal. And if there is persistent elevation in the pulsatility index or optic nerve sheath diameter, or of course, if there are issues pulmonary wise with your PEEP, you're going to stop. And once you identify that best PEEP for that patient, then you're going to keep those vent settings on for a little bit and check an ABG and make sure that those vent settings are actually helping your lungs, right? But I think that whatever algorithm you decide to choose or whatever piece of the ultrasound you're going to do, I think it's very helpful to sort of think about this in a stepwise manner, right? Every intervention that we do has negative effects. And I think as neurointensivists, we think all the time about the brain, but I would argue that there are a lot of different patients, including cardiac arrest patients, right? Or patients with hyperammonemia and liver failure who may be at risk of having elevated ICP and we just don't know because we're not looking for it. And with that, I want to thank you for your attention.

neuroultrasound

complex patient care

stroke-like symptoms

thrombolytic treatment

point of care ultrasound

giant vegetation