SCCM Resource Library-Caring for the Critically Ill Transplant Patient

Video Transcription

Hello, everyone. My name is Michael Shashadi. I'm from the University of Pennsylvania. I want to thank the SCCM for inviting me here to moderate this session entitled Caring  for the Critically Ill Transplant Patient. Transplant patients are some of the most complicated patients that we care for in the intensive care unit.  They are on multiple different medications, from immunosuppressives to antimicrobial medications, and oftentimes they can develop syndromes that are unusual or particular to  their patient population that we don't see in non-transplant, non-immunosuppressed patients.  The talks in this session will review some of the basics of immunosuppressive medications, immunosuppression prophylactics, and basic management and dealing with those medications  in the setting of critical illness, as well as an overview of how to manage stem cell transplant patients and the particular critical illness syndromes that may affect them from  respiratory failure to other organ dysfunction syndromes. So whether you see many of these patients in your clinical practice or if you just see  them from time to time, we hope that this will be a practical review of how to manage these patients. I thank you for joining us, and now I'm going to hand it over to our speakers.  Hello. My name is Allie Killian. I'm the pharmacist in the Surgical Transplant ICU at Emory University Hospital in Atlanta, Georgia.  Today my talk is entitled So Many Transplant Drugs, So Little Time. I have nothing to disclose today.  The objective of my presentation today is to explore the array of immunosuppressive medications and infection prophylactics in transplant patients and management in the  setting of critical illness. The epidemiology of the reasons transplant patients get admitted to the ICU is very wide.  Of course, in the immediate post-transplant period, ICU admission is routine for heart, lung, and most liver transplants, even if it's just for a short stay.  At our center, kidney transplant patients only come if there are complications. If it's a fresh transplant, of course, you will be dealing with the initiation of new  immunosuppression, and you'll have a transplant team of providers to work with. Also, there could be surgical complications in recently transplanted patients requiring  ICU admission. However, once a patient is further out from transplant, the long-term exposure to immunosuppression  does carry a risk of a variety of events that can bring them to the ICU, such as cardiovascular  events, severe infections, drug-related toxicities, and immunosuppression-associated malignancies, any of which might bring them to the ICU.  A review article published in CHEST in 2016 compiled data from 13 studies to describe the admission diagnoses and corresponding etiologies in kidney transplant recipients  admitted to the ICU. Many reasons for ICU admission are either related to immunosuppression in general, such  as infection, which you see here at the top portion of the slide, or may actually be directly  related to the immunosuppressive agents themselves, such as serolimus-induced pneumonitis here, or PRESS syndrome, which can be seen with the calcium urine inhibitors.  It's important to separate reasons for ICU admission into infection-related examples  of those at the top of the graphic, or non-infection-related at the bottom of the graphic, because that may dictate how you handle immunosuppression.  As you can see, acute respiratory failure and shock are the main reasons for ICU referral, but these reasons can be due to a wide variety of etiologies.  We'll dive right into immunosuppression right now and do an overview of the agents that are most commonly used.  Starting off with induction immunosuppression, the goals of immunosuppression in general are to optimize combination regimens, minimizing rejection and toxicities.  The idea is to use agents with different mechanisms and different toxicities, improving long-term graft survival while trying to minimize the risk of infection.  In general, you start with more immunosuppression initially, and then you'll decrease over time.  Related to induction immunosuppression, this is the early agents that are administered perioperatively.  The goal of induction is to induce allograft acceptance by suppressing T-cells. This is useful in a variety of patients, but most often in high-risk patients, such as  those with acute cellular rejection, those who have received multiple transplants, or those who are highly sensitized.  For example, in liver transplants, it's not necessarily routine to use induction immunosuppression except for those who are high-risk or who have renal insufficiency.  Another reason to use induction agents might be a renal sparing protocol. This might allow the delay of the use of calcium urine inhibitors, which could minimize the  risk of nephrotoxicity. You might also use a renal sparing protocol if you have expected delayed graft function in situations such as a long ischemia time or a marginal donor.  On this slide are the agents used most commonly for induction. The most common are the IL-2 receptor antagonist monoclonal antibodies, which is basaliximab.  Basaliximab halts T-cell proliferation, and it provides 30 to 45 days of IL-2 receptor blockade.  It's generally well-tolerated, has been associated with a reduced risk of acute cellular  rejection, and it has very rare hypersensitivity reactions, but you should be aware that those have been described, anaphylaxis, urticarial reactions, hypotension, and bronchospasm.  And if you knew a patient had had these in the past, you would want to premedicate. A less commonly used induction agent is thymoglobulin.  It's a polyclonal antibody, and as you'll see, although it also reduces or delays the onset of acute cellular rejection, it has a more significant safety profile compared  to basaliximab. It's most commonly used in high-risk patients and also in kidney transplant patients, but  there is a pretty widely described cytokine release syndrome, which has symptoms such as fever, chills, headache, malaise, dyspnea, arthralgias, and even pulmonary edema associated  with a capillary leak syndrome. This is generally a first-dose effect, however, and it can be premedicated with medications  such as acetaminophen, diphenhydramine, and hydrocortisone, and also the infusion rate can be prolonged to try to minimize the risk that this occurs.  Another adverse effect associated with thymoglobulin is serum sickness. This is fevers, arthralgias, and rash, potentially cardiovascular symptoms.  This is more delayed and can develop one week or more after administration. With thymoglobulin, you can also see leukopenia and thrombocytopenia, and immune reconstitution  could take as long as six months. Even if patients don't receive induction with either basal lipsomab or thymoglobulin or  one of the other agents, they often will receive a dose of methylprednisolone, at least one dose in the operating room, typically a rather high dose, and then that would be tapered  over time. Associated with methylprednisolone, of course, are adverse effects that we're much more attuned to in the ICU, including hyperglycemia and the risk of delirium.  It should be noted that there are transplant protocols that are steroid-sparing or completely steroid-avoiding.  One example of that is patients who have a history of hepatitis C, because it's been shown that steroids, specifically the high doses associated with induction, can increase  your viral load. With the advent of the treatment of hep C, often done before transplant, this has become less of a concern.  Transitioning on to maintenance immunosuppression, this or some combination of these agents are what patients will be on lifelong to prevent them from rejecting their graft.  You have to, of course, prevent that rejection, but also balancing toxicities and infections. I've circled the three most commonly used agents at our center anyway, which would be  tachycolimus with mycophenolate and prednisone. The calcineurin inhibitors really are the mainstay of a maintenance regimen.  They have poor to variable absorption, and therefore you have to really closely monitor trough levels.  Goal trough levels will be widely variable, and depending on patient-specific factors such as timing from transplant, history of a previous transplant, or history of rejection,  history of infections, and what other immunosuppressant medications they're on. Of note, it is metabolized by the CYP453A4 isoenzyme, so carries with it a number of  drug interactions, which we'll discuss in a subsequent slide. Tachycolimus, because of its variable absorption, PO, can be given other routes, which might  be especially useful in the critical care setting, such as sublingual, which is what we typically do in our ICU patients who can't swallow.  You might need to decrease the dose as much as 25% since there is increased absorption. The IV would be used rarely because of the difficulty in getting accurate levels.  Tachycolimus is another calcineurin inhibitor that you might see utilized, second is tachycolimus.  There are two formulations, a modified under the brand name Neural or GenGraf, and a non-modified under the brand name Sandimune. These are not interchangeable.  There's a liquid available, which does adhere to the nasogastric tubing, so you could see erratic absorption there as well.  And again, similar to tachycolimus, the IV is rarely used. The side effects of the CNIs are pretty significant, and might be some of the reason that patients  are brought to the ICU, specifically nephrotoxicity and neurotoxicity, which can range from tremors all the way to posterior reversible encephalopathy syndrome, or PRESS.  PRESS and some of your other more severe neurotoxicities may actually necessitate holding the calcineurin  inhibitor, and maybe even trying to switch to the alternative calcineurin inhibitor, and sometimes they won't have recurrence of their symptoms.  Endocrine adverse effects are also significant, and we certainly can see them in the ICU with hyperglycemia and new onset diabetes after transplant.  There are some situations which can increase risk of toxicity with the CNIs, specifically  other nephrotoxic agents would be concerning, potassium sparing, diuretics, or supplementation of potassium as there's an increased risk of hyperkalemia.  Statins can increase the risk of rhabdomyolysis, and interestingly, diarrhea can actually increase  absorption and potentially result in higher levels of calcineurin inhibitors, because in a state of diarrhea, more villi are being expressed, and due to that increased surface  area, the mechanism of absorption of CNIs can actually increase to more absorption, which is counterintuitive.  Listed here are a number of drug interactions that I mentioned due to its CYP415 metabolism. Some of them, as you can see, can increase the level of calcineurin inhibitors on the  left side of your screen here. Others might decrease the level of calcineurin inhibitors. It's not that you can't use these medications in combination with calcineurin inhibitors,  it's just that you have to anticipate what it may do to your serum levels and make dosage adjustments accordingly.  When the medications are used more chronically together, this is easy to do, but in the acute setting, if these medications are stopped and started, it may be difficult to handle  the changes that can occur with the calcineurin inhibitors, and consultation with a transplant pharmacist or a critical care pharmacist would be useful.  A second agent is mycophenolate. It can be utilized oral or IV. However, it does have a number of adverse effects, specifically diarrhea in the gastrointestinal  category as well as pancytopenia, which may respond to a dose reduction but could ultimately result in changing your immunosuppressive regimen.  Some patients tolerate mycophenolate sodium or brand name Myfortic, however, those two, they're not interchangeable.  Drug interactions with mycophenolate are less than with the calcineurin inhibitors and generally have to do with separating administration from cations.  I'll briefly mention the co-stimulation blocker Belatacept. It's approved only for kidney transplantation, and you might use it over time to minimize  exposure to calcineurin inhibitors and the adverse effects associated with those, specifically  long-term cardiovascular and renal function at three years and five years have been shown to be better in the Belatacept group than in those who continue to receive CNIs, and  in fact, our kidney transplant patients often come off CNIs at around a year post-transplant.  Our liver transplant and lung transplant programs use these, but much less commonly than the kidney program.  So now that we've briefly talked about all the immunosuppressive agents, how do we manage them in the ICU? The answer is really that it's a highly patient-specific management.  There are a number of considerations you have to take, baseline graft function, time from  transplantation, immunological risk, severity of infections, and whether they have a difficult to treat pathogen.  All these things can go into deciding what sort of immunosuppressive regimen you're going to continue in the ICU.  If infection is known or suspected, then generally you might reduce your overall level of suppression, but certainly there is no consensus around this.  Absorption concerns are common, so utilizing alternative routes of administration for each agent with appropriate dose adjustment will be important.  And then consideration of acute kidney injury, especially with calcineurin inhibitors where you could increase NIFR toxicity.  There is one small retrospective evaluation of kidney transplant recipients admitted to the ICU in Turkey over a five-year period.  These were 31 patients who were admitted for severe sepsis, an average of eight and a half years after their transplant.  All were on triple immunosuppression with TAC, MMF, and a steroid. Overall mortality was just over 50%, and most of these patients died with a functional graft.  Of note, there was no loss of a graft among surviving patients. This is a descriptive study, so really it just goes through each regimen.  The majority of patients, as you can see here at the bottom, were downgraded to steroid alone, and you can see here, interestingly, that most patients who were non-survivors  received that regimen of steroid alone. I don't think that you can determine any causality here, as patients who were the most sick from  their severe sepsis were most likely to be downgraded to the least immunosuppression, which would be a steroid alone regimen.  There were a handful of patients who also received MMF plus steroid or TAC plus steroid.  But it should be noted that there really is no study evaluating different immunosuppressive regimens in the setting of critical illness.  Briefly, this slide talks about anti-infective prophylaxis. There's a lot of information here, and there's a lot of variation between the different organs and different centers.  Generally, you should know it's acceptable to hold prophylaxis for brief periods of time in critical illness or if you have adverse effect concerns or absorption concerns.  Overall, patients will receive prophylaxis in these three categories, PJP, viral, and fungal, from anywhere from three months to 12 months, depending on the organ transplanted  as well as the protocol.  First line for PJP prophylaxis is trimethoprim sulfa.  It can cause bone marrow suppression and renal injury. Viral prophylaxis is going to be dependent on CMV risk.  The lowest risk will only receive an antiviral covering HSV and then be monitored for CMV viremia.  Those of the highest risk, donor is positive for CMV and the recipient is negative will actually receive valgancyclovir for usually six months.  And then fungal prophylaxis is even more variable. Some patients receive only thrush prophylaxis with nystatin, all the way up to lung transplant  patients which might receive something with aspergillus coverage such as posaconazole. It should be noted also that if a patient gets treated for rejection, it's important  to typically reinitiate prophylaxis as their risk for these opportunistic infections have gone up after the increased immunosuppression they get for their rejection.  In summary, immunosuppression is tailored to each individual patient. It will be very important to contact the patient's transplant providers to determine how to proceed  with managing immunosuppression in the ICU setting. You must balance efficacy with side effects which can be very difficult to do, especially in a critically ill patient.  Critically ill patients often require reduced immunosuppression, especially in the setting of infection.  And as a pharmacist, I would have to say, remember to consider absorption concerns in choosing your route of administration and making any necessary dose adjustments.  Here are selected references from my talk today. Really appreciate your time. Have a good day. Thank you.  Thank you so much for allowing me to talk to you today about critical illness after stem cell transplant.  I have no financial disclosures, however I will be briefly discussing medications that are used off-label.  My objective today is to help you develop an approach to patients with critical illness after stem cell transplant, specifically those that involve respiratory failure.  We'll first start with talking a little bit about transplant basics and then spend most of our time talking about complications of stem cell transplant that require critical  care support as well as developing an approach to respiratory failure in these patients. A little on transplant basics, when these patients come to your ICU, you really do  want to know what the reason for their transplant was and whether or not it was autologous or  allogeneic because that will help you understand which complications they're most at risk for.  There are some really interesting and eloquent things that transplanters know about how they manipulated the graft and where the stem cell transplant source came from.  And while very interesting, they're probably not going to help you that much with what you need to know for the complications they're having and managing those in the ICU, and  the transplanters can help you more with that. What you do really want to know is how far out of transplant they are because the timing  of when they develop the complications will give you a clue as to which complications these may be.  Infections can happen throughout the transplant course, months to even years later. These patients can be still at risk for viral and fungal infections particularly.  As far as management of these infections, a lot of the same things that you would do for an otherwise healthy patient, you would still do, cover some more specific things  for transplant. We follow PCRs for particular viruses such as CMV and EBV. We may be doing beta D glucan or serum galactomannan tests, kind of screening for infections.  We may do CTs earlier to look for fungal infections, and we may be doing BALs very early on to  try to really hone in on what the underlying organism is causing the infection, and even  doing things such as next generation sequencing to pick up infections that you might otherwise not pick up.  Treatment is similar to otherwise healthy patients, however, we more aggressively manage particularly the viral infections that healthy patients would be able to get rid of on their  own. So we use antimicrobials, we may use IVIG, and there are even viral-specific T-cells that are directed at particular viruses that we sometimes use in these patients.  Graft-versus-host disease is another important complication we see, although because the transplanters have advanced their knowledge and management and prevention of this so much  more, we don't see it quite as much. GVH typically involves the skin, liver, and gut, and that is something that we do still see in the ICU.  The best treatment is to never get it in the first place, so like I said, some very eloquent ways to manipulate the graft these patients are getting.  Many patients are on calcineurin inhibitors such as taprolimus or cyclosporine to prevent it, and if all those things fail, there are many more options for managing and treating  graft-versus-host disease today that we didn't have a decade ago, and the transplanters are very well-versed in how to manage this.  Another complication that is gaining more notoriety, it's probably been around forever,  but we just have more recently recognized it, is transplant-associated thrombotic microangiopathy. You can see this in auto or allotransplants.  In particular patients undergoing their second transplant are more at risk for it, but in the autotransplant population where we're seeing it particularly are those that are  getting tandem autotransplants as part of their protocol. The cause is likely from injured endothelium causing complement activation in microthrombi in the vasculature.  The diagnosis is a clinical one, so there's not a particular test that tells you absolutely they have it.  There are some screening tests for complement activation that are a little bit more specific  and helpful, but they are not readily available at many places that do transplant, so you're left with your clinical acumen.  The patients we see with this typically have very difficult to treat hypertension. They're on two or three or more agents.  They have evidence of hemolytic anemia, and they may have multi-organ involvement, serocitis  throughout things like GI bleeding and ileus, diffuse alveolar hemorrhage, and renal failure is another thing we commonly see.  The treatment for this is to treat underlying causes you may find, stopping calcineurin  inhibitors if they're on it, because we know that can lead to this, and then for more severely  ill patients complement blockade with epilizumab has been used, and that data is published out of Cincinnati. You know, occlusive disease has gained more interest recently.  It's also been around forever. The reason people are thinking about it more, though, is in 2016, diffibrotide was approved  for use in treatment, and in fact, in Europe, diffibrotide is even approved for use for prophylaxis.  One of the things that came out of us thinking about VOD more is realizing that children are different from adults.  This has led us to think about the fact that pediatric patients are much more at risk for VOD than adults are, and we have redefined the diagnostic criteria for VOD in children.  The EBMT, as well as the PBMTC and PLESI have gotten together and agreed on these criteria. They're similar to old criteria, however, what's notable is that in children, you do  not have to have hyperbilirubinemia anymore to be diagnosed with VOD. Children currently do not have that. There's also no timeframe requirement.  We know that children can get this later out of their chemotherapy or transplant course, so that has been taken away.  There's been more interest in management, and in 2017, the PLESI-PBMTC group together published guidelines on how to diagnose, treat, and manage VOD.  What is of interest to the intensivists is that there's really a stress on fluid management.  There's always been, but this has stressed even more use of early renal replacement therapy  if needed to control fluid balance, more aggressive management of ascites using paracentesis to prevent abdominal compartment syndrome and renal failure, and also more attention to  pleural effusions leading to respiratory failure and more aggressively managing those. VOD can also occlude in the lungs, however, much less is known about this.  The gold standard diagnosis is through biopsy or heart cath, however, those are really risky undertakings in these patients because these patients are really sick.  There has been a paper published looking at CT findings and finding there's some perhaps  characteristic CT findings of pulmonary VOD, but the numbers are very small, so it's difficult to say how accurate that really is. We don't really know what the treatment would be.  There is some thought that diffibrotite may help this population, but it's not really known for sure.  Other non-infectious pulmonary complications of transplant can be divided into early and late because it kind of helps you think about what you should be worrying about.  Engraftment syndrome is probably my favorite. It happens around the time of engraftment. It's caused by cytokine release with engraftment.  You can see it, surprisingly, in auto or allo transplant, and I've even seen it really in oncology patients, particularly AML patients that have been neutropenic for quite a while  and then suddenly their cells start to come in. The thing that's great about this is it's very treatable. It responds to steroids, and the patients really do quite well.  Not as fun of a complication is diffuse alveolar hemorrhage. There are many different reasons people may develop diffuse alveolar hemorrhage, but you  kind of get into this pathway of alveolar epithelial injury, inflammation, dysregulated cytokines, and capillary endothelial injury.  There has been some advancement in DAH management lately. One of those things is understanding these complications of transplant better, so realizing  what underlying diseases they may have and treating those, and the other thing is also we've gotten a little better at controlling the bleeding. We have always used high PEEP.  We use a PEEP of 10 or higher, and we keep it there for quite a while and wean it slowly over time, and we've always tried to correct any coagulopathies we found, but more recently  we've been using topical therapy with inhaled TXA or inhaled recombinant factor 7A. There are a few case reports of using this that are published, and we have started using  it at St. Jude, and this is kind of our St. Jude approach to DAH, which anecdotally seems to be helping, and hopefully we'll have a paper out soon on our experience with it as  well, but we start with inhaled TXA. If the patients are not responding to that, then we move on to adding inhaled recombinant factor 7A.  If they didn't respond to those two things, I'm not sure what we do next because so far everyone's responded at least at some point in that pathway.  Not to say we won't meet a patient that doesn't, though. Idiopathic pneumonia syndrome is another typically early complication, although it can go out  as long as to day 120 or perhaps even longer. The cause is thought to be from toxicity with conditioning leading to activated T cells and inflammatory cytokines.  Part of the definition is it's idiopathic, so there's an absence of infection, so usually people do a BAL to rule out infection.  However, many people recognize that it is possible that some of these patients have undiagnosed infections that we just haven't found.  Treatment has been shown to be helpful with using either FAM with steroids or TNF-alpha blockade with steroids, and there's some promising results with both of those.  The later complications we see are cryptogenic organizing pneumonia or bronchiolitis obliterans syndrome, so both of these typically happening after 100 days.  COP tends to present a little earlier than BOS, but they both overlap quite a bit. They're both associated with chronic graft-versus-host disease.  Their CT findings are quite different. COP is a restrictive problem, whereas BOS is obstructive.  If you had to pick one, I guess COP would be the better one to pick because these patients actually can get better, whereas with BOS, the best you can hope for is to stop their  progressive decline. They are both treated with things aimed to decrease inflammation, such as steroids and  azithromycin or FAM and BOS, and those are the CT findings between the two. They're notably quite different.  Right heart dysfunction is also increasingly recognized as a complication of transplant. Our colleagues at Cincinnati Children's Hospital started doing screening echocardiograms at  day seven on all transplant patients as well as every time these patients are admitted  to the ICU, and they found that many of these patients have abnormalities on their echocardiogram that may have otherwise gone unnoticed.  Most commonly, they're seeing right heart dysfunction and pericardial effusions, some of which these are actionable items.  We all know that right heart strain goes along with ARDS, and recognizing this and trying to manage it is most likely going to be helpful for our patients.  So our St. Jude approach to respiratory failure can be sort of summed up in go big or go home, which is, I know, kind of cliche.  We either have to be really aggressive or we have to go the palliative route. Getting somewhere in between is really not helpful.  So we aggressively search for infection and other underlying causes. We do BALs early on to find infection or bleeding.  We do CT scans early on if patients are stable enough and we think they may help us. We do echocardiograms quite routinely, and we do all the other great ICU care that we  do for every other patient, so lung protective ventilation, trying to protect the kidneys, meticulous fluid management, good nutrition, and trying to prevent other adverse events.  There's a big debate in these patients is noninvasive versus invasive mechanical ventilation.  With some people feeling noninvasive, ventilation decreases your risk for later associated infections,  whereas others feel that noninvasive is just delaying the inevitable intubation, and when you delay that, your mortality rate is increasing.  SEARCH was a study done by the Polizzi Group. It had 222 patients out of 12 centers. It was a retrospective study looking at lots of different ventilation data.  What we found was that the longer you were in ICU prior to being intubated, the worse you did. So the longer you were on high amounts of oxygen, the worse you did as well.  In terms of our noninvasive patients, we also found with these patients that the longer you were on noninvasive ventilation prior to being intubated, you had a higher mortality,  so those on it more than 48 hours did worse. Alternative ventilation, such as high frequency or APRV, the numbers are small, but these  patients had very high mortality rates, but maybe they were sicker. ECMO is another thing we debate.  Many think it is futile, but it is increasingly being used and looks a little more promising than we previously thought. We definitely need more research.  There's a joint conference of the NHLBI, NICHD, and NCI that said we need more research, and  in fact, they came out with a notice of scientific interest recently asking for this as well. So in conclusion, advances in transplant have allowed us to take care of higher risk  patients. We have a better understanding of their complications and their outcomes are improving, but they're still not great, and more research is definitely needed.  Thank you for allowing me to talk today.

Video Summary

The video transcript discusses the care of critically ill transplant patients. The first speaker emphasizes that transplant patients are complicated to care for due to the multiple medications they require and the unique syndromes they can develop. The talks in this session focus on the basics of immunosuppressive medications, prophylactics, and the management of stem cell transplant patients. The second speaker discusses the array of immunosuppressive medications and infection prophylactics used in transplant patients, particularly in the critical care setting. The speaker explains the goals of immunosuppression in optimizing combination regimens, minimizing rejection, and toxicities. Different induction immunosuppressive medications are mentioned, such as IL-2 receptor antagonists and thymoglobulin. The speaker also discusses maintenance immunosuppression, which often includes calcineurin inhibitors, mycophenolate, and prednisone. The management of immunosuppression in the ICU is emphasized, taking into account factors such as patient-specific risks, infection concerns, and absorption issues. The second presentation focuses on critical illness after stem cell transplant, particularly respiratory failure. The speaker mentions complications such as infections, graft-versus-host disease, transplant-associated thrombotic microangiopathy, and non-infectious pulmonary complications. The management of these complications, including the use of antimicrobials, steroids, and targeted therapy, is discussed. Finally, the speaker presents an approach to respiratory failure in stem cell transplant patients, emphasizing the importance of early diagnosis, treating underlying causes, and providing aggressive supportive care.

Asset Subtitle

Transplant, 2021

Asset Caption

The Society of Critical Care Medicine's Critical Care Congress features internationally renowned faculty and content sessions highlighting the most up-to-date, evidence-based developments in critical care medicine. This is a presentation from the 2021 Critical Care Congress held virtually from January 31-February 12, 2021.

Learning Objectives Explore the array of immunosuppressive medications and infection prophylactics in transplant patients and management in the setting of critical illness Develop an approach to sepsis in transplant patients, including recognizing atypical sepsis presentations, initiating appropriate diagnostics, and implementing empiric therapies to treat the broader range of infections affecting this population Develop an approach to unique critical illness syndromes in stem cell transplant (SCT) patients, including graft-versus-host disease and SCT-specific syndromes resulting in respiratory failure

So Many Transplant Drugs, So Little Time Alley J. Killian Critical Illness After Stem Cell Transplantation Jennifer A. McArthur

Meta Tag

Content Type Presentation

Knowledge Area Transplant

Knowledge Level Advanced

Membership Level Select

Tag Transplant

Tag Stem Cells

Year 2021

Keywords

transplant patients

immunosuppressive medications

stem cell transplant

critical care

respiratory failure

complications

supportive care

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