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This podcast will examine a retrospective, observational cohort study that found an association between excessive oxygen supplementation in the first day of mechanical ventilation with multiple organ dysfunction syndrome on day 7 of admission and in-hospital mortality in critically ill children. Host Elizabeth H. Mack, MD, MS, FCCM, is joined by L. Nelson Sanchez-Pinto, MD, MBI, to discuss the study’s findings. (Sanchez-Pinto LN, et al. Pediatr Crit Care Med. 2022;23:89-98). Dr. Sanchez-Pinto is a pediatric critical care physician, data scientist, clinical informaticist, and healthcare technologist at the Ann and Robert H. Lurie Children's Hospital in Chicago, IL.
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Category: PCCM Podcast
Dr. Mack: Hello and welcome to the Society of Critical Care Medicine’s Critical Care Podcast. I’m your host, Dr. Elizabeth Mack. Today, I will be speaking with Nelson Sanchez-Pinto MD, MBI, on the article “Excessive Oxygen Supplementation in the First Day of Mechanical Ventilation Is Associated With Multiple Organ Dysfunction and Death in Critically Ill Children,” published in the February 2022 issue of Pediatric Critical Care Medicine. To access the full article, visit pccmjournal.org. Dr. Nelson Sanchez-Pinto is a pediatric critical care physician, data scientist, clinical informaticist, and healthcare technologist. Welcome Dr. Sanchez-Pinto.
Dr. Sanchez-Pinto: Thank you for having me.
Host: Do you have any disclosures to report?
Dr. Sanchez-Pinto: Some NIH funding for the research that I do, but nothing related to this article.
Dr. Mack: Wonderful. Thank you so much. Great contribution to the literature, I really enjoyed reading this. Tell us a little bit about how you came up with the idea for this study. What were you seeing clinically or in your research that led you to attempt to answer this question?
Dr. Sanchez-Pinto: I have this fascination with some of the excesses in critical care. A little bit about some of the part of the theme of my research has been focusing on some of those. We’re intense people, it’s in our job description as pediatric intensivists. Sometimes we like to do things, and we like to do a lot of those things, and sometimes we overdo it, I think. The history of critical care, and certainly the history of medicine, is full of interventions that were not there before. Then when they became available, we have a learning curve of how to use them appropriately. A lot of these things are U-shaped relationships. Too little is bad. Too much is also bad. And we just have to find that balancing point where therapies are effective and not harmful and things like tidal volume and excessive pressures when mechanically ventilating patients, thresholds for blood transfusions in anemic patients, when to give antibiotics to the child who is going to die from sepsis but not give it to the child who’s going to have a disruption of the microbiome or develop resistant bacteria. Fluid resuscitation is a huge one. Sustaining patients is key to their survival when they’re in shock but when we overdo it, we cause fluid overload and then we’re dealing with the tremendous impact that has on outcomes.
We’ve done some work on some of those things, working on antibiotics and fluid overload and some of our other projects. Oxygen is right there in the middle and sort of a huge component of what we do every day. And again, that’s what we’re talking about—the U-shaped relationships. Oxygen has been on that completely left side of that relationship. Going back to oxygen, certainly that U-shaped relationship is huge. Most of our job definitely in pediatrics and definitely in the pediatric intensive care unit is about providing adequate oxygen and delivery of oxygen to the tissues.
That’s what critical care is all about. A lot of pathologies are respiratory pathologies. Oxygen is 99% of the time our friend, is what we’re trying to provide for our patients, but anything else it can be harmful, like a lot of history of medicine. I love this quote from Paracelsus that the poison is in the dose, the idea that everything can be a poison and it only depends on the dose that you’re providing, and oxygen is certainly one of those big ones. Within our own field of pediatrics, oxygen has also had a little bit of this duality to play out historically. The first-ever report of the use of oxygen as a medical therapy was in a young patient with pneumonia. I don’t know the age of the patient, it’s not in the report, but I like to think that it was an adolescent, also we can say it was a fully pediatric report and it was used for a young patient with pneumonia, oxygen therapy in the mid-1800s with a lot of success.
The recognition of the benefits of oxygen to certain medical therapy is happening within the realms of the specialty of pediatrics. And of course, as we intimately know as pediatricians in the mid-20th century, some of the toxicity of oxygen was first described in pediatric patients, specifically neonates, with the the realization that the epidemics of blindness in premature children were due to retinopathy of prematurity, which is of course caused by excessive use of oxygen and the development of vasculature in the retina of these patients, as well as the direct admission of the influence of oxygen therapy in the development of bronchopulmonary dysplasia in those kids too. We’ve also seen that duality of the goodness and the badness of oxygen play out in pediatrics. I’m fascinated by the excesses. Oxygen particularly is one that fascinates me because of that huge influence in our history and in our everyday jobs as intensivists in the intensive period.
Dr. Mack: Thank you so much. Can you share a little bit about the institutional database that you used in this study? Some of us might be a bit jealous that you were able to mine all of these data from your local patients.
Dr. Sanchez-Pinto: I’m actually very lucky to have access to a lot of this clinical data from our electronic health records. As you described at the beginning, my main roles are as data scientist and clinical informaticist. So I spend a lot of my scholarly time learning how to do the data science and clinical informatics and understanding the digital infrastructure in which we are practicing medicine in the 21st century. It’s not an easy job, a lot of what we do when we do big data analysis is about really understanding the data structures, cleaning the data, standardizing data elements, especially when you’re merging data sets from different institutions like we did here, we’re using data from two different institutions. That whole process is very time consuming. People say that data scientists spend 80% of the time cleaning the data and 20% of the time complaining about cleaning the data, or I guess 20% of the time analyzing it. And it is true. And if you don’t do it right, then it’s the classic garbage in, garbage out.
If you don’t spend the time ensuring that you have solid, high-quality data to do your analysis, then your results are going to be meaningless. In my research lab, we spend a lot of time thinking and doing a lot of this data harmonization and data quality assurance. There’s a few very exciting projects coming down the line. I’ll put a plug in for that through the pediatric data analytics and data science and analytics group of the policing network, which I’ve been part of for many years, we’ve been doing a lot of data collaborative projects. We have the PICU data collaborative posted by Rhonda Wetsel in Los Angeles of which I’m part of, we’re engineering these large aggregated anonymized databases to do this kind of research.
I think the age of data science and research using large electronic health record databases in pediatric critical care is just now starting to flourish, and we’re going to see a lot of really cool stuff coming down the pike, and I’m really excited about that. Rhonda Wetsel was a huge inspiration in my career as a data scientist. He talks about the natural experiments. If you think about it, in critical care, in medicine in general, but in critical care certainly, we’re constantly doing natural experiments in our patients since a lot of what we do is trial and error. We have a reasonable physiologic explanation of why we’re going to do something to a child, but oftentimes you’re doing it and seeing what happens and then changing course, if what we did did not make a difference.
Those are all small natural experiments that we’re doing on a daily basis. Thousands of natural experiments are being done across hundreds of pediatric intensive care units in the country at the same time. We have an opportunity—I would say an obligation—to learn from those natural experiments that are happening. The best way that we can observe those experiments and gain insights is by collecting that data from patients through the electronic health record data that’s already being collected, but cleaning it and merging it, ensuring that it’s good quality, improving the quality of that data over time as we continue to collect it in that routine care and build systems so that we can improve that collection of data and then learn from those natural experiments so that we can gain the insights that may help us determine what are the best treatments for certain groups of patients or what are the harmful therapies that we should be avoiding or balancing out a little bit more. The theme of our work in our research labs is to collect these databases and spend a lot of time building those infrastructures to then be able to answer some of these very important and critical questions.
Dr. Mack: Great. Thank you so much. I’m wondering if you can just share a little bit about how confident you are that pulse oximetry is an adequate proxy for arterial oxygen saturation, one of the core tenets of this work?
Dr. Sanchez-Pinto: Absolutely. I think the use of noninvasive pulse oximetry as a proxy for arterial oxygenation, PaO2, is intimate to the pediatric critical care field. A lot of work has been done around using SpO2 as a proxy in this regard because of the fact that we don’t collect blood gases as much as our adult colleagues. Over time, that’s becoming even more and more of a reality now in our specialty. Robbie Kimani, who has been an external mentor of mine for many years, has done a lot of work around the use of the S/F ratio as a proxy for the P/F ratio. We see the work in the PALICC guidelines for pediatric acute respiratory distress syndrome, introducing not only the oxygenation index as a measure of severity of ARDS, but also the oxygen saturation index, which uses SpO2 instead of PaO2. It has been critical in being able to classify patients, even when they don’t have invasive arterial blood gases in them.
Obviously, this is the oxyhemoglobin dissociation curve, the steep vertical part of the curve, where that relationship is linear, where we do a lot of that work, where we assume we’re doing a lot of that work, but obviously SpO2 has its limitations all the way from the quality of the sensors, the location of the sensors, the quality of the profusion of the patient to achieve adequate reading recordings, but it is what we have, and we have a lot of it. Every child who goes to the intensive care unit will have an SpO2 measured, probably for most of the time that they spend in the ICU. Even though it might not be the perfect measure, we have a lot of it. A lot of it is good quality, and I think we can learn a lot about these measures that we’re collecting routinely but oftentimes forget to look at a little bit in more detail.
Dr. Mack: Great. Thank you so much. Tell us a little bit about the cumulative excess oxygen exposure, CEOE, that mean hourly FIO2 above 21%, when the corresponding hourly SpO2 was 95% or higher, maybe just give us an example to get us in that mindset that really is an anchor in your article.
Dr. Sanchez-Pinto: Absolutely. Our goal was to try to come up with a way to noninvasively measure the amount of oxygen in excess that patients were being exposed to. The traditional way that this has been done is using PaO2 recordings. Most of the literature in hyperoxia in adults and so far in pediatrics has been on measurements of PaO2, and it’s usually a one-time measurement. So it’s really one snapshot in time or maybe a couple of measurements over the course of a day, where you get a PaO2 and you find some threshold, usually people use 200 or 300 PaO2 as the threshold for hyperoxia and then look at the association with outcomes. And that’s a really very nondetailed way or very broad way of looking at hyperoxia. So we were really interested in two things—on the one hand, to figure out how to measure oxygen exposure in a noninvasive way. And the second one—how to quantify that exposure in a more robust and continuous way, as opposed to one snapshot in time, since we know that we have this data over time.
So the idea was, if we know that certain oxygen levels are adequate for normal function and there’s actually normative data showing that up to 25% of healthy children that are undergoing anesthesia for a routine procedure have saturations of 95% or above, or 96%, so 25%. So the vast majority of patients having saturations at that level or above. So we figured, if that’s normative data, these are normal, healthy children undergoing routine procedures, and that’s a normal saturation, then you don’t need more than that. So if you are receiving FIO2, extrinsic oxygen above room air, when you’re already at 95%, you don’t need it, that oxygen is already in excess. So the way we did it is, for every hour, we would look at the oxygen saturation and we would look at the amount of FIO2 that patient was receiving. If the patient was at 95 or above, any percentage of oxygen above 21 counted as a point in this score of CEOE, cumulative excess oxygen exposure.
Say a patient is on 40% FIO2 and, for that hour, they were 96, 97, 98%, probably 100%. We love 100% in the ICU. I don’t know why it should terrify us as a number. But we love seeing 100% for some reason. It’s reassuring to us but probably very harmful for our patients. So anyway, imagine the child’s on 40% FIO2 and saturating 100% for that hour, that patient would have 19 percentage points above 21 for that hour. So that CEOE score for that hour would be 19 for that patient. If that patient was on, say, 40% for half of the hour and then on 21% the other half of the hour, then instead of being 19 points, it would be half of those points, it would be 9.5 points for that hour.
We did this for the first 24 hours. The patients were on mechanical ventilation and we would add up all those scores, every one of those scores over the course of those 24 hours and then average them out. That would give us the final cumulative excess oxygen exposure. If a patient in a given hour had no excess oxygen exposure, they were receiving 21%, that score would have been zero at that point, or if the patient was saturating below 95%. Say the patient was 90%, 91, and they were receiving oxygen to help them maintain those levels, then that score would also be zero for that hour because we would consider that oxygen above 21% was not in excess, it was necessary to keep the patient within that range that was being targeted to avoid hypoxemia.
I would also have to say that, before we did the cumulative oxygen exposure calculations, we removed all patients who had overt hypoxemia during that first 24 hours. So patients who were desaturated at any point, we would consider that they, regardless of how much cumulative exposure they may have had in other hours, the fact that at some point they were hypoxemic, we put them in their own group because of the huge confounding variable of hypoxemia in those kids. We were really interested in those who were not hypoxemic but were receiving some degree of oxygen and calculating that cumulative exposure to oxygen and estimating how much of that was in excess of what they physiologically needed.
Dr. Mack: Awesome. Thank you for explaining that. I was a bit surprised to see that 15% of your patients in those first 24 hours of mechanical ventilation had zero cumulative excess oxygen exposure. I’m just curious, was it common during the study timeframe to have patients on 21% in your unit?
Dr. Sanchez-Pinto: Yeah. I think we are a relatively oxygen-averse unit, and maybe part of it is because of this interest in excess oxygen. But a lot of those patients, if you look at Table 1 of the paper, for the majority of those patients, about 70% of those patients were patients with tracheostomies. As many ICUs around the country do, we serve a large population of patients who are home ventilated, who receive mechanical ventilation at home for, say, children with bronchopulmonary dysplasia or neuromuscular diseases. A large population are those patients. In our population, oftentimes their FIO2 is 21%. So I think that group that was largely 21% was largely driven by those patients. We did not include those in the main analysis, as you may have seen in the paper. The main analysis was in those who had some degree of cumulative oxygen exposure and then comparing that to the hypoxemic group. But we thought that this unique group of patients at 21% that were largely these tracheostomy home-ventilated children, was a very special subgroup of patients that we didn’t want to influence the main analysis of the paper.
Dr. Mack: Gotcha. If you don’t mind, just share a little bit about your findings in this manuscript.
Dr. Sanchez-Pinto: What we did with the cumulative oxygen exposure measures, we divided patients into four quartiles Any patient that had any CEOE, any score above that 21% during the first 24 hours of mechanical ventilation, were divided into four groups based on the quartiles of the total cumulative excess oxygen exposure. The way it panned out is the first quartile was patients who had a score about 9%. So these are patients around 30% FIO2. The second quartile was nine to 17%, so this would be 30 to 45%. The third quartile was 17 to 25% CEOE, so that’s a gestalt of up to 45 or so and 55 or so. Then the fourth quartile was about that range. And what we found is that we used the first quartile of patients, so patients who were on less than 9% excess, so 30% FIO2 or less cumulative over the course of 24 hours, we used those as a reference, and then we compared the second, third, and fourth quartiles against that first group to see whether they had a decreased likelihood of having poor outcomes.
Of course, how much oxygen you receive is confounded by many variables. Things like your age, whether you are sick or how sick you are and some other potential confounders. In the analysis, we adjusted for several potential confounders, including obviously age, the presence or absence of an immunocompromised state, so whether you have an oncology diagnosis or transplant diagnosis, and whether you’ve had multiple organ dysfunction during that first day of mechanical ventilation. Then we did add some additional sensitivity analysis, adjusting for whether you have had a cardiac arrest and measuring severity of illness as a continuous variable of the degree of organ dysfunction, as opposed to a yes-no multiple organ dysfunction. We did a number of sensitivity analyses to ensure our results were robust, and they were.
The results were essentially that there was this apparent dose response, dose relationship, between the amount of cumulative excess oxygen exposure, and these poor outcomes that we’re interested in, mortality and multiple organ dysfunction syndrome at seven days. We’re interested in this idea of looking at the persistence of organ dysfunction or the presence of organ dysfunction at seven days of ICU stay as a measure of the impact of this therapy on organ dysfunction because we believe in this idea that the pathophysiology of oxygen toxicity and that causal pathway, this organ dysfunction, is a big part of it. The excessive oxygen causing reactive oxygen species, causing this damage, obviously molecular patterns that are recognized by the immune system that activates some degree of inflammation that causes some dysfunction of multiple organs, and then that leads to organs failing and ultimately increased mortality.
We believe in this continuum between organ dysfunction as a result of excess oxygen and not leading to death because mortality in pediatrics and pediatric critical care thankfully is not that high. We wanted to have an outcome that was more frequent than death. Our mortality for these mechanically ventilated patients was about 5 to 6% whereas our incidence of multiple organ dysfunction at seven days of ICU was about 17% or so. So we really were looking at the larger number of patients having poor outcomes that we could study with this modeling approach. Indeed we saw that sort of step-wise increase in the risk of multiple organ dysfunction at seven days, the patients going from the first to the second, to the third, to the fourth quartile of the cumulative exposure.
We also saw that relationship with increased mortality, which was more evident, not surprisingly only in the worst group, in the fourth quartile, compared to the first quartile. Those patients, after adjusting for confounders, had a higher likelihood of mortality. In the second and third quartiles, we didn’t see that difference, but again, probably because of the low rates of mortality, whereas with the multiple organ dysfunction outcome, we did see that relationship was true for all the quartiles, the second quartile of cumulative oxygen exposure, those patients who were a little bit above 30 to 35% FIO2, already had an increased rate of multiple organ dysfunction compared to the kids in the first quartile, which were 30% or lower, so the the third and fourth quartiles. So essentially, through the number of sensitivity analyses we performed, we saw the same relationship stay consistent.
We also did a really interesting sensitivity analysis that was not part of the original manuscript but was requested by one of the reviewers, a PCCN, and the results I think are very enlightening, which is: We took out all patients who had multiple organ dysfunction on the first day of mechanical ventilation. Obviously a huge portion of our patients have multiple organ dysfunction when they’re receiving mechanical ventilation in the ICU. So we actually removed those kids for that sensitivity analysis and only looked at the cumulative excess oxygen exposure in those patients who had no multiple organ dysfunction during that first day and looked at whether the degree of oxygen exposure led them to develop multiple organ dysfunction and have persistent multiple organ dysfunction at seven days after their admission.
We saw that relationship stay true for that outcome of multiple organ dysfunction at seven days. There was no relationship with mortality at that point because of the very low mortality for those patients who don’t have MODS on the first day of mechanical ventilation. But for the multiple organ dysfunction, we did see that relationship, which was very enlightening in the sense that it is possible—we’re not saying that this is causative—but it is possible that some degree of this multiple organ dysfunction that developed in those patients who did not have it on the first day of mechanical ventilation may have been in part because of excess oxygen exposure causing some of the pathophysiology leading to organ dysfunction and having poor outcomes.
Dr. Mack: Wonderful. Thank you. I’m curious, have these findings led to different practices in your institution? For example, might you be using more or less arterial lines? Might you have hired more respiratory therapists or have different technology or different weaning parameters? What’s changed?
Dr. Sanchez-Pinto: I wish we had hired more RTs, respiratory therapists. We are in a huge crisis in this country of RTs due to the COVID pandemic. We definitely need more of those. We actually tend to use a lot of arterial lines, I would say, in our institution traditionally. And we definitely are seeing a drop in the rate of arterial line usage. But I think this is common across the pediatric critical care field, that we’re getting more and more comfortable with noninvasive modes of monitoring and noninvasive modes of organ support. So I don’t think that may be related directly to our findings. I would say though that we’ve traditionally been very cognizant of the potential deleterious effects of oxygen. We talk about oxygenation and oxygen FIO2 levels often, our nurses are very adept at weaning oxygen when adequate oxygenation is achieved. I think in part that may be an inspiration for this work but also that trend has been reinforced by our findings. One of our fellows does good quality improvement projects, and one of the quality improvement projects that was implemented in the last few years was a weaning FIO2-type approach in all patients with adequate oxygenation. So we’ve done some work around that. I think that could be done better and more robustly, but definitely I think we’ve traditionally been very oxygen averse, and these findings have definitely reinforced our approach.
Dr. Mack: Well, thank you so much for that. I’m curious, what are your thoughts on closed-loop feedback systems and systems that might automatically adjust the FIO2 based on pulse oximetry?
Dr. Sanchez-Pinto: That’s a fascinating question. As a clinical informaticist and technologist, quote unquote, I love the idea. I think that would be the future of a lot of the oxygen therapies that we provide. There’s been a reasonable amount of work in the neonatal space, in the NICU space, around developing those automated approaches and some of them with some degree of success, obviously in the experimental research setting. None of those are in wide use in clinical care. I think we have this tremendous amount of attachment to oxygen therapy, and I think people are scared about machines removing that vital air from our patients. So I think there’s a little bit of an emotional component to allowing some of these closed-loop systems to make those decisions. I will remind the intensivists listening to this podcast that one of the mainstays of the therapies that we provide, which is mechanical ventilation, is full of closed systems, right?
If you do a volume-guaranteed PRVC, for example, that’s a constant closed-loop system, determining the degree of pressure that you’re going to be delivering to patients to achieve a targeted volume. And that’s a very well-regulated, well-studied, closed-loop system that works great for our patients. Many of the other parameters within the ventilators are actually closed-loop systems. So this is not a foreign thing for us, I think, whereas we’re a little bit more cowboyish with our pressures, perhaps we’re a little bit more attached to our FIO2, and we’re not willing to let go of that manual control. So we’ll see where the culture of oxygen therapy goes and how this evolves.
I want to say though that a big limitation of this work, and it has to be emphasized, is that our priority already removed patients who had overt hypoxemia from our analysis. We did compare to the hyperoxia groups, but a priori we had already removed patients who were hypoxemic. So we don’t know if, by being overzealous in reducing the FIO2 exposure, we may cause more patients to go to the other side of the pendulum and be hypoxemic, and what those effects may be, if that hypoxemia is going to cause as many problems as hyperoxia may be causing. So there’s definitely that U-shaped relationship, once again, being extremely important here. Systems that are just dumbly going down on the FIO2 but don’t have a good regulated way of increasing the FIO2 rapidly when needed may cause us to suddenly have many more children who have hypoxemia and we don’t know the outcome of those, or we don’t know the outcome of those in comparison to the tradeoff of those that don’t have hyperoxia. This has to be prospectively studied.
There’s currently a large clinical trial in the UK, the Oxy-PICU trial. There was a feasibility trial in 2018, and now there’s a larger one ongoing of targeted ranges of oxygen. So 95 to 98% target versus 88 to 94% target. I think these are the kinds of studies that we need to do in pediatric critical care to determine what ranges we should be targeting, which ranges are safe, similar to the whole literature around glucose levels. We know that hyperglycemia was bad. We did a lot of work in developing systems to treat hyperglycemia and measure hyperglycemia, to reduce hyperglycemia rates. Yet we found that when we did that in excess and caused hypoglycemia, we had poor outcomes, and that literature is marked by that duality of glucose.
I think oxygen is very similar in that regard. So we have to learn from that glucose literature and figure out how we can study these prospectively to not do things in excess but also not do them too little when they’re actually necessary. So when we talk about these closed-loop feedback systems, I think we’re too early. We still need to fully develop that science and understand what are those target levels that we need to achieve before we let the machines do the work for us.
Dr. Mack: Awesome. Thanks. Is there anything else that we haven’t covered that you’d like to touch on?
Dr. Sanchez-Pinto: No, I think this was a lot of fun. It was a lot of fun to write this article and I want to acknowledge my coauthors. Bria Coates was the other senior researcher that also thinks a lot about oxygen and helped me develop a lot of these ideas. Daniel Balcarcel, who was the first author, he’s a fellow, he was a resident at the time when we wrote this at Emory Children’s and is now a fellow in critical care at CHOP. I think you guys are going to be hearing about him in the future, I’m sure, he’s a very bright young man. Grace Chong, a former colleague from the University of Chicago, is our partner in having availability to this work with more than one database. Thank you for having me on the podcast and having this fun conversation, and to the readers of PCCM, we’re a growing field, a growing community, and it’s a lot of fun working here and getting to know people and continuing this work.
Dr. Mack: Thank you so much. I certainly learned a lot. I enjoyed the historical pieces as well. It really puts it into context. This concludes another edition of the Critical Care Podcast. For the Critical Care Podcast, I’m Elizabeth Mack.
Elizabeth H. Mack, MD, MS, FCCM, is a professor of pediatrics and chief of pediatric critical care at Medical University of South Carolina Children’s Health in Charleston, South Carolina, USA. Dr. Mack received her bachelor of science and medical degrees from the University of South Carolina. She completed her residency at University of South Carolina Palmetto Health and her fellowship at Cincinnati Children’s Hospital Medical Center. She also completed a master of science degree with a focus on epidemiology and biostatistics at the University of Cincinnati. Currently, she serves as chair of the American Academy of Pediatrics Section of Critical Care and is past chair of SCCM’s Current Concepts in Pediatric Critical Care Course.
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