Transcript
Speaker: Welcome to Critical Matters, a sound podcast covering a broad range of topics related to the practice of intensive care medicine.
Speaker: Sound provides comprehensive critical care programs to hospitals across the country.
Speaker: To learn more about our programs and career opportunities, visit www.soundphysicians.com.
Speaker: And now your host, Dr. Sergio Zanotti.
Speaker: Fluid overload is common in critically ill patients.
Speaker: Although it's a frequent finding, a better understanding of its potential harms has renewed interest in properly managing fluid overload in the ICU.
Speaker: Today's podcast will focus on this topic.
Speaker: Our guest is Dr. Michael J. Conner, a practicing intensivist and nephrologist.
Speaker: He is a professor and senior physician of critical care medicine and nephrology
Speaker: at the Divisions of Pulmonary, Allergy, Critical Care, and Sleep Medicine and Renal Medicine at Emory University School of Medicine.
Speaker: Additionally, he serves as the Director of Critical Care Nephrology at the Emory Critical Care Center at Grady Memorial Hospital.
Speaker: Dr. Conner's clinical and academic interests are heavily focused on critical care medicine, particularly acute nephrology issues in critically ill patients.
Speaker: Dr. Conner is an internationally recognized expert on acute renal replacement therapies, acute kidney injury, volume management, and hemodynamic support of the critically ill, intra-abdominal hypertension, abdominal compartment syndrome, and extracorporeal blood purification techniques, including extracorporeal membrane oxygenation.
Speaker: Dr. Conner has been on our podcast in previous episodes, and today we welcome him back to Critical Matters.
Speaker: Hi, Michael.
Speaker: How are you?
Speaker: Hi, Sergio.
Speaker: It's so great to be back.
Speaker: Thank you so much for having me.
Speaker: I really always value and enjoy these conversations that we've had together.
Speaker: And I learned so much from you and from your audience.
Speaker: So I hope I can share a few things.
Speaker: Same here.
Speaker: And today we chose a topic that I know is of great interest and passion for yourself, but also happens to be a very common occurrence.
Speaker: And sometimes I think people kind of don't pay it as much attention as they should.
Speaker: But in your words, why is this topic of fluid overload important for clinicians in the ICU?
Speaker: Yeah.
Speaker: Yeah, you know, this is a topic that has evolved so much over the course of the last 20 years.
Speaker: And please don't get me wrong.
Speaker: I believe very much that, you know, we should be resuscitating our patients.
Speaker: But the question then becomes, you know, how do we manage the fluid moving forward after that resuscitation and when do we remove it?
Speaker: And, you know, we have a wealth of data now that fluid overload is very harmful for our patients.
Speaker: It prevents
Speaker: our patients' recovery.
Speaker: It limits and slows the recovery of our organ function and our overall survival, not the least of which is that it also contributes to organ dysfunction.
Speaker: So we as intensivists are in the business of trying to help facilitate our patients' recovery.
Speaker: And as you know, Sergio, right, there's the sort of reality of critical care medicine is that aside from treating infections and sort of addressing the primary problem,
Speaker: We provide life support, but the patients ultimately have to fix themselves.
Speaker: And there's not a lot of stuff that we can actively do that can really help foster recovery.
Speaker: But managing fluid overload properly and resolving fluid overload is one of those things that we can actually do on a day-to-day basis that does actually improve
Speaker: our patients' chance of recovery.
Speaker: So I think it's a really important topic that we can't just accept that fluid overload is sort of the consequence of critical care these days.
Speaker: We need to work to resolve it and return our patients to uvolemia as soon as possible to help foster their recovery.
Speaker: Perfect.
Speaker: Michael, could you tell us about the overall frequency and the pathogenesis or how do patients become fluid overload in the ICU?
Speaker: Yeah, well, let me take the first one because I think it's pretty simple that pretty much it's unusual that a patient is not fluid overloaded at some point during their ICU stay.
Speaker: I think the data has been pretty clear that
Speaker: We tend to, as a side effect of our resuscitations, make everyone sort of fluid overloaded.
Speaker: We're rapidly expanding volume status in almost every critically ill patient when they arrive in the ICU to resuscitation.
Speaker: Maybe a few neurologic indications for ICU admission.
Speaker: Maybe patients don't get as fluid expanded, thinking of the seizure patient or the stroke patient.
Speaker: But almost every other indication for ICU admission generally requires us to do some form of resuscitation.
Speaker: And so, you know, the frequency, the incidence is quite high.
Speaker: It's going to vary from patient, from population to population, and different ICUs are going to have different cultures surrounding this.
Speaker: You know, easily 50% of our patients, if not significant more, will have some period of time in which their fluid overloaded, you know, following admission.
Speaker: Why it happens, you know, the mechanisms are sort of, I would say,
Speaker: twofold.
Speaker: The first is, you know, we're giving resuscitation volumes to patients, whether that's crystalloid, colloids, blood, you know, patients are being resuscitated and we can't really necessarily avoid that.
Speaker: I know that, you know, we might not really get into this too much, Sergio, but I know that, you know, many of your audience and you have probably seen these various, um, studies that have looked at a more conservative approach to fluid resuscitation, like in sepsis, um,
Speaker: And I don't really want to get into debating, you know, the merits of conservation of fluid when it comes to resuscitation right now, but that's a big reason.
Speaker: But, you know, there's other studies that really talk about that a lot of the fluid accumulation and fluid overload is really fluid creep.
Speaker: You may have heard that term before, Sergio, but, you know, we get a lot of fluids through, you know, various medications, all the antibiotics we're giving, all the, you
Speaker: carrier fluids for all of our drips, all the infusion volumes, you know, all of that really sort of adds up.
Speaker: And, you know, regardless of sort of what study you look at, there is generally in the adult patient population, around two to two and a half, up to three liters of obligate intake every day between infusion volumes and medications and, you know,
Speaker: and carrier fluids.
Speaker: And it's really this fluid that really leads to the sort of inexorable gain of fluid if we're not sort of actively managing it, if we're not really sort of paying attention.
Speaker: And we're not, you know, so these are the fluids that we really have to pay most attention to.
Speaker: It's these sort of hidden fluids that we don't think about, you know, our non-bolus fluids.
Speaker: Analogy that comes to mind immediately, Michael, is what happens with sedation often, right?
Speaker: It's more likely over time or especially over a night shift that sedation go up as opposed to go down unless we actively intervene and have an intentional approach to reevaluating and bringing that down.
Speaker: So like you mentioned, this is very common in the ICU situation.
Speaker: It is unlikely that somebody who's been in the ICU for several days is not going to be fluid overloaded, and we just need to manage that a little bit better.
Speaker: Yeah, and, you know, I think that you're absolutely right, and there have been some studies that have really tried to, in a very granular way, look at the sources of fluids for patients throughout their time in the ICU, and
Speaker: and had been able to sort of, and then sort of create like a pie graph as to where these sources of fluids come from.
Speaker: And by far the biggest portions of those pies
Speaker: are the sort of hidden creeped fluids.
Speaker: In these studies, they oftentimes even look at how many of the pre-filled flush syringes are being used for patients.
Speaker: And you can see that it's really, the piece of the pie that's the resuscitation volume in most patients
Speaker: is somewhere around a third to 40% of the fluid.
Speaker: But the majority of the fluid ends up being all of these other hidden areas.
Speaker: And if we're not cognizant of that, if we're not being mindful of those, then our patients become fluid overloaded quite easily.
Speaker: You know, just to piggyback one quick thing, one, you know, one common, you know, scenario is, is, you know, you need to provide your patients some dextrose.
Speaker: So people order, you know, D5W or D5, you know, something or other.
Speaker: when we could easily just disorder D10, or if they have a central line, D20, at which point we're decreasing the volume of fluid by twofold or fourfold compared to D5, yet still providing the same amount of sugar.
Speaker: So it's small little things like this that can really make a huge difference when you look at the arc of our patients' time in the ICU over the course of a week or 10 days or God forbid longer.
Speaker: I would like to talk about the consequences of fluid overload in our patients.
Speaker: And maybe we could start by talking about the general impact of fluid overload on patient outcomes, specifically mortality.
Speaker: What do we know today, Michael?
Speaker: What have we learned over the last decade or more that maybe has changed our approach to fluid overload?
Speaker: Yeah, well, I mean, Sergio, I think it's pretty well known now that there have been many, many prospective and retrospective studies that have demonstrated that there is a very strong association between
Speaker: The development of fluid overload, depending on how you define that, of course, each study defines a little bit differently.
Speaker: We can get into the definition in just a couple of minutes, but there's a very strong association between the development of fluid overload and, for that matter, the persistence of fluid overload.
Speaker: and mortality in the ICU.
Speaker: Now, I'm very much on record as saying that, you know, I think it's very clear from other studies that we can talk about, you know, over the course of the next few minutes, that this isn't just an association of fluid overload with worse outcomes, it's actually causative of worse outcomes.
Speaker: And we can talk about, and we will get into, I think, in a little bit why that is.
Speaker: But
Speaker: even when you look at this association, many people will come to me and say, well, this is just a marker of disease severity, Dr. Connor, that the more sick you are, the more likely you've gotten a lot of fluid, you've gotten a lot of resuscitation volume.
Speaker: And there have been several studies that have
Speaker: sort of demonstrated that that is not entirely accurate, that the severity of illness does not correlate very strongly with the amount of fluid that people accumulate, and that in several studies in which they look at
Speaker: SOFA scores or Apache scores or other sorts of severity of illness retrospectively, oftentimes they are either equally as sick between the two groups or sometimes the fluid overloaded patients actually have lower SOFA scores and lower Apache scores.
Speaker: And so there really is no correlation between the severity of illness and how much fluid that people are accumulating.
Speaker: So
Speaker: Fluid overload is not just a marker of more sick patients.
Speaker: There is clearly something, there's clear mechanisms by which this venous hypertension and fluid overload causes organ failures.
Speaker: And we can get into that over the course of the next few minutes.
Speaker: Just if I can put on one other quick hat, which is to say that patients who have acute kidney injury, this is a particularly profound effect that fluid overload is really fatal in patients who have acute kidney injury.
Speaker: And we need to work to mitigate that as much as possible.
Speaker: If I may, let me just take your audience for one second and say we need to define what fluid overload is.
Speaker: There are many ways to do that, but increasingly the most accepted way to do that is to calculate a percent fluid overload.
Speaker: In other words…
Speaker: You know, are you 10% fluid overload, 5% fluid overload?
Speaker: And the way that we do that is you take your current weight minus your admission weight and divide that by your admission weight and multiply that, you know, by 100 then to get a percent.
Speaker: So in other words, if you are...
Speaker: If you are currently 77 kilos, your admission weight is 70 kilos, then you are 7 over 70.
Speaker: You are 10% fluid overloaded.
Speaker: Does that make sense?
Speaker: It does.
Speaker: And it's an objective or more objective way for our clinicians to think at the bedside.
Speaker: And what I would imagine, based on my own experience, is that once in a while when you do calculate that, you'll be surprised, right?
Speaker: Like, whoa.
Speaker: Yeah.
Speaker: Yeah, I mean, it wasn't that long ago that I had a patient transfer or lateral into my ICU who was 50% fluid overloaded.
Speaker: Like literally, they had gained 50% of their weight with volume and they were obviously not doing well.
Speaker: And studies have looked at that percent fluid overloaded both as a dichotomous value, you are above or below a certain benchmark, 5% or 10% fluid overloaded, but it can also be looked at as a continuous variable as well.
Speaker: So 2%, 5%, 7%, 10%.
Speaker: And different studies have taken a little bit of a different approach.
Speaker: And this concept of percent fluid overloaded, I do want to really give credit to the people that came up with this because this was really our pediatric colleagues in both pediatric critical care and pediatric nephrology that really have been on the vanguard over the course of the last 20 to 30 years, recognizing
Speaker: how important and how much morbidity their pediatric patients experience from fluid overload.
Speaker: And they're really the ones who have taught us as adult doctors how important this topic is.
Speaker: And I think credit should be given to our pediatric colleagues on this concept.
Speaker: And they really invented this idea of percent fluid overload.
Speaker: And it really has held true between both pediatric and adult literature.
Speaker: You mentioned the impact that fluid overload has on outcomes in patients with AKI.
Speaker: There's also been similar studies in specific populations such as severe sepsis, septic shock, ARDS, respiratory failure, and post-op patients.
Speaker: What I would like to do instead of reviewing that literature is to go a little bit more into the mechanisms and to talk about the specific impact fluid overload has on organ systems.
Speaker: Yeah, well, so first of all, you're absolutely right.
Speaker: I mean, I don't know a patient population.
Speaker: I haven't seen a report of a patient population who does better with fluid overload.
Speaker: It holds true in trauma, ARDS, sepsis, cardiac surgery, abdominal surgery, AKI.
Speaker: You know, I haven't seen a patient population that that that, you know, it's beneficial for.
Speaker: So but the mechanism, you know, it primarily has to do, at least in my opinion, and I think the literature backs this up.
Speaker: is that this really comes down to a blood flow problem.
Speaker: And I remind your audience that, you know, blood pressure is not the same as blood flow.
Speaker: And while we agree that we have lots of studies that we don't need to just, you know, give every organ
Speaker: massive amounts of perfusion.
Speaker: You know, we don't need to maximize delivery of O2.
Speaker: We do need to have organ perfusion.
Speaker: And the underlying physiology has to do with fluid overload leading to venous hypertension and leading to other compartment pressure problems like abdominal hypertension.
Speaker: And as we get venous hypertension, that impairs blood flow.
Speaker: So just if we step back for one second, Sergio, we, um, to sort of, you know, very basic stuff, right?
Speaker: Flow of anything, fluid air or anything flows from high pressure to low pressure.
Speaker: And that pressure gradient from high pressure to low pressure drives the, the, the, um,
Speaker: the, what's the word I'm looking for?
Speaker: The quantity of the flow, how much something flows is a function of that pressure gradient from high pressure to low pressure.
Speaker: And so if your audience remembers, in normal individuals like you and me, hopefully sitting here right now, we don't have a lot of venous hypertension.
Speaker: Our right atrial pressure, depending on where we are in our spontaneous respiratory cycle, is anywhere from minus two to four.
Speaker: And so our veins of our organs are basically draining into a pool in which the blood drainage has no resistance.
Speaker: And as our blood leaves our various organs, we've lost a lot of the pressure gradient.
Speaker: So in our capillaries, our mean capillary pressure is only around 12, 15, 18 millimeters of mercury.
Speaker: And so the pressure gradient on a normal circumstance is somewhere between 15, 18 at our venous capillary to essentially zero in our central venous circulation.
Speaker: And so our organs have this sort of pressure gradient of around 18 to 20 millimeters of mercury to drain out blood.
Speaker: And when venous hypertension develops, when CVP goes up, especially acutely from its sort of baseline, then the pressure gradient to allow the blood to drain out of the organs decreases.
Speaker: And then that leads to organ congestion.
Speaker: And as we get organ congestion, that leads to perfusion problems because we oftentimes impair the blood entry into the organ
Speaker: if we're unable to drain blood out of the organ.
Speaker: So, you know, many of your audience will have heard of things about like, you know, congestive hepatopathy, but it's the same physiology that drives kidney dysfunction,
Speaker: We get organ edema in our heart, in our lungs, in our brain, in our viscera, all of which leads to impairment in function of those organs.
Speaker: Did that crystallize it at least simply enough without being able to show diagrams?
Speaker: That was excellent.
Speaker: And I believe that it's important to reemphasize some of these specific organ failures because most clinicians are familiar with what pulmonary edema looks like.
Speaker: And if you give too much fluid to certain patients, they become more hypoxic.
Speaker: You diurese them and they get better, right?
Speaker: I mean, pulmonary edema is a very common complication.
Speaker: Let's call it a fluid overload.
Speaker: But sometimes...
Speaker: we are not as aware of cerebral edema and the impact it might have on the patient's mental status.
Speaker: We're not, we're not, we, I remember very vividly one of my first patients I took care as an attending is like over 25 years ago, 20 years ago.
Speaker: And a septic shock, ARDS, obviously massively fluid overloaded and then kind of stuck, right?
Speaker: Not getting better at one point off pressers, still on the vent, not responding.
Speaker: And we started diuresing aggressively, and you saw every single organ get better.
Speaker: All of a sudden, tolerating nutrition better, waking up slowly, weaning down the ventilator, renal function starts improving.
Speaker: And it's just a crystallization at the bedside of everything you talked about in that mechanism.
Speaker: And I would like to hear more about the kidney specifically because...
Speaker: The story of intra-abdominal hypertension and intra-abdominal compartment syndrome is an interesting one that evolved significantly over the last 20 years, and probably because we also started giving massive amounts of fluid to non-surgical patients and started seeing this more commonly in the medical ICU and elsewhere.
Speaker: But the impact on the kidneys is quite significant.
Speaker: quite special and probably much more frequent than people realize.
Speaker: Yeah, well, first let me just piggyback on what you said before.
Speaker: Every organ is impacted by this.
Speaker: And when you said cerebral edema, a lot of people think about pathologic amounts of cerebral edema and intracranial hypertension leading to herniation.
Speaker: But that's not exactly what we're talking about here, Sergio.
Speaker: You know, this is just subtle amounts of cerebral edema that cause delirium and cerebral dysfunction and some confusion problems.
Speaker: But yes, you're absolutely right.
Speaker: Every organ system is impacted and the kidneys are very susceptible to this for a variety of reasons.
Speaker: You're right that if we develop intra-abdominal hypertension or on its most severe forms, abdominal compartment syndrome,
Speaker: which is very common in patients that are fluid overloaded, even in non-surgical patients, that impairs arterial perfusion into the kidney.
Speaker: But fluid overload has a much more insidious problem on kidney function, which has to do with organ edema,
Speaker: and congestion.
Speaker: And I'm going to try my best to verbally describe this process.
Speaker: It's best illustrated, I think, with some pictures.
Speaker: So I'm going to try my best to verbally discuss this.
Speaker: But
Speaker: But as we get venous hypertension, that leads to an impairment in drainage out of the kidney.
Speaker: The kidney, unlike your liver, is an encapsulated organ.
Speaker: So it has a very tough capsule around the outside.
Speaker: It's similar to your brain that is encapsulated by our skull.
Speaker: And so acutely, the kidney cannot really swell.
Speaker: You can get nephromegaly over time.
Speaker: The kidneys can get larger over time with infiltrative diseases and slow processes like lymphoma or diabetes.
Speaker: But acutely from congestion, the kidney cannot really swell that much.
Speaker: And so as you get impairment in drainage out of the kidney,
Speaker: that leads to interstitial edema and an increase in pressure
Speaker: inside the interstitium of the kidney because the kidney can't swell to relieve that pressure.
Speaker: And as that pressure goes up, it starts compressing the individual nephrons because the nephrons, like the ventricles in the brain, the nephrons are the compressible structure.
Speaker: And so the pressure starts compressing the nephron, which thereby raises the pressure inside the nephron
Speaker: and the nephron is contiguous with Bowman's space, if you remember the nephron anatomy, and so the pressure in Bowman's space then increases, and that then drastically impairs our ability to filter at the level of the glomerulus, because the glomerulus filtration is driven by a pressure gradient from the glomerular capillaries into Bowman's space.
Speaker: And so if you can't, if that pressure gradient decreases, now your filtration gradient decreases.
Speaker: You're not filtering as much at the level of the glomerulus.
Speaker: And the patients become oliguric.
Speaker: And when you look at the urine, it's very highly concentrated.
Speaker: It has a very high specific gravity or osmolarity.
Speaker: The urine sediment will oftentimes be very bland, so it won't show any signs of ATN.
Speaker: Creatine will be increasing sort of slowly every day.
Speaker: And if you're inclined, I don't believe in this necessarily, but if you're inclined to measure fractional excretion of sodium, it would be very, very low.
Speaker: And so this is venous hypertension causing a very intense perfusion mediated acute kidney injury, what some people would call sort of a pre-renal AKI.
Speaker: But this is not necessarily a problem with inflow.
Speaker: This is a problem with outflow.
Speaker: And unfortunately, many, many times, this physiology of this slowly creeping up, increasing creatinine,
Speaker: oliguric concentrated urine, bland urine sediment is oftentimes misinterpreted as this patient must have total body fluid overload but intravascular volume depletion, when in reality this is really all just venous hypertension and fluid overload that's causing this problem.
Speaker: And this has been known for quite a while, several decades.
Speaker: And we have animal models that have shown this on kidney biopsies and such.
Speaker: But Sergio, as you know, you're a big proponent of POCUS.
Speaker: POCUS has really allowed us to prove this physiology over time.
Speaker: As you know, we'll get into some assessments, but we've been able to prove with POCUS that you do get sort of impairment and drainage of these renal veins, of your portal veins, and that this is venous hypertension that's causing this problem.
Speaker: And so, you know, we can move past this idea of association
Speaker: and really show that this is a causation problem.
Speaker: So we established that it's extremely frequent and that this is not just a marker of severity, but can actually cause problems, organ failure, and lead to worse outcomes for our patients.
Speaker: So let's move on to what can we do at the bedside and start with the recognition of fluid overload and its assessment.
Speaker: You defined a little earlier fluid overload.
Speaker: Are there any other useful definitions you want to share with us before we talk about fluid status assessment?
Speaker: I think in terms of useful definitions, no.
Speaker: I think the percent fluid overload is a great way of being able to do that.
Speaker: I think obviously, you know, cumulative fluid balance and daily fluid balance is very important.
Speaker: I'm not going to say that they're not.
Speaker: There is some accuracy questions, I think, that go into all of those, you know, over time.
Speaker: But, you know,
Speaker: I think combining, you know, what is our cumulative fluid balance, how's our daily fluid balance been, combining that with these percent fluid overload definitions is really probably the best way to define this situation.
Speaker: How do you evaluate an ICU's patient fluid status?
Speaker: I think we all do it.
Speaker: Yeah, I mean, I think we all probably have many different ways that we do it.
Speaker: I think the most important thing, Sergio, if I can stress, is we have to get away from this sense of sort of conjecture
Speaker: or sort of feeling, you know, I feel like my patient is fluid overloaded.
Speaker: We need to be objective about it as much as possible.
Speaker: And fortunately, in the ICU, we have so many tools at our disposal that can help us move away from using intuition and objectively sort of
Speaker: deciding what someone's fluid status is.
Speaker: And that includes looking at things like fluid balance, daily fluid balance, looking at the weight trends and the percent fluid overload.
Speaker: That's the really great place to start.
Speaker: And then you can use other tools, other objective tools to help confirm
Speaker: what you're thinking and to triangulate information.
Speaker: It's not to suggest that any one definition or any one tool is perfect or infallible in all patients.
Speaker: We usually have to sort of triangulate assessing the volume by several different tools, make sure that they all sort of agree that
Speaker: and move forward from there.
Speaker: I'm still a big believer in physical exam.
Speaker: It is exceedingly uncommon for me to have a patient that is anisarkic and has 3, 4-plus pitting edema who has an IVC that's collapsible or has a CVP that's low or has a positive passive leg raise.
Speaker: So physical exam, I think, still remains very important.
Speaker: But I will say that I don't think we all agree on what these definitions of 1 plus, 2 plus, 3 plus are.
Speaker: I don't think there's a lot of good inner observer variability on this because many, many patients that I've been told...
Speaker: hey, this patient by my APPs or resident has one plus edema, you know, I go in there and I would say, you know, wearing my nephrology lens that this patient has, you know, four plus edema or anisarca.
Speaker: So we need to, we need to probably define these things a little bit better.
Speaker: But then, you know, as you know, right, we have things like passive leg raise, we have POCUS, we have chest x-rays, we have, you
Speaker: Things like CVP we can talk about, other forms of dynamic fluid monitoring like stroke volume variability, dynamic cardiac output assessments, all sorts of different hemodynamic monitors that look at this type of question is, is this patient fluid responsive or are they fluid overloaded?
Speaker: And so we need to think about using all of those different tools to help us recognize the problem.
Speaker: Is there anything you want to mention on labs?
Speaker: You know, I don't know that there is a lot.
Speaker: I mean, I'd be curious what your experience is.
Speaker: I don't think we have a real good data on any particular lab biomarker that's very reliable for this.
Speaker: I don't think that BNP or pro-BNP are particularly useful in the critically ill patient population.
Speaker: It's not to say that it's not, but I certainly don't use it that way, and I haven't seen any studies on its pro-
Speaker: predictive value to define fluid overload in a critically ill patient.
Speaker: And I'm not really aware of many other biomarkers along that pathway.
Speaker: Is there anything specific that you were thinking about?
Speaker: No, just wanted to get your impression.
Speaker: And I agree with you.
Speaker: BMP, I find it more useful when it's normal.
Speaker: And usually earlier in the context of my caring of a patient when they show up as opposed to a week into the ICU.
Speaker: Yeah, I agree.
Speaker: But I was just curious if there's anything out there.
Speaker: I know there's been a lot with biomarkers, but that's more renal function.
Speaker: And I was just curious if there was something that I was missing.
Speaker: But like you said, part of this for me is also having the...
Speaker: the intention of evaluating a patient as objectively as we can and utilizing all these tools at the same time to kind of inform our assessment.
Speaker: And then, like you mentioned, we can quantify it by just looking at the percent fluid overload because a patient who's been in the ICU for a week or two weeks did not gain weight because they're munching down McDonald's hamburgers, right?
Speaker: No, you're actually right.
Speaker: Yeah.
Speaker: You're only gaining weight in the ICU by getting external fixators attached to you or, you know, gaining fluid.
Speaker: You're not gaining muscle weight or fat weight in the ICU.
Speaker: That's for sure.
Speaker: Yeah.
Speaker: For those who like movies, I don't know if they saw this is the end.
Speaker: There's a very famous line of one of the guys caught in the rapture.
Speaker: They're trying to survive.
Speaker: And one of them is gaining weight.
Speaker: And there's like, oh, everybody's complaining.
Speaker: The
Speaker: The mother F is gaining weight and everybody else is losing weight.
Speaker: What is he doing differently?
Speaker: And he was, he was eating the secret stash of food.
Speaker: Yeah.
Speaker: But, you know, I think battling this problem of fluid overload, recognition is really half the battle.
Speaker: Um, you know, we have to look at this and, you know, I would say that, um, there are a few things I think that hand string us, you know, number one is, um,
Speaker: we have to insist that we have accurate I's and O's.
Speaker: We have to help the nurses.
Speaker: We have to design systems to help the nurses keep track of this easier and more accurately.
Speaker: Urine output is oftentimes viewed as this extra thing that people don't – it's just some excrement.
Speaker: Why do I have to measure this or why are people so caring about this?
Speaker: I mean cardiac ICUs are religious about documenting urine output.
Speaker: you know, all ICUs need to be religious about documenting urine output.
Speaker: It's not just because urine output can give you an insight into the development of AKI, which I'm, you know, obviously a big believer in.
Speaker: But if we're not measuring the urine output, where there's no way we're going to be able to keep a sense of, you know, how we're doing on an eyes and nose perspective, we have to look at the graphs, right?
Speaker: Every EHR system
Speaker: not only tracks ins and outs, but can actually display it for you on a daily basis on graphs, what my cumulative or what my daily net fluid balance is.
Speaker: And so if you have many days in a row where your net balance is positive,
Speaker: That's important.
Speaker: And I think a lot of times in the new era of critical care, at least in the US, where there's a lot of shift work, you know, people don't, we might not have people who have had three or four or five days straight with the patient where they know, oh yeah, three days ago, we were also positive.
Speaker: Five days ago, we were also positive.
Speaker: So when we're rounding and reviewing things, we have to look at those graphs, you know, more carefully.
Speaker: And then we have to use these tools.
Speaker: So we say, hmm, I think my patient might be fluid overloaded.
Speaker: They look like it on exam.
Speaker: Their I's and O's are positive for many days.
Speaker: Their weights are up.
Speaker: Now let's confirm this by some other mechanisms.
Speaker: Let's look at our POCUS.
Speaker: Let's look at our VEXUS.
Speaker: Let's look at our
Speaker: you know, our CVP.
Speaker: CVP is not predictive of who is fluid responsive, but it certainly can tell you what the venous pressure is like.
Speaker: And if the CVP is 15 or 18, then it's either fluid overload or your right heart has failed, you know, either way.
Speaker: So, you know, I think we have these tools that we can use, but we should use them to help confirm what we're already thinking by reviewing the data.
Speaker: Let's talk about fluid overload management.
Speaker: And we could start with some general concepts.
Speaker: I still recall the first time I heard somebody talk about de-resuscitation.
Speaker: And it was 20 years ago, Dr. John Marshall, who's a surgical intensivist from Toronto, he was talking about this concept.
Speaker: And I was like fascinated because at that point,
Speaker: we would just abide by the rule that to get well, you have to swell and we would give tons of fluid and then see what happens.
Speaker: But I know that that thought has evolved and now people talk about rows or other frameworks in terms of fluid management.
Speaker: And maybe we could start with a general overview of those concepts.
Speaker: Yeah, you know, I agree.
Speaker: I mean, I think there's a lot of debate about what's the right term, de-resuscitation, evacuation.
Speaker: You know, I personally like the word de-resuscitation because it implies that we have to actively do something as clinicians.
Speaker: Yeah.
Speaker: And I think what's clear is that in the absence of actively doing something, patients just gain weight.
Speaker: And I'll come back to that in a second.
Speaker: But we really have been a proponent for the last 10, 12 years with this concept of phases of fluid management or this ROSE model, resuscitation, optimization, maintenance, or stabilization, and then evacuation or de-resuscitation.
Speaker: And this was first, I would say, conceptualized by the Acute Disease Quality Initiative, the ADKE group of critical care nephrologists and intensivists that created a consensus around this concept.
Speaker: With the idea being that when our patients come in, in the first few hours or days, most of them are gonna be resuscitated.
Speaker: We should be rapidly increasing our volume status.
Speaker: But that at some point in the first 12 to 24 hours, resuscitation and optimization should end.
Speaker: And we should transition into a state of stabilization in which the entire goal is to no longer accumulate volume for the patient.
Speaker: That the patient may have developed and accumulated three, four, five, six, seven liters, but the goal at that point is to no longer continue to accumulate volume.
Speaker: And then at some point, you transition to a period of time after you've plateaued here to a period of time in which you're actively evacuating or de-resuscitating the patient's volume through various means.
Speaker: And so this model should look like a steep rise, a plateau, and then a fall with the various slope in the volume over time.
Speaker: What's clear is that if you're accumulating volume very quickly in this resuscitation phase and you continue to just rapidly accumulate volume because you can never transition out of the resuscitation phase and the patients just rapidly develop really profound fluid overload, those are the patients that are just likely going to die because you've never really been able to
Speaker: you know, exit your resuscitation phase.
Speaker: Resuscitation does not mean like transitioning to stabilization does not mean being liberated from vasopressors.
Speaker: It just means that you have achieved an appropriate fluid balance and the patient is no longer fluid responsive.
Speaker: You know, they have an appropriate cardiac output and such.
Speaker: But what's equally as seen is that if you do not transition into this plateau period, but you do sort of exit out of resuscitation, you sort of get into stabilization phase of illness,
Speaker: but that the fluid balance just sort of continues to go up and up and up, you know, very slowly throughout their course in the ICU.
Speaker: These are the patients that end up with a lot of morbidities like prolonged time in the ICU, disability, failure to recover, tracheostomy insertions, post-intensive care unit syndromes.
Speaker: And so really we need to transition very quickly.
Speaker: We need to actively make a decision as a team, okay,
Speaker: This patient is no longer needing resuscitation.
Speaker: Our goal for today, for tomorrow, for the next day, you take it on a day-by-day basis.
Speaker: Our goal is to no longer accumulate volume.
Speaker: We want ins equal to outs.
Speaker: And then at some point, we transition into taking that fluid away and giving the patient a net negative fluid balance.
Speaker: And I think that this sense, this concept of
Speaker: of phases of fluid can be really helpful and is something that I really advocate a lot, is that we need to actively have these conversations on rounds as to what our fluid balance goals are.
Speaker: The problem is, Sergio, is as you know, most people, at least in the U.S. and for that matter around the world,
Speaker: oftentimes discuss patients and review patients in this sort of systems-based approach in which we talk about the brain and then the heart and then the lungs, and then most people jump to the GI system.
Speaker: And so by the time they start getting into kidneys and fluid…
Speaker: our attention has sort of waned.
Speaker: And I think that's part of the reason why we end up not conversing and having clear discussions about what we want to accomplish as much as we should.
Speaker: So, you know, please continue to prioritize fluid management, you know, high up in your talk.
Speaker: And I think you'll in your discussion about the patients every day.
Speaker: And I think you'll see that a strategy focused on fluid management and fluid evacuation will improve your patient's outcomes.
Speaker: And clearly, as you stated, there is active interventions that we should be implementing in the R, the O, and the S phases to try to control this and improve the outcomes of our patients.
Speaker: But I would like to dive in further into the E or evacuation phase of our fluid management.
Speaker: When you get to that point and you say, okay, it's time to evacuate some of this fluid, I'm seeing some of the effects of fluid overload.
Speaker: And my patient now is probably being hurt by this fluid overload as opposed to help by the fluid we gave him in this phase of his disease.
Speaker: How do you start by setting some goals and explain to the team how you will monitor efficacy and safety?
Speaker: And then we can go into the actual interventions.
Speaker: Yeah.
Speaker: So first of all, we have to recognize, Sergio, that oftentimes given our patients have an obligate intake of, you know, say two and a half liters a day between meds and nutrition and other sorts of stuff, we actually oftentimes have to start thinking about active strategies to evacuate fluid, even when we just want to keep them net even.
Speaker: So even before we actually want them to be net negative, we oftentimes have to introduce some
Speaker: assistance to the patient to even just keep them net even.
Speaker: And I think this is a really important concept because many, many times, especially in ICUs that care for younger patient populations, be them pediatric patients or trauma ICUs, where
Speaker: The patients tend to have a skew younger.
Speaker: Even when the kidney function looks normal, the creatinines are low, the patients are urinating, it's very easy to overwhelm the kidney's ability to excrete salt and water.
Speaker: And I have, you know, you hear this all the time where someone says, well, I wasn't giving a diuretic because their kidney function was normal.
Speaker: I assume their kidney could do this on their own.
Speaker: And the reality is, is that even kidneys that are quote unquote healthy or normal,
Speaker: can easily be overwhelmed and will struggle to excrete that salt and water.
Speaker: I remind your listeners that every one liter bag of 0.9% quote unquote normal saline contains around 3.6, 3.5 grams of sodium.
Speaker: That's the same amount of sodium as in one and a half pounds of Ruffles potato chips.
Speaker: And you can understand that our kidneys are not designed to be able to excrete three grams of sodium in
Speaker: You know, especially if we give five liters of fluid in that day, you know, now we've given, you know, 20 grams of sodium.
Speaker: Our kidneys are not designed to be able to excrete all of that.
Speaker: And so oftentimes, even just to maintain a net even fluid balance, we need to start thinking about not only decreasing our intake, but how can we augment the output to keep the patient sort of net even.
Speaker: But switching directly to the evacuation phase, as you discussed, you know, most patients are going to end up needing some sort of help for this.
Speaker: It is the exception rather than the rule that spontaneous urine output alone can help evacuate the volume.
Speaker: The most common situation where spontaneous urine output alone might be able to do this is
Speaker: is like a patient who might be polyuretic when they're recovering from an ATN episode, or if we have demonstrably improved cardiac output.
Speaker: We've started somebody on ECMO or we inserted an Impella or something like that, and now cardiac output and perfusion has increased significantly.
Speaker: And the kidneys that, you know, might be able to then suddenly say, wow, I can get rid of all of this volume now.
Speaker: But it's really the exception rather than the rule that our patients are sort of spontaneously polyuretic and spontaneously net negative.
Speaker: So we have to establish, we have to discuss what is our goal going to be.
Speaker: is it the right time to start evacuating?
Speaker: And then if we're going to evacuate, how are we going to do this?
Speaker: In the overwhelming majority of patients, we should initially think about, you know, making them urinate more and potentially augmenting their urine output with diuretics.
Speaker: And then, you know, we'll consider other strategies for fluid removal if augmenting urine output is unsuccessful.
Speaker: In terms of helping them with active medical interventions, obviously, you already mentioned diuretic therapy.
Speaker: Can we talk more about this?
Speaker: Which drug?
Speaker: Is there really a difference?
Speaker: Is there a delivery mode, bolus versus continuous, that you prefer to use and why?
Speaker: And how we should think about these diuretics?
Speaker: And maybe we could start with something I've heard you say multiple times.
Speaker: Diuretics are not nephrotoxic.
Speaker: Yes, diuretics are not nephrotoxic in the classic sense of the word.
Speaker: So I just, you know, it's a matter of nuance here, but nephrotoxic agents are agents that are directly toxic to the tubules or the glomerulus.
Speaker: They directly cause cytopathies.
Speaker: Diuretics do not do that.
Speaker: Under very, very rare circumstances, most of our diuretics contain a sulfamoiny, and there will be some patients who can develop an interstitial nephritis due to our exposure to the sulfa of diuretics.
Speaker: But that is really very rare.
Speaker: I cannot recall the last time I diagnosed interstitial nephritis quite frequently in my ICU.
Speaker: I cannot recall the last time I have blamed a diuretic as the cause of that.
Speaker: So in the classic sense, diuretics are not nephrotoxic.
Speaker: But it is – I am –
Speaker: I recognize that when we give a diuretic, you know, that that can cause people to be a little bit nervous, especially when there is some change in creatinine concentrations that occur when we give diuretics.
Speaker: But I remind most of your listeners that, you know, as we give diuretics, if we're successfully removing volume from the patient,
Speaker: we're going to be lowering total body water.
Speaker: And since creatinine is dissolved in total body water, there will be a concentrating effect in that situation.
Speaker: So if we have three liters less water, but the same amount of creatinine, concentration will have to go up.
Speaker: And so we have to be a little bit more nuanced when we see the creatinine going up and we're giving diuretics.
Speaker: The creatinine could be going up because they have ATN and the kidney function hasn't gotten any better.
Speaker: The creatinine could be going up because we're concentrating the creatinine down.
Speaker: The diuretics are almost never to blame for the situation.
Speaker: It is very hard to have overdiures the patient.
Speaker: You will have other signs that you've overdiures the patient.
Speaker: So that's the first thing is diuretics are generally, you know, no nephrologist views them as nephrotoxic.
Speaker: We also have to remember that kidneys that are sick, in other words, whether they have AKI or even if they are sort of have subclinical AKI, kidneys that are unwell will need more diuretics.
Speaker: And there are some patterns of care that have been looked at that tend to suggest that as kidneys get less well, many ICUs prescribe less diuretics.
Speaker: And really, they should be potentially using more diuretics, not less diuretics.
Speaker: So generally, I teach that in the overwhelming majority of patients, diuretics are safe.
Speaker: They're very efficacious.
Speaker: I'm not going to stand here and tell you one type of diuretic, you know, furosemide is better than bumetanide or this or that.
Speaker: What matters is whether or not it's effective and meeting your goals.
Speaker: And we should be dosing the diuretics to achieve certain goals.
Speaker: We shouldn't just say, let's give Lasix twice today, 40 milligrams twice today, and then we'll follow up tomorrow and see how they did.
Speaker: No, we should be giving diuretics to achieve a certain goal.
Speaker: So the discussion on rounds should be, let's give Lasix, you know, to have our patient net negative two liters by tomorrow.
Speaker: And you start with, you say, I'm going to try, this is the first time we're exposing a patient.
Speaker: I don't, you know, I think they're going to need 80 milligrams of Lasix.
Speaker: And then you look and see how well did they respond to that 80.
Speaker: And that will then make a decision as to what your second dose or your third dose is going to be.
Speaker: There have been lots of studies that have looked at bolus versus continuous, Sergio.
Speaker: I think you probably are aware of these.
Speaker: That generally speaking, there is no clear benefit to a continuous infusion of a diuretic over high-dose bolus-dose diuretics.
Speaker: That being said, there are a couple of situations where I might lean more towards a continuous as opposed to a bolus, but these are sort of more nuanced situations, specifically surrounding mechanical circulatory support.
Speaker: If I give a bolus of a diuretic, the patient may make one liter of urine in an hour,
Speaker: And that might lead to some dynamic changes in intravascular volume as we are re-recruiting volume from the third space back into the intravascular compartment.
Speaker: And that could disrupt the function of maybe my mechanical circulatory support device or my ECMO device.
Speaker: And so sometimes, not always, but sometimes...
Speaker: in my ECMO patient, I might lean a little bit more towards a continuous diuretic just to sort of smooth out the hourly variation in the fluid removal as opposed to the sort of up and down that you get with bolus dosing.
Speaker: But outside of those sorts of more
Speaker: nuanced mechanical circulatory support devices, there's really no demonstrable difference clinically between bolus versus continuous.
Speaker: And certainly bolus is easier and generally speaking cheaper and generally speaking associated with a lower total daily dose of diuretic needs.
Speaker: In terms of monitoring your therapy, obviously, you're going to look at the urine output.
Speaker: You're going to continue to look at the weight and calculate the percent fluid overload.
Speaker: You mentioned CVP, obviously, as an example.
Speaker: Another tool that I have read about in the literature, and I wanted your input, is we talk a lot about fluid responsiveness.
Speaker: And when somebody's being resuscitated or somebody's fluid responsive, it doesn't necessarily tell you that clinically they need more fluid.
Speaker: But patients who are fluid overloaded technically would not be fluid responsive.
Speaker: So if you recover fluid responsiveness by any way that you measured, is that a good sign?
Speaker: Is that a good goal?
Speaker: You know, that's a great question.
Speaker: I'm not aware of any problems.
Speaker: of any prospective studies that look at the reacquiring fluid responsiveness as a endpoint for when you've evacuated enough fluid.
Speaker: Does that make sense?
Speaker: I'm not aware of any studies that look at that.
Speaker: I am aware, however, of a number of studies that have looked at the absence of fluid responsiveness
Speaker: as being a predictor of patients who are ready to have fluid removed.
Speaker: Does that make sense?
Speaker: Yep, perfect, yeah.
Speaker: So in other words, if you do a passive leg raise before you do a session of intermittent hemodialysis, for example, if they do not respond on the passive leg raise,
Speaker: they tend to tolerate their session of intermittent hemodialysis without generating interdialytic hypotension in the ICU, as opposed to the patients who have a positive class of leg raise at the start of hemodialysis are more likely to get interdialytic hypotension with fluid removal during dialysis.
Speaker: There's a few other studies that have sort of looked at that.
Speaker: So, you know, I don't want to get too far
Speaker: off tangent, Sergio, because we could, you know, I don't, I'm not espousing, I need to come back to have this discussion, but, you know, you could have a whole podcast on hemodynamic monitoring, right?
Speaker: And, um, and there's so many different tools like change in end tidal CO2, passive leg raise, um,
Speaker: cardiac output.
Speaker: But what I think is important for your audience to recognize is that when we are testing somebody's fluid responsiveness, we're not looking at whether or not their blood pressure is going up in response to the challenge.
Speaker: What we care about is whether their cardiac output is changing.
Speaker: Okay.
Speaker: And so when you test any of these things, you don't really want to test and just look at blood pressure because that does not predict patients who need more volume.
Speaker: Change in blood pressure does not.
Speaker: What matters is a change in cardiac output.
Speaker: So I tend to, I tend to just to finish that thought, I tend to look at some of these tools.
Speaker: For example, if we're diuresing somebody and we happen to have a dynamic, a pulse wave or stroke volume variability tool, hemodynamic monitor that we're using, and let's say we are taking fluid away by diuretics or by dialysis, and we see that the patient at the start
Speaker: had a stroke volume variability of 7%.
Speaker: And now we're taking fluid away and they've become more hypotensive and their presser needs have gone up.
Speaker: Well, if we have over-diurese them or if we've evacuated fluid too quickly with CRT,
Speaker: We should see, therefore, if it is related to low intravascular volume, we should see that the stroke volume variability is going up and that cardiac index and cardiac output are going down because preload is going down.
Speaker: And many, many times you'll see that the pressure needs might have gone up, but there's been a slightly, but there's been no change at all in any of these other objective measures of preload.
Speaker: And in that situation, I would say that we haven't overly done this too quickly, and we just need to keep taking volume away.
Speaker: Perfect.
Speaker: That makes a lot of sense.
Speaker: I would like to ask you about extracorporeal therapies, Michael.
Speaker: When do you bring them to the bedside for your patients with fluid overload?
Speaker: Okay.
Speaker: Yeah, this is a great question, because I think that increasingly I recognize that there is a little bit of controversy, and some of this comes around some of the question of timing of dialysis.
Speaker: But, you know, there is pretty good consensus globally within the nephrology community that we should not be starting dialysis with
Speaker: for the indication of fluid overload absent any other indication for dialysis.
Speaker: We should not be starting dialysis purely to manage fluid unless we cannot achieve
Speaker: our targets, our goals, of fluid balance goals with non-dialysis means.
Speaker: So we have no data that suggests that dialysis is superior to spontaneous or augmented urine output.
Speaker: And there has been some
Speaker: increasingly this sort of sense of, oh, I don't want to use diuretics.
Speaker: I'm just going to put my patient on dialysis.
Speaker: Dialysis comes with CRT, you know, but any form of dialysis comes with its own set of complications and risks.
Speaker: You and I discussed that in our most recent podcast about, you know, diala trauma and, and, and insults to patients that dialysis itself causes patients.
Speaker: And so we really should never introduce that unless we cannot achieve the goals for that patient by urine output or some other means.
Speaker: But if I've given high-dose diuretics, if I'm doing these things and I'm not reaching the goals that we need to reach, then it's very reasonable to introduce dialysis in that situation.
Speaker: Excellent.
Speaker: And as you mentioned with hemodynamic monitoring, renal replacement therapy could be another series of podcasts.
Speaker: And we did discuss this topic earlier in a previous episode.
Speaker: So I will definitely link that episode to our show notes so our listeners can refresh their memory on that.
Speaker: As we move towards our closing moments,
Speaker: Michael, could you summarize some pearls and pitfalls about fluid overload for our clinicians before we move to non-clinical questions?
Speaker: Yeah, well, can we start with the pitfalls?
Speaker: I mean, I think the pitfalls is that we don't recognize this.
Speaker: We assume that it's cosmetic instead of being causative of a lot of bad outcomes for our patients and that we have a lot of, I think,
Speaker: pass down a generational dogma that leads us to be less aggressive than we should.
Speaker: There is this dogma that we swell to get well.
Speaker: Well, we need to probably think about, we need to, as one of my former pharmacy residents said, we need to pee to be free of the ICU.
Speaker: And we need to give diuretics.
Speaker: We need to think about using diuretics.
Speaker: I think most intensive is due, but we need to not be afraid of diuretics as a means to achieve fluid goals.
Speaker: From a Pearl's perspective, you know, I think we covered a lot of them.
Speaker: The first is, you know, make sure that you're objectively assessing the volume.
Speaker: Use the tools that you have available.
Speaker: Don't use intuition.
Speaker: Talk about it every day.
Speaker: Establish what every day's fluid balance goal is going to be once you leave that first 12 to 24 hours of resuscitation.
Speaker: It needs to be a key part of the conversation.
Speaker: And then, you know, think about how we're going to evacuate and monitor how well it's being tolerated.
Speaker: I usually show a graphic that I created where it's sort of a circle.
Speaker: We have to, every day we start at the top of the circle where we're strictly monitoring I's and O's and measuring urine output and documenting daily weights.
Speaker: Then we need to discuss every day and establish what is our daily fluid balance goal.
Speaker: We need to stop excessive IV fluid administration because we talked about how much mission creep there is in IV fluid exposures.
Speaker: We, or at least decrease excessive IV fluid administration.
Speaker: And then we need to stop and ask ourselves, is the patient fluid overloaded and are they ready for fluid removal?
Speaker: If they're not ready for fluid removal or they're not fluid overloaded, well, then we just stop and go back to the first step of measuring everything and talking about this every day.
Speaker: If they are fluid overloaded and they are ready for fluid removal, then we probably need to use vasopressors a little bit more liberally.
Speaker: What I mean by that is that we should prioritize a return to uvilemia and a liberation from the ventilator before the
Speaker: prioritizing liberation from vasopressors.
Speaker: And I think we oftentimes, as intensive as many of us think, oh, let's get off the pressors as quickly as possible.
Speaker: It really should be a race to liberate from the vent, which oftentimes needs us to be uvolemic, than race to liberate from pressors.
Speaker: And then we need to remove volume by some means and monitor for tolerance.
Speaker: You know, how is this patient tolerating this fluid removal?
Speaker: And then sort of keep going back and going through that every day, that same sort of workflow.
Speaker: Excellent.
Speaker: You've been a guest on the podcast before, so you know how we roll, Michael.
Speaker: And I would like to close with a couple of questions unrelated to the clinical topic.
Speaker: Would that be okay?
Speaker: Absolutely.
Speaker: So the first question, it relates to any books that have impressed you since we last spoke on the podcast or any specific music album that you're really into these days.
Speaker: Good question.
Speaker: Book, I will say a book that I'm very fascinated about, but I have not finished yet, is a book called Think Again.
Speaker: I'm trying to remember who the author is.
Speaker: I want to say Adam something or other.
Speaker: Adam Grant.
Speaker: Adam Grant.
Speaker: Yeah.
Speaker: Think Again.
Speaker: It is
Speaker: not light reading.
Speaker: It really challenges us as clinicians, I think, and as scientists to, you know, really think through things and understand how we think in our daily lives.
Speaker: So I really like that.
Speaker: I look forward to hopefully making more progress with that.
Speaker: Music.
Speaker: I've been listening a lot recently to the most recent, um,
Speaker: album by Mumford & Sons called Rushmere.
Speaker: I've enjoyed that quite a bit.
Speaker: Excellent.
Speaker: So we will definitely check them out and also share them in the show notes.
Speaker: And Think Again by Adam Grant.
Speaker: I agree.
Speaker: It's a great read on how we think and how the true sign of intelligence is being able to change our opinions based on new information.
Speaker: And reading that book, what struck me
Speaker: is that our colleagues and myself as physicians tend to think about our group as being scientists, yet we don't behave like true scientists.
Speaker: I completely agree.
Speaker: I completely agree.
Speaker: And you'll probably see the politician analogy and the preacher analogy.
Speaker: That seems to be much more common among physicians and clinicians than true scientists who are really humble and questioning what they believe, right?
Speaker: Yeah.
Speaker: Right.
Speaker: And I probably have sounded a little preachy and politic-y in going through this topic.
Speaker: But, you know, I think I've, I've hope, I hopefully have stimulated some ideas that, that, that this is really what I'm saying has really come out of scientific understanding that has evolved over the course of the last 30 years, that we really have gone back and looked at some of the assumptions that we made about fluid and what we had been teaching each other, you know, for decades in medicine.
Speaker: And that we have really changed this over the course of the last 10 to 20 years and have really evolved, I think, in a new paradigm.
Speaker: But that doesn't mean we shouldn't be continuing to question what we've done on this topic.
Speaker: Absolutely.
Speaker: The second question relates to the same idea of learning from our experiences and learning from failure.
Speaker: So if you could share with us your favorite failure and what lesson did it teach you?
Speaker: Well, if it's okay, I'm going to actually share maybe two.
Speaker: The first is that, you know, as it pertains to this topic specifically, I will say that when I finished fellowship and, you know, became and started my life as an attending 16 years ago,
Speaker: I very much did not prioritize return to uvilemia.
Speaker: It was in the era where everyone was swollen, and we didn't really think about that.
Speaker: And it was my own failures of my patients not getting better that really asked me to question sort of what I was doing.
Speaker: Some conversations I had with some colleagues of mine who worked at LTACs, you know, that really got me thinking more and more about, you know, how do we accelerate the removal of fluid and does that improve our patients outcomes better?
Speaker: And so my own failures stimulated my interest in this topic and my clinical care has improved greatly as I've evolved my position.
Speaker: But my other failure is, you know, I would say that we've all had patients that stick with us.
Speaker: Oftentimes, either really good outcomes that were unexpected or really unfortunate and tragic outcomes.
Speaker: And I think the tragic outcomes that, uh, where we failed, um, uh, or modern medicine failed, maybe not, I didn't fail, but just the Royal we failed to, um, you know, uh, foster and allow that patient to recover.
Speaker: Um, it really has taught me that, you know, we don't, we need not only humility, um,
Speaker: and a willingness to accept when we're wrong and re-explore our diagnostic or our diagnoses and make sure we don't have diagnostic errors.
Speaker: But we also need to accept at some level a degree of helplessness that we as intensivists have things that we can do, but there's many things that we can't do.
Speaker: that we can't make our patients get better.
Speaker: We can't make them survive.
Speaker: We can try to create the environment in which their body can recover, but we can't make them actually recover.
Speaker: And this sort of helplessness is an idea that I use and a framework I use a lot when I talk to families and to say that, you know, we're going to work very hard to create that environment.
Speaker: We're going to work to resolve fluid overload and provide nutrition to your loved one.
Speaker: We're going to try to get off sedation and help their strength improve.
Speaker: But I don't have any medicine that can make them get better.
Speaker: I don't have any medicine that can make them heal themselves.
Speaker: And we have to accept that there is a level of helplessness and we should not feel angry or disappointed or carry trauma with us as physicians for cases that we did what we could, but we were helpless to really allow them to survive.
Speaker: I think that's a perfect place to stop, Michael.
Speaker: I really want to thank you for sharing your expertise and your time with us in the podcast.
Speaker: I'd love to have you on as a guest.
Speaker: We'll definitely invite you back and maybe you already suggested a great topic.
Speaker: But as always, thank you so much for sharing your expertise.
Speaker: I learned a lot and really enjoyed the conversation.
Speaker: Well, Sergio, it is always a pleasure.
Speaker: You are a fantastic interviewer and such a knowledgeable colleague.
Speaker: I always learn so much from you whenever you and I get a chance to talk as well.
Speaker: And thank you so much for the honor of being a repeat guest on this podcast.
Speaker: Absolutely.
Speaker: Thanks.
Speaker: Thank you for listening to Critical Matters, a sound podcast.
Speaker: Make sure to subscribe to Critical Matters on Apple or Google Podcasts and share with your network.
Speaker: Sound's transforming the way critical care is provided in hospitals across the country.
Speaker: To learn more, visit www.soundphysicians.com.
