All right, everyone. I am Brandon Odo, a critical care PA from Connecticut, and what I'd love to get in with you today is really just a couple things. Why we seem to have a hard time effectively diagnosing a lot of our patients in the ICU, and maybe a couple tricks for doing it better. We don't have time for more than a quick review, certainly don't have time for a whole lot of data, but the data that you will find is probably going to be in autopsies, and there have been a number of ICU autopsy studies looking at ICU deaths and comparing their pre- and post-mortem diagnoses, and to summarize, regardless of the population you look at, we seem to be missing a fair amount, both missed and missed diagnoses. That being said, I'm not really sure what this can say about the patients who don't die, because really I think the most common error we might be making is neither missed or missed diagnosis, but just failure to fully unpack diagnoses. How many patients are in your ICU right now with labels like this, sepsis, we don't know why, respiratory failure? What disease is acute hypoxic respiratory failure? Can you show me that in a textbook? But a lot of patients never really get beyond these labels, and I don't know if that's a problem. You could say that if you treat them supportively and empirically, and they get better, maybe that's okay, but I don't know. First of all, some patients won't get better if you don't offer them a specific treatment, but even the ones who do, if you never identify what you're treating, the best you can do is over-treat it, which means that you're giving too much, and we all know that there are complications associated with that. Some diseases will occur again if you don't identify them. How can you meaningfully engage in shared decision-making and prognostication if you don't know what you're treating? Doc, what are my chances? I don't know. I don't know what you have. There are public health implications to some diagnoses, like toxicologic exposures, communicable diseases that could affect other people. Imagine being the first person to see COVID-19 and waving it away as respiratory failure. And I think there's just something toxic to what it does to us when we stop treating diseases specifically and mechanistically, and we get in the habit of treating symptoms supportively. The original diagnostician, Sherlock Holmes, who was, by the way, based on a physician, said there are just three things you need to make a diagnosis or solve a case, observation, knowledge, and deduction. Observation is the ability to look at the patient or the crime scene and glean the data from that. Knowledge is the other data, the background knowledge you have of how the world is, in our case, what diseases are like. And deduction is the ability to put all of that data on the table and connect the dots, see the pattern it's forming, and make a leap. So let's look at each of these steps and see where we're falling short. When it comes to observation, the most important tool you have is still the patient's history. They want to tell you what's wrong with them. But it is hard, right? Our patients are often confused, comatose, intubated, sick. So what do we do instead of good histories? We try to do these broad tests. We scan everything. We send chemistries and cultures. But they just don't take the place of it, do they? If you've ever seen this show House, you've seen this team of crack diagnosticians spend an hour doing bizarre tests to solve a medical mystery. A lot of the time could have been solved in the first couple minutes if you just asked the patient a couple questions. It's also true that our patients are sick, and often we have to prioritize treating them instead of diagnosing them. And sometimes treating helps. A trial of therapy can tell us something useful. But if it doesn't answer the question, it could also muddy the waters. Knowledge is why diagnosis is a lifelong journey. We just can't take the place of a really deep and broad base of knowledge of what diseases are like. And if you don't know what a disease looks like, you're never going to make that diagnosis. And yet, what do we focus on in critical care? When you walk around at this conference, the diagnostic focus, if there is one, is going to be on our ICU problems, ARDS, sepsis, delirium, most of which really are just syndromes that occur in the setting of other diseases. And those diseases are not our focus. They're another specialty's problem. But of course, the patients don't know what chapter they're in. Finally, deduction. Well, it probably never seems like the right moment to sit down and sink your teeth into a medical mystery, right? We're all busy. But I think that's often an excuse more than anything. We just don't try a lot of the time. We're happy with these fake diagnoses and empiric treatments. And what this really ends up looking like is data collection is not a snapshot. You look at what you have. It generates a hypothesis, and that suggests the next test you need. And if we ever do this, we ever try, what it looks like is standing around on rounds, stroking our chins. We have an idea and say, could it be X? And so we check another box or two. We send a test. But a lot of the time, what it should suggest is asking another question. But do we do that? How often do you go back for more history after the patient's admitted? I think even in the Star Trek future, when we can run a tricorder down the patient, scan every cell in their body, we're still going to need to ask these questions. How are you feeling? If you had weight loss, how's your breathing? So in the real world, what do we do? We try to test everything. And it doesn't work, not because it's costly or inefficient, which it is, but it just doesn't work. There's too many things to test for if you can't get into the right ballpark first. We try to consult our way out, which doesn't work either. The consultants know additional things, but they don't have the continuity we have. They probably don't care as much. They have a lot of other patients. So if you have a specific question for them, they could be helpful. But if your question is just what's going on, they probably don't have much to say. We say somebody else will diagnose this patient on the floors or in the outpatient setting. How often do you think that happens? These people have their own problems, they have a lot more patients, and now the problem has aged. And we try to do it the same way every time. And just as you can't treat every patient in your busy unit like a medical mystery, I also don't think you can treat the ones that seem a little off as if they are a bread and butter case. You need the ability to switch modes a little bit and slow down and be more systematic. So you kind of have to start over in many cases. Use the data you have, but discard the differential you have and look at things with fresh eyes. Kind of admit the patient new and go from there. The hypotheses you've had so far have gotten you where you are, which is not good enough. And I think a practical way to do this a lot of the time, in again the busy worlds we live in, is to make day two of ICU the day you diagnose. It's not practical to think that you're going to diagnose everyone fully when they're admitted. They're sick, they're being resuscitated, you don't have all the data back yet, and oftentimes it may be after hours, skeleton staffing. But day two, the dust has settled, you're in the light of day, you can look at what you found, decide what you still don't understand, make a fresh differential, and then as part of that process, expect to go and get more history. Don't get in that cycle of just trying to send a test. Plan to go back and ask some more questions. And if you really make that a habit, I think you'll make a lot more diagnoses than you are now. It's kind of like the tertiary survey the surgeons do. They know they're going to miss things initially because so much is going on, so they plan for it. As you go through all this, you're going to expect that you're going to be very fallible as we all are. So rather than trying to remember everything, you're going to write things down, the abnormalities, your differential. You're going to try to label what you're looking at as specifically as you can, so you can trigger those pathways and buzzwords you've learned about, because that's how you're going to engage your pattern recognition. You're going to really reflect on the test characteristics of those tests you use, so you don't falsely rule something in or out when that test didn't really have the power to do that. And that can be subtle and may involve looking things up, talking to experts. And you're going to use whatever tools you can to back you up, because this is hard. And just like the airline pilot's not going to assume he remembers every step of his preflight checklist, you're going to assume that you might miss things. You probably have cognitive biases you're bringing to the table. Now it's not particularly clear from the data whether acknowledging these helps. You can't make them go away. I think that you can maybe take the edge off if you acknowledge them. The common ones are going to be anchoring, sticking with one diagnosis longer than you ought to. Availability or recency bias. Every diagnosis you hear about at this conference, you're going to try to go make for the next week or month or year. And if you have an interest in diagnosis, which perhaps you do if you're in this room, you're probably always going to be a little bit drawn towards the good diagnosis. The fun one, the rare one, the elegant explanation. Even if it's not the most likely, just based on prevalence. If you acknowledge that, then you can try to mitigate it a little bit. Here are some checklists. These QR codes will take you there. I put these together. They're not perfect. You're going to have to optimize them for you. I would suggest you either put it on your electronic device so you can pull it up or just dump it into your EMR as something like a dot phrase. That would be very easy to get. This first one is just questions. It's the elements of the history you might not always remember to make use of. You see the ones that are applicable and you say, oh, I should ask that. The second one is the same for physical exam maneuvers. And the last is diagnoses. The things you may not always remember that are perhaps high yield, morbid, specifically treatable and easily missed. You don't use these in place of your reasoning. You use them to supplement at the end of it. You get as far as you can and then you check your lists or your tools and you say, what might I have missed here? So where does this leave us? I think the first step to a lot of this is just making an effort to diagnose. And if you just do that, I think you'll get a lot farther than we are on a lot of our patients. And a lot of the next steps is just tools you already have. We all learned in school how to take a good history, do a good exam, build a differential. To some extent, I think we just forgot. We got into the real world where it's busy. We saw common things a lot and we focus, especially in critical care, on treatment over diagnosis. So you have the tools in your toolbox, it's just maybe a matter of using them. And finally, I hope you can let yourself be a little bit excited by all this. Diagnosis is still one of the most complex and I like to think the most interesting things we do in medicine. Perhaps the last thing we'll lose to the machines. And really one that requires us much more than a lot of treatment, which can often be somewhat protocolized. It's my opinion, I'm sticking to it. This is me. I'm happy to answer any questions. Or if you missed a checklist or something, just reach out. I'll give you over to Kasey here. We'll do questions at the end of all three speakers. So our next presenter will be presenting My Patient Won't Wake Up, Now What? by Kasey Albin. Hi there, everyone. And congrats to all of you for being here so bright and early. So I'm a neurointensivist by training. I spend most of my time in the neuro ICU seeing patients with mostly cerebrovascular disease. But I have the luxury in that position to get to do a lot of ICU consults as well. And I think this is a frustrating and common occurrence that we get called for all the time. You know, the patient was sick, and now, you know, we made them better, and they're still not waking up. And how do you approach that patient? There's no disclosures, nothing relevant. So delirium, as we know, is incredibly common in the ICU population. You know, maybe a third of patients who are not on the ventilators, up to 80% of vented patients if they are formally screened. Common problem. However, 10 to 15% of non-neurologically admitted patients, so patients who did not come in with meningitis or stroke or something else, will develop a neurologic problem during the course of their ICU admission. That's actually kind of a lot of patients, right? And so I think when we think about reducing a problem to a syndromic diagnosis, they are delirious. They have toxic metabolic encephalopathy. We have the potential to really miss reversible causes that could be treated. And so today, we're going to talk about, you know, this is a very broad topic, but a little bit of an approach that I use when I'm seeing these patients, when I get called from other ICUs to kind of think about why is the patient not waking up. So first, who does this apply to, and who does it not apply to? So this is not the patient population that was specifically admitted with a neurologic problem, right? This is not a patient with meningitis. This is not a patient who came in with a stroke or interstitial hemorrhage. This is not a patient that's at high risk for a neurologic infectious complication, not someone who's had a recent neurosurgical procedure, not someone who's got an open skull. This is a patient who is altered beyond what you think would be appropriate for whatever systemic illness they came into the ICU, right? They came in with liver failure, and that's kind of been corrected. They came in with sepsis. You treated that. They came in with some other syndromic diagnosis that's very common in critical care, and they still just aren't waking up. And so you've also done the base work. You know, by the time I get in consulted, people have already checked the ammonia level. People have already looked to make sure that their BUN is not 150. They're not hypoglycemic. They're not hyperglycemic, right? You've done the basic work here. So how do you approach those patients where it's not clear just from your typical metabolic screening what is going on? You have to be really thorough in these patients, and so you have to dot your I's and cross your T's. So we're going to use this nice mnemonic, dots, okay? So starting from the beginning, D for drugs. I know you're all thinking, duh, I looked to make sure the patient wasn't on fentanyl. They're not on a sedative anymore. But I think there are a ton of things that we can do from the medication list. And I see the pharmacist shaking their heads here, yes. This, I have to tell you, is at least half of the consults we get. We dig through the medical record. We look at what drugs they were exposed to or not exposed to. And that's a really clear, a really important thing to do is to go back to the patient's home medication list and think, did you not restart their levodopa, right? Like this Parkinson's patient is going to look terrible without their support. Are they off their antidepressants? Are they off their baclofen? Are they off their anti-seizure medications? I think a lot of time we think about what patients are exposed to and forget to think, what have we left off? I think for all the pharmacists in the room, I know that you know this, half-lives really matter. I think we as clinicians sort of say we stopped the drug and now it's gone. This has really been drilled into me in doing brain death testing. When you think about the five half-lives that you need before you can clinically clear someone, it is a long time for a lot of the sedatives that we are giving. So just be mindful that just because you stop something doesn't mean it's not on board. And then reviewing their kidney function, their PRNs, you know, this is like bread and butter but it's good practice to do this. And then antibiotics, right? I think we have sunk in more and more to cefepime neurotoxicity, but it is not just cefepime. In fact, when you think about antibiotics, basically any class of antibiotics has a potential for neurotoxicity. This is particularly true of metronidazole and isiazid. The cephalosporins are chief offenders of which cefepime is a major culprit, but it is not the only one. And so, you know, the mechanism here is probably inhibition of synaptic transmission that leads to excitotoxicity and delirium and then potentially seizures. But this is just something, you know, to be very mindful of. And if nothing else, this is sort of like, you know, drug fever type thing where you're like if the patient's still altered and they're on a class of antibiotics, think about is that a class of antibiotics that we could switch to and give them a different exposure. It is more common in the elderly and is more common in patients who have impaired renal function. So really, antenna up for those patients. This is not common, but I think it gets missed and the reason I'm bringing it up is because it's not going to be seen on a head CT and you're going to have to potentially go back. So osmotic demyelination causes the syndrome of central pontine myelinolysis or extra pontine myelinolysis. This is something that we see, I would say, once every maybe two years. This is a very unfortunate case of a liver transplant patient where you can see that trident sign in the pons, which is the classic finding in this disease. It is specifically thought of or traditionally thought of in patients who have a rapid correction of their sodium, but it can occur from a lot of different other things. It's been reported in hypokalemia, in DKA. It's incredibly, or our patients who are peritransplant are at higher risk of this condition. The reason I bring it up is because specifically with sodium, usually the team that is aware when this rapid correction of sodium happens is horrified. they know that this happened. Central pontine myelinolysis presents in a delayed fashion. So the team that was really worried about it is probably rotated off service. And now it's a second team that's like, why is this patient not waking up? It has a sort of biphasic appearance. So the patients first come in with seizures, encephalopathy. They get a little bit better. And then all of a sudden, they have dysarthria. They have gaze restrictions. They become locked in. Right? So this is something that is not, fortunately, very fortunately, not that common. But I always think about it. And I go back and I look at the sodiums. I go back and think about, was this DKA patient? In stage renal disease patients, it can be observed in patients who have rapid sodium and rapid concentrations of urea shifts. So this is one of those things to keep in mind and go back. Because the team that is going to diagnose this is not necessarily the team that saw the insult happen. And it's not going to be seen well on your head CT. T for thiamine deficiency. I love thiamine. I just give thiamine like DVT prophylaxis. And the reason is that thiamine repletion is pretty much harmless. So thiamine deficiency results in increased dopamine, which causes delirium. In extremes of this, you actually see Korsakoff psychosis, which is just really incredible neurologic diagnosis of confabulation. It decreases acetylcholine, which causes this cognitive impairment. And the triad, this Wernicke's encephalopathy of ophthalmoplegia, ataxia, and confusion, not often seen. What we're mostly seeing is confusion, plus minus maybe a little bit of impaired lateral and upward gaze. MRI is actually pretty sensitive for this and is specific for it as well. You see this T2 hyper intense signal around the cerebral aqueduct in the periaqueductal gray, as well as in the mammillary body, as in sometimes in the thalamus. What's really important to know is sending a thiamine level is not going to be helpful. So patients with the blood and plasma concentration of thiamine does not reflect your tissue concentration of thiamine. Your blood level can be rapidly normalized if, say, you get a banana bag in the ED. That does not reflect the true tissue concentration of thiamine. You can send a blood thiamine diphosphate level, which is a little bit more sensitive. But again, this to me is a clinical diagnosis and one that has a very low risk of repletion. You might expect it in patients who've been adequately resuscitated but still have a high lactate and an elevated anion gap. I like this study of end-stage renal disease patients who were in the ICU with encephalopathy. They gave them high-dose thiamine and 90% improved. Now, do I think it's confounded by other things? Could they have gotten better by other things? Sure. But is this harmful? No. And I think that this is one of those things that when I consult for patients who've been in the ICU for a long time, one of the first things I do is high-dose thiamine replacement. I love the first part of this algorithm because it has involved no testing. All you've had to do is sit down and go back through the drug list, go back through their home medication list, think about what they have and have not had in terms of metabolic fluctuations, and give them some thiamine. At the end, we're now going to get into two tests that are going to be helpful. So the next thing you have to think about is structure. Most ICU patients are complicated. It's harder to get them to an MRI. So what you're going to do to evaluate the structure is the classic head CT. And I think it's important when we're thinking about this to know that the diagnosis of this is actually fairly good. When we send patients down, I hear complaints of like, what are we going to see with a head CT? But actually, you can see a lot. And in 10% to 15% of patients in the ICU, this actually has the potential to change management. So again, it's a humble test, but one that I think is a good one. So what are you going to see? When we think about this non-focal, what looks like toxic metabolic encephalopathy, it can be that they've had a vascular event, specifically in the PCA territories or in the right parietal, sort of posterior MCA territory on the right, and the thalamus. So those syndromes don't present with a lot of weakness, gaze deviation, language deficits that are easy for us to pick up on a screening neurologic exam, but can make a patient very encephalopathy. Press and vascular dysregulation makes patients look very confused, seen on a head CT. Subdurals, global cerebral edema, and hydrocephalus, all picked up by the humble CT scan. So actually, I think this is a really helpful test, and I think we can get a lot of information. It's really important to know what you are going to miss, which is acute stroke. So if there is focality, or it is an abrupt change in consciousness, you must, you must, you must think about, is this a basilar thrombosis? Please, if you have any, if this is an abrupt onset change, or you have any lateralized symptoms, send the patient for CT angiogram the first time around. Nothing is more annoying to everyone involved than getting a head CT and then sending them right back down. Neurons over nephrons, I don't care what their kidney function is. If you think that this is an intervenable lesion, please just get the contrast. All right. Finally, seizures. All right. So non-convulsive seizures and non-convulsive status epilepticus is probably very under-recognized in critical care patient populations that are outside of the neuro ICU. This is a simple test. Even a routine EEG, if you can get two to three hours, you're probably going to pick up at least a whiff of that something is abnormal. Longer is better. If you have the ability to do continuous EEG, 24 hours is going to catch 95% of things. If you do not, still getting a couple hours of routine will give you at least sort of a, is this a high risk or does this just look like a little bit of triphasic, a little bit of attenuation. This is really important to diagnose because this is treatable. We can intervene. It's important, though, that not every spike needs to be treated. I think when you get the reports back from our encephalographers, sometimes they can make it sound like it's a really active EEG. And there is a delicate balance of not over-sedating patients with anti-seizure medication while taking this seriously and treating seizures. Again, maybe depends on the series used, but somewhere between 3% to 17% of patients who are screened from a non-neuro ICU, so in a MICU or in a SICU. All right, so takeaways here. Kidney functions, medication list. Honestly, this is basic stuff, but this is really where the most of our solving comes. Head CT and EEG. There's a reasonable diagnostic. You're going to get bang for your buck in those two tests, and they're simple to do, and they're pretty cheap. Always consider vascular imaging for abrupt onset changes. And think about thiamine. Just give them thiamine. Like, I don't think you're going to hurt them. So with that, I will turn it over to our next speaker. So thank you. Thank you. All right, our last speaker will be discussing sick people deserve a diagnosis, identifying infections in the ICU by Dr. Jan de Waal. Thank you. Thank you very much. I think the previous speakers already nicely showed how complex it can be to come to a diagnosis. I'm afraid in infections and sepsis, this is no different. These are my disclosures, none of them, in fact, relevant for this presentation. I don't think I have to convince this audience that sepsis is important. And well, if you want to treat sepsis properly, then an infection diagnosis is actually very important. And I'll explain you why. Well, the first and simple reason is that by diagnosing infection and diagnosing it early, well, you avoid progression from an infection without any organ complications to sepsis and eventually septic shock. So trying to break this vicious cycle early is quite easy and straightforward if you get your infection diagnosis early and correct. Organ dysfunction, of course, may have multiple causes and is definitely one of the confounders. And in our approach to sepsis, we need to understand there's two important elements. There is, on the one hand side, the organ dysfunction that is quantified in the sepsis tree definitions. And we have the tools. We use the SOFA score. But the infection is often taken for granted. There's no guidance in the sepsis tree guidelines about how you diagnose an infection. There's even barely mention of that. And I'll come back to that in a minute. Very importantly, better infection diagnosis leads to better sepsis treatment. And there's two important reasons why I think this is the case. Not every patient with sepsis will get the same antibiotics. If a patient is suspected of suffering from meningitis or an abdominal infection, well, you will be administering different antimicrobials. And more importantly, and this is a topic dear to my heart, source control. You need to have an infection diagnosis, an anatomical diagnosis, in order to be able to control the source of infection when necessary, of course. And only if those two things are right, then you can start thinking of treating sepsis with any new sepsis-specific drug you are interested in. In the end, also, better sepsis diagnosis, better infection diagnosis, will lead to better sepsis research. Because let's be honest, a lot of those patients in sepsis studies, they come down with what we call a culture-negative infection. We assume an infection is there, but actually we cannot document it. I'm not saying that those patients will never have an infection, but I'd rather see a microorganism identified when I treat a patient with sepsis or septic shock. So this search for a reliable sepsis infection diagnosis has been going on for quite some time. But we made very little progress, I think. This is coming from a Dutch study. The Netherlands, as you know, this is a country where the threshold for giving empirical antimicrobials is quite high. But they looked in this study, patients admitted to the ICU through the ER, and they checked three days down the road whether the initial diagnosis of infection was correct. You can see in this figure that one out of six patients, it was very clear there was no infection at all. On the other side of the spectrum, one out of three patients, it was very clear. And the rest was, well, somewhere in between. It could be infection, but it could be something else. So we need to be aware that we are not very good at diagnosing infection. We're good at diagnosing sepsis, at least the organ dysfunction associated with sepsis. But the infection part itself, it's much more challenging. And the reason why, well, there's so many diagnoses that look like sepsis. I'm sure you can add many more to this list. And often also, once we make a diagnosis of sepsis, we are often happy. We are in a busy ICU. Once we have this diagnosis, we just switch off our brain. We move on to the next patients. And we do not consider, we do not revisit this diagnosis. It's a lot of confounders. I already mentioned symptom overlap. But we have to admit that patients may be admitted with pulmonary embolism, which mimics in many ways an infection. Patient comorbidities make it more difficult, and especially this ultra sensitive and probably overused imaging. We scan everybody. We echo everybody. And then we come up with, well, things that maybe are totally irrelevant. But we try to use it in our construct of an infection. And finally, the information coming back from the lab. Increasingly sensitive tests are being used. It gives us more information. And it tells us that a pathogen is there. But you don't just need a pathogen to have an infection. It should be an invasion by a pathogen, multiplication, and causing the disease. This is what constitutes infection, and not the mere presence of a pathogen. And especially distinguishing colonization, because you can culture your patients and you always will get a number of pathogens back from the lab. But that necessarily doesn't mean that an infection is present. So two important distinctions need to be made. Of course, we need to diagnose sepsis. But the focus there is on host response and the quantification of organ dysfunction. But when it comes to diagnosing infection, we need to take a different approach. We need to look for signs and symptoms of this infection. Because if you have a skin infection, well, then you will have signs and symptoms of that infection. And always use a contextual approach. If a patient is admitted three or four days after elective abdominal surgery, with abdominal pain and signs of sepsis, well, it's not that likely that this patient will have meningitis, if you see what I mean. SIRS, there's been a lot of SIRS bashing, of course, in the past years. And we all feel a bit awkward when we still would even mention it. But let it be clear, also in the sepsis three guidance, it was explicitly mentioned that, of course, we don't use SIRS criteria for the sepsis diagnosis. But non-specific criteria like SIRS will continue to aid in the general diagnosis of infection. And this is something that we need to remember. These are tools that help us to diagnose infection. But above all, I think we need to look at our patients. We need to use the tools. So that means our brain, our eyes, our hands, our ears. And go and look at patients. This is very important. Look at a patient's history. Often, there are clues hidden there. Clinical evaluation, very simple, very simple things, but all too often forgotten. Why? Because we often skip and we go for echo. We want to scan. And we just, well, we'll see what comes up from the scan. And it's not about just one of these items. It's about integrating all this information and revisiting when necessary. Of course, that brings you to a diagnosis. This is one of the big problems in this context. We forgot about physical examination. We like all the other stuff, the biomarkers, very exciting, changes in biomarkers and the ultrasounds. But physically examining your patients actually will help a lot, I think. And I often see residents these days, they're behind their computer ordering the tests. But actually, did you look at the patient? I will do it. I will do it in five minutes. But they are not using that to actually inform the tests. I'm not saying it easy. It is very complex in ICU patients. And I think we've discussed a number of the reasons why. But that should not chase us away, I think. I like to use a simple, practical approach. It doesn't need a lot of time. Again, your hands, your eyes, your ears, just focus on the most plausible sources of infection. The most plausible sources of infection is pulmonary, first of all, OK, 2 thirds of our patients. And then abdominal, urinary tract, catheters, neuro, not very often. If it's a surgical patient, you look for the skin and wounds. And actually, this in 60 seconds or less, you can already have a good idea where the problem is located and what it can be. And maybe you will be stuck, indeed, with undetermined infections or bacteremia or candidemia, indeed. But often, again, this can really help you. Of course, we all like the new fancy biomarkers and the new diagnostic tools, often hoping that it will bring more information. As far as I'm concerned, often this is information overload. We get more microorganisms reported from the lab. We get more detailed biomarkers. But actually, quite often, they are not contributing in a relevant way. So in conclusion, I hope I've convinced you that diagnosing an infection is very important for treating patients with sepsis. Again, quite difficult and challenging in the ICU. But clinical examination with contextual thinking can actually already bring you quite far. But using this integrated approach, all this information, going at the bed of the patient. And I do realize we need better tools. We need better strategies, better biomarkers. But I'm not sure if they are around the corner. With this, I would like to end. Thank you for your information. And I'm happy to take questions. Thank you.

ICU diagnosis

critical care

sepsis

respiratory failure

patient history

clinical deduction

diagnostic process