Good morning, everyone. I have nothing to disclose. The objectives of this talk are to review the rationale of incorporating vexus in day-to-day practice, whether nephrology or ICU or essentially any medical practice, and to summarize the key evidence that's behind vexus. So why do we care about venous congestion? As you know, vexus is a way to quantify venous congestion. So why is it important, or why elevated central venous pressure is important? It's because organ perfusion grossly depends upon both forward flow and central venous pressure. So for example, in the context of kidney, the mean perfusion pressure is the difference between mean arterial pressure and central venous pressure, or intra-abdominal pressure when it's elevated. So you can view central venous pressure as the outflow pressure of the organ or organ afterload. So even if the mean arterial pressure is well preserved, elevated CVP drops your perfusion pressure. That's why we care about it. So going back to vexus, what is it? Vexus or venous excess ultrasound involves performing inferior vena cava ultrasound to estimate the right atrial pressure. And once you did that initial step, it involves doctor ultrasound of hepatic vein, portal vein, and intrarenal vein. And where does this concept of vexus come from? It comes from a post hoc analysis of a prospect to cohort study performed in cardiac surgery patients where they found that in patients with a big IVC or dilated IVC that is more than or equal to two centimeters, that is in patients with elevated right atrial pressure, if they demonstrated severe flow abnormalities in at least two of the previously mentioned veins, that is two of the hepatic, portal, and intrarenal, the risk of development of acute kidney injury was substantially high. So basically we are saying that vexus predicts organ injury. So you may ask, why not just do inferior vena cava ultrasound? IVC ultrasound tells you about the right atrial pressure. And we know that elevated right atrial pressure is bad for the organ perfusion. But as you know, the correlation between inferior vena cava ultrasound and right atrial pressure is not really that great. It's modest at best in spontaneously breathing patients. And in mechanically ventilated patients, which most of us deal with on a day-to-day basis, it's essentially poor. And in addition to that, IVC ultrasound has several pitfalls. We are primarily looking at the vessel in a long axis to measure the diameter, right? So we are using a two-dimensional modality that is ultrasound to slice a three-dimensional structure. And your beam could be slicing the vessel in the center, as in the first image, where you get the correct diameter. Or it could be slicing at the periphery, where you get falsely low diameter. That would be even more problem if you are following upon the same patient or a different colleague of yours comes and scans the patient and falls prey to this false effect, which you call the cylinder effect. And also, say, for example, in spontaneously breathing patients, you are relying on patient's sniff, which means it is determined by the strength of breath, so to look at the collapsibility of IVC. And as you know, the strength of breath varies greatly among patients. Even if everybody is sick, a 30-year-old male's strength of breath is different than an 80-year-old female's strength of breath. And in some conditions, like pulmonary hypertension, the IVC might never get small. It's always plethoric. And it's not at all uncommon to confuse inferior vena cava with adjacent structures, whether it could be aorta or a carotid lobe of the liver or distended duodenum. So it depends upon the clinical context and patient's body habits and so on. So even experienced operators fall prey to these technical pitfalls. And other important reason, apart from IVC technical pitfalls, is that vexus outperforms central venous pressure alone to predict organ injury. In this original vexus study, they compared severe grade vexus, that is, these flow abnormalities, with just elevated central venous pressure of more than or equal to 12 millimeters mercury. And the post-test probability of developing acute kidney injury was substantially high when they used these Doppler parameters in addition to central venous pressure alone. And so what are the individual components of vexus? So you have hepatic vein, portal vein, and intrarenal vein. First, it's very important to understand that everything is in this hemodynamic circuit, right? We are assessing the backward limb of hemodynamic circuit. So you have the hepatic vein here, and it's very close to the right atrium. And it has this systolic wave and diastolic wave representing the venous flow into the right atrium during systole and diastole. And the small blub here is the atrial contraction, so you call that A wave. So this S wave and D wave are similar to X descent and Y descent of your central venous pressure waveform. And we always try to use EKG whenever possible, that way we can correctly identify what is S and what is D. The wave that follows the R wave of the EKG is the systolic wave. And when you go to the portal vein, portal vein is separated from the main systemic circulation by hepatic sinusoids. So instead of displaying those S and D waves, in normal state and in patients with normal right atrial pressure, the portal vein is relatively continuous. And same is the case with intrarenal vein. When we say intrarenal vein, we are primarily referring to interlobar vessels within the kidney. So those vessels are within the kidney parenchyma. So if you have the consequences of elevated right atrial pressure, these veins are going to feel the effect rather than main renal vein. That's why we are stressing that intrarenal part. And in normal state, the intrarenal vein is continuous. So in this waveform here, above the baseline, this pulsatile thing is the intrarenal artery, and below the baseline is the venous waveform. So what happens to these waveforms with elevated right atrial pressure? The hepatic venous waveform with elevated right atrial pressure, the gradient between the venous retina and the right atrium decreases, so there is more resistance to the systolic wave. Normally, the systolic wave is bigger than the diastolic wave, as x descent is bigger than the y descent. And with further elevations in right atrial pressure, the systolic wave becomes smaller and smaller. Finally, it goes and sits above the baseline. It typically happens when you have concomitant functional tricuspid regurgitation, which is not at all uncommon in fluid overload states. Because during systole, the tricuspid regurgitation jet is going back into the right atrium. And portal vein, normally it's continuous, and with increases in right atrial pressure, it becomes more and more pulsatile. You can calculate the pulsatilitye fraction by just going into one particular cardiac cycle. You go to highest and lowest points and see by how much they are pulsatile, whether it's more than 30% or more than 50%. Typically more than 50% pulsatility is considered significant or severe congestion. And coming to the last component, intrarenal venous Doppler, normally we said the venous waveform is continuous, like in the first waveform here. And as the right atrial pressure increases, the venous waveform becomes more and more pulsatile. Ultimately, you see two distinct venous waves here below the baseline, one corresponding to systole and other corresponding to diastole. In hepatic venous waveform, we said you need to have EKG. But in intrarenal venous waveform, the above the baseline waveform is arterial waveform, so it's like a built-in EKG. So that tells you what is systole, what is diastole. And ultimately, similar to hepatic venous waveform, the S wave gets reversed as the right atrial pressure increases. Just because there is arterial waveform, that wave is not visualized. So leaving only D wave, or the diastolic wave, below the baseline in severe congestion. So in the original study, all the severe waveforms that I showed, the S-reversal in hepatic vein, D-only pattern or monophasic in renal vein, and more than 50% pulsatility of portal vein, these are the patterns that correlated with organ injury. And very important thing about vexus, the key role in day-to-day practice is that these waveforms are so dynamic. Like if you are removing fluid or addressing the pressure overload, these waveforms change. For example, this patient had a prolonged ICU stay. And the fluid balance was positive 12 liters. And the patient did not have significant pain or edema. But the point was he had a lot of sacral ulcerations and edema. It's hard to know the person's fluid status. The question came because the patient was not tolerating dialysis well. But when we did vexus, the portal vein was 100% pulsatile. As you can see, there is even below the baseline flow. That's the first one. So I put this patient on continuous renal replacement therapy, removed about 4 liters. You can see that it's still pulsatile, but it's much better than the first waveform. I removed 3.36 liters compared to the prior exam, and it almost normalized. Now the pulsatility is about, say, 30% or less. But this patient developed AFib with RVR, so the surgical team gave some fluids. As the patient became positive again, you can see that the pulsatility has increased compared to the previous waveform. And on the right, again, I removed 5 liters with CRRT, and the waveform has essentially normalized. And the patient was taken to the OR for some debridement surgery, got a lot of fluids during anesthesia, was positive 4 liters. And as you can see, the waveform went back to that almost 100% pulsatile state. And we removed further fluid and normalized the waveform. So I'm just saying, like, it's really a visual depiction of how hemodynamics are changing in everyday practice. Apart from that, these waveforms carry prognostic significance. For example, in this study in the ICU, pulsatile portal vein at the admission to intensive care unit and monophasic waveform of the intrarenal vein at ICU admission portended worse prognosis in terms of organ injury or acute kidney injury. And in this non-ICU study, looking at heart failure patients, so these are two different studies. So prior to discharging these patients from the hospital who were hospitalized for heart failure exacerbation, they did this intrarenal venous waveform assessment and followed these patients to assess prognosis. And in both these studies, as you can see, patients with monophasic intrarenal venous waveform, that is D-only pattern, or discontinuous intrarenal venous waveform, did poorly compared to overall cardiac event rate. And it's not just about cardiac surgery, though the original surgery was in cardiac surgery patient, which is the ideal cohort to study vexus, right? So there was this recent study in CHF patients, sorry, in septic patients who are all mechanically ventilated in the ICU. They found that the discontinuous pattern conferred worse prognosis in terms of organ injury and death compared to continuous intrarenal venous waveform. And another study in acute coronary syndrome patients found that patients who had severe vexus grade, the last part, the third bar there, the fourth bar, so all these patients who had severe grade vexus developed acute kidney injury, or in other words, congestive nephropathy. And another recent study in non-selected ICU cohort in 90 patients who developed acute kidney injury. So this acute kidney injury was grade two or higher, which means that serum creatinine was at least twice that of baseline. And vexus was performed at enrollment and 48 hours later. And what they found was if they tried to normalize these waveforms by decongesting these patients, if the waveforms did improve, it conferred good prognosis in terms of renal replacement free days. And one common criticism is that vexus takes a lot of time, right? It's a pulse wave Doppler application and you assess three waves. It might not be worthy of your time. But I don't think that's true because if you really do critical care ultrasonography, you know that all these veins are just in the right upper quadrant. You go to the lateral aspect, mid-axillary line, you fan the transducer anteriorly, you get portal vein. Fan the transducer posteriorly, you get hepatic vein. You sweep the transducer posteriorly, you get the kidney right there. The kidney is technically difficult because as it moves with breathing, it can be a little difficult. But again, if both hepatic vein and portal vein are abnormal, that itself is severe grade vexus. You don't need to do renal vein. And all these waveforms have limitations, right? Yeah. I mean, hepatic vein, you need EKG and it's affected by arrhythmias, it's like atrial fibrillation. You can have inherently smaller S wave and so on. And in liver disease, you can have abnormal portal vein and hepatic vein at baseline. In chronic kidney disease, in advanced chronic kidney disease, we don't know exactly how these waveforms behave at baseline. So these are the limitations. But that's the point of doing this combination score and evaluating multiple veins to offset the limitations of individual veins. And that's another reason why we have this PROCON debate, otherwise there is no scope for PROCON debate, right? And more veins are being studied. It's not just like these three veins because in cirrhotic patients, it might be difficult. So one of the veins that has garnered a lot of attention is femoral vein because femoral vein is easy to do. But one caveat is that femoral vein is relatively far from the heart. So the right atrial pressure, the correlation between RAP and femoral venous waveform is not so great. But a recent study found that the agreement between femoral venous Doppler and vexus was pretty decent, if not great. And vexus does not distinguish between volume and pressure overload. Yeah, that's true. But do organs care about it? So if you have pulmonary hypertension and organ congestion, do organs behave differently as opposed to you have fluid overload and organ congestion? Probably not. It's just you have to take into consideration the clinical context and give the patient whatever is appropriate, diuretics or dialysis or pulmonary vasodilator, lung transplant, heart transplant, whatever is appropriate. And in summary, vexus aids in the diagnosis of congestion. It aids in quantification of severity of congestion. The waveforms carry prognostic significance. Vexus helps in monitoring the efficacy of decongestant therapy in real time. So I don't want to glorify vexus, but this is what it is doing. And it is just giving you information about the one part of the hemodynamic circuit. That's my machine. The sticker is always there to remind myself and my fellows that the machine doesn't have a brain. Use your own and interpret the findings in the right clinical context. With that, I rest my case and I let Dr. Navita Ramesh give us some con aspect of vexus. Dr. Ramesh is a program director for Pulmonary Critical Care Fellowship at UPMC Harrisburg and she'll take over. Thank you. Thank you, Dr. Kauratla. Yeah, I realize I'm up against a huge uphill task, but I'll try my best to go over the cons of vexus. So I do not have any conflicts of interest related to this presentation. My topic is actually vexus is vexing. It is really vexing, right? So I'm just going to go over some of the slides focusing on this. So the first time I saw this, this picture was on Twitter about vexus. That's the first time I'm hearing it. And this is exactly what my expression was. So then I decided I need to dig deeper and try to understand this a little bit more. So in the next couple of minutes, I'll talk about, again, what is vexus? What is venous congestion? We'll go over the grading system, scoring. This is just to add on to what Dr. Kauratla had already mentioned. I'll focus more on the limitations and where exactly can we use vexus in our ICUs. Before going on to that, it's important to go over some of these facts. So hypoperfusion is not always accompanied by hypotension. Fluid overload is not good, increases mortality and morbidity. As the venous congestion is increased, it impairs organ perfusion. And venous congestion has extensively studied in a cardiology context, as in cardio-renal syndrome, cardio-hepatic, or cardio-intestinal syndromes. So with that background, we're going to look at the pressures at different points in the circulatory system. So we focused a lot on our arterial waveforms. We all know that. But my focus is going to be on the venous side of things. So the venous side has long played second fiddle to the arterial side. So now there's more focus coming on to the venous circulation. So if anybody asks me, what is perfusion pressure of an organ? I used to say it's MAP minus CBP, which is actually the wrong answer. So perfusion pressure is the pre-capillary arteriolar pressure minus the post-capillary venular pressure. So that's something that's very important for us all to understand. When in a normal collapsed state or in the unstressed volume, the veins are distended. But they're just full. They're just right. So when the veins collapse, they do not contribute to the venous return to the heart. However, when the veins are fuller or they're in the stressed volume, they're more distended. And when those veins collapse, they do add on to the venous return and add to the work in your right atrium. So we have to understand physiology. It's important to look at this, where the Frank-Starling mechanism, it says, based on where you are on the curve, as you increase the preload, the stroke volume will increase up onto a point. But when you reach the flat portion, the stroke volume responsiveness decreases, the variation. So the concept of fluid responsiveness comes here, which is basically, if you give a fluid bolus, will you increase your stroke volume or not? That is the question we are asking. Will the blood pressure increase? What will happen to the congestion? Will your stroke volume increase or not? So just a raise of hands, or you can shout out the answer. What percentage of critically ill patients that we see in our ICUs are fluid responsive? 50, 60. Yeah, you're about right. It's only 50%. So we are operating in a zone of complete uncertainty, maybe 50-50 chance of whether they'll respond to fluids or not. And with that concept of fluid responsiveness comes fluid overload, where it's not a good thing, not only what's physiologically happening to your body, but also fluid overload increases duration of mechanical ventilation, increases hospital length of stay, and also mortality. So that's not good. So what do we have available? POCUS assessing all these metrics that have been looked at to assess the volume status in the ICU patients. WEXIS focuses on these four things, analysis of the IVC, the IVC size variability, hepatic and portal veins, and renal vascular congestion. So this is the very first study that Dr. Korotella had mentioned. It was done in 2020. It was published in 2020. The main question was to determine the risk of acute kidney injury in cardiac surgery patients. So it was a small study, 145 patients. The question was, these patients undergoing cardiac injury, can we use WEXIS to predict whether they'll have acute kidney injury or not? Again, this is from the study, the first picture that I had put in initially. And as Dr. Korotella mentioned, they graded these patients from WEXIS-A to WEXIS-E. And they looked at grade 0 to grade 3, based on the number of organs that were congested. This was, again, discussed previously. Instead of seeing the regular waveform for the hepatic vein, the S and D, as the severity of congestion increases, the S wave is inverted, the portal vein becomes more pulsatile, and the renal wave kind of follows the hepatic congestion, like the S and D pattern. So the rationale for using WEXIS, why they brought up this thing, this topic, was under normal circumstances, again, the venous system is highly compliant, has high capacitance. But when we have patients with right ventricular failure or intravascular volume overload, the venous system becomes congested, the compliance is reached, and these pulsations are transmitted back into the smaller veins and eventually go back to the heart. So this study concluded that the presence of at least two alterations of the hepatic vein, portal vein, or intravenous flow, in the presence of a dilated IVC over 2 centimeters, correlated with post-operative acute kidney injury in patients undergoing cardiac surgery. And the higher WEXIS means higher risk of acute kidney injury. WEXIS grade 3 outperformed CVP, which we are used to looking at. So that's a very focused population, cardiac surgery and who goes into acute kidney injury. The WEXIS steps were described, IVC, hepatic vein, portal vein, renal vein. The reason I put this up is because I want to take them apart. So when you look at IVC, this study came out in 2019, looking at ultrasound assessment of IVC for fluid responsiveness. And they did point out some of the downsides of IVC measurement, not only the technical limitations but also the confounding factors of why we should not be using IVC as the go-to for fluid assessment. So when you look at IVC in spontaneously breathing patients, the study that looked at IVC measurement to look at volume responsiveness, they used an emergency department patient cohort. Only 124 patients were there in that cohort. And they actually, those patients had a standardized and quantitative inspiratory effort. So patients were trained to do a particular inspiratory effort and then their IVC variation was noticed. That's not a regular population in our ICUs. And when you look at mechanically ventilated patients, they looked at the IVC distensibility and they found this gray zone, right, like between 13 millimeters and 25 millimeters of IVC. We don't know. They may or may not be fluid responsive or not. And in that study, over 71%, 71% of the patients were in the gray zone of between 13 and 25 millimeters. That's where the data is coming from. So I just put it up here for you to read about the conclusions of the various IVC studies. But the conclusion here is the evidence supporting IVC analysis is controversial, complex, and it's subject to interpretation. Now moving on to the hepatic vein, like taking them apart one by one, right? So the next one is hepatic vein flow. The hepatic vein flow basically depends on the interaction between the venous-driven mean systemic filling pressure and the pressure in the right side of the heart. So just to make it simple, if your right atrial pressure is very high, higher compared to the mean systemic filling pressure, the blood will go away from the heart. If your right atrial pressure is less than the mean systemic filling pressure, the blood will flow towards the heart. So in a normal state, that's the first wave form is the hepatic wave form. As Dr. Korosola mentioned, you have the normal S and D pattern. As the filling pressures increase, get more congested, the S wave gets more inverted. So that's just taking apart the hepatic veins. Just the physiology of hepatic veins totally depends upon the systemic filling pressures. Now portal vein pulsatility. So portal veins in a normal state should not be pulsatile, right? This was studied basically about 30 years ago in the setting of, again, heart failure, but that never got incorporated into comprehensive point of care ultrasound assessment. The portal vein, it should be undulating, phasic in nature, but as we get more congested, it gets pulsatile. Same thing with intrarenal, when the arterial and the venous flows, they're supposed to be seen in two or more cardiac cycles, and usually the venous flow is monophasic below the baseline, but as the congestion increases, it becomes similar to the S and D waves in the hepatic vein flow. So this is the ideal world, right? Your IVC is less than two centimeters, you forget vexus. No grade zero, no congestion. And then when the IVC is greater than two, you look at the other three categories, the hepatic vein, portal vein, and interlobar veins. How much of the IVC is in the gray zone, that's a significant number. So just switching gears a little bit more, I want to talk to you about this 2009 guidelines between American College of Chest Physicians and their French equivalent, giving recommendation about competence in point of care ultrasound. They divided it into two, general critical care ultrasound, looking at thoracic, abdominal, and vascular, and echocardiography, again, divided into basic and advanced critical care echo. So these are the competencies, general, everybody knows that, those five general ones, plural, lung, abdominal, vascular, for vascular access, and for venous thrombosis. When you move on to advanced, there's IVC distensibility index, SVC collapsibility index, respiratory variation, looking at Doppler velocity and cardiac output following passive leg raise. So again, we all, I'm sure we are all familiar with basic critical care echo, but to get competence in advanced critical care echo is still, not all of us are, and then vexus is like one step above this. There's more literature coming out about vexus, since this is supposed to be an evidence-based topic for discussion. Most of the studies described as positive studies for vexus had limited number of patients, about 30 patients, or 90 patients, or 145 patients, so that's a limitation. We are eagerly waiting for this Andromeda vexus study to come in, that's looking at the Andromeda shock population, which is a multi-center prospective randomized control trial in multiple countries, they're currently being recruited, looking at our main bread and butter in the ICU, septic shock patients, looking at septic shock patients, and within about six to 12 hours of randomization into Andromeda shock, they look at vexus in those patients, and the outcome is need for renal replacement therapy or mortality in those patients. So that's a very good study to look out for, that's coming up. And they're adding more complexity or more protocols to this, while adding the lung ultrasound along with vexus, right? So first you should know vexus, and then you incorporate lung ultrasound to see if that improves your diagnostic accuracy. So the caveats for me, while looking at vexus, when you look at the IVC number one, it can be compressed by increased abdominal pressure, independent of the right atrial pressure. Hepatic vein may not show significant alterations if your patient has severe tricuspid regurgitation. The portal vein may be pulsatile in normal, healthy individuals. And also it may be non-pulsatile if the patient has stiff liver, such as cirrhosis. Interlobar renal veins are technically difficult to obtain, and as Dr. Korotila mentioned, the renal parenchymal, those who have parenchymal renal disease, we don't know how much of a use the intrarenal Doppler studies are going to be. So with all this evidence, is it vexing yet for anyone? Yeah. So yes. It does not specifically identify the source of congestion. It should not be used exclusively, but used as an adjunct. There are no robust studies on all comers admitted to the ICU. The main studies that have looked at vexus is increased predictive value of acute kidney injury in cardiac surgery patients. We don't have answers as to what about the systemic congestion with an IVC less than two centimeters, with an IVC less than that cutoff of two, and below, does that mean there is no systemic vascular congestion? We don't know. It may provide a point to stop fluids when you're resuscitating a patient, and those who might benefit from fluid removal. Just like Dr. Korotila mentioned, he went through his case where it gives him an indication as to this patient's fluid overloaded, let me remove fluids. So my conclusion, you should look at the right patient population while doing vexus. It's primarily studied in heart failure and cardiac surgery patients. The operator expertise and ultrasound knowledge is important because, again, it's an advanced ultrasound technique, so you can't get to advanced before getting to the basic. Requires appropriate training and also appropriate understanding of the pitfalls of the various components of vexus scan. The potential value that I see in vexus is serving as an early warning sign for stopping further fluid therapy, and signs of congestion in multiple solid organs can give a much stronger picture or prediction of higher risk of potential harm with additional fluid therapy. So basically it will tell you when to stop fluids. That's what I'm taking away from this. So I saw this tweet from Nephropocus. He said, who said cardiologists and nephrologists can't be friends, right? So my question to him is, it's not just cardiology, now it's time for pulmonary critical care and nephrology friendship. So it begins here with CHESS 2023. Thank you, everyone. So with that, I would like to introduce Dr. Taro Minami, who is our expert in diaphragm ultrasound. Thank you for the nice introductions, and it's always a pleasure and honor to be here to work with all these awesome people. And thank you, everyone, for coming to our session, and I hope I'm not wasting your time. So I have a disclosure. I am a consultant to Fujifilm, which is an ultrasound company, and AA Health Dynamics. The reason I am a consultant is because I am teaching point-of-care ultrasound in Kenya, so that's Japanese government funded this activity, so that's why I'm a consultant. So the learning objectives, understand why we should consider diaphragm ultrasound, meaning you're just selling this new technology, or not, learn how we assess and understand the weakness and pitfalls, hey, I do recognize a weakness, and recognize the evidence not only for, but also, I'm a fair person, so I'm going to bring up some evidence against diaphragm ultrasound. And so, again, it's a disclosure, I'm teaching point-of-care ultrasound in Kenya, Africa, so I'm a consultant to these companies. But the real disclosure, I would say, is I'm a strong proponent of the diaphragm ultrasound, and Dr. F. Dennis McCool, those who haven't read the article, review article from New England Journal of Medicine 2012, Diaphragm Dysfunction, you should read his review article, and recently we wrote together the review article, so that's my bias, obviously. So to begin with, so this is my disclosure, three, I'm not telling you that use it for every single weaning trial, right, because I always get the questions when I present this, hey, are you doing every single weaning, no, I'm not. So a diaphragm dysfunction would explain every single excavation failure, no, I'm not saying that, why, because excavation failure is multifactorial, right, it's a respiratory system compliance, airway problem, it's a cardiac dysfunction, respiratory muscle weakness, there we go, or mental status, or a fluid balance that we just talked about, and we are just looking at the one factor, so I'm not saying that this would solve every issues in a weaning problem, no, I'm not saying that. But what I do think is that the diaphragm ultrasound should be considered because it's an accurate way to assess the diaphragm functions, and it's easy to perform, hopefully I could convince you, and there is evidence, good evidence, I would say. So what do you mean accurate? So there you see Dr. Boone's and Dr. Sekiguchi's paper 10 years ago from Mayo Clinic, they checked a diaphragm ultrasound could detect phrenic nerve dysfunctions, and the sensitivity is pretty high, 93%, and specificity is also quite high. And with all these things combined, and this is the table that I created by reading Dr. Boone's paper, it's also easy to use, and it's not invasive, and you do not have to transfer patients to the CAT scan. So why not is my opinion, and how are we going to do that, and here I hope I could convince you that it's relatively easy to perform, there's two ways to do that, one is to take a look at the diaphragm dome excursion, and number two is diaphragm thickening by vascular probe, and this is my real clinic, I'm also a pulmonologist, more than intensivist, so this is my real clinic, real patient, I'm doing what we call the diaphragm clinic or chest wall clinic, so I let the patients sit on the chair, and facing in front of the ultrasound machines, and I'm using the phase array probe, the cardiac probe that we use for echocardiogram, then we could simply take a look at the dome of the diaphragm to move to the right side, which is the tail, and the left side is the head, and the diaphragm is an inspiratory muscle, so when you breathe in, the dome of the diaphragm should go down, which it is. So when you do take a look at the M-mode, so this is kind of the demonstration of how I could quantify the movement of the diaphragm, I simply put the M-mode, and while the patient is still sitting on the chair, looking at the ultrasound machine, and it's surprisingly, sometimes patients, patients can tell, oh, my right side is not working, oh, my left side is not working, right? So even patients can tell that the diaphragm is working, and it's a very intuitive process, and this is from my textbooks, in case you're interested in reading, so it's like, you know, TAPC, tricaspid aneupline systolic excursion, so how much excursion we could quantify, but basically, eyeball method, you could see the diaphragm dome excursion, and you could tell if the diaphragm is working or not. It's relatively easy to locate, and easy to measure, however, there are some pitfalls, like a fluid presence may impair the movement of the diaphragm, so even though the muscle is working, the movement could be impaired, so that's, you've got to be careful about that. Now, how about diaphragm thickness? So here, you're going to use vascular probe, the same probe we are putting in the central line, and you put at the zone of opposition here, and I'm going to show you in a moment, and this, so this is what we are looking, right? The diaphragm is a muscle sandwiched by the pleura and the peritoneum, and the depth is around four to six centimeters, so this is, I don't know if you notice, that my left hand is now holding the vascular probe, so I'm doing the thickening flexion, so this is basically what I'm going to see, so when you take a look at the diaphragm here, when she breathes in, the diaphragm is getting thicker, very simple, right? Any skeletal muscle in action gets shorter and thicker. My bicep is not a good example, but anyway, so that's a principle. So the diaphragm is working, it gets shorter and thicker, right? It's very simple to take a look and get the idea of if the muscle is working or not. This is from Dr. Dennis McCall's article in New England Journal of Medicine 11 years ago, so we check at the zone of opposition where the diaphragm is apart from the chest wall, like here, right? So then we could do the measurement, yeah, but it's a little bit cumbersome. A little bit tipful is that the structure looks very similar. Can you tell which one is the diaphragm? Like one, two, five, all look similar? Four, ah, there you go, you're proving the point. Yeah, so it's diaphragm, right? And above is intercostal muscle and two is serratus and surface muscle, so it's a little bit tough to say and a little bit tough to measure this thickness at the end inspiration and the thickness at end expiration, but sometimes you don't need to do the calculation. So when you take a look at the left diaphragm and the right diaphragm, which one is not working? I hope it's quite obvious to you, right, and am I convincing you? So sometimes you do not have to do the calculation. People say, oh, calculation is so cumbersome. Yeah, I have to agree, but you do not have to do that, you know, qualitative assessment over quantitative assessment, but what about the evidence? So my fellow, Arnie DeNino, did this study at Brown when he was a fellow 10 years ago, at 2014, and they assessed the diaphragm thickening for weaning, so that's one of the first of its kind, and you put the patients on spontaneous breathing, you know, people five and pressure support of five, and you measure the thickening, so how much that's going to be thickened during the spontaneous breathing, and you could see a significant difference. So if the thickening fraction is more than 30%, meaning that when the breathing diaphragm gets thicker, then sensitivity and specificity for successful extubation is quite high. Then my colleague, Dr. Atul Parker, says Corny Paul Mayo, Eric Gottesman, he's actually from Brown, did the study also five years ago about excursion, and excursion also would accurately predict the successful extubation. I mean, sensitivity is 85%, and specificity is 65, and it's not a bad number, but even more so, 2017, CHESS published a review article about diaphragm excursion and diaphragm thickening, both are quite helpful to predict the successful extubation. It sounds like there's lots of good evidence, until 2019, the French people published this article. It's very hostile, right? It's an inability of diaphragm ultrasound to predict excavation failure. Hey, you guys are talking about this diaphragm ultrasound, and we're going to prove it's nothing, right? They actually kind of did that. So dome excursions, okay, and left excursions, and thickening, how about thickening fractions? Because I was looking, oh, they did the dome excursion only, but they also did the thickening fraction too, and they kind of proved that, oh, hey, these guys are talking about nothing. So there is no difference between the successful and unsuccessful group. Diaphragm ultrasound is not helpful. Four years ago that they say from France, but you know what? So I read this article, so I got to see from top to bottom. Then I realized that it's not necessarily the orange to orange, you know, orange to maybe apple. So first of all, the definitions of excavation failure is so different. So Arnie De Nino, Atul Parker, both define as 48 hours, and Dr. Viviere from France, excavation failure is seven days, which is 168 hours compared to 48 hours, right? So that's not fair. And how they weaned the patients, they did the T-piece trial. So it's not really, you know, apple to apple, orange to orange, right? So then finally, here comes a guideline from intensive care medicine two years ago, and they actually do support, hey, guys, we do recommend the diaphragm excursion for diaphragm function assessment. Okay, good. So now you guys admit diaphragm ultrasound is helpful. However, we are unable to provide recommendation on the evaluation of diaphragm thickening fraction because it's techie, and I have to disagree, you know? And so I asked the writer of this guideline, why you said that? And oh, there are a few people from France who are strongly against that. Okay, all right, now I see why. Why do I think diaphragm ultrasound is helpful for weaning populations? One is accurate, and it's relatively easy to perform. Diaphragm excursion is relatively easier, really, so just to take a look at the diaphragm dome, and diaphragm thickening, okay, I admit, it might be a little bit more techie, but it's definitely worth it. And there is a good evidence, there is a conflicting evidence, I have to admit, but there is a good evidence to support that. With that, I thank you for your attention. That's it. Thank you. So, and next is my friend and colleague, Dr. Michelle Voivin, who just went back to University of New Mexico for professor, and we've been working together for the innovative use of the ultrasound usage, which is not here this year, but maybe in the future. So how should I close it? Oh, escape board. Okay, so now we can close the board. Of course. Yeah. Hi, my name is Michelle Voivin, and I'm hostile. So I don't have any disclosures. I'm here to talk about why not to use diaphragm ultrasound in weaning. I'd like to thank Dr. Ramesh for inviting me, and really, Dr. Manami has been instrumental in teaching me diaphragm ultrasound. I really learned a lot from him, but when I went out into the real world, I found some new knowledge that made me a little question my beliefs, and so I've come back to discuss them with him. I'd like to review the guidelines briefly and to describe how diaphragm ultrasound does not provide additional benefits, but I think there's a couple things that we've agreed upon. We all know that delays in extubation are associated with worsened outcomes, so it's really important to extubate our patients timely, but at the same time, reintubation is associated with really poor outcomes. So it's really important for us to have tools to try and find those patients who are at risk for reintubation while at the same time getting people extubated quickly. We all know this. Diaphragm ultrasound is the best test to monitor diaphragm function, and diaphragmatic dysfunction is an under-recognized cause of extubation failure and prolonged weaning. This next study is actually from 2018 in the Blue Journal, but if we look at diaphragmatic weakness and respiratory failure, there's actually a bimodal distribution, and if you look at on the left, it's a little small, but it's a thickening fraction on day three compared to time on the ventilator, you can see that a reduced thickening fraction, the bars on the left, or an increased thickening fraction, the bars on the right, lead to prolonged time on the ventilator. And if we look at the graph on the right side, you can see that a change in thickness over time on the ventilator, the blue and the red bars representing both atrophy and hypertrophy, both of those are bad, and both of those lead to prolonged time on the ventilator. And the thought was that if you're either not using your diaphragm enough while you're on the ventilator or using it too much, then you're going to be on the ventilator for a long time. So I think we can both agree that diaphragmatic weakness is important in prolonged respiratory failure. If we look at where we're at with our current guidelines for weaning, how many people use diaphragm ultrasound prior to extubation in all their patients? Ever? Seriously? Yeah. Thank you. Yeah. Thank you. Exactly. I love you. So I think most of us are doing spontaneous breathing trials with pressure supports of five to eight as a standard for the ATS-ACCP guidelines. The cuff leak test in high-risk patients, which is an extubation test, and protocol-driven spontaneous breathing trials, you know, coupled with sedation awakening have become, you know, the accepted standard method. But in terms of what actually we use to decide whether or not to go forward with extubation is not decided, right? There's a lot of what we were calling weaning parameters back in the day or tests of liberation or tests of extubation success, if you will. The classic ones, and I think the ones that are most used are the RSBI. MIP or NIF is commonly used and other things. But there's been lots of other studies and lots of different groups that other scores have used. There's more complicated scoring systems. There's cough tests. And there's patient factors that predict extubation failure that aren't really modifiable as well as the cuff leak. The white card test, which I had forgotten about, but is the test where you put a white index card in front of someone's ET tube and see if they cough three inches away. And you see if they cough on it. And if they get any sputum on it, they're likely to be extubated. Now this seems like a somewhat crazy test, but it actually has a really good sensitivity and specificity. And so there's lots of different tests you can use to determine whether or not to extubate your patient. Is diaphragmatic thickening or excursion a better test than what we, all these tests that we currently have, which would be kind of the standard to replace what we currently use. So if we look at the RSBI, in most studies and in a combination, you're looking at sensitivity of around 74 to 73% for sensitivity and specificity. That's okay. But like I said before, this is a high risk undertaking that we're taking. And so we should think about whether we can do better. When we look at excursion, I've actually combined the multiple meta-analysis here to give you an average sensitivity of 70% and a specificity of 80%. So it's not really much better than doing the RSBI. If you look at diaphragmatic thickening, there's a lot of variation. The meta-analysis were done at different times and they included different studies. So there's a bit of a range. Some of them are saying that the sensitivity is 70, others up to 90%. And then the specificity is running around 70 to 85%. So this has the potential to be better than what we're currently doing. There's only one randomized trial from the Brown group. And they, interestingly, what they did was they gave the information to half the subjects in the study. They randomized a small group of patients, 30 patients who are on prolonged ventilation. And they gave the information of the diaphragm ultrasound to the clinicians looking after them in half the cases, but they did them in all of them. And what they found was that if you gave the teams, the treating teams, the information that the diaphragm ultrasound was good and told them that they had a 90% chance of success, they extubated them faster. But the thing I didn't understand is that when they gave them the information that the diaphragm ultrasound was bad, they also extubated them faster. So it was a little confusing. But I think the important thing is that they're on the right track here, that we need to systematically do studies that involve giving people the perspective information and seeing if we can get better outcomes. So my criticism is that there's significant heterogeneity here amongst all the studies. We're not looking at apples to oranges comparisons. These are a fruit salad of different tests. Mostly medical ICU patients. It's almost all single center studies, except for perhaps the VVA study. Fewer single operators. Most of the tests are being done by experts, the local experts in diaphragmatic function. And different thresholds are used, 20% for thickening, 30% for thickening, and 25% different transducers. The definition of weaning failure and extubation failure change, as Tara was mentioning. And then it performs better in the subgroups that have more diaphragmatic dysfunction. So patients who fail weaning, if your patient has failed their weaning tests, or who've been longer on mechanical ventilation, have a higher instance of diaphragmatic dysfunction, and it's going to perform better in those groups, which might explain some of the differences in the studies where some studies show it not to be useful and some show it to be incredibly diagnostic. There's other challenges when you're measuring really small numbers on ultrasound. For example, the diaphragm is about two to four millimeters thick and you're measuring a small change of 10%, you're talking about tenths of millimeters. This is really prone to errors. And when you have someone who's got a very thin chest wall, then you're able to zoom in on that image. If you have a thick chest wall, you're measuring further away, your image is smaller, much more prone to measurement errors. You're somewhat dependent on having someone who's really good at diaphragm ultrasound, and these studies have all been performed by experts. And it is, again, it's going to take time to do this. I think we have to remember that our patient populations are very different across ICUs and think about which patients we'd like or could potentially apply this to. In the difficult airway patient, I'm really focused on the cuff leak. In my cardiac surgery patient, I might be focused on whether they're bleeding or not and hemodynamically stable. In the neuro ICU, what's their mental status? The diaphragm ultrasonography is going to be particularly helpful in your pulmonary patients or your patients who are intubated for a long time. That being said, I think we really don't know which patient populations will really benefit from this. And I think there's a danger in, or at least there's statistical problems in using multiple tests to make a decision. If you consider each extubation test to be a hurdle, whether it's cuff leak or RSBI or diaphragm ultrasound, if you add them on sequentially and someone only has to fail one to not get extubated, you're going to be very sensitive for successful extubation, but you're going to miss a lot of patients who could potentially be extubated. And I'm not sure that anyone knows how to combine these tests and in what order to use them. I think in real life, we wind up looking at all these things and trying to add them all together, but I don't think we can really say that we have data how to do that properly. So I'd say, what do we do about diaphragm ultrasound? Do we ignore the RSBI? That information is there in front of us. It's going to be hard to ignore it and only do another test. But if we do it sequentially, do we take patients who pass their SBT and then ultrasound their diaphragms? If they fail, are we going to leave them on the vent? I find that a little hard to believe, but I think there may be the group that most interests me are the people who fail in RSBI, but really have strong diaphragms who could potentially be extubated and the improved sensitivity of diaphragm ultrasound might be identifying some of these patients. So I think there might be a role there with further study. So in conclusion, I'd like to say that diaphragm ultrasound can predict extubation success in selected populations likely, but it's time-consuming, highly operator-dependent, and right now we're not really sure which groups would really benefit from this study, and particularly those with a low risk of reintubation. I thank you all for coming here today to listen to our talks. I want to leave a little bit of time for people who had any questions about any of the four topics or the two topics. Hi, this was an amazing session. I have not received so much ultrasound education in one hour ever in my life. I happen to be a POCUS champion and I was formerly at Brown, left there about 15 years ago before you guys were there. So the question about diaphragmatic ultrasound, firstly, was have you used it in post-sarcotomy patients for diaphragmatic paralysis and wouldn't that be a good population? And secondly, how would you break the news to a cardiac surgeon? So that to me is the most difficult challenge I've had in my life. And thirdly, the biggest controversy in POCUS that I have seen in my life trying to teach POCUS for the last 25 years is we're the choir and we're preaching to ourselves. And when I'm in a hospital and I have an internal medicine residency and a critical care fellowship and trauma critical care fellowship and everybody else, how did you convince people around you that this is the new stethoscope or this is the new way to examine patients? Well, thank you so much. I guess I'm going to answer the questions. I believe we have three questions and I think a second one is the easiest one. How are we going to deliver bad news to a cardiothoracic surgeon? It's quite simple. I'll send an epic message. So it's easy, you know, whether you read it or not, it's up to you, but you're supposed to. Yeah. So that's, that's the easy part. So now, so do I, do I, well, joking, joking and I call. Yeah. But joking aside, do I see a diaphragm dysfunction after the CT surgery? Absolutely. We do have a, our hospital does not have the cardiothoracic surgical department, but we are strongly connected with Brigham and Women's, which is one of our way. So we see a lot of patients who did the CABG or ABL, MBL at Brigham comes to a hospital or clinic. And I do diagnose a lot of diaphragm dysfunctions. Oh, holy cow. That's, you know, I don't know how many I picked up and, and, and I send a big message, but anyway, I do. So that's also a belief that I think it's really, you know, most of the introduction for the diaphragm ultrasound, that's, we probably missing quite a bit of the diaphragm dysfunction. And this is a modality we should really, you know, utilize more and more. How are we going to, so this is a complex technology and I have to admit, and I've been preaching this almost 10 years and I see slowly that the, you know, people start using the diaphragm ultrasound, including HCCP core faculties has been growing up, but I have to admit, so most of the question could be translated, how we could convince or how we could share the knowledge or experience more easier to the folks. And one of the ways that's, that's why we have this session, but the, that's a struggle, but that's definitely a rewarding process as I observed for the past 10 years. Yes. Hopefully I'm answering to some of your questions. Tara, I want to add to, so Tara and I, I'm Frank Chamber from Boston. Tara and I taught a course just in August and we gave the residents a pretest. And what was the mean score on the pretest? Uh, pretest was at 23 out of 25. So, so people are coming out of residency adopters. Yeah, that's the older ones. Right. So thank you, Frank. Yeah. So, you know, over the past 10, I've been teaching a point of care since 2006 here at the HCCP. Holy cow. That's why my hair is so gray, but the, um, over 20 years, I'm absolutely seeing the difference. So like, like some fundamental question, like a Vex says, like, you know, how the first things first, like we have to teach them how to differentiate IBC to aorta, for example, or a portal vein to hepatic vein. So that's a first step, but I think we are catching up, uh, to the points that's coming to the point that we are ready to teach, for example, diaphragm aorta center of excess. So that's how I take it. So thank you. Thank you everyone.

VEXAS

Venous Excess Ultrasound

venous congestion

organ perfusion

ultrasound scans

inferior vena cava

flow abnormalities

diagnosis

therapeutic interventions

research