SCCM Resource Library-Year in Review: Anesthesiology

Video Transcription

Hello. Good morning, everybody, and welcome to our anesthesiology year-end review. I'm Ranjit Deshpande. I'm moderating this session, and we have three great speakers. Our first  speaker is Dr. Sudarshan Sethi from Minnesota, and he's going to talk about lung transplant for the generalist intensivist. Our second speaker is Dr. Jarwa Chow from Chicago, and  she's going to talk about top articles in anesthesiology from 2019. And then Craig Jabeli is from Emory. He's the division chief of critical care there, and he's going to talk  about cardiopulmonary resuscitation and emergency airway management. So with that, I'm going to invite Dr. Sethi to come up and start his talk.  Good morning. I'm Sudarshan Sethi. I'm an assistant professor at the University of Minnesota,  somewhere in the cold north from here. Today, I'll be talking about lung transplants for the general intensivist. I would like to thank the organizers, the education committee, for  the opportunity to speak here. I have no disclosures. Objectives for this talk. So talking about  lung transplants in 15 minutes is next to impossible. So I'm going to highlight a few things. Then I will talk about a few other things that I feel is important for the intensivist  to know in a little more detail. So we'll go over some select surgical and interoperative details and how that can affect your patients in the ICU. We'll talk about primary graft  dysfunction and ventilation strategies for the newly transplanted lung. And if there is time, I'll talk about the other stuff, other critical care issues and immunosuppression  and antibiotics. So this is the database from ISH-Healthy. That's the International Society for Heart and Lung Transplantation. And do they have a laser pointer? No laser  pointer. I'm going to hover my mouse around here. Hope you guys can see that too. Yep, you can. All right. So the bars in green is North America. And if you see from like the  mid-'90s to now, this is the number of centers reporting lung transplants. And it has not changed much. So the overall number of centers across the world has come down a little bit.  What about the number of transplants that have been performed so far? So this is data from like 2017 to 2018. And they did close to about 4,000 lung transplants. And from  the day we started doing lung transplants to 2018, it's about 70,000. So I'm proud to say that the University of Minnesota celebrated its 1,000th lung transplant a couple of years  ago. So we are probably at like 1,100 now. So as intensive as you might come across patients  pre-transplant when they have respiratory failure or after they get their lung transplant,  I'm not going to like dwell too much into the pre-transplant part of it because that's more of the medical ICU. I think like it's more important for us to know like issues with  like post-lung transplant. It could be either the single lung or double lung transplant.  Some select intraoperative details. The incision. How do they put the lungs in? Either a clam shell, which is like bilateral subcostal, thoracotomies, one side or two sides,  or a median sternotomy. And why is this important to us? It'll influence like how pain is managed  post-operatively. You can imagine, you know, if the patient has like a bilateral clam shell or  a thoracotomy, patient is doing great, gets extubated, has pain issues, and doesn't breathe  well, atolactasis, so on and so forth, versus median sternotomy, which is reportedly not that  painful. What we do in our center is we put in like bilateral paravertebral catheters on the  day of extubation and keep them in for seven days post-op. What affects the choice of incision?  Surgeon preference, whether they want to do this procedure off-pump or on-pump, or they're doing  like a single lung or double lung. Intraoperatively, they do three anastomosis. So if you  come from posterior to anterior, that will be the bronchus, the pulmonary artery, and the pulmonary  vein. What is not anastomosis? This is probably more important to know. The bronchial artery is  not anastomosis. Why is this important? It can cause a lot of complications after the transplant  is done. It can cause bronchial anastomosis, dehiscence, necrosis, infections. This is an  artist's rendition of the left hilum of the lung, not color-coded. Don't go with the color here. So  most posterior is going to be a left bronchus, and anterior to that is your pulmonary artery,  and then you have the two pulmonary veins. And so when they reperfuse the lung, it's kind of  important. There is some data to suggest that if the lung is reperfused slowly over 10 minutes,  the incidence of primary graft dysfunction is reduced. Again, small studies from a single  center. The other issue that we have to think about when you get a patient in the ICU is you  have to find out whether this procedure was done on ECMO or cardiopulmonary bypass. Why do patients  need to go on any kind of circulatory support bypass for ECMO when the transplant is being performed? About 40% of them require the cardiopulmonary bypass support for circulatory  reasons. They don't do well. Their pressures are dropping. You have to support the pressure. You  put them on cardiopulmonary bypass. Interoperative TE. Our center, we are not big on using TE  intraoperatively, but we do use it when patients have pulmonary hypertension, right heart issues,  and to check the anastomosis on the pulmonary venous anastomosis. If they have performed a  TE, it's good to know because if you have higher velocities on the pulmonary venous anastomosis,  they're more likely to have stenos and cause issues in the postoperative period. And when  you are doing this procedure, usually we have to do lung isolation, so we place big double lumen  tubes. At the end of the procedure, though, when the patient is being shifted to the ICU, we usually switch it out to a single lumen tube, a big single lumen tube, like 8 or 8.5,  so that they can do a seated bronchoscopy as easily in the ICU. This sometimes becomes an issue. There's so much edema, sometimes like massive blood transmission that's performed,  that it's not safe to take the double lumen tube out. So what do you do in those situations? What  we have done is we have converted the double lumen tube to a single lumen, if possible. If not,  you just pull the tube back and leave the tip in the trachea. It'll essentially work like a single  lumen tube, but you have to inform the ICU faculty or ICU team to treat it like a single lumen tube,  and when the edema subsides in a couple of days, we can switch it out to a single lumen tube safely.  Inhale nitric oxide, inhale prostaglandin, mildenone, sometimes used for oxygenation  issues or to support your right ventricle. This is a big issue, ECMO versus cardiopulmonary bypass.  How many of you are familiar with these two modalities in the operating room? Good, about half of you. So what's a big difference between these two? Cardiopulmonary bypass and  ECMO, the circuit is the same. You're draining blood from the right side and putting it back onto the left side of the heart. They get oxygenated, provides blood pressure support.  What is different is the length of the tubing between the two. The ECMO circuit is smaller,  and the ECMO circuit doesn't have a reservoir. There's no venous reservoir. How does this change  things? If you have a venous reservoir, there's something called a cardiotomy suction. From the  surgical field, if there's bleeding, the surgeon puts in a suction cannula. That's the cardiotomy  suction. The blood comes directly into the venous reservoir, and when you need volume,  you can ask your perfusionist to pump the blood back in. Advantage of this, whole blood goes in,  whole blood goes into the venous reservoir, and you can put it back into the patient. The disadvantage, though, is the inflammatory cascade is activated more if the blood is just  sitting there versus the ECMO. In ECMO, what happens is there is no venous reservoir. So  from the surgical field, all this blood goes to a suction canister, a cell saver. What happens  to the cell saver is whole blood goes in, only PRBCs come out. So you're losing platelets. You're  losing clotting factors, but the inflammatory response is much lower. So what does that mean?  Primary graft dysfunction, renal complications, AKI leading to renal replacement therapy, tracheostomies, and requirement for higher anticoagulation goals. So that's with the  cardiopulmonary bypass. If you see here, higher ACT goal, inflammatory cascade activation is  higher, higher PGD, renal complications. All this is lower with VA ECMO. So the trend across the  country and across the world is to do these procedures on ECMO. The operative time and  ischemic time is similar in these two modalities. What is primary graft dysfunction? So we'll look  at the incidence, how you diagnose that, what is factors you can kind of predict to see if the  patient's going to develop PGD, and how do you treat this. The incidence overall of some grade  of primary graft dysfunction is about 30% after lung transplant. How do you diagnose this? Simplest  terms, hypoxia, infiltrates on the chest x-ray. This is a chest x-ray from a patient who got  bilateral clamshell incision. This is like two days later. The patient was not doing well, hypoxic,  and you see like the infiltrates. And the red arrow there is the VV ECMO cannula. This is the  veno venous ECMO cannula. So blood sucked out from the right side, gets oxygenated, and then put back  into the right side. There is a scoring system that the ISHLT has put forward for primary graft  dysfunction. So this is the scoring system. And if you see, you look at the scores at 0, 24, 48,  and 72 hours. And you look at the presence or absence of infiltrates on the chest x-ray and  the P by F ratio. It's more or less like ARDS. You look at the ARDS data and like this one,  you look at the P by F ratio and the absence or presence of infiltrates, and then you can grade  them. If the PGD is worse, grade 3 is being worse than grade 0 or grade 1. And as we saw, the outcome can be very different. Great. So what are the risk factors for primary graft  dysfunction? In the recipients, if you have a patient whose primary diagnosis is sarcoidosis,  IPF, pulmonary arterial hypertension, or the patient has like higher pulmonary artery pressures,  is obese, higher risk for developing primary graft dysfunction. What about the donor? Most of this is very intuitive. If the donor has been smoking or has an aspiration, pulmonary  contusion, chest trauma, has like purulent secretions and bronchoscopy, traumatic brain injury, has prolonged mechanical ventilation, they are more likely to develop PGD in the  transplanted lungs. But more often than not, it's not easy to find this information when your  patient is not doing well. Why do we need to worry about PGD? Mortality goes up. Worse the PGD,  mortality is worse. And all-cause mortality goes up in patients who have primary graft dysfunction. And as you all know, the interaction of like the different organs in the body,  one is not doing well, you do things to support that, side effects, some other organ fails. And  it's not just that acute period where you're talking, you're trying to take care of the patient in the ICU. If the patient makes it out of the ICU, the incidence of chronic lung  dysfunction is also higher in patients who have primary graft dysfunction, immediate post-operative.  How do we prevent this? Can we prevent this? There are some ways we can minimize or reduce the incidence of primary graft dysfunction. Starting with management of these lungs in the  donors. EVLP, ex vivo lung perfusion. Lungs are kind of unique that these organs are more prone  to ischemia. It's harder to find. About a third of the lungs that are posted for harvesting,  like they don't make it to the recipient because something will come up like contusions or they  don't survive the journey, the ischemic time is too long. So this is where like the ex vivo lung  perfusion will matter. I will talk about this in the next slide. The other big thing is donor-recipient  matching. So currently the matching from the donor and the recipient is based on like a couple of  things. Blood group and the predicted total lung capacity. What does the predicted total lung  capacity based on? The gender, age, and height. Now think about this. You have a patient who has  idiopathic pulmonary fibrosis. If you look at the predicted total lung capacity, it will give you a  number. Let's say like two liters. But because the patient has had idiopathic pulmonary fibrosis,  his lungs are small, his chest cavity is small. Now the predicted total lung capacity for the  patient with IPF is similar to one who doesn't. So you take lungs which are bigger. Let's say  the donor has like big lungs but somewhat similar predicted TLC. You get those lungs, put it in this  patient with IPF. Now you end up with lungs which are too big for that cavity. As a result, sometimes  it's not easy to close the chest. And we have seen sometimes patients will come back like in a couple  of days for lung reduction surgery. They'll take out like one lobe or like a segmentectomy and then  close the chest. On the other hand, you have a patient with COPD who is the recipient, has like  huge lung cavities, and you end up with like smaller lungs. Both situations are bad. But which  is worse? If you put in smaller lungs in a bigger chest cavity, they tend to do poorly because of  higher incidence of primary graft dysfunction. This we know from our ARDS data. If you use like  high tidal volumes in smaller lungs, they don't do so well. So judicious use of blood transfusions and as I mentioned earlier, like Cell Saver, which is part of ECMO, is better than  cardiotomy, which is part of cardiopulmonary bypass. And use lung protective ventilation strategies in the post-operative period. So this is ex vivo lung perfusion.  I have five more minutes. Let me see if I can get through the rest of it. So there's like a couple  of FDA approved commercial products for ex vivo lung perfusion. So in a nutshell, this is what it  is. You take the donor's lungs, and if they're marginal for whatever reason, the patient has  like not been doing well, oxygenation is poor. You try to optimize that. How do you do that? Avoid  the ischemic time or minimize the ischemic time. You are pumping around either, you know, warm blood  or like a perfusate using like some kind of like mechanical device. It's similar to what is done  for like kidney transplants, but this is for lungs. And then you get the lung on this machine to your  recipient site, and then you take a look and see if the lungs are improving based on like  oxygenation, the airway pressures. And if they're improving or stable, then you put them into the  recipient. So they found that the long-term survival and lung function, even on these  marginal lungs who have gone through this ex vivo lung perfusion, is the same as conventional lungs.  And this is what one of them looks like. This is the transmedics machine. What do you do for treatment for primary graft dysfunction? In many ways, it's similar to treating ARDS.  Use fluid carefully. Inhale nitric oxide and epiprostenol. Improves oxygenation. We don't know  about like the long-term outcome if it changes mortality. And if this doesn't work, we also turn  patients prone if they're hypoxic. And if these don't work, you put them on some kind of like  extracorporeal life support. We know venous or we know arterial ECMO. And if everything else fails,  you can consider them for retransplant. If you retransplant earlier in the course, then they do much better than retransplants much later in the course. And this is a slide on like  normal therapy. Surfactants, complement inhibition, platelet activating factor antagonists have some  benefit, but not widely used. There was more interest in this like a few years ago than now.  What about ECMO and lung transplants? You can run into these patients pre-transplant or post-transplant. You can use this as a bridge to transplant or a bridge to recovery.  In the bridge to transplant, there is something called as awake ECMO. So these are patients who have like a big venous scanner on the neck, are extubated, sitting up in a chair. And  when the lungs become available, you put the lungs in. Mechanical ventilation.  So you have to use like some kind of ideal body weight to calculate the tidal volumes. Which one  would you use? The donor versus the recipient. Based on what I told you and like what I've  seen earlier. So if you use the donor ideal body weight, you will probably be better off.  But even then, like it's very controversial. We don't know like how to ventilate these lungs.  And challenges with assessing volume. This is good like not just for lung transplants,  but any other patient in the ICU. Your chest X-ray is not a good way to assess volume status of a  patient. You can use like dynamic indices of volume responsiveness, which may be challenging  in these patients. Sometimes they leave the chest open because the lungs are not doing well.  Then some of these are like off. And if the patient has pre-existing RV dysfunction, you should account that also into your fluid management. This is a slide from like a patient  who had severe pulmonary hypertension pre-transplant. And if you see that red arrow is measuring the thickness of the right ventricle. It is usually like way lesser  than the left side. But if you can see here, like this is about like three and a half centimeters,  which is like a very thick right ventricle. This is how the right heart looked post-transplant.  Now all of a sudden, the right heart is like completely decompressed because the pulmonary pressures are lower. And it looks like it's not moving at all, but it was doing its job.  The left heart was getting like the flow.  Other critical care issues. Atrial arrhythmias are very common in patients after lung transplant  for like various reasons. They anastomose the pulmonary veins there  that can set off the atrial arrhythmias. Atrial fibrillation is very common in up to half of the patients. So what do you do with these patients? You do like rate control  in the immediate early post-op period, and then rhythm management maybe with amiodarone.  Long-term anticoagulation is still very controversial. And airway complications, depending on like which study you look at, between 15 and 70% of the patients at some point  in the post-transplant care will develop some kind of airway complications. Could be necrosis  or dehiscence, or could be infected. And sometimes like stenosis, which presents usually later.  A lot of these lung transplant patients present to you with a lot of anxiety pre-transplant. They have this feeling of dyspnea that usually sometimes doesn't get better after  the lungs go in. It takes a lot of like TLC to assure them that the new lungs are in, they're  working. Sometimes showing them objective data will help, saying that your saturation is better,  you're not on oxygen. And delayed chest closure. You will hear probably hear this like from your  surgeons when they say, you know, we'll close the chest on Monday. Today is Friday. We'll come back  on Monday and close the chest. They found that it's an independent risk factor for surgical  site infection. So if your surgeon tells you this, like maybe you can use this data to tell them,  like maybe you can do this on Friday, don't wait for Monday. Acute kidney injury in up to half of  the patients. And what are the risk factors? Use of vasopressors, intraoperative hypertension, post-operative hypertension, nothing new here. Pulmonary hypertension.  All right, so infectious complications. Let's skip this. And so immunosuppression, last slide.  So it's induction, maintenance, and treatment of ejection. The ejection is highest in the first  six months after transplant. So you induce with like different agents and maintenance depending  on what the renal function is. So the idea is you use like some of like many medications so that  the complications are and side effects are reduced. All right, in summary, they're complex  patients to care for. PGD can be difficult to manage. Use mechanical ventilation strategies similar to ARDS.  Anyway, that's all I have for you. Just want to say something about the last slide in 10 seconds. Minnesota is farther up north. It's really cold. Winters are like on a good day,  it's like minus 20. I'm just kidding. But we do have a lot to offer. This is on a frozen lake in Minnesota, in downtown Minneapolis. You can also get to take some pictures with  some luminescent penguins. Thank you.  Thank you, Dr. Sethi. I'm going to have Dr. Chow, who's from Chicago, come and talk about the top articles in anesthesiology from last year. She's an assistant professor of  anesthesiology at the University of Chicago and does a lot of work in the surgical ICUs and works with liver transplants.  Hi, good morning. We don't have a lot of time to cover 10 articles. I'm actually just going to jump right into it.  First we have bagged mass ventilation during tracheal intubation of critically ill adult patients.  The authors hypothesized that bagged mass ventilation would increase the lowest oxygen saturation during the interval from induction to two minutes after tracheal intubation versus  no ventilation. So this was a multi-center parallel group unblinded randomized trial.  They included adult patients undergoing induction and tracheal intubation, and they had standard exclusion criteria for their protocol for bagged mass ventilation.  They used a flow of 15 liters per minute, PEEP of 5 to 10. The intubating provider utilized a two-handed mass seal with a head-to-chin lift, oropharyngeal  airway, 10 breaths per minute with the smallest volume required to generate a visible chest rise.  As you can see, the primary outcome of median lowest oxygen saturation was statistically  significant at 96% in the bagged mass ventilation group versus 93% of the no ventilation group. This is a graphical representation of that same thing, and hypoxemia was also lower.  So the authors concluded that in critically ill adult patients undergoing tracheal intubation, patients receiving bagged mass ventilation during the interval between induction and  laryngoscopy had higher oxygen saturations and lower rates of severe hypoxemia versus no ventilation. This study was not blinded, so that was one of the major limitations.  Next, we have the effect of a fluid bolus on cardiovascular collapse among critically ill patients undergoing tracheal intubation.  So it's estimated that about a quarter of critically ill adult patients experience cardiovascular collapse during intubation.  So these authors wanted to look at whether or not a fluid bolus would reduce the incidence of cardiovascular collapse versus no fluid bolus.  This was a multi-center, unblinded, randomized trial done in the United States. They included all adult patients undergoing tracheal intubation.  They excluded patients where there was a planned awake intubation, if the patients were too sick to be randomized, or if the treating clinician thought that a fluid bolus  was either indicated or not indicated. In terms of the intervention, they used a 500cc crystalloid bolus that was administered before the induction of anesthesia.  In the no fluid bolus group, they didn't give any more fluids between enrollment and until two minutes after they were intubated.  Cardiovascular collapse was defined as you see there. In terms of the primary outcome, there was actually no difference in any of the components  either except for pleural effusion, which was not different. In terms of subgroup analyses, they didn't find any differences except that in patients  who had pre-intubation positive pressure ventilation, there was a favoring towards the patients that got a fluid bolus.  So the authors concluded that the administration of a fluid bolus prior to tracheal intubation  in adult patients did not affect the incidence of cardiovascular collapse compared with no fluid bolus.  Limitations for this study, they didn't know what was the optimal amount of fluids, whether or not 500cc of crystalloid would be the correct amount or when to give that fluid.  The study was actually not powered, and they didn't assess how much fluids patients got prior to enrollment.  Next we have the effect of a resuscitation strategy targeting peripheral perfusion status versus serum lactate levels on 28-day mortality in patients with septic shock.  So this was a multicenter international randomized controlled trial. They included adult patients and early septic shock were randomized within four hours of fulfilling criteria.  Early septic shock and fluid responsiveness were defined as you see there. In terms of the peripheral perfusion group, they measured cap refill every 30 minutes  until it was normal, which they defined as less than or equal to three seconds, and then hourly after that.  In terms of the lactate level group, they measured it every two hours until it was normal. Although the primary outcome of death within 28 days was not statistically significant,  the p-value was actually 0.06. It was lower in the peripheral perfusion group at 34.9 versus 43.4 in the lactate group. This is the Kaplan-Meier.  And in terms of subgroup analyses, they actually found a favoring towards the peripheral perfusion group in healthier patients with lower APAGI-2 and SOFA scores.  So in conclusion, the authors found that in patients with septic shock or resuscitation  strategy targeting, normalization of peripheral perfusion as measured by cap refill time versus serum lactate did not reduce 28-day mortality.  Limitations for this study, it wasn't blinded. There was no true study prior to this to calculate a sample size.  Interrater variability for cap refill was not evaluated, and the assessment frequency between the two groups was different.  Next, we have conservative oxygen therapy during mechanical ventilation in the ICU. So this was after a 2016 study, the oxygen ICU trial that was stopped early because of  enrollment issues, where they actually found more vent-free days and lower mortality in patients who received conservative oxygen therapy.  So this was a multi-center, bi-national study done in Australia and New Zealand looking at adult patients who were expected to receive mechanical ventilation in the ICU.  They excluded patients who received over two hours of mechanical ventilation or non-invasive ventilation.  In terms of the study protocol for the conservative oxygen therapy group, the FiO2 was decreased  to 21%, or supplemental oxygen was decreased or discontinued depending on the saturation. They actually set an alarm to minimize any exposures to SATs greater than 97%.  And in the usual oxygen therapy group, no additional alarms were set, and they did not allow an FiO2 to go below 30%. In terms of the primary outcome, there was no difference.  This is the Kaplan-Meier. And so the authors concluded that conservative oxygen therapy versus usual oxygen therapy  did not significantly affect the number of vent-free days in patients undergoing mechanical ventilation. This study was not blinded.  It was actually not powered, and they utilized a different oxygen therapy protocol than in prior studies.  Differences from the 2016 trial, they did not have a high oxygen saturation limit. The minimum FiO2 was actually 40% versus 30%.  And although this study was not powered, it had a much larger sample size. Next we have the effect of post-extubation high-flow nasal oxygen with non-invasive ventilation  versus high-flow nasal oxygen alone on re-intubation in patients at high risk for extubation failure.  So this was a multi-center randomized controlled trial done in 30 ICUs in France. They included adult patients who were intubated for over 24 hours, passed an SBT, and were  considered at high risk for extubation failure. They excluded patients who required non-invasive ventilation chronically or had a contraindication to non-invasive ventilation.  For the control group, they utilized high-flow nasal oxygen for at least 48 hours with a flow of 50 liters per minute and an FiO2 that was adjusted for SATs greater than or equal  to 92%. For the intervention group, non-invasive ventilation was started immediately after extubation.  The first session lasted for at least 4 hours with a minimal duration of 12 hours per day for the 48 hours following extubation.  They utilized a pressure to target tidal volumes of 6 to 8 cc per kilo of predicted body weight,  PIPA 5 to 10, and again, that FiO2 was adjusted for SATs greater than or equal to 92%. High-flow oxygen was administered between the non-invasive ventilation sessions as in  the control group. The primary outcome of re-intubation at 7 days was statistically lower in the high-flow oxygen group with non-invasive ventilation.  It was also significant at 48 and 72 hours. This is the Kaplan-Meier. And so in critically ill adult patients requiring mechanical ventilation at high risk for extubation  failure, high-flow oxygen with the use of non-invasive ventilation immediately after extubation decreased the risk of re-intubation within the first 7 days versus high-flow oxygen  alone. The study was unblinded. They didn't standardize how the spontaneous breathing trials were conducted for these patients.  And it was unusual that they utilized high-flow oxygen in both groups. Next, we have early neuromuscular blockade in the acute respiratory distress syndrome.  So this was a study done by the Prevent and Early Treatment of Acute Lung Injury or the PETAL network.  They wanted to look at the efficacy and safety of early neuromuscular blockade with heavy sedation versus usual care with light sedation on 90-day in-hospital mortality.  They utilized a protocol that was consistent with the 2010 ACQURISYS trial. They included mechanically ventilated patients with ARDS, 48 hours.  For the control group, they targeted light sedation, so for a RAS score of 0 to negative 1.  For the intervention group, again, they utilized the ACQURISYS protocol for neuromuscular blockade and deep sedation with a RAS score of negative 5.  All patients had lung protective ventilation and then changes in PEEP and positioning were at the discretion of the treating provider.  In terms of outcomes, there was no difference in the primary outcome of in-hospital mortality at 42.5 versus 42.8. This is the Kaplan-Meier.  And so they concluded that in patients with moderate to severe ARDS, the administration of neuromuscular blockade early did not result in significantly lower mortality at 90 days  compared with usual care and lighter sedation. This study was not blinded. They excluded many patients who did receive neuromuscular blockade who may have benefited from this.  And the study was actually stopped early due to futility.  This is from the 2010 trial. Patients were enrolled much earlier. Across the board in both groups, patients received higher levels of PEEP and lighter sedation.  Next, we have intensive versus standard treatment of hyperglycemia and functional outcomes in patients with acute ischemic stroke.  Because hyperglycemia in patients with acute ischemic stroke is associated with worse clinical  outcomes, including increasing infarct size and hemorrhagic conversion, the authors wanted to look at the efficacy of intensive versus standard blood glucose control in patients  with hyperglycemic acute ischemic stroke. This was a multicenter, blinded, randomized clinical trial looking at adult patients who  presented within 12 hours glucose level of greater than 110 in diabetic patients or 150.  They excluded type 1 diabetics and any patients that required an insulin infusion for whatever reason and had any clinical condition that may have confounded a stroke assessment.  In the intense treatment group, they used an infusion. They maintained a blood glucose of 80 to 130.  In the standard treatment group, they used subcutaneous insulin on a sliding scale, and they targeted glucoses of 80 to 180.  They checked the sugars hourly in both groups initially and then 1 to 2 hours in the intense treatment group and 3 hours in the standard treatment group.  There was no difference in any of the outcomes that they looked at except for severe hypoglycemia, which was higher in the intense treatment group.  And so the authors concluded that in patients with acute ischemic stroke and hyperglycemia,  treatment with intensive versus standard glucose control did not result in improved functional outcomes at 90 days. The study was not powered.  It was actually stopped early due to futility. In the 63 sites, 6 of them enrolled over 40% of the patients, and there was a difference  in how frequently they monitored sugars in both groups. Next we have early sedation with dexmedetomidine in critically ill patients.  Because dexmedetomidine is associated with decreased time to extubation and less delirium, the authors wanted to look at dexmedetomidine as the primary sedative versus usual care  in patients receiving ventilatory support on all-cause mortality at 90 days. This was a multicenter, multinational, open-label, randomized control trial.  They included adult patients who required mechanical ventilation and were receiving sedation.  In the dexmedetomidine group, the goal was to use dexmedetomidine as the primary sedative and, if possible, the only sedative.  They started it at 1 and titrated it up to a max of 1.5. If they required additional sedation, propofol was the most commonly used, and they discouraged benzodiazepines.  In the usual care group, the provider could use whatever sedative that they wanted, and rescue dexmedetomidine was also allowed.  In terms of the clinical outcomes, there was actually no difference in primary or secondary outcomes.  In terms of pre-specified subgroup analyses, they did find a favoring towards dexmedetomidine in older patients and higher mortality in younger patients.  And so in critically ill patients undergoing mechanical ventilation, the early administration  of dex as the primary sedative did not result in lower 90-day mortality compared with usual care. This study was not blinded.  They actually excluded patients who acquired deep sedation who may have benefited from dexmedetomidine, and daily sedation interruption was not mandated in any of the patients.  Next we have the effect of intraoperative high PEEP with recruitment maneuvers versus low PEEP on postoperative pulmonary complications in obese patients.  So this was a study looking at whether or not a ventilatory strategy with high PEEP and recruitment intraoperatively could decrease the postoperative complications in obese patients  in the first five days post-op. Previous studies looking at this issue were not adequately powered, so this was a multicenter international randomized controlled trial.  They were looking at patients with a BMI of greater than or equal to 35 who required general  anesthesia for over two hours who were at intermediate or high risk for developing postoperative pulmonary complications.  In the high PEEP group with recruitment, they used a PEEP of 12, and recruitment maneuvers  were performed after intubation, repeated hourly after any disconnection from the ventilator before the end of surgery.  They standardized recruitment maneuvers to increase the tidal volume in PEEP until they reached a plateau pressure of 40 to 50.  The low PEEP group used a PEEP of 4, and postoperative pulmonary complications included the following. In terms of the primary outcomes, there was actually no difference.  Pleural fusion, which is one of the components of the primary outcome of postoperative pulmonary complications, was actually higher in the high PEEP group.  There was no difference in any of the secondary outcomes. However, in terms of adverse events, there was more hypotension and bradycardia in the  high PEEP group and more hypoxemia in the low PEEP group. So the authors concluded that in intraoperative mechanical ventilation with high levels of  PEEP and alveolar recruitment, it did not reduce postoperative pulmonary complications versus low PEEP and no recruitment in obese patients. This study was not blinded.  The recruitment maneuver, although there were limitations into how high the plateau pressures could go, how they actually conducted the recruitment maneuvers were not standardized.  And individualized PEEP for the patient or the procedure was also not done. Finally, we have the effect of cellopressin versus placebo on ventilator and vasopressor-free  days in patients with septic shock. So this was a phase 2b3 trial of cellopressin in critically ill patients with vasopressor-dependent  shock who were being treated with norepinephrine. They wanted to see whether or not cellopressin could improve vent-free days and vasopressor use versus placebo at 30 days.  This was a multicenter, multinational, blinded, randomized, placebo-controlled clinical trial looking at adult patients with proven or suspected infection in septic shock.  There were four groups. There were actually three cellopressin groups at different doses and a placebo group. There was no difference in any of the primary or secondary outcomes.  This is the Kaplan-Meier. And so the authors concluded that in patients with septic shock receiving vasoactive support,  cellopressin did not improve any outcomes for vent-free days or vasopressor-free days versus placebo at 30 days.  Limitations for this study, on average, the patients received a median of eight hours of norepinephrine prior to enrollment.  And one of the primary benefits of cellopressin was that it reduced pulmonary edema, which was not looked at in this study.  So I know I went really, really fast, but we got through the 10 articles on time. If you have any questions or comments, let me know. Thanks. Thank you.  So I can tell you this is the hardest talk, because you have to get through so many articles. I have done it in the past two years, and guys, we'll have questions in the end if we  have time. But now I'm going to call Dr. Craig Javoli here. He's from Emory. He's the division chief of critical care medicine.  And he's going to talk about a pretty interesting topic of cardiopulmonary resuscitation and emergency area management. All right. Good morning, everybody.  Thanks for sticking with us. So kind of like Ranjeet said, oh, I have no relevant disclosures.  We will discuss off-label use of both medications and some medical devices, so just keep an eye out for that.  Over the span of the next 15, 20 minutes, I'm going to go over some updates related to CPR and the area management within the context of CPR.  I'm also going to talk a little bit about resuscitation science. Where possible, I'll try to cover literature from 2019 or more recently.  I guess another potential disclosure to make would be it's been said that anesthesiologists who are good at CPR should probably not be trusted.  I mostly do critical care, so I'm going to put that out there. We're going to focus primarily on in-hospital cardiac arrest in the United States.  That's probably what the vast majority of us are doing because of the way our pre-hospital care works.  I think we all realize that in-hospital cardiac arrest is both common, and although the outcomes are better than out-of-hospital cardiac arrest, the outcomes are still not great.  Some things differentiate in-hospital from out-of-hospital cardiac arrest clinically and also make it difficult to apply lessons that we learn from out-of-hospital cardiac  arrest to what happens in the hospital. In the hospital, we know that there are additional contributors to arrest in these patients, typically respiratory and etiology.  On an out-of-hospital basis, the etiology is primarily cardiac in origin. Having said that, there are also some opportunities that we have with in-hospital cardiac arrest  that are covered elsewhere during the sessions here at the Congress, specifically relating to the recognition of deteriorating patients.  About a half of in-hospital arrests occur in highly monitored settings, the ICU, the operating room, the emergency department, where we have an enormous amount of continuous  physiologic data about these patients that offer us the opportunity to detect something going wrong and intervene earlier.  So it's a mixed bag with in-hospital arrest, some good news, some bad news. A lot of the science these days is about out-of-hospital arrest, as we'll see in a little bit.  But having said that, we have some real opportunities when it comes to in-hospital arrest. If anyone feels like it's difficult to stay up to date in this domain, there's actually  some evidence-based literature to suggest that you should indeed feel that way. In 2018 alone, there were about 1,200 publications related to cardiopulmonary resuscitation that  came out in the medical literature. Of that, the vast majority, by which I mean about a quarter, were about prognostication and neuroprognostication after arrest.  Again, over the span of the next 15 minutes, we're going to primarily focus on guidelines and some publications related to the management of in-hospital cardiac arrest.  Everyone's probably familiar, thinking back to the five-year update cycles that happened  with the resuscitation guidelines, where the American Heart Association and its international partners would get together every so often and re-review the literature.  As the amount of literature in resuscitation science is really ratcheted up, to the credit  of the AHA and its international partner organizations, they moved to a more continuous evaluation of the literature.  And indeed, we have the 2019 update published by the International Liaison Committee on Resuscitation.  The good news, and I'm going to walk off the stage now, I'm kidding, is that they said that there are no major changes in adult treatment recommendations.  But having said that, when you go through the three areas of focus for the 2019 update,  which were advanced airway management, vasopressors, and extracorporeal CPR, I think that there are some trends that we can tease out and some things that we can see if we look into  the future that I want to talk about today. 2018 was a great year for randomized control trials about airway management during CPR.  All three of the large trials, and we covered actually all three of these last year, all three of these trials were in out-of-hospital environments.  And if we drill down and we look at the success of tracheal intubation in two of these studies, it was really quite low.  And although we don't know what the average success rate of tracheal intubation is during in-hospital arrests, I would certainly hope that it's probably better than 70% in most  of our institutions. There was one trial that had a relatively high success rate that we'll focus on in just a second. I do want to set the stage and just rewind to 2017 real quick.  A lot of people may have seen this publication in JAMA. I remember when I read it, so just to set the stage a little bit, this was a large retrospective  study that utilized a registry that's maintained by the American Heart Association called the Get With The Guidelines Resuscitation Database.  And many of your institutions and many of you indeed may be reporting data back to the AHA. Our institution is actually about to start doing that.  And what Anderson and his colleagues did in this particular investigation was to look back and to examine exactly what happens to patients who got definitive airway management,  meaning endotracheal intubation, during their code. And I remember when I first was looking at the results of this study, I said to myself  like, oh, yes, shockable rhythms, maybe we should see if we can defibrillate them out of those before we instrument the airway.  Medical non-cardiac, those are probably respiratory arrests, yes, they should probably have endotracheal tubes. Patients with respiratory insufficiency, yes, this makes good sense.  Patients in the ICU. And then I saw, oh, wait a second, Unity's way over there, way over there.  So the bottom line summary of this trial was that it suggested that definitive airway management  during codes can be potentially risky for our patients due to probably the interruption of chest compressions in some instances.  So with that being the stage about in-hospital airway management, I want to focus on this trial by Patricia Jaber and her colleagues that came out late in 2018.  And again, pre-hospital study, looking at randomized control trial comparing bag mass ventilation to endotracheal intubation, really with a focus on neurologic outcomes.  Primary function, or sorry, neurologic function at 28 days being the primary outcome. As we talked about earlier, the rate of airway failure in this trial was very low.  And that's because, probably, they used a physician-based pre-hospital care system in France and Belgium where the trial occurred.  They randomized 2,000 patients, which is very impressive. And again, the bottom line summary is that the neurologic outcomes were equivalent.  They had more ROSC in patients that were intubated, but 28-day survival was, again, equivalent.  Like I said, very low failure rates for definitive airway management and bag mass ventilation.  Bag mass ventilation was associated with more complications, like aspiration, which I'm sure we've all had the pleasure of witnessing in our clinical practices.  These findings have also been supported in other large retrospective investigations using big data registries.  Again, I'll highlight another one, this one also using the large registry that's maintained by the American Heart Association.  So if we take a look here at our first outcome, which was survival to discharge, essentially what they did was they looked at institutions and they divided them in quartiles by the  likelihood of patients getting tracheally intubated during their code. And they divvied them up into one, two, three, and four, one being the quartile of hospitals  that had the lowest rate of tracheal intubation during codes, quartile number four having the highest incidence.  And interestingly, survival was more likely in hospitals where you were less likely to get intubated during your code. So I'll highlight some of these.  Ditto with ROSC, and we see a relatively clean association as we move across these quartiles. And ditto with 24-hour survival, which is very interesting, very interesting.  So to summarize quickly, you know, we as, show of hands, anesthesiologists in the room?  Hopefully a good number, yes, we as anesthesiologists, sometimes when we're not wearing our critical  care hat, our primary role at codes is airway management, the kind of traditional thought that every patient who's coding needs a definitive airway.  Maybe we should challenge, this led, and I won't read these, but this led to these recommendations from the liaison committee in 2019, which I think is very interesting. All right.  On the subject of airway management, Jarva just covered the PREPARE and the PREVENT trials. Again, just to summarize very quickly, PREPARE trial, 500 cc's of fluid, no difference in  adverse cardiovascular outcomes. Some suggestion trial was stopped early for a variety of different reasons, largely because of how enrollment happened.  Some suggestion that patients who are on positive pressure mechanical ventilation could benefit from a crystalloid bolus.  Again, not in the bottom line summary of the trial, so I'll leave that there. PREVENT trial suggests that if you squeeze the ambu bag, patients desaturate less often.  Bottom line summary of that trial. One trial I do want to highlight about, again, out-of-hospital emergency airway management,  which was published in JAMA back in December of 2019, randomized control trial of Sucks and Rock for out-of-hospital airway management of patients that had coded.  They gave a good dose of Rock, 1.2 mg per kg, 1 mg per kg of Sucks. This was a power designed to be a non-inferiority trial.  Interestingly, findings of the trial favor succinylcholine, higher first pass success rate when it came to intubation, and also some difference at the subgroup level as well.  And as a Rock uranium fan, I felt very sad. So I'll just leave that out there. So we covered airway management. That was area number one.  Pardon my phone check while I make sure that we don't take too much of our collective time.  I want to move on to the subject of vasopressors. So I think we all know that for a long time, we did not have good randomized clinical trials  to really inform the question of whether or not giving high-dose vasopressors to people who have coded is a helpful intervention.  I know it sounds silly because it's so ingrained in our routine management of these patients. Over the past few years, there have been a few trials.  I don't want to focus too much on that. But one suggestion that has come out of these trials is that there may be a differential  effect of vasopressor administration in patients who code with a shockable rhythm and patients who code with a non-shockable rhythm.  So the authors of the Paramedic 2 study did a meta-analysis of their data and the data from another trial.  Interestingly, like a very weird thing in medical publishing, the authors provided their pre-hospital data, or sorry, provided their pre-publication data to the AHA, who did their  own meta-analysis. The authors then went on to do their own meta-analysis separately, something about the least publishable unit maybe. I'm not sure. But it's interesting.  So we had these two competing meta-analyses. Interestingly, the trials or the two meta-analyses are a little bit different. So I focused on the one that was done by the authors.  And if we compare ROSC and looking at shockable rhythms versus non-shockable rhythms, we see  that there was a little bit more of a treatment effect, if you will, looking at these odds ratios and confidence intervals, a little bit more of a beneficial treatment effect  with epinephrine in patients with a non-shockable rhythm compared to a shockable rhythm.  And ditto, if we look down here at survival, we see that the impact of epinephrine on survival  in patients with a shockable rhythm was different than the impact of epinephrine on survival in patients with a non-shockable rhythm. So this was a little bit of a course analysis.  I think it was pretty well done. This was recently re-evaluated in another paper that was published in Critical Care last month, actually.  A little bit more of a, I think, kind of nuanced analysis, again, looking at the difference between placebo and epinephrine in patients with shockable rhythms over there on screen  left, non-shockable rhythms over there on screen right, which I think is fascinating. We see in patients with shockable rhythms, we don't really see a divergent treatment  effect until somewhere in the maybe five-minute range, suggesting that, again, if you've got a shockable rhythm, you can get defibrillated out of it quickly.  Maybe some benefit to holding off, or maybe at least some equivalent treatment effect with holding off from epinephrine for a little bit of time.  You've got a patient with a non-shockable rhythm, it seems important to get them the epinephrine as quickly as is humanly possible. Don't just take these studies' words for it.  These have been studied in kind of other large registry studies, retrospective investigations. I won't highlight this for too long, other than to say that we have a growing body of  evidence to suggest that there may be a differential treatment effect of high-dose vasopressors amongst patients with shockable rhythm, non-shockable rhythm.  And then, to my knowledge, for the first time, this has started to emerge in the bottom line summary from the International Liaison Committee.  Whether or not this will be reflected in ACLS 2.0, we're due for another ACLS update relatively soon, remains to be seen.  But we're starting to see some change of thought about the role of epinephrine in shockable versus non-shockable rhythms.  For those of us who work in cardiothoracic-heavy ICU environments, we have now some relatively  well-evidenced-based guidelines about resuscitation, starting to delay epinephrine administration in these patients.  And I'd be curious to see, like I said, if that bleeds over into ACLS territory after a period of time. All right. So that's airway, vasopressors.  That brings us to number three, which is extracorporeal CPR, eCPR. Quick show of hands, patients with eCPR, formal eCPR programs at their hospitals. All right.  More than I would have expected. Yeah, correct. Hand-waving for us at Emory. Yeah, if we use the term formal loosely.  So eCPR has certainly become a lot more common around the world. I'll make just a blanket statement and say that Western Europe, I think, is kind of farther  ahead than North America, broadly speaking. The question of the impact of eCPR on clinical outcomes in patients who have obviously arrested  has been the subject of a lot of publications, retrospective publications, a lot of different outcomes. These were systematically reviewed recently.  There was a plan to do a meta-analysis, but there was too much heterogeneity between these different investigations to where the authors of the review really felt like they couldn't  definitively determine what the pooled treatment effect was. Again, the literature, pretty mixed.  If we look at just a subset of the outcomes that were examined in the systematic review, we have up here on the top long-term survival.  We have on the bottom favorable neurologic outcomes at discharge, some mixed effects in these different trials.  There was a new investigation published, I think, five days ago in Intensive Care Medicine that I want to highlight.  This is a very interesting investigation, I think, for a number of reasons, and we compare it against a lot of the other retrospective investigations that have been done.  Comes from five hospitals with a formal eCPR program, sharing kind of similar clinical guidelines, similar activation and initiation criteria, offers a lot of information about  patient-specific comorbid conditions and demographic factors that don't exist in a lot of other retrospective investigations in this domain.  Also a relatively large study, so I want to highlight it. I think it's both recent and I think it's extremely relevant to this question.  Spoiler alert, and we'll get there in a minute, the liaison committee had a very difficult  time identifying good literature in this domain to really inform their recommendations, and I think that this particular five-day-old investigation really offers something new.  So like I said, five European centers, 2012 to 2016, out-of-hospital cardiac arrest comprised about 268 patients in the study. In-hospital cardiac arrest comprised 155.  They did a post-hoc analysis of what they called good candidates. There is actually some literature out there to suggest what a good candidate for eCPR  might be, the commonly accepted criteria being witness arrest with CPR within five minutes of the code, refractory arrest, meaning that you haven't gotten ROSC after 10 minutes,  patients who are under the age of 65, no severe comorbid disease, which is defined by these  criteria up here, and that also the initiation of extracorporeal support within 60 minutes is feasible.  And when they examine, again, I want to focus a little bit on in-hospital cardiac arrest, I think it's the most clinically relevant for the majority of us, in examining in-hospital  cardiac arrest, about two-thirds of patients, interestingly, had an initial shockable rhythm,  which does not really match our demographics about in-hospital cardiac arrest in the United States very well, so I'm going to leave that there.  Eighty percent of patients who were arrested in the hospital did receive eCPR, the average time from arrest to initiation of full support was 44 minutes, pretty good, interquartile  range of 30 to 60 minutes, first lactate on ECMO was 10.9, again, pretty good, and their survival statistics in this series are not bad, 34% survival to ICU discharge, and of  those, 36% had favorable neurologic outcomes, which if you remember way back 15 or 20 minutes ago, beats the odds for what we think the kind of overall outcomes in this cohort of  patients are. So again, I'll show you some survival curves, screen left, survival, screen right, survival with favorable neurologic outcomes.  As always, the good stuff is buried in the supplement, so if you read this paper, it's in the supplement.  They broke down the outcomes further amongst patients who are considered to be good candidates,  this is a very confusing figure, the bottom line summary is that patients who are considered  to be good candidates, roughly speaking, had a mortality rate of 44%, and they had a favorable  neurologic outcome rate, or sorry, unfavorable neurologic outcome rate of 38%, meaning on  the flip side, 56% of patients who are considered good candidates survived to ICU discharge, which is pretty good, pretty good.  So again, if we go back to the bottom line summary from the International Liaison Committee, they say, well, we need to do a little bit more work in this domain.  I want to take one more of your minute to talk about something that could be coming soon. Quick show of hands, who's heard about heads up CPR?  Heads up CPR, okay, an emerging concept in resuscitation science. Right now, some evidence from porcine and canine models that doing closed chest compressions  with the head elevated may be associated with more favorable cerebral perfusion pressures. Your supine, you have no cardiac output, you develop venous and arterial stasis, your ICP  starts to go up, and in animal studies, so again, at the bottom here, we have standard positioning, these purple and green plots.  At the top, we have heads up positioning, and again, kind of worrisome, this is in porcine models, but around 15 minutes, we start to get a cerebral perfusion pressure of zero  in conventional supine closed chest compression CPR, which is worrisome. That might explain why patients who get coded for longer than 15 minutes tend not to do well.  The question has been, how in the world do you translate this into humans? And there are actually, in the United States, here in Florida, believe it or not, there  is a pre-hospital system that has done this. And they published their experience, again, relatively recently in critical care medicine,  using an automated chest compression device, head of the patient elevated, and again, this was a feasibility study, but their outcome data are very interesting.  They basically just did before-after study here, and you see here in the blue plot, their survival numbers before they started doing this, their transition period in red, and  the green plots are their survival after they implemented this in their single pre-hospital EMS system. You will see more publications about this over the next two to three years.  It's coming at you. Thank you to everybody for your attention. Thank you.  Thanks, Greg. So we barely have time for maybe one or two questions at the max. Any questions? Thank you, everybody.

Video Summary

In this video transcript, Dr. Sudarshan Sethi from the University of Minnesota discusses lung transplants for the generalist intensivist. He covers surgical and intraoperative details of lung transplants, including incision options and anastomosis techniques. He also talks about the risk factors for primary graft dysfunction and its management, as well as infectious complications and immunosuppression. Dr. Jarwa Chow from the University of Chicago talks about the top articles in anesthesiology from 2019. She discusses studies on bag-mask ventilation during tracheal intubation, fluid bolus during tracheal intubation, targeting peripheral perfusion status versus serum lactate levels, conservative oxygen therapy during mechanical ventilation, and early sedation with dexmedetomidine in critically ill patients. Finally, Dr. Craig Javelli from Emory University discusses cardiopulmonary resuscitation and emergency airway management. He covers updates on airway management, vasopressors, and extracorporeal CPR. He highlights studies on the impact of definitive airway management during cardiopulmonary resuscitation, the use of vasopressors in different rhythms, and the outcomes of extracorporeal CPR.

Asset Subtitle

Pulmonary, Transplant, 2020

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 2020 Critical Care Congress held February 16-19, 2020, in Orlando, Florida, USA.

Learning Objectives

Recognize immediate complications after lung transplantation and develop strategies to manage them
Review impactful literature in anesthesiology critical care medicine for the year 2019
Evaluate recent literature on emergency airway management
Summarize current concepts in the conduct of cardiopulmonary resuscitation

Lung Transplants for the Generalist Intensivist

Sudarshan Setty

Anesthesiology: Year in Review 2019

Jarva Chow

Cardiopulmonary Resuscitation and Emergency Airway Management

Craig S. Jabaley

Meta Tag

Content Type Presentation

Knowledge Area Pulmonary

Knowledge Area Transplant

Knowledge Level Intermediate

Membership Level Select

Membership Level Professional

Membership Level Associate

Tag Ventilation

Tag Airway Management

Tag Organ Transplantation

Year 2020

Keywords

lung transplants

surgical details

anastomosis techniques

primary graft dysfunction

infectious complications

anesthesiology

tracheal intubation

conservative oxygen therapy

dexmedetomidine

cardiopulmonary resuscitation

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