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SCCM Pod-458 CCM: Association of Catecholamine in Patients With Septic Shock

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Catecholamine is used in patients with septic shock to augment hemodynamics and achieve goal mean arterial pressure. Ludwig H. Lin, MD, is joined by Gretchen L. Sacha BCCCP, PharmD, to discuss this retrospective observational study to evaluate the associations of catecholamine dose, lactate concentration, and timing from shock onset at vasopressin initiation with in-hospital mortality. (Sacha G, et al. Crit Care Med. 2022;50:614-623). Dr. Sacha is a critical care clinical specialist at Cleveland Clinic in Cleveland, Ohio. This podcast is sponsored by Sound Physicians.

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Category: CCM Podcast


This podcast is sponsored by Sound Physicians, the employer of choice for critical care physicians, where we seek to transform acute episodes of care. At Sound Physicians, we ensure physicians have the time and resources needed to deliver compassionate care that measurably improves quality and lowers the cost of healthcare for patients in the communities we serve. For more information, please visit

Dr. Lin: Welcome to another edition of the Society of Critical Care Medicine’s iCritical Care Podcast. I’m your host, Dr. Ludwig Lin. Today, I will be speaking with Gretchen Sacha, BCCCP, PharmD, and we are talking about the article, “Association of Catecholamine Dose, Lactate, and Shock Duration at Vasopressin Initiation With Mortality in Patients With Septic Shock.” To access this full article, visit Dr. Sacha is a critical care clinical specialist at Cleveland Clinic in Cleveland, Ohio. Dr. Sacha, welcome and thank you so much for doing this. Before we start, do you have any disclosures to report?

Dr. Sacha: I do not. None regarding this content.

Dr. Lin: Okay. Good. Let’s get started because this is a great topic and I’m sure we will have lots to discuss. The most basic question for you is, how did you and your group decide to focus on this clinical topic?

Dr. Sacha: Great question. Also, thank you for having me. I’m so excited. How we came up with these questions actually goes back to when I was a pharmacy resident at the Cleveland Clinic. At that point, my research project focused on determining predictors of response to vasopressin in patients with septic shock. We developed this database to answer this question, and this database and the question that we were looking at really opened my eyes to many different questions that we could look at with vasopressin. I want to briefly say what we found in that study was that we were looking at patients who had a response to vasopressin’s initiation. We found that about half of patients who received vasopressin had a positive hemodynamic response to its initiation, meaning their MAP improved and they did not require further up-titrations of their catecholamine doses.

What’s important is that we found that this was associated with nearly a 50% reduction in the odds of ICU mortality. What I take from this is that it showed us there was a subset of patients who respond favorably to vasopressin, and this is associated with improved mortality. But it left us with many questions, like who responds and why did they respond? So we looked at this and multiple other questions.

What led to this particular evaluation is that we paired all of that with the findings that I’m sure we all know—and maybe, if you’re like me, love—which are from the VASST study. We know that VASST did not reveal an improvement in clinical outcomes when looking at norepi compared to vasopressin with norepi, but they did find that, in the subset of patients who were deemed to have, quote, less severe shock, which is what they defined as a catecholamine dose at randomization less than 15 mcg per minute, they found that those patients who received vasopressin had improved 28-day and 90-day mortality. They also saw the same thing in those who had a lactate less than, I think it was 1.4 at randomization. Although these were just subgroup analyses, they really made me and my study team think about it and wonder if timing was one of those pieces that mattered when it came to vasopressin’s utilization. So this is what led us to studying it further.

Dr. Lin: Can you tell us what you found? How did you design your study and your conclusions about it?

Dr. Sacha: Absolutely. What we wanted to look at specifically was the association between different timing variables in vasopressin’s initiation and mortality. But first, the question is what timing should we look at? We thought, when it comes to septic shock, especially clinically at the bedside, because we wanted it to be applicable to the bedside provider, timing can be thought of in different manners. You can think of the actual temporal time from shock onset or how many hours have passed since they were diagnosed with shock to when they were initiated therapy, here vasopressin, or how severely ill they are. Like with VASST, how are they progressing from a vasoactive needs standpoint? What dose of catecholamines are they requiring or what’s their lactate concentration?

We set out to examine the association between each of these three factors on mortality: timing, catecholamine dose, and lactate concentration. We set up this observational study that included patients throughout our Cleveland Clinic enterprise, eight included hospitals. We looked at just noncardiac ICUs between 2012 and 2017. We utilized our screening criteria and our definition, utilizing the CDC definition for an adult sepsis event. Patients had to be receiving vasopressin, so all patients received vasopressin. Then we evaluated these three variables of interest: norepinephrine dose, lactate, and timing, and we created three different models to evaluate their association and adjust for known confounders and providing predictive mortalities across the way, which we’ll talk about.

We included over 1600 patients in this evaluation, found a very wide range of timing of vasopressin initiation. But on average, patients were initiated on vasopressin when the norepinephrine equivalent dose was around 25 mcg per minute, which is what we see in VASST and when they initiated it, and when the lactate concentration was 3.9 millimoles per liter, and then within about five hours from shock onset. Now, breaking each three of these down briefly, when we looked at the norepinephrine equivalent dose, we found that the odds of in-hospital mortality increased by about 20% for every 10 mcg per minute increase in norepinephrine dose at vasopressin initiation. There was a cap, so this was only up to initiation dose 60 mcg per minute. After that, I like to say it was probably futile and they didn’t need to add vasopressin at that point.

When we look at lactate and timing, it gets a little bit trickier because there was an interaction between these two variables. To evaluate their association, we have to look at them together. There was actually no association detected between timing of shock onset and mortality, but there was a linear association with lactate, again corroborating what we’ve seen in prior studies. When vasopressin was initiated two hours from shock onset, the odds of mortality increased by 12% for each unit of lactate concentration increase. So, every time the lactate went up one millimole per liter, mortality increased by 12%. The same was found when we looked at different timing. We had to break this down in timing because of the interaction. When initiated within 12 hours from shock onset, mortality increased by about 18% with each increasing lactate concentration.

In a nutshell, that’s what we found, lower mortality rates when vasopressin was initiated earlier and earlier, meaning lower norepinephrine equivalent doses and lower lactate concentrations, again corroborating the findings from the VASST study that we talked about.

Dr. Lin: Right. Wow. That seems pretty significant. How do you feel clinicians should use this information?

Dr. Sacha: I think that this is telling us that if a clinician is standing at the bedside and deciding, this patient needs vasopressin, because again, we can’t compare this to no vasopressin use because that’s not what this study looked at. It looked at only those who were going to receive vaso. If you’re even thinking, I need to initiate vaso on this patient, or, I think this patient is going to be one who requires vasopressin, you should start it earlier. Timing of its initiation really does matter. So in my mind and how I’m going to practice and what we’re trying to implement at our institution is recommending initiation of vasopressin when the norepinephrine dose is around 10 mcg per minute. I utilize the norepinephrine dose because I think it’s the most easy variable of the three that we looked at to apply at the bedside. I think it’s the easiest for clinicians to talk about and utilize, but you could also consider initiating vasopressin when the lactate concentration is around or below 2.3.

Dr. Lin: Okay. Those are really good guides. Let me ask you a couple of questions about this. One thing that came to my mind when you were talking about the study design is that it’s a retrospective study. So these are all associations rather than, for example, knowing that intervening at a certain time point changes the outcome. Is that correct?

Dr. Sacha: Correct, no causality. Correct, it’s just an association.

Dr. Lin: Right. I would think that some people would find it, well, I don’t know what the word is, I think some people would rather know that there is a causality involved, rather than just that some people just weren’t meant to get better. If somebody asked you that at a conference, what would your answer be?

Dr. Sacha: I think what I would say is that I acknowledge and accept the limitations of this study. I totally agree with that. We did the best that we could with our resources to account for as many differences in characteristics of these patients because we know some patients are going to receive vasopressin at different time points because of differences in their characteristics. We had accounted for as many as we could in our model. So when I say these associations, they have been adjusted for factors like age, gender, race, weight, even things like immune suppression and ICU location, because we treat patients differently in different ICUs. Whether or not they utilize stress-dose steroids, their fluid balance, and severity of illness, we utilize the SOFA score and APACHE-III score to account for differences in severity of illness. I would say that I acknowledge the limitations, but we adjusted for as many known confounders as we could in our models, and these results are reflective of that.

Dr. Lin: Got it. Another question I have for you is, I think one of the sentences in the article mentioned that people who were intravascularly depleted would respond differently to the initiation of vasopressin. Does that sound familiar?

Dr. Sacha: Yeah. We always wonder if there are differences in response based on many factors, including fluid balance. I might not have mentioned it, but that was another variable that we accounted for in our models. We looked at both fluid balance at the time of vasopressin initiation and what their fluid bolus receipt volume was in a specified time period around when vasopressin was initiated. I agree that that may impact the way they respond and its use, but it’s something that we accounted for as well.

Dr. Lin: I was curious about that. I would personally like to have a little bit more information about that part of your study. How did you guys determine that somebody was, for example, quote-unquote, under-resuscitated or potentially hypovolemic? Or were you looking more at the total amount of resuscitation volume that they had received prior to initiation of vasopressin?

Dr. Sacha: We looked at both. We looked at how much volume in an mL standpoint or liters did they receive before vasopressin initiation, and we looked at the fluid balance, and the way that we looked at fluid balance was just a continuous variable. What was their fluid balance, positive or negative? We looked at the documented ins and outs in the electronic medical record. We have Epic here at the Cleveland Clinic, so we used Epic and took their entire cumulative fluid balance at the time that vasopressin was initiated. Everything the nurse charted as ins and outs, we combined that together to get what their fluid balance was. Now, I will be the first to admit that the electronic medical record recording of ins and outs, we all know has its limitations, but it was the best that we could utilize and come up with for this variable.

Dr. Lin: Okay. That is a great answer to my question. My follow-up question for you is: We have available to us more and more technology, and there are some clinicians and, for sure, researchers, who really advocate advanced ways of real-time assessment of a patient’s intravascular volume, filling volume. Did you guys look at any of those, by any chance? Do you have any thoughts about that part in terms of how it relates to vasopressin?

Dr. Sacha: Yeah, I think, for our study first, it wasn’t something that we were able to account for. Even if we’re talking about other markers, like you might be referring to, even, say, cardiac function or fluid responsiveness, things like that, markers like that are not something that are captured within our medical record right now. Every data point that we captured for this evaluation was captured directly through the electronic medical record. There was no manual data collection. Some of those less discrete variables we were not able to capture, unfortunately. I do think that I agree this should be, for lack of better terms, the way of the future, in which we’re able to capture some of those more complex hemodynamic variables that we don’t necessarily know right now whether or not they impact the benefit of vasopressin or any of our other catecholamines but should be looked at further. I definitely think that this is something that should be incorporated in the future as it’s able. But when we talk about these large observational studies that rely on electronic medical records, I think at this point in time it becomes very difficult to capture those pieces.

Dr. Lin: Very true. And there are so many different out there, in terms of new technologies. I think the proof is in the pudding and we’ll see which one actually does wind up working. But in the meantime, it sounds like you can start taking the most common variables that most clinicians will have available for their clinical decision-making. That makes a lot of sense. Let me ask you another question. You talked about how you looked at a lot of different types of clinical scenarios in septic shock, different types of ICUs. You are a pharmacist. We, as intensivists, cannot live without you guys. We totally live by your recommendations. Do you ever have scenarios where you consider it a strict contraindication to vasopressin administration? Or are there clinical scenarios where you would not recommend it as strongly?

Dr. Sacha: There are some that I consider, I guess it would depend on and go back to the type of shock that the patient has. When I think of situations in which I would avoid vasopressin, it’s patients who truly have some type of cardiac compromise, particularly left ventricular dysfunction is the situation in which I might be more hesitant or cautious to utilize this agent because it is pure afterload, it increases afterload in a more pure manner than our other agents like norepinephrine or epinephrine. Patients that have that cardiac dysfunction, it can be detrimental potentially to continue to increase our systemic vascular resistance and increase our afterload. Those are the scenarios in which I start to think a little bit more about my approach to my vasoactive agents and would be a little more cautious with the utilization of this agent. I think that’s what, I’ll use the point of individualizing our pharmacology for our patients with any type of shock state is going back to, what type of shock do they have, how is this specific patient responding, how are their hemodynamics and their cardiac function, to design the correct regimen for them.

Dr. Lin: Okay. What I’m hearing from you is that in patients with cardiogenic shock, you would definitely be a lot more careful and think about red flags in that patient’s clinical scenario to make you not want to use vasopressin.

Dr. Sacha: Correct.

Dr. Lin: If it’s a patient with septic shock, even with cardiac comorbidities, would you feel okay about vasopressin?

Dr. Sacha: Yeah, I guess it would depend on the specific scenario, but the presence of a cardiac history in most capacities, as I said, wouldn’t preclude me from utilizing this drug. It would be, how is their cardiac function in this moment? If their LV is functioning fine and you think they have no systolic dysfunction, then I would say it would be fine to utilize vasopressin in that scenario. It would require acute real-time monitoring to determine.

Dr. Lin: Sounds great. Ties back into the whole picture, which is what we do. So yes, thank you for that answer. You and I had talked before we started about some of the changing economics of the different medications that we have available. How do you think economics factor into the way we utilize different vasopressors in the setting of septic shock? Does that influence or impact the way we think about patient care?

Dr. Sacha: Yeah, I think this is a really great question. I’m assuming if someone listening in is a vasopressin lover like myself, they’re very familiar with the fact that the price of vasopressin has really exponentially and unfortunately increased over time. It was rebranded by Par Pharmaceuticals in 2014. Since that time, its cost has increased over 50-fold from, I think it was about $4 per vial, up to, now I recently asked one of our buyers here, it’s over $200 per vial. So it’s really a significant increase.

Dr. Lin: Oh, my gosh.

Dr. Sacha: My thoughts exactly. I know that this has resulted in many institutions looking at vasopressin use and designing cost savings initiatives. We’ve done this too, internally, as well. In spite of this, we recently evaluated this. I’ll put in another little plug. In the same issue of Critical Care Medicine, we looked at the rebranding of vasopressin and its use despite its increase in costs and found that, despite the cost increase, the use of vasopressin for vasodilatory shock continues to increase. From our conclusions, vasopressin has an inelastic demand or price inelastic demand, meaning that demand does not decrease as its price continues to increase. What I think, when it comes to vasopressin, is that I would argue that drug cost is not as important as it might be perceived.

In, I think it was 2020, a few members of my study team conducted a cost-effectiveness analysis of second-line vasopressors for the treatment of septic shock. They looked at vasopressin, they also looked at ang 2, and then just utilizing norepinephrine alone. What they found was that vasopressin utilization was actually the most cost-effective strategy of the three. So rather than just continuing to increase that dose of norepinephrine and thinking you might be saving drug costs and avoiding vasopressin use, vasopressin use was actually associated with lower total ICU cost and higher ICU survival. I will also say that, despite all this, thank God, the cost of the drug is finally starting to come down, not significantly and not quickly, but I do hope and anticipate that it’s going to continue to go in the right direction. So I think economics in this discussion is really important. But with all of these studies that we’ve done, it actually hasn’t changed my practice now. I feel comfortable recommending it earlier, despite that high drug cost because it appears to be the most cost-effective solution.

Dr. Lin: That’s really good to know that, despite the really inappropriate costs of vasopressin, even with that, the amount of savings in ICU utilization justifies its use. I’m glad that we talked about that. I think that’s important for all of us to know. I had some questions about the physiology of vasopressin that I was hoping we could discuss briefly since we’re on the topic of everything about vasopressin. We obviously use vasopressin to manipulate the renal system, using its impact on sodium and water management. In your study, did you see any of these volume changes or electrolyte changes from vasopressin use or are those effects seen at a different dosage level for vasopressin?

Dr. Sacha: What you’re referring to is vasopressin’s V2 receptor-mediated actions in the renal collecting ducts. Again, like you said, while it results in free water resorption, which is its action, as the hormone in our body is also known as antidiuretic hormone and, because of this, it can result in hyponatremia. But thinking about this, it actually wasn’t something at the forefront of our minds when we designed this study. I will be honest, it wasn’t an outcome that we looked at. If I recall, in VASST, this occurrence is actually really rare in the trials that looked at vasopressin for specifically vasodilatory shock at these lower doses. I think it was only about one, maybe one patient in the VASST study who developed hyponatremia. So, because the risk appears to be so low, particularly at this dosage and this regimen and in this shock state, it wasn’t an outcome that we specifically sought to evaluate. When we’re looking at utilizing it as a vasoconstrictor and in someone with shock, it actually might be attractive to have that increased free water and maybe increase your preload a little bit and assist in that manner, but I will admit it wasn’t something that we looked at or had the capacity to, because it hasn’t been seen prevalently in the septic shock trials.

Dr. Lin: Thank you. That’s really good to know. Again, I think we should all be aware, but what you’re saying is these are not clinically significant. I think that’s really good information for all of us. Another clinical use of vasopressin is in the ACLS algorithm, of course. For example, I was taught that using vasopressin as a bolus induces this momentary increase in coronary perfusion during PEA arrest, so that is actually quite helpful. I was wondering if that effect could be clinically significant in septic shock patients or are the vasopressin concentrations so different in terms of the infusion rates versus that bolus in the ACLS protocol that these are totally different phenomena?

Dr. Sacha: I think this is an interesting question and insight that, again, I will admit wasn’t something that we had considered when writing our manuscript in developing this project. So, just thinking out loud, as a vasoconstrictor, vasopressin will increase your diastolic and mean blood pressure, therefore potentially increasing coronary perfusion pressure, like you’re mentioning. But this is what’s so funny to me about, I say vasopressin, but it’s really many drugs that we use in the ICU and how much we really don’t actually know about it, because if I recall right, I’ve looked at and read some animal models of vasopressin that showed vasopressin can have a concentration-dependent coronary vasoconstriction and potentially reduce coronary perfusion. So I think it goes back to telling us how little we really know about the nuances of these drugs. But I will say, I think it’s a really great thought but it wasn’t something that our study was able to assess or designed to assess. I think that, since all our patients receive vasopressin at this relatively lower dose, I’m assuming coronary perfusion is probably not a contributor to our mortality findings at least but definitely something to think about as we move forward with additional vasopressin studies.

Dr. Lin: Thank you. Like I said, we’re just talking about all things vasopressin, so I think it’s great. I love it. Speaking of genetic heterogeneity, I had a follow-up question for you about this study design. I already mentioned this before. It’s a retrospective study. Do we know why some of these patients in the Cleveland Clinic database had initiation of vasopressin at a lower norepinephrine concentration? Was there something else about their clinical picture at the time that made the clinicians involved decide to do that? A follow-up question to that is, could something else about those patients have had confounder characteristics that separately impacted them without any outcomes?

Dr. Sacha: These are the discussions and the thoughts that I have in my head all the time. To answer the first part of the question, why was there such variation in practice, actually, the answer to that is we do have such variation in practice, in general for a couple of reasons. One, we have this dataset of patients, including providers from our large academic medical center, the main campus, and then our regional facilities too. So there are different providers among all the institutions and they all have their own manner of practicing. We did not, for the majority of the time frame of this study, have any recommendations on when to start vasopressin. It left it completely up to the provider, which I think is really beneficial for this study design because if it’s just the provider determining, I like vasopressin and I started it earlier, or another saying, I don’t think it works, I’m going to start it later or not at all, I think that gives us a little bit more of a random sampling of occurrence, which I think is beneficial in this study.

I will also pair that with: There was a little bit of a practice change where, in late 2016, we did recommend to hold vasopressin and restrict it until the norepinephrine dose exceeded 50. That’s also why we saw some later initiation of vasopressin in this sample. Again, because that was a practice change and not a difference in patient severity, that also helps us with our study design and lessens the potential confounding.

But with all of that said, underlying all of that, is the potential that vasopressin could be started earlier because they were sicker or started later because they thought it was futile. I think there are a lot of things that could be occurring, like we talked about. We mentioned that we accounted for as many known confounders as we could, but that leads to the second part of your question, which is, there are very likely unknown confounders that we couldn’t account for, such as what you alluded to, which is genetics or other things like cardiac function, which we didn’t have echo data on all of our patients to be able to account for this. I think there are definitely unmeasurable confounders that should be thought about and should be the focus of future trials, looking into and teasing out a little bit more. We know timing matters, but why and who responds to vasopressin and why did they respond to vasopressin?

Dr. Lin: That sounds really good. You’re talking about future studies and I know from our conversation that you definitely consider yourself a vasopressin aficionado and you’ve done these great studies already, so of course I have to ask you, what are the different questions that you would like to continue to ask about vasopressin and its use in septic shock?

Dr. Sacha: Yeah, it’s great. I don’t know if I would refer to myself as an aficionado, maybe more a fanatic or very passionate. I’m just someone who happens to study it. But I agree. I think that this stems into a lot of need for future evaluation. So I acknowledge that this is a retrospective study. We need stronger data that can show causality. I think that should be something that is thought about when we move forward, how do we make this data more robust and a stronger study design? Is this a randomized control trial or something like that? I think that’s definitely something that should be thought about further. I definitely would like to continue looking into the timing aspect. I think we don’t really know what timing matters the most. So we looked at these three variables, but are these the right variables, and which one matters most? Is it norepi dose? Is it lactate? Is it actual time? So I think that there are definitely a lot of further questions that can be teased out from these data. And then, of course, like I mentioned before, just continuing to tease out who responds to vasopressin and why did they respond, is something that should be the focus of future trials.

Dr. Lin: Very cool. I look forward to all that. I feel like we’ve been talking a lot about using cutting-edge technology to help us make decisions and talking about this entire aspect of timing. For example, even one of the criteria you use is a norepinephrine equivalent dose of vasopressors. All of this makes me feel like this is a perfect way to utilize something that is, I would say, somewhat controversial in modern healthcare and actually in the ICU, which is electronic health medical systems, informatics, artificial intelligence. But those things could really help us in terms of making sure that we are timing the vasopressin initiation correctly, for example. It sounds like you work pretty closely with Epic at your institution. You are also a pharmacist who deals a lot with automation. Tell me your thoughts about this.

Dr. Sacha: I think it’s interesting when you talk about future state, because you start to get into that mode of like, I can’t even fathom what would come next, because we already have such great technology, so how can it advance? But I think the future is so bright and it gives me so much excitement. I think of how we can integrate that electronic medical record, like you’re saying, and integrating things like closed loop titration and closed loop systems where you have such technology where you have your pumps connected to the telemonitor and you see the patient’s MAP is low and it increases their blood pressure, or it increases their vasopressor dose, or it meets X threshold and then it initiates another drug for use. I think that the future is limitless, and I look very much forward to seeing what closed loop titration and that integration with the EMR a little tighter than we have it now is going to hold for us. That’s what I think I’m most excited for.

Dr. Lin: Very cool. I look forward to that. I would like to ask you if you have any additional concluding thoughts about this topic before we draw this podcast to a close.

Dr. Sacha: My only conclusion, and what I hope that the reader and the listeners of this podcast take away from this, is I think that maybe timing matters, timing of our interventions. We know that timing of antibiotics matters. I think that there’s no debate there. So I hope in the future that this article and this research is able to stem at least some people thinking, hmm, timing of antibiotics matters, but timing of other interventions in septic shock matters too. And if we’re going to use vasopressin, we should use it right away. I encourage people to read this article, apply it to their practice, and think, do I agree? Should vasopressin be started earlier? Because I definitely am a proponent of, we’re going to use it, let’s start it earlier.

Dr. Lin: Great. I think that’s a really nice way to form a nice conclusion about this entire topic for all of our listeners and for me as well. I really want to thank you, Dr. Sacha, for joining us for this and for providing us with your thoughts about this. Thank you for doing the study. Thank you for posing these questions. I would like to say that this is going to conclude yet another edition of the Society of Critical Care Medicine’s iCritical Care podcast. Thank you all for joining us.

This podcast is sponsored by Sound Physicians, the employer of choice for critical care physicians, where we seek to transform acute episodes of care. At Sound Physicians, we ensure physicians have the time and resources needed to deliver compassionate care that measurably improves quality and lowers the cost of healthcare for patients in the communities we serve. For more information, please visit

Ludwig H. Lin, MD, is an intensivist and anesthesiologist at Sutter Hospitals in the Bay Area of Northern California and is a consulting professor at Stanford University School of Medicine, where he teaches a seminar on the psychosocial and economic ramifications of critical illness. Join or renew your membership with SCCM, the only multiprofessional society dedicated exclusively to the advancement of critical care.

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Knowledge Area: Sepsis