My name is Andre Holder. I am an assistant professor at Emory University, and I'll be moderating this session here today. So for those of you who are unsure or maybe not sure where you are, this is the challenging cases in the ICU session. So if you wanted to stay for this one, please, and I invite all of you to stay. The first thing I will ask is if everyone, since we're in a kind of a large room, and I just want to make sure that everyone can see and we can engage each other. If you can come a little closer to the front, we'd greatly appreciate that. So we have four speakers, and they are going to be focusing on different types of units and the questions that arise in different types of units. So the theme of this session will be threefold. So either you'll see rare cases that present in any particular ICU. You may see unusual presentations of a common thing, or you may see situations where patients have common disease processes in which the treatments may, the treatment for one may be problematic for the other. All right? So that's the general theme. So first up to bat, I'd like to introduce Debra Cools. So Debra is currently a faculty at UNLV in Las Vegas. She's a trauma and general surgeon and is the chief of the section of critical care in the Department of Surgery and the program director for the Surgical Critical Care Fellowship Program. She has served in numerous capacities in various organizations, including the American College of Surgery, where she serves as the national chair of Injury and Prevention Committee, amongst many, many other claims to fame. She currently serves on the executive committee at UNLV Faculty Senate as well. So without further ado, I'd like to introduce Dr. Cools. Good morning, I'd like to thank you all for coming to the session, supporting SCCM and I'd really like to thank my fellows who helped with these presentations, helped with the selection of interesting cases as well as the preparation. So the first case I'm going to talk about involves blunt cerebrovascular trauma among other types of traumatic injuries. So this patient, young patient, 26-year-old, and for any of you who are rock climbers, Red Rock Canyon and our state park is really famous. People just fly into Las Vegas just for hiking. So anyway, he was hiking and he fell 50 feet. He really came in and as you'll see, he was awake and he really didn't have any significant past medical history, past surgical history, allergies and so forth. He did initially attest to THC use. We didn't really get a timeline on that, but he was a GCS of 15. So for those of you who know GCS, 15 is kind of normal. He came in as a full trauma activation because of his mechanism. He fell 50 feet and we were expecting major injuries. During his workup, he had difficulty really holding still for his diagnostic workup and so he was intubated. And during his initial resuscitation, he did have periods of hemodynamic instability. And among his findings of many plane x-rays and CAT scans, when he had a CT of his abdomen and pelvis, it revealed complex pelvic fractures and active extravasation of contrast. So we are right next to our own angio suite. So we quickly called those folks in to angio and embolized his pelvic bleeding. During resuscitation, he received seven units of Pacro blood cells, seven units of FFP, trying to maintain a one to one to one ratio. He also got one unit, which is actually 10 of cryo and one single donor platelet transfusion. So we have a designated trauma ICU. So he was admitted there and we called our various specialty consultations. So these are his injuries. And for those of you, you know, we all have scoring systems. On the trauma side, we use injury severity score. And an injury severity score of 50 is extremely high. Most trauma programs actually consider, and when we're site reviewed, anything over an ISS of 15 is potentially an ICU admission. So among his injuries, he had a subarachnoid hemorrhage. He had a small interventricular hemorrhage, an occipital skull fracture. He also had a comminuted transverse fracture of the inferior tip of the clivus. And he also received a CTA of the neck at that time. And there was a possible left vertebral artery injury. He had rib fractures, pulmonary contusions, and that was another reason that we saw this on some of our initial x-rays, and that was part of the decision to intubate him as well. He had a right hemothorax, he got a chest tube. We mentioned the pelvic fractures, and he got embolization emergently. He had a right adrenal gland hemorrhage, a scapula fracture, which is a very large bone and indicates that there was a lot of force. And of course, he fell 50 feet. And he also had some fairly minor extremity fractures. So I'm going to bring up some of the key images. He had a lot of imaging done on admission. But this is imaging that really demonstrates his clivus fracture on several different views. And this, along with other basis skull fractures, was very worrisome to us, even though he was, interestingly, a Glasgow Cohen score of 15. So pretty with it, if you will. Again, some enlarged images, again, demonstrating that we really need to look carefully at our own scans, as well as waiting for the radiology reads. In our institution, the entire trauma team goes with the patient to CAT scan, and we initially can pick up a lot of these injuries as well. On the CT of the brain, I'd like to just, you know, point out that we did have some areas of what were called subarachnoid hemorrhage. And they're kind of odd, initially. When we think of traumatic injury and subarachnoid hemorrhage, it's usually more peripheral than deep. And so, again, that was an area of concern. And we were all pleasantly surprised that he remained neurologically intact. So as is the case with injuries like this, we will get our neurosurgeons involved. And so, first, we got a repeat head CT. And it showed a new subarachnoid hemorrhage along the occipital lobe and bilateral parietal lobes. And, again, this is not unusual for a repeat head CT after traumatic injury. Some of the original subarachnoids we saw were mildly improved. And he had some effacement of his basal cisterns. And this was concerning. His neurological status was not changing at all during this time. And there was a question of, in looking at all of his scans, that there was this question of initially what was thought to be a left vertebral artery injury. The recommendation from our neurointerventionalists was to get a four-vessel angiogram. And I'm going to show you that in a minute. And kind of surprisingly, what it found was a pooling of contrast from both of his carotid, internal carotid arteries, as well as both of his vertebral arteries. And it was suggested, we talked to multiple interventionalists, and they thought it was probably a dural tear due to a stretch during his initial injury. And these are the images. And so we can see pooling of contrast in multiple locations all at the base of the skull. Actually, during this time, I don't know how your institutions are, but if there are thought to be significant findings, we actually get a call in our trauma ICU. So one of the calls we got was, you know, is this patient alive or dead? And we're like, he's alive and he's following commands. So we were tipped off early on of how serious this could be. So one of the management decisions that came up through his course, he obviously had multiple sources of bleeding, including some active extravasation. How should we address this base of skull extravasation? So when we talked with our neurosurgeons, we talked with our neurologists, we talked with our interventional neuro folks, and it's really, really difficult because he has four vessels. And if we were to consider stenting any of them, and I think probably no one would consider stenting all four of them at the base of the skull, it requires some degree of antiplatelet therapy, if not further anticoagulation. It also sort of brought up the issue of what should we do about DVT prophylaxis, other than SCDs, and what are our options, if there are any? And I would say, I was attending to him. I was the admitting surgeon, and I was attending to him in the ICU. And so he had very involved parents. At that time, he was intubated. But what should we tell them about his prognosis? Because, again, we'd gotten a call, like, was he alive or dead? So I'm going to save that for part of the discussion. So we planned out the rest of his course, and it was decided that he should get a repeat CTA. And so that demonstrated stable hematomas and no active extravasation on hospital day nine. We were still not giving him any DVT chemoprophylaxis. So we were doing sequential surveys for DVTs. Patient was extubated. He had been in 11T all the time, which is the most you can be when you're intubated. And again, he was awake and alert when we extubated him. On hospital day 16, we got another four-vessel angiogram, again, after consultation with multiple specialists. And it showed, and I'll show you in a minute, a skull-based fistula arising from the branch of the right vertebral artery, which was subsequently embolized. He was discharged to rehab neurologically intact. And he's a fairly recent case, and I have not seen him in follow-up. So I will be querying. But here is the AV fistula, and you can see that it was coiled. And I think we're very pleased that the extravasation stopped after a period of time from all four vessels, and that we were able to follow up enough to actually detect this complication. And he will be following up with also neurosurgery and so forth. So just a couple of things. It takes a lot of force to fracture the base of the skull, particularly the inner portions and the clivus is considered the deepest bone. And that is one of the tip-offs for a blunt cerebrovascular injury, particularly when they're transverse-oriented, there's an even higher incidence of these types of injuries, many times with cranial nerve deficits, which to the best of our ability, he did not have any on examination. So this is kind of our summary, and clivus fractures are not very common. And so we as trauma surgeons, we really need to know that this is a tip-off for further investigation, starting usually with CTA. And it depends on the protocol of your hospital, but you want to be sure to include the circle of Willis as well. And the natural history of these injuries can be very complex, as I hope I've demonstrated, and really require follow-up as well. These are our references. And I think our plan is to present two cases, and then we'll take a little bit of a break, and then we'll do Q&A on both of them. So just be mindful of this is the first case, and then I'm going to go on to my second case. And it's a case of severe ARDS in a patient with a traumatic pneumatic seal and a splenic laceration. So many of our patients have multiple injuries. So this is a 34-year-old man going 100 miles an hour, which is very typical in Las Vegas, on a motorcycle, right? Okay, no problem, right? So what we always find is that the significant others of these people have been pleading for years for them to stop the motorcycle. So anyway, he was a little tachycardic on primary survey, secondary survey, and otherwise, you know, no obvious external injuries. Secondary survey, he had tenderness in his left chest wall, and he also had some abdominal tenderness. And past medical history, which we find it sort of buried deep in the record, but there was a history of vaping nicotine, which was not initially disclosed. So this is his initial chest X-ray. We can see haziness in the left chest. And if you look closely, you can see rib fractures as well. So for us, again, significant mechanism, you can see has a clavicle fracture as well. It's a tip-off that we should really get a CTA of the chest. Among his other injuries, he could have a transected aorta, which he does not in this case. But this is his admission chest CT, and there are several findings. One is this area of active extravasation, right, in his left lung of concern. And at this point, he was just requiring some supplemental oxygen. And then we see this pneumatic seal, which is fairly unusual for a man in his 20s. And he's a former smoker. Now he's vaping. So on the CT of the abdomen and pelvis, we can see he had a spleen injury with active extravasation. And so you can see this is spleen in the bucket, right. So he went to the OR. And this guy had an ISS injury severity score of 51. For those of you who might have come after my last presentation, ISS greater than 15 often gets admitted to the ICU. So he had a splenic laceration. He had this traumatic pneumatic seal with the question of active bleeding, a left pneumohemothorax, pulmonary contusions, rib fractures, and a spleen injury. So his ICU course, this is a follow-up chest x-ray. So he really developed bilateral pulmonary contusions. You can see he has a fresh clavicle fracture. And from a prior motorcycle crash, he had a right clavicle fracture. And so he started to have some bloody secretions, which initially were not really significant. The surgeon who admitted him took out a spleen, and he wasn't really actively bleeding. We didn't think from his pneumatic seal. So that was not embolized as well. I was attending to him early in his course. And I noted the active extravasation in his chest on the initial study. So I, again, consulted with radiology about what's the best study and so forth. And they thought the CT of the chest was. It showed no active extravasation at this time. But on and off again, we would have bloody secretions. We had, we did, we performed bronchoscopies to clear his secretions. They were not initially very voluminous as well. And then he went on to develop moderate ARDS and proceeded to severe ARDS, which required paralysis proning. We used Floland because he was very hypoxemic. And multiple modes of ventilation. And we do not provide ECMO at our institution. But we did consider transferring him to an ECMO center. What I wanted to say, and I'll point this out a little later on, is he had this active bleeding off and on from his chest. And there was one time when I started him on Lovenox. And a day and a half later, I got a report that overnight, there was about a half a liter of blood out of his endotracheal tube. So we had a really difficult time managing him in terms of prophylaxis. And on ECMO, we really felt that he would probably bleed. And he was in such bad shape from ARDS that really at one point, when I was on trauma call at night, I called the family and didn't think he was going to make it through the night. But we used permissive hypercapnia and so forth. He ended up having recurrent large pneumothoraces from his, one was thought to be from his pneumatocele, which ruptured. And then the family came to us and said, hey, you know, we've heard about this vaping problem. You know, he's an active vapor. And early in his ARDS course, we had multiple people really deciding whether to believe spotty literature again, whether steroids would be helpful or not. We decided to give him a short course of steroids. He also had multiple bouts of pneumonia. He had some GI bleeding that was pretty minor and did not require any intervention as such. But again, our challenges in DVT chemoprophylaxis, so one of the questions I have for you is, what would have you done? And again, I started it early on and he definitely had bloody, increased bloody sputum. We called CVT surgery at that time. Should we resect part of his lung? They said nothing really to do. And I just wanted to point out, I know there was a very nice talk on Ivali yesterday. And that is, was not his probably presentation. He didn't have the prodrome and so forth that you normally see with that. But we felt that that might have contributed to some of the ARDS problems that we had. And again, it's debated whether steroids would be helpful in this group. And those are our references. So, I'd really like to open it up for questions from the audience. And I'm just going to bring up some of, in case you forgot or missed case number one, just the questions I asked there. So, I'll open it up for discussion and questions. And I'd be really curious, would people have done things differently? And my question, does the IVC filter have a role on these patients who are very high risk of bleeding as a DVT prophylaxis? So, that is a very, very good question. I kind of purposely didn't include that on my slide. So, the person with case number one with the Clivus fracture, I was actively in the ICU at that time having discussions with his family. And even though he was awake, I wasn't quite sure of his cognition. So, I did not include the patient in these discussions. But I really, I recommended an IVC filter. But this person was so injured, we got at least one call, like was he brain dead or not brain dead, that I felt that I really wanted to engage the family in decision making. But I did recommend an IVC filter on him. They did not agree. And he's a patient, the patient who did not get a DVT. So, they wanted to just proceed, you know, without that. And I really needed to explain, like we really couldn't start him on chemoprophylaxis. We were afraid that his bleeding would increase, which could really lead to his demise. So, good question. One of the comments I wanted to make from the, this is Cheryl Chang for Neurocritical Care. I'm looking at the microphones. Thank you. Yeah, I'm sorry. It was just that when people are a little surprised at the neurologic status of the patient, the key to remember is that whether it's intracranial hemorrhage or extracranial. So, those were extracranial vessels. And so, even though some of it is at the base of the skull, and that is an important comment. And I have, as you know, a companion case to that talking about blunt cerebrovascular injury. But just to remember that what you're doing, the more life threatening is going to be somebody who's intracranial. And when you're imaging people, it's important to remember the intracranial vault when you're imaging patients where you're worried about blunt cerebrovascular injury. But he was still doing okay and not brain dead because the blood was at the base of the brain, not higher. He did look tight, his brain scan. But fortunately, he had a good GCS. So, it was easy to monitor that by mental status by keeping him awake enough. Yeah. Any other comments or any comments on the second case? Just curious. We had this inner kind of overlaid history of vaping along with ARDS. Sorry. So, oh. Yeah. I have a question for the first case. Sorry. Do you think TXA or EMICAR could have a role to prevent or decrease the extravasation in the first case? So, is that regarding both cases or just one of them? The first case. So, I think TXA could. And we use it as part of our massive transfusion protocol. And he did not really meet that criteria. So, we did not use TXA. And its use is also somewhat controversial. And so, as new studies come out on TXA, I think it is not really clear. I mean, there's some incidents of hyperfibrolysis syndrome as well, which can actually exacerbate ongoing bleeding or possibly can contribute to it or cause it. So, right at our institution, unless you really meet that criteria. And on his way in, EMS and so forth, he was hemodynamically stable. He only really dropped his pressure in the hospital and not immediately after intubation. But, you know, throughout as he required ongoing transfusion. Also, surgically, one of the other things that you can see in a case like this, because he did receive quite a bit of blood initially, there's a fair amount of evidence that as an alternative, he could have been taken to the operating room and have, we could have done pre-peritoneal packing to, again, occlude the NE arteries and veins. And it's mostly venous bleeding usually. And a lot of pelvic fractures, it will tampon out that bleeding. And so, that would have been an alternate strategy. Had he really been hemodynamically unstable, that's likely what we would have done. So. Hi, Debra. One other, one last question. And specific to the second case. So, in your review of the literature with vaping, with surgical vaping related injuries, have you noted if perhaps the CT surgeon was right? Were there case theories that show that, you know, removing, you know, doing a pneumonectomy in a patient with pneumatic seal didn't change outcomes? And I guess the second follow-up would be, is there anything medical that could have been done, any sort of medication that could have been given to help mitigate some of the longer-term consequences? So, in terms of surgical, when I think the biggest issue, quite honestly, was initially bleeding. And they felt that, you know, he was already heading an ARDS. He wouldn't really have tolerated single lung ventilation. So, that was a contraindication. On repeat imaging, he didn't, we never were able to, it's a little like a GI bleed, right? Sometimes they have GI bleed, you do all your studies, and you still don't find the source of bleeding to really know exactly what you should do. But I think angioembolization, although it's very uncommon in chest injuries, could have been an option if we really found some active bleeding. Yeah. Steve Hollenberg, Hackensack. So, this isn't really a surgical question, but I wonder, as in this case, you often don't get a history of vaping, or you don't get an accurate history of vaping. So, I don't know, we have some non-surgeons in the room, maybe opinions. So, if we're doing bronchoscopy, should we be routinely looking for foamy macrophages and lipoid pneumonia in patients with ARDS in complicated settings where you can't really be sure what is or isn't going on? Any takers to that? Looks like that's a challenging question for everyone. Well, on that sort of bittersweet note, I thank Debra for giving her talk. Thank you. All right. So next up will be myself. So again, I'll be talking about challenging cases in the medical ICU. For those of you who came a little late, my name is Andre Holder. I am assistant professor at Emory University and Emory Center for Critical Care and also Division of Pulmonary Allergy and Critical Care in Sleep Medicine. I have no financial disclosures to report. So I already mentioned the general themes for all of the talks at the beginning. The general themes for my two cases is sort of this push and pull. So I'm going to present basically very common things that we see in medical ICUs, but things that are presenting simultaneously and also have very different treatment modalities, which may affect the other disease process. So the first case is a 60-year-old man. He has a history of hypertension, diabetes, COPD, CAD, and presents with worsening shortness of breath and chills for about two to three weeks. And this is in late September. Obviously, I'm giving you that for a reason. So on review of systems, he had some diarrhea, may have had a sick contact, but his wife improved. She had a runny nose, cough, et cetera. So in the ED, his vitals were noted to be he was febrile. He was a little bit tachypneic. He was tachycardic, but his blood pressure was normal. On chest X-ray, he was found to have multifocal pneumonia. He received two liters of IV fluids and was started on appropriate antimicrobial coverage. Later on, he was found to be influenza A positive from the screen they did in the emergency department. And he was started on Tamiflu and then admitted to medicine. So he then decompensated after that, developed worsening respiratory distress, became hypotensive, rising lactate, altered mental status. He was given four liters of fluid by the hospitalist team as well as his antibiotics were broadened to zosyn and vancomycin, and then he was transferred to the medical ICU, whereupon he was promptly intubated based on how he looked and was started on vasopressors. While he was in the MICU, from the time he was intubated, his oxygen requirements kept going up and kept going up. The ABG that we received about three hours after that, you can see that he's now hypercapnic as well as hypoxic. So his chest X-ray went from that, from the time that he presented and was intubated, this is a post-intubation chest X-ray, to that. So I think we all have a pretty good idea of what's going on here. In addition to that, his hemodynamics got worse. So he went up to norepinephrine 40 mics per minute. We use non-weight-based at my hospital, but that would be equivalent to .6 mics per kg based on his weight, and he was on vasopressin as well. He continued to get worse. So his vasopressor and ventilator requirements increased. So the very first thing that we thought about doing was proning him. But at the time when we tried to prone him, we got him the ronoprotein bread, he was placed in it, was placed at about 30 degrees, and was promptly aborted because he abruptly became bradycardic and more shocky, and thankfully did not have a cardiac arrest, but that was because we were very quick to actually push epinephrine in him before that happened. So that was aborted. He was then deeply sedated and paralyzed. He appeared fully responsive once a resident actually hooked the patient up to an arterial line. They looked at SVV and saw that his SVV was 25. So here's the first dilemma. What strategy would you use for fluid or hemodynamic management? So remember, this patient, just to summarize here, is a guy basically in septic shock, and it looks like fluid refractory septic shock since he got about six liters of fluid already, still with worsening both ventilatory and vasopressor requirements. So just a show of hands here, how many people would give more IV fluids based on the data that we have? All right. So a couple people. So how about diuretics? Just show of hands. I don't see anyone here doing that. So maintaining uvulemia? All right. Now, what about using pulmonary vasodilators in this patient? So a few hands there. What about none of the above? Would you do something else? No, they're not mutually exclusive. That is absolutely right. But of course, for the sake of demonstration, I have to make it as such. How many people would say that they need more data before they can even act? You'd give steroids. All right. All right. So I'm going to bring up the second dilemma here. So I'm not going to give the spoiler alert as to what I did because that sort of takes away from the general theme of the talk. But based on whatever you decided to do, the ventilator settings are now slightly worse. We've dropped his tidal volume. His PEEP is now up to 14. But he's on the ARDSnet ladder. So his FiO2 is 60%. ABG is somewhat improved, maybe about the same. His pH is maybe a little bit better. His norepinephrine dose was decreased down to 20. And then his vasopressin was down to 0.04. But it was slowly increasing again. So separate and aside from the prior question, what strategy would you use for managing his PEEP to optimize his both oxygenation and perfusion? How many would you use? I mean, well, would you use more or less? And this is not a question I'm throwing out right now for an answer, but more so to ponder on. And how would you titrate it and by how much? So again, the case here actually that I'm referring to is a guy with septic shock and ARDS in the setting of actually decompensated RV failure and acute corpulmonality. So he had a history of COPD, as you recall. And he was on rather high PEEP settings. I didn't mention this, but his driving pressure was, excuse me, was about 20 at the time that he initially presented. So I think the first lesson here is that stroke volume variation, we have to be very careful, or pulse pressure variation for that matter. We have to be very careful with how we use it to predict fluid responsiveness, especially in RV failure. So if you recall, this is usually measured by looking at left ventricular function and stroke volume for the LV. And certainly I don't have to tell many of you in the room that looking at the LV to determine what's going on with the RV can lead you down a dangerous path. So specifically in patients who have very high pulmonary vascular resistance, and this patient will be one of them given his history of COPD, as well as his very high PEEP settings at this point, that's going to provide high RV afterload. And in that setting, even though the RV is full, the LV looks fairly empty. And of course, based on that, in someone who's being mechanically ventilated, that's going to look like someone who's volume responsive. And in fact, if you do that, you may actually put this patient in a dangerous spot because, excuse me, because they are not, there's something, there's a concept in physiology called ventricular interdependence. And essentially it says that the septum is going to bow in whatever direction there's least resistance. So in this particular case, if your RV is overloaded, your LV is going to start getting smaller and smaller, and eventually you may have functional tamponade. So this is a very potentially dangerous situation. So the take-home point here is that literally the LV does not know what the RV is doing. And it's very literal to this translation of this old adage that the left hand doesn't know what the right hand is doing. Second point is that ruling out, it's probably important to rule out other causes of hemodynamic compromise during proning because in general, proning is actually potentially beneficial to the RV in reducing afterload. So there are some small studies that have looked at this. And then looking back at the PROSIVA trial back in 2013, when a separate study was done on this, when they looked at the patients who had, who undergone proning versus those who had not in the control group, the PF ratio had not changed within the first hour of proning compared to the group that did not receive proning. So the question is, is it really the oxygenation that actually brought that 32 down to 16% mortality benefit that they saw in the PROSIVA trial? Or is it something else? And I would submit perhaps that it might be that this particular point right here. Although, again, it wasn't too clear how many of those patients had corpulmonale. So, and then the third point I would make is that optimizing your, whether you're in volume control, your tidal volume, or your pressure, if you're in pressure control mode, as well as your PEEP, of course, together being your driving pressure, as well as VQ match, can actually help to optimize hemodynamics. So I don't probably have to go over this slide with you. This is, of course, a picture of the West Zones, looking at the areas that are very well aerated here, but not properly perfused, and going down to the areas that are well perfused and not properly aerated. So, there is this concept of, possibly we need to undergo RV protective ventilation, particularly in patients who are either at risk for, or are giving you signs that they have acute corpulmonale. And some literature has quoted plateau pressure less than 27, a driving pressure less than 18, and a PCO2 of less than 60, if you can facilitate that. And then, of course, optimizing VQ match is what proning helps to do, which is why it might be beneficial, both for the oxygenation piece, but also, again, for offloading the RV, because now you have those areas that were not properly oxygenated, being oxygenated better, because you've proned them, as well as those areas are getting properly perfused. So, the proper perfusion and relief of that pulmonary vasoconstriction can actually help offload the RV, and you can inadvertently, or actually, in addition to oxygenation, you can also potentially improve your hemodynamics. So, what happened to this patient? I will tell you that this case happened a few years ago when I first came out of fellowship, and I was very squeamish about trying to prone this patient again after he decompensated. But instead, what I did was I used a pulmonary vasodilating agent, and my strategy was let's try to improve the oxygenation as best we can so we have some room to actually go down on the PEEP so that we can offload his RV. And in fact, that actually did work, and we were eventually able to start this patient on CRRT. He's developed AKI as a result of his disease process. He was started on CRRT, and we were able to get some fluid. We were able to get about 15 liters off, and he eventually got trached and was transferred to an LTAC. So similar to the prior presentation, I'm going to hold all the questions until the very end. So case number two is a 70-year-old functional woman with a past medical history of stage three breast cancer, hypertensive diabetic, and she has some remote CV in the past admitted for shortness of breath. When she came to the ER, she was tachycardic to the 120s. Her CT angios showed that she had a multi-segmental PE and hemodynamically stable from a blood pressure standpoint, but her troponin was .2, and her BNP was 530. When the ER saw this, they did a point-of-care ultrasound, and there was question about whether or not she might have had RV dilation. Her CT head was normal, and she was started on heparin. When they got a formal echo, they asked for this rather quickly, and she showed some mild RV strain with a little bit of dilation. So they promptly called interventional cardiology and CT surgery, who both said there was no intervention needed and they admitted her to the medical ICU. I will say that's a point of contention for me, but this was what was decided prior to presenting to us. So in the medical ICU in hospital day three, she now developed new large melanotic stools. Her hemoglobin went from 10 to 8. Her heparin was held, and GI was consulted. So I should mention also that we recontacted our cardiovascular surgeons to find out if she might be a candidate for embolectomy, and without going into too much detail, they said due to her age and her function, they would not. I think there was a misunderstanding of how functional she was. So this is her CT scan. So you can see that she has rather distal PEs, and that actually was one of the other reasons why she was not a candidate as well. But there was disagreement amongst our CT surgeons about whether or not they would have actually tried to go for it anyway. So this was, of course, just a slight example of what her bloody stools looked like. So rather large and bloody. So when GI did the EGD and the colonoscopy, it was unremarkable. So she had a bleeding scan that was negative, as well as CT angio. We waited for about 24 hours, and then restarted the heparin, and then within about 12 hours after that, she started having more melanotic stools. Repeat imaging and repeat EGD were negative. She had a pill endoscopy that was negative. Basically, her entire workup was negative. And on top of that, she also was found to have a right lower extremity popliteal DBT. So without going into too much detail about whether or not we thought this patient might have been appropriate for surgery, presuming this is someone who is not functional, how would you manage the anticoagulation in this person? Would you stop it? Show of hands. All right. So a few. How many would stop and reverse her anticoagulation because of the significance of her bleeding? All right. And how many would continue? So it looks like the majority of folks are saying that they would continue. So the interesting thing is is that there's really not a lot of evidence or guidance, for that matter, in terms of how we should best do this. So this is a quote from the Gastroenterology Society as to whether or not we should restart anticoagulation in someone who is receiving it and has a GI bleed. So clearly it's not super helpful, and we indeed did this and weighed the benefits and the risks. She had a submassive PE and needed anticoagulation. So because, again, we have this situation where this patient needs a particular treatment that is really contraindicated based on her other disease process, should we be having goals of care conversations with this patient, I think is the other question that came up. And when would you do that? Would you do it now, you know, when she's, after she's rebled after two negative workups for her GI bleed? So I will tell you that in this particular case, when I went back to our CT surgeons, I did talk to them about this case, and the understanding actually was that she was not as functional as she let on. This was functional by history. And also, more importantly, they were saying based on the location of where her, where her, her PEs were, it was going to be difficult for them to access to do actually a thrombectomy. And also, our cardiologists do suction thrombectomy as well, and they actually said the same thing. So really there was no other option for this patient. So I will tell you that my threshold for having this conversation was after her second bleed, when we realized that we really didn't have much more of an option. And I should also mention that the patient declined an IVC filter. So what eventually happened is this patient actually spoke to our palliative care folks and was eventually taken to palliative, to the palliative care service. So with that, I will conclude. If there are any questions, any feedback, I would actually be very curious to hear your thoughts about particularly the latter case and how you might have approached that. But certainly, any feedback on either case would be appreciated. Yes, sir. The second case is really interesting that, you know, many patients, they decline IVC filter. I think part of that is the media. Do IVC filter have side effects? They're retrievable. So some patients, they agree with anticoagulation which may have serious complications, but they decline IVC filter. The second case, I think, you know, with I know surgical embolectomy is high risk, but you can do interventional, mechanical embolectomy, or you can use the most recent ultrasound-guided catheter which gives very small dose with thrombolytics. Right. And probably can be successful on more proximal. And this is not even probably, you know, it's submassive. So on this probably patient who's not candidate for anticoagulation, it will be combination in addition to IVC filter. But I mean, another comment on the first case, I mean, you know, many times with the interventricular dependence, many patients, they just do not do well. I mean, I had a recent case, scleroderma ARDS, nothing really worked except after. I mean, we did not have Flolan. We started Milrinone, which is a pulmonary vasodilator. Right. As well, and patient improved. And thank you for those comments and the questions. So I have also used Milrinone particularly in settings where I know that their kidney function is not going in the wrong direction. And this is in part because I had a patient dial me from Milrinone toxicity when he developed progressively worsening AKI in the context of using Milrinone. But I have used it in patients who are on CRRT, for instance, which this patient was on, so he technically could have. But at the time, my priority was trying to improve his oxygenation so that we can try to wean his PEEP down. To your second point about the, to the other point about the second case, yeah, I think, so we do have access to many of those modalities at our institution. Unfortunately, our interventional cardiologist was unusually demure about this case. He's usually fairly aggressive, but I think he got scared because of the large volume of bleeding that she had and actually didn't want to use ultrasound-guided catheter-directed lytics. And also said that the access, again, the access for the, to do a thrombectomy was too foreign. If there are any CT surgeons, by the way, in the room, I'd be curious to hear your thoughts about the location of that, of that PE and if there's any, anything you would have done differently. Yes, sir. Just a question about the first case and a suggestion or thoughts about the second one. I'm going to start with the second one. Sure. We had a large discussion in our group about submassive PE, which basically what you're describing. Have you guys thought or anyone dealt with interventional radiology asking them to just put a catheter and then TPA directed to the area? One of my colleagues basically have dealt with it and that was his suggestion. And I thought that probably could save lives because eventually our patient and our institute ended up dying with, with, with that case. Mind you, he came on to the hospital being on CPR from, from, from the ambulance. Sorry, go ahead. No, it's going to be for the second case. Okay. Or the first case. So, so yeah, and in fact, yeah, again, that, so our, our interventional cardiologists are the ones who generally do those, those types of, of procedures. So the, and as you probably know, some of this gets a little territorial between the cardiologists and the radiologists. So because the cardiologists have taken such a lead at our institution, our radiologists have taken a step back. So we, when we, you know, approach our interventional cardiologists about this, we sort of have to take their word and really have no other recourse. And frankly, I understand the, the dilemma in that particular case. But yeah, so we, we, we only have those, those particular experts who actually do it here. For the first case, we've been always taught about the treatment for pulmonary hypertension at the same time to avoid four things, hypercarbia, hypoxia, acidosis, and hypothermia. I didn't see in your slide if you guys kept those patients at least euthermic because this is part of something that I felt that I'm becoming more strict. I don't want to use another word about this patient that I need to keep them warm. This is part of the treatment. Keep, yes, so the patient was not hypothermic. The patient was actually, he initially had a temperature of 39 when he first came in. But when he first came into the ICU, that is, after transfer. But after, after, interestingly, after expanding his treatment, we, to, to Peptozo and Vanco, his temperature curved effervesced. So, yeah, so, so certainly we, we, we did think about that. But it wasn't actually an issue in this particular case. Yes, sir. Hi, very good presentation. My name is Tony Relock, and I'm a pharmacist. So in the second case, you were at the proverbial rock and hard place, right? Right. And I think what you guys did is probably right. But my question is, is did you try lower, targeting lower PTTs or, you know, anti-10A levels? Because we've had multiple patients like that. And I can say there's some that once you go above a threshold, they start bleeding again. Now if you can temporize them, I think the point too is sometimes we also forget sub-Q treatment dose heparin is also an option in those people, especially for long-term therapy. And you minimize zine fluids, which was something that I think we sometimes forget about as well. Is, I'll actually ask you a question. Is the sub-Q heparin, is that, is that generally, has that been shown to have less bleeding risk? Well, typically it would be more for long-term use. So you think about like long-term therapeutic enoxaparin, for example. In this case, it's more, you know, where they're supposed to be and they're stable. Then you can convert it to a subcutaneous heparin that might be more than the 5000 standard Q8 and stuff for long-term use. Especially, you know, the downside about heparin too is, you know, in these patients you have a lot of fluid. And sometimes we do that because that's what we used to do, you know, 20, 30 years ago. Right. So I think great points. We, so to answer your first point about the heparin ranging that we used. So unfortunately at our hospital, I'm not really sure why, but there's a lot of overlap between the low-intensity and the high-intensity heparin. So we actually did do the low-intensity heparin, but, and I didn't mention that, but that was the second time that we restarted the heparin. It was at a low intensity. And, you know, the patient still bled. So unfortunately, yeah, we did think about that. But in her case, it wasn't effective. So we'll take, so this will be the last question. But go ahead. You, sir. So in the first case, when the patient deteriorated requiring intubation and developed worsening shock, I'm sure you did do the present cardiac workup to rule out LV problem. Because the chest X-ray, when you showed the difference between the initial chest X-ray and the next X-ray, actually there was, it was like central bilateral infiltrates, which could indicate pulmonary edema from LV failure. So basically, just echocardiac biomarkers, EKG, to rule out. Yes. And I apologize. I didn't have that in the slide. But, so we did do an echocardiogram, and it showed that the LV function was normal, but the RV was the one that was mildly dilated and had dysfunction. The other point is that when we, I apologize. I lost my train of thought. Yeah, I apologize. I lost my train of thought. But we did rule out a cardiac cause. Very quick. What was the outcome of the second patient? Did she eventually die in palliative care or? The second patient? Yes. Unfortunately, I'm not sure. I didn't follow up after she was transferred, but I would presume so. But I'm not 100% sure. I apologize. Yes, sir. Hi, my name is Nader. I'm a second year fellow at Montefiore. About your first case, I just have a question. You did ask if anyone would go for more tests, but I don't think we talked about that later on. And as he was asking an echo, so did you end up doing a bedside echo to find out about the RV, or it was just a high clinical suspicion about the situation that pointed you towards? It was both. We initially had a suspicion. We had initially had a clinical suspicion. I didn't mention this, but because the SVV was 25, this happened overnight. My resident actually gave the patient the bolus. And he told me that the blood pressure got worse, which, of course, is what you would expect in someone who has RV failure. So it was based on a clinical suspicion. But we did get an echo the following morning, which confirmed what we suspected. Thank you. Thank you so much. Thank you. So at this point, I'd like to introduce Dr. Cheryl Lee-Chang. So she is the medical director of the Neuroscience Institute and Neurocritical Care at the Queens Medical Center in Honolulu, Hawaii. She is a clinical professor of medicine and surgery and is a council member of SCCM in the neuroscience's designated seat and is a past president, immediate past president? Immediate past president, right? Oh, past president for Neurocritical Care Society. So without further ado, Dr. Chang. Thanks, Andre. And thanks to the organizing committee to ask me to speak today. So I'm going to take you through some cases. I have a few. I have actually four, but we'll probably maybe do two or three. I just have some fillers just in case. I do have to do disclosures. I sit on the ABIM critical care medicine board exam committee and we're required to put this up that I'm not going to be disclosing any exam questions during this presentation. So we'll be asking questions, but you won't see them on the board. All of this is confidential. So our first patient is a 19-year-old man who dove from a wall into the surf and struck the top of his head. Unfortunately, in Hawaii, we get a lot of these quadriplegic and he was pulled from the water awake. When he gets to us, he's awake, he's alert, and his motor exam, he's moving only his biceps, his deltoids, and then his cranial nerve exam, a very astute nurse practitioner had noticed he had very tiny N-gazeni stagmas. You can have N-gazeni stagmas, but it seemed a little more than usual. Otherwise, the rest of the cranial nerves were fine. So I'm going to ask the group, what imaging would you perform next? So would you get, who wants a CT scan of the neck? Who wants a CT scan with an angio of the neck? And most people want to do that. Who wants an MRI? Okay, so some people go straight to the MRI. So our usual trauma protocol is to go straight to the CT scanner, and typically when there's, and I'll talk about what the triggers we use to image these people, but this is a CTA of the neck as well as the CT. And what you can see here, and I didn't put the laterals in, but there's some jump facets. He has a scoliosis already, but you can see that the vertebral artery is nice on the left side, and this is a separate cut, this in and out division. But you can see that the vert here in this view is not there. You can see a tiny trace of it, and on this cut too, you can see that the vert is filling the basilar very nicely, dominant vert from the left side, nothing here. But actually, I have to tell you that typically on the angio, our cerebrovascular people want to see if it's going to be atretic, it's actually better to be occluded than atretic just because of the risk for emboli. So after this, what is your next study? Does anyone want to look at the spinal cord with an SSEP, a sensory somatosensory evoke potential? Any electrophysiology people? Okay, digital subtraction angiography, so this is where you're getting a conventional angio. So, and then the other is MRI at that point. So at this point, the concern that you should be having, and this is the thing that I always warn when we're teaching the residents is that when we get spinal cord injury patients, everybody's focused on the spine, but you have to look at the cranial nerves because remember what the vasculature that this goes to is the posterior circulation. So actually, he did have an MRI of the head and of course, the surgeon wanted the neck, but he did have going along with his nystagmus, this cerebellar stroke. So it's really important to look for these. Also, we're looking at the brain stem if there's any findings, but remember to do your cranial nerve exams when you have a spinal cord patient. It may change, you know, that those of you who manage acute spinal cord injury, 85 millimeters of mercury for seven days is what we typically augment the map to. So in this case, if you're pushing the mean arterial pressure up and you have, and this is a fairly small cerebellar stroke, but if you have a larger one, you may actually be causing more edema and causing more problems. Also, if you know that there's a stroke there, you might think about if there's an indication for anticoagulation for some reason, would you want to put this patient on full anticoagulation while you're pushing the map up as well. So you need to think about it. So this is not this patient fortunately, but in a patient who does have a cerebellar infarct, it can develop into a full infarct like this. And the next thing you know that you have brain stem compressions. So if you're not examining your patient every day and they're on a ventilator and not seeing these happen with the cranial neuropathies, then obstructive hydrocephalus as you occlude that fourth ventricle, then you may have a patient who herniates and dies. So you have to think about it. They may need a suboccipital craniectomy. So think about that when you're dealing with your spinal cord patients. So as I mentioned with Dr. Kuhl, this is your other blunt cerebrovascular injury. The incidence is about 3%. Untreated, the stroke incidence can be as high as 30 to 40% in carotid and 10 to 15% in vertebral artery. So you have to look for this. Sixty percent of these strokes that do happen, most of them happen in the first couple of days. Eighty-five percent typically in the first seven days. But you have to think about this. Again, because about only 37% may have stroke symptoms when you're examining them. So when they first come in. So important to think about. Important to screen these patients. If you treat these patients, it decreases your risk for going on to have stroke. Now this is a little hard to see, but the reference you'll see when you go online. But the preferable screening tool for these patients and what they say is that anything greater than a 16 slice CT scan. So most of us do have 32, 64, even higher slice scans. So as long as you have something that gets good resolution, then the choice is a CTA with us to look for this. And then otherwise, the secondary would be a digital subtraction angiography. So that's what we typically do first is a CTA. Typically the patient is getting pan-scanned. We're looking for signs and symptoms. So if you see obvious bleeding, then that's somebody you'd think about. Most don't listen for cervical bruise. But if you see an expanding cervical hematoma, things look late, that's going to be someone who's transected. And then focal neurologic deficits, like we saw in our patient. And then looking for something on the imaging that you do. The risk factors, anything high impact. So Dr. Kohl's talked to you about someone with a clival fracture that had 4,300 newtons of force to break something. So any with a high energy transfer with the fall, any type of mid-facial fractures, mandibular fractures. I forgot, on the next patient I'll show you a different fracture that had this. And then anything complex fractures, anything through the spine that goes through the vertebral foramen. You need to worry about near-hanging patients as well, close-line type injuries, or even people with seatbelt injury signs. And then again, high energy force. So if you've had cardiac rupture, upper rib fractures, scalp declubbing, you have to think about it. Now how do you treat these patients? And this has been in great debate. And there aren't a lot of trials out there. This particular CADIS trial that came out in Lancet looked at, and it wasn't all trauma patients. This was all comers of dissection. And they randomized patients. It ended up being 118 carotid and 132 vertebral. Within the first couple of days and randomized into three months, it was once you were randomized by telephone to either antiplatelet or antithrombotic with anticoagulation, it was dealer's choice of the investigator which agent they actually used. And there was no difference in these patients. So the stroke was fairly rare, though. We saw it was more frequent. And when you look at the different case studies, but this was about 2%, much rarer than you typically see. And then these patients were treated for three to six months, some went a little longer. So to summarize that, the way that we grade these dissections is one, that you see a little irregularity. So that's a grade one. Two, intraluminal thrombus or intramural hematoma. Three, you have a pseudoaneurysm. And four, you have a total occlusion. And they're treated, those four are treated pretty much all the same, all a choice of either using an antiplatelet or antithrombotic for typically, and I had seven to 10 days. So some investigators say reimage at that point. If it's gone away, then you might think about not doing anything or maybe changing. If you've chosen from an antithrombotic agent like heparin, then you might want to go to an antiplatelet. Then endovascular, a lot of people think, well why aren't you doing endovascular? The guidelines for stroke, acute stroke is that only if they're having recurrent ischemic events despite doing your adequate medical therapy with one of the agents that we talked about. If it's transected, obviously they need to go to surgery. So you hold pressure as best you can if you can and get them to surgery. So any questions about that? This is sort of, okay. So patient two is going to be our 41-year-old intoxicated male passenger in a motor vehicle accident. Came to the ED, GCS at 12. Extensive cranial facial trauma with a large bleeding frontal scalp laceration. And it was stapled shut without washout. I should mention that on Twitter there was a question of whether you staple or you suture. And I was going to leave it to my surgical colleagues. I don't know if one of you want to pick up the, Dr. Cools, you want to pick up the mic and talk about whether you would staple or suture. I think it really depends on how much the patient is bleeding. But many times there can be a small arterial bleed and you would suture ligate that and then after that you can staple. Okay. So this patient had GCS at 7. They're intubated now. Most of the imaging CT was all negative. But their brain scan and the CT angio, the head and neck, were revealing. So this patient had significant bifrontal injury. Had air, so pneumocephaly. So you know there's got to be a breach in the skull. As you go higher and more superiorly you see that there's a skull fracture with traumatic subarachnoid hemorrhage. Already have midline shift. You can see that we look for the basilar cisterns here to see how open they are. He's a fairly young guy and these are closed down. So someone who's very tight. So also again, because of the force, we do a CT angio on these patients. And again, we don't just do the neck. It's the neck as well as the head. Because we want to, as Dr. Kuhl pointed out, you want to be able to see the base of the brain, the circle of Willis. So you need to get CTA of the head and neck in these patients. And you can see that on this left side, one there's a fracture through here, fracture. And then here you can see that there's an abnormality in the vertebral artery as it's entering here right at the base of the skull. And a close-up again here. So here you have a patient with a lot of bifrontal injury. You have a dissection. We're going to talk about how you treat that. But in addition now, you have a depressed skull fracture. And this is on the sagittal cuts. And you can see the sagittal sinus is thrombosed as well. Okay. So now you have a couple of things. So here's the question now. You have the sagittal sinus thrombosis. So what do you risk for? You risk for having venous infarcts and more edema in those patients, which will mean higher ICP. So that's something you want to try and avoid in this patient if you can. And with the vertebral dissection that we saw, we have risk for ischemic stroke. So, but they have these hemorrhagic cerebral contusions. So here's who wants to, now the first thing obviously is they're going to get a monitor, right? So we all agree that they need a monitor. And that was Fison on the first day. So who wants to at this point observe, because treating this patient with an antiplatelet, antithrombotic is going to make them bleed more. And they want to just observe. Anyone want to do that? Okay. So a lot of people want to do that. How about endovascular treatment? We talked a little bit about endovascular treatment. We're not going to treat this sagittal sinus thrombosis with that per se. But it looks like nobody's a taker on that. And then also that you can't really stent the vert where it is. Who's going to vote for an antiplatelet agent at that point? No takers. You can't reverse that very well either. So good. Unfractionated heparin infusion. Any takers on that? And low molecular weight heparin. So and a lot of people are not weighing in, but that's okay. So we actually know that the literature, the guidelines, and these are older guidelines that talk about a cerebral vein thrombosis and what the risks are for those patients. And what they showed for patients that had these, they show that people do worse overall and have more likely to have bad neurologic outcome unless you treat them with either unfractionated heparin or low molecular weight heparin, even in the presence of intracerebral hemorrhage. That it's important to think about this. We don't do endovascular treatment unless they've failed anticoagulation. So knowing this, that the risk is it's something we could turn off in case the patient's going to bleed. And there is a risk also for that dissection going on to having a thrombosis. We chose to use low molecular weight heparin. So in our shop, we use a low dose, no bolus, and aim for a PTT of 40 to 60. So we actually have a protocol where there's no bolusing if you have a low PTT. So as I mentioned, the thought is that with cerebral vein thrombosis, there's a fairly high mortality rate of 5.6%, it goes up to 15. But overall, poor neurologic outcome can be seen in about 10%, especially if they're not treated. Also, when we look at the guidelines, so then you go back also when you're talking to your trauma surgeons, they're like, well, you want to anticoagulate this person. What do our guidelines say? For traumatic brain injury, if you remember in 2016, and it's a little too small to say, they didn't weigh in on full anticoagulation. They talked about DBT treatment and that we would be using low molecular weight heparin or low dose unfractionated. And they kind of went down and said there's insufficient evidence to support recommendations regarding the preferred agent, dose, or timing, but most of us use the 24 hour, 48 hours. Trying to go through all the literature of any kind of guidelines, I found one that came out from Austria this last year. And I'm not going to go through all those guidelines, but just specifically, they did talk about what most of us do and who do start, who does start anticoagulation or DBT prophylaxis within the first 24 hours as this would recommend. Any takers? Yeah. Then you could do. 48 hours is what Dr. Menden uses. Okay, great. And then as far as therapeutic anticoagulation, I think this is what all of us can say is case by case. Do we have any, Dr. Menden, do you have any comments about that? We have our distinguished investigator here from Cambridge, so I might as well pick his brain. So I just, I mean, heaven forbid that I should argue with the speaker, but I wouldn't anticoagulate this patient because the context that people describe using anticoagulation is in spontaneous cortical sinus thrombosis. And they're treating the thrombus will actually reduce the risk of further bleeding because it reduces venous pressures. But here you've got an independent source of bleeding in the frontal contusions, which has got nothing to do with the venous pressures. So unless they were stable, I wouldn't start even sort of light anticoagulation. So the reason why I think, and this is where again, we're practicing not evidence-based medicine, is we've had patients with this before that weren't treated. It went on to have venous infarcts and having high CP. So we're trying to prevent the secondary that we haven't seen yet. So, I mean, we see these patients so infrequently, but our experience is that they have more problems with raised intracranial pressure. But about 14, 15 days, suddenly it breaks and I think they spontaneously recanalize or maybe what's happening is some of this venous obstruction is because of the edema and there may be still a sliver of lumen left. And once the intracranial pressure starts to settle, they undeniably have more problems with raised intracranial pressure, but I'm stealing a thunder. So, yeah, no, the good point because actually that's the next part is Dr. Menon was a plant, I guess, is because in the nine days later, so when I come on service, I notice the ICP still elevated at this point. It's up to the 30s and they're treating with mannitol and 3% saline. So at that point, you're thinking, well, what's going on? So the decision to anticoagulate wasn't mine, but it was, I mean, that was the rationale to do it. But so now, who votes that we think these are seizures, I need to get EEG and Dr. Menon's going to say they're not all mutually exclusive, but your first choice, I guess, would be, would it be an EEG and takers for that? Yes. I know you're going to vote multiple times. So the hemorrhage, who's going to get a CT scan because you're worried about a hemorrhage because we start on anticoagulation. Edema, you're worried about edema, get a CT scan. You're worried about hydrocephalus. So you're going to get a CT scan. Yeah, I get a lot of the people involved here. How about DAI? Now I think there's DAI. I want to get an MRI. Any voters for that? Okay. Yeah. And then meningitis, getting an LP. Yeah, kind of dangerous at this point, right? The ICPs are high. So we did what you would do is get a CT scan. You saw that was up for three times. This you wouldn't see again on the board. So there's three different, when you look at this, you see that there's three different reasons to look for whether there's a problem in the CT scan. Not a lot of hydro that's compressed, but a lot of edema. The hemorrhage is not much bigger at that point. And of course, we had held the anticoagulation when we were worried about this. So I got the scan, saw what was going on here. So now I have to ask, why is there so much edema? So this is what my thought was at the time is that if you remember our auto-regulation is so key. When you're standing at the bedside with a traumatic brain injury patient, you should be thinking of three things, the Monroe-Kelly hypothesis where you've got brain, you've got fluid, which some of it's CSF, and you have blood. Or you also have to, and then you have to think about your CPP equals MAT minus ICP. And you have to think about what's going on with auto-regulation. So if you remember your auto-regulation curve, as our blood pressure is going up, the brain is so smart that it's vasoconstricting to actually decrease the compartment that's happening inside. So it's trying to keep the blood flow. Sorry, this is the cerebral blood flow. This is arterial. It's trying to keep your cerebral blood flow the same, right? So it's going to vasoconstrict to do so. And as you're all here and starting to fall asleep and your blood pressure is dropping down, you're going to vasodilate. So you can imagine with your Monroe-Kelly hypothesis as your box is only a certain size. If you vasodilate, you're filling that box, the ICP actually is going to go up with auto-regulation intact. The ICP will go down as you vasoconstrict. And at the other ends, as you remember, you're going to get ischemia. And then with the pressure passive dilation, you're going to have edema. So this is actually the pressure reactivity index. And there's a lot of studies going on about looking at people when this is inverse, the ICP is inverse to what's happening with your blood pressure, that's telling you with your auto-regulation is intact. And I know that Dr. Menon is working on the COGITATE study that's looking at the pressure reactivity. But the key thing to remember is, remember those horrible contusions we saw in our patient, or if you have a patient with a spontaneous intracerebral hemorrhage or a big stroke. In that area, there's defective auto-regulation. So it's a straight line. So the higher you drive the blood pressure, let the blood pressure run, you're going to have more edema in that area and potentially more bleeding, especially if you have anticoagulated that patient. So you can imagine that if we look at this patient's curve, so I went back and looked at it, and you could see that this is the systolic blood pressure is kind of going up and down, the cerebral perfusion pressure kind of up and down and up in the 60s, it's very high, almost near 100. And some of this sometimes is being driven by trying to keep the brain oxygenation a little bit high. And you can see here's the ICPs. If you remember our guidelines, we want to be below 22. And all this time, this patient is on a lot of midazolam. He was like 70 kilos, a lot of fentanyl, actually up to 200, getting lots of boluses. He was normal thermic, and he was very well sedated on this. And so I came on service, and I looked at some of this, and I thought, well, I need to do something. So I did the something, and the ICP came down, and he did very well after that. So my question to you folks is, what is that something? So here's how I think about treating, and everybody has a different way of thinking about how they manage ICP, and some are in stepwise. I think of it sort of as a board game, is that you want to keep that ICP less than 22. And actually the goals are to keep the, if you look at the guidelines, it's 60 to 70 for your CPP, depending on whether you're, what your auto-regulation is doing. We think of the first tier as your head of the bed is up, keeping, making sure they're not orthostatic, because you want to keep your CPP good. So fluid should be euvolemic. You want to keep their brain, how much blood they're needing, how actively metabolizing the brain is. Not having any pain, so opioids. And then making sure they're well sedated, whether you're using benzodiazepines, propofol. I was talking to Dr. Menning yesterday. He uses a lot of propofol. Typically we shut it off earlier because we usually use it when patients are more waking up, but some places are using propofol for a longer period of time. And then these were all happening as second tier. These, I think of when we hyperventilate somebody, it's really rescue. We only do it for a short time. If we're using rescue osmotics, we should be doing it for a short time. Paralytics, typically if it doesn't work a lot, but if someone is hyperthermic or if they're shivering a lot and you have them well sedated, there's cooling. So how many would vote that I was, I cooled the patient? Okay, how many would vote that I put the patient on Pentavarb? Okay, how many would vote that I had the neurosurgeon put an EVD in? Okay, and who says I went to hemicraniectomy? Okay, so I actually, going back this slide, let's see if I can go back. So actually what I did was put the patient on Penobarb at this point. And what we found is that despite his BIS was looking good, he just responded a lot better to Penobarb. And just by having not all these spikes and a lot of osmotic, so some of you may recall that with Manitow, if you have a bad blood-brain barrier, some of that will extravasate into bad brain. So the more osmotics you use sometimes, the more problematic and you begin to fight yourself. So I think he was just not adequately sedated. But any of the things that we talked about here, definitely we would have been able to see that drop. So fortunately, it was just sometimes finding, and some places don't use barbs. And I know that I've spoken to some of my German colleagues, and they think it's a killer. But if you manage it very carefully, then patients can do okay. So I think I have a little time to go into my next one. So this is one where we get Dr. Zimmerman to wake up a little bit, because it's a little kid. So we have a three-year-old, which is in our neuro-ICU, unfortunately, we're also the trauma center for the state that has to take kids, and none of us are truly pediatric trained. So I would like any input from you folks about this patient. So this was a three-year-old, 18 kilo, very healthy boy, and went to his folks early in the morning complaining of a headache. And they did something, maybe gave him a little Tylenol, put him back to bed. And then he was unresponsive when they went to wake him up. They took him to a local, another hospital. And his general exam's not too remarkable. He was afebrile, he was, heart rate was 100, blood pressure 90 over 50. And he was a little tachycardic, had some arousal. He was unresponsive. He was not blinking to threat, but his pupils were reactive. He did have some brain stem findings. So his corneal was present on the right, but not left. And he had no movement to pain on the right side, but left a little bit of withdrawal. So you're localizing it, probably something's going on near the brain stem. So the CT scan of the brain shows intraventricular blood, subarachnoid blood near the foramen magnum. And the question I have is, if you folks were out there and taking, or trying to figure out where to send that patient, if you had the choice, because not all of us have the perfect pediatric place, trauma center to go to, would you go to the pediatric hospital that has no neurosurgeon on call versus an adult level one trauma center that's a comprehensive stroke center with a 24-7 neurosurgeon on call? This is a scan you have in your hand on PACS. So who would choose the pediatric hospital, no neurosurgeon? No, nobody. Adult hospital? Okay. Pretty much everybody agrees. So that's what was done. The patient was sent to our hospital. And the first thing that they're going to need, he is going to need also is, you can see how tight his brain is, his basal cisterns are closed down, he's got hydro, so he's going to need an EVD. So everybody picked up that he's going to need a neurosurgeon. He also came to us because we're looking to see why is this, sorry, where is this blood coming from? And so the CT angio of the brain was suggestive of abnormal blood vessels at the base of the brain. There was some early tangle. Our interventions were looking at it, but nothing they could really pick out. And he was too sick to go to MR or to go to conventional angio, and he's little, so they're kind of not that happy with doing little kids that are shot for angio as well. But interestingly enough, on his low cuts of his head CT, because he's small, we could see there was already something going on in the lungs, and some of this is dependent. So this is what we were dealing with. He came in, so he was at the outside hospital, and I say that because you'll see a chest X-ray from the outside hospital, came to us, he was very tachycardic to 200 at that point. His blood pressure, and for those of you who don't manage little kids like I don't a whole lot, so we put this all up there and we look at our Breslo tapes, that our pulse rate should be 90 to 150. This is up at 200. The respiratory rate was okay, but normal systolic blood pressure should be 99 to about 120 or so. He was about 120, and then low is less than 70. So he had unreactive pupils. We used pupilometers and also noticed that he was, that the MPIs were zero. So he got some 3% saline and also got some fentanyl, and the blood pressure promptly dropped, probably because we dropped his intracranial pressure a little bit too. So his blood pressure was coming down. Then he got fentanyl on top of that, which was unfortunate. So blood pressure now is low, so what do you do when they're low? You give fluid, and then you give norepinephrine. Neurosurgeon comes in, puts in an EVD, drains a lot of CSF, which also, so here at this point now we have our ICP monitor going on, and this is somewhere around, at this point, it's reading about, it was a lot of drainage. So it was now down to our pop-off number of about 10 or so. And then you can see the CPP here climbed a little bit and then started coming down. Patients started desetting later that night, which is the details I want to get into. He'd gotten the 3% saline here. So his repeat scan did show this, a nice decompression of the ventricles, his EVDs in good place. And then his chest X-ray, so this is at the outside hospital, this feeding tube was taken out and replaced. This is his follow-up at 1355. You can still see opacities of the lungs here, heart not too big. And then you can see, as we head into the code situation, you can see the pads here. The chest looks very whited out. So this is what was going on at 2045. This is way out here. He was starting to actually, if you look at this, starting to show that there was something going on, but the ICPs didn't seem too high. I think he was 18 at this point here, 15 to 18. CPP was dropping a little bit though, but he had this abrupt hypotension. Norepi was increased. He was tachycardic and febrile, so he was given a saline bolus. And then with this, just a few minutes later with these findings, went on to get another, even though the ICP was okay, was given another 3% saline that was appropriately dosed. Does anyone have any comments about that point, about giving more fluid? Please, 5 minutes, okay. So he's hypoxic, no pneumothorax, bilateral chest congestion, and then he has dopamine, Lasix, and chest tubes, the code was called at that point. So these are what his gases looked like before the PHs. This is going in the chronology, 74024273, and then the abrupt drop-off that happened at this point here at 2133, acidemic, rising PCO2, dropping PO2. And he was in full arrest at that point. So you can see that this continued to get worse despite all the different things that were being given, Lasix, chest tubes were put in, and this continued to worsen until the code was called. So this actually looked like it was a case of neurogenic pulmonary edema. How many of you have seen this, encountered this in your, yeah, so pretty frequent. That we think about in neurologic disease, you can get aspiration pneumonitis because they aspirate, but when you have poor pulmonary status, you have to think about this neurogenic pulmonary edema. It can be early, which is classic, so minutes with the head injury. They come in foaming. There was a guy who died in a ski resort who got hit by another skier, wasn't wearing a helmet. You know, he was dying on the slopes with foam coming out of his, bloody foam. And this is a little bit delayed, not quite 12 hours, but close to that. Most commonly associated with something hugely adrenergic, a head injury, subarachnoid ICH seizures, and then clinical findings are all the things that we would expect to see in someone who has significant pulmonary edema. What's happening is that there's a huge sympathetic surge that's coming out and into the lungs causing vasoconstriction, and they did this very nice study that showed in a rabbit model when they put a latex dye into it and whacked the little animal in the head, they were able to see in the post-capillary venules that there's these constrictions. Interesting enough, when they tried to actually inject the dye after they had done the blow, they couldn't even inject dye because, or this cast fluid, because this was so, like a constriction was so significant. So you can imagine that if you're looking at the arterioles, then the capillary hydrostatic and you have this venial resistance that there's going to be a problem with pulmonary edema. And studies have shown if you, this is bronchial and alveolar, you not only have fluid, but you have red blood cells in there. There's also, it's not just hydrostatic, but there's actually a breakdown of the pulmonary permeability. So in this pathogenesis, and this is a long time ago, we're talking about there's a hypothalamus is disturbed, massive alpha-adrenergic discharge causing the sympathetic vasoconstriction, increased arterial pressure, decreased LV compliance, increased LA pressure. And then all this is going into this pulmonary side, but also blood is being shifted into the pulmonary, increased pulmonary blood volume. And you have this pulmonary vasoconstriction, venous pressure is high, this unbalanced Darling forces with acute pulmonary edema. This is all going to damage the structure, and so you have the red blood cells here, as well as the pulmonary edema here. So some of the things we think about then, you just need to support them. Unfortunately, I think the only thing that would have saved this little guy would have been ECMO if we had been in a pediatric hospital capable of ECMO. You may have to use high PEEP, which he was already on at that one point. And remember that people often say, well, I don't want to use PEEP because the ICP is high. But in animals, what they've shown is that in order for PEEP to be significant as far as increasing ICP, you have to transmit that pressure from the lungs. So you have to have a very compliant lung and a very restrictive chest wall. So to mimic or to try to get PEEP to affect ICPs in dogs, they actually had to wrap their chest, making a constrictive lung disease, and then put them supine or upside down. So you'd use whatever PEEP you need in order to be able to manage your patient, fentanylamine potentially, or ECMO in this case. So thank you very much. Before we move on to Dr. Zimmerman's talk, are there any questions or comments from the audience? Hi, there. I'm Krista Swisher. I'm a neurointensivist at Duke. Thank you, Dr. Chang. One of my jobs here is to monitor Twitter to ask some of the questions from the audience. And there was an audience member that asked about the use of DOACs for cerebral venous sinus thrombosis. So if you could comment on that for the audience. Thank you. So just a year ago, we didn't have any data using DOACs, though there have been case reports. And I think more recently, there was a little case study, a larger case study that's showing that DOACs can be used, and not in this setting, clearly, because it was a fairly acute setting, but in someone who's chronic with a cerebral vein thrombosis has shown stability on unfractionated heparin, then you might want to use a DOAC. There are data out there to use one, and none preferable to the other. So it can be used in a chronic setting. I would just like to ask a question with regards to grade 1 and grade 2 cerebrovascular injuries that are traumatic in origin. I think it's always important to weigh the overall literature and mixed populations. In the trauma populations, when often we don't feel that we can anticoagulate patients, and we've gone on to study what the natural progression is, particularly the grade 1s tend to resolve without any treatment. So I think it's really important for people in the audience to really look at the specific patient populations as well as the overall larger studies. I think it's always important to weigh risk-benefit. So starting aspirin in a patient who's got multisystem trauma obviously wouldn't make a whole lot of sense, or even anticoagulating those. So that's why there's that thought at seven days you might just re-image, see if things are worse or better. All right, thank you, everyone. So we're going to move on to our last and final presentation. Home stretch, everyone. So two hours. So I know it's fairly long. So Dr. Jerry Zimmerman is faculty in Pediatric Critical Care Medicine at Seattle Children's Hospital and was past president of SCCM. So without further ado, Dr. Zimmerman. All right, thanks for staying, everyone. You don't think you're going to get out of here without some kids. Well, Cheryl had one. So here's a couple more. I don't have any disclosures that are relative to this presentation. So here's the case. There's been a lot of trauma this morning. And here's another one. This is a five-year-old involved in a high-speed motor vehicle collision in the backseat where she was supposed to be belted in, strapped in, but maybe not properly strapped in. So here is what this child looked like in the ED shortly after arrival. And the initial assessment showed these injuries, clavicular fracture, subarachnoid hemorrhage, right hemothorax, common carotid artery injury also on the right, acute respiratory failure requiring intubation basically at the scene of the accident, retroperitoneal hematoma and bladder rupture, which were surgically fixed, and then a cervical spine injury. So this is what the initial lateral C-spine looked like. And then with further imaging, which I'll show you, the additional information provided this summary of this complex cervical spine injury from C1 all the way through C3. Here is another view on CT imaging with significant distraction of the cervical spine high up. And you may not be able to see this very well, but on the bottom are the vertebra, vertebral bones high up and the fixation, surgical fixation from the occiput to C3 not long after the patient arrived at the hospital. So the fallout of all of this is shown here. This patient was unfortunately quadriplegic, so now acute and chronic respiratory failure, so required a tracheostomy airway that was placed early on, a gastrostomy feeding tube placed early on. There actually following the surgery unfortunately was a surgical site infection with an associated CSF leak. This was a big deal for about three weeks, and eventually an EVD was placed to take the pressure off the surgical site leak and this fixed. And eventually actually this EVD was replaced with a ventricular peritoneal shunt. But the big deal, and I don't know, maybe you don't think this is as exciting as what you've heard so far, but the big deal with this patient, and I just have never encountered this, and I've been around for a while, acutely is this child had this persistent abdominal distension, pain, and feeding intolerance, and you can see the x-ray on the right. And this is what this child's x-ray looked like basically every day. And this was this catch-22 that this child and the care team was in. This child would become agitated, had pain, and when she was crying she would swallow air, and just as you might expect, this led to more abdominal distension, more abdominal pain, and so this is what her x-ray looks like every day. And this is 24 hours a day, and then you can add on in a third dimension another interaction that was going on, and this was grandma who was the primary caretaker, the child adding anxiety to the caretaker, grandma and the grandma feeding back anxiety, and this just went around and around. And so this was a, this is an x-ray with that gastrostomy tube open, and this is what the patient looked like. So this patient had this persistent abdominal distension, did not tolerate feeding. The feeding tube was transitioned eventually from a G-tube to a GJ-tube, but still issues. We eliminated anything that had any anticholinergic activity. We weaned and actually discontinued all of the opiates. Actually for a while, we, this patient was actually started on methanol naltrexone while we were weaning the opiate. Magnesium citrate from above, and we learned to give that slowly over an hour instead of over five minutes so she wouldn't vomit it. And then things like every day, twice a day, these rectal mini enemas, digital stimulation, continuous venting of the gastrostomy tube now, and at one point we had to stop enteral nutrition because she just vomited it all up, and it became a risk factor for aspiration pneumonia as well. So here is this on one of these x-rays, a fecal impaction in the right ascending colon. This is exactly where it happens on almost all of these patients. I looked this up because I haven't thought about this for a long time. And for this patient with a high cervical cord injury, the problem was a hypotonic bowel throughout and a hypertonic external sphincter on rectal exam. You could understand why this patient was distended because she was not passing stool or flatus. So we've seen a couple cervical spine injuries already. There's 12,000 more or less annually in the United States, and almost all of these patients have what I am describing acutely and then chronically. It is a big deal with respect to their quality of life. And at least if you talk to adult patients with this injury, this is a bigger deal than bladder dysfunction, sexual dysfunction, chronic pain, fatigue, and even overall body image having to be in a wheelchair, maybe hooked to a ventilator. This is the major thing that impacts their long-term health-related quality of life. So the complications of this, I guess more chronically, is fecal impaction, which is recurrent, megacolon, perhaps associated with even bowel perforation, volvulus, hemorrhoids, rectal prolapse, diverticulitis. And then this is a trigger acutely as well as chronically for autonomic dysreflexia. And that's why it is actually really important to figure out how to get this bowel cleaned out and get a nutritional regimen that will work for the patient. So here is a high-power magnification of this fecal impaction in the right ascending colon. And this autonomic dysreflexia, if you've taken care of these patients, this can happen at any time. You think about the bladder being full, but you also need to think about the bowel being possibly full. So hypertension to the extent that this can actually be a trigger, an antecedent for intracranial hemorrhage, and then this sympathetic response, flushing, chills, skin blotching, nasal congestion, and headache. Now this was a child, and actually a lot of chronic diseases in adults can really augment this picture of dysfunctional bowel and may have a significant, I can't think of any word but impact, but diabetes, Parkinson's disease, multiple sclerosis, this is not uncommon. Severe spina bifida in a child, stroke, irritable bowel, lactose intolerance, inflammatory bowel disease, rectal bleeding, chronic medications, all can have an impact on this severe constipation following a cervical spine injury. So the signs of what we're talking about, again, are abdominal pain, abdominal distension, fecal incontinence in the long run, difficulty in stooling, and this ongoing risk for autonomic dysreflexia. So in this patient, while she was in the intensive care unit, we did all of these things. We discontinued the anticholinergic drugs. We used stimulants. We used osmolar agents, bulking agents, stool softeners, and as I said, she was on a course of methyl naltrexone while we were weaning the opiate for initial pain control. So additional things that actually I needed to look in the literature but that we employed that are helpful, one is abdominal massage sort of from the right colon over the top and this has been described as useful by a lot of patients, rectal suppositories, digital stimulation, enemas, and then this idea of transanal irrigation. You can imagine if you were a patient and you had to do this every day, but of all of these things, this is the maneuver that works and adult patients have actually described that this does improve their quality of life. But it takes a lot of work and determination to do this every day. And lastly, there are surgical treatments for chronic significant neurogenic bowel dysfunction. The first is this Malone Antigrade Continence Enema and this is where you take the appendix if you still have one, bring it up to the belly button, not the umbilicus, and create a conduit for giving an antigrade enema, which sounds more pleasant to me than the irrigation from below. So this is well described and it's used in other settings as well. The second is sacral nerve stimulation. And then lastly, some adult patients will actually opt for a colostomy or ileostomy just so they can deal with this more easily long term. So that is the first patient. The reason I presented this is this was a big deal for this child and the family and the care staff because everybody was doing what they were trying to do and nothing was working. Eventually, we were able to, after about two weeks of TPN, reintroduce enteral nutritional support, get rid of a lot of medications and the patient gradually is better. But still, the problem is recurrence. So I think it's going to be a chronic issue for this child. All right, I'll go on to the second one, second case. This is an 8-year-old who is generally healthy except she had obsessive compulsive disorder and she was being treated with a valproic acid derivative, Depakote. No other chronic medications. She had been complaining of some vague abdominal pain for a month. No history of trauma here, immunizations up to date, average student in the third grade, no one else at home, no recent travel. This is pediatric history. So this was this generally healthy child except for she was taking one drug. When she came in with complaints of abdominal pain, this is what was going on. Her heart rate is elevated for an 8-year-old. Her blood pressure is not terrible but it's low for an 8-year-old and the pulse pressure is wide and she had trouble with oximetry saturation, breathing room air. She had nothing in terms of skin findings. She was agitated because she was confused and had abdominal pain, I believe. So her Glasgow Coma score was a little bit abnormal. For the moment, her airway was patent, no obstruction but she did have a moderate increased work of breathing and if you listen, she was diffusely noisy. Her heart seemed to be fine. Her liver at this time was not enlarged. Her capillary refill was prolonged and if you look at her temperature demarcation, she was warm down to her elbows and then cool. Same thing on the lower extremities. No bowel sounds, abdominal pain. Maybe it was left-sided but I think that's a stretch at least initially. So here are her initial laboratory studies. Her CRIT was 30, platelets 80,000, white cell count 25,300 and the leukocyte differential was 55 cegs, 20 bands, 20 lymphs and 5 monos. The electrolytes are unremarkable except the chloride is a little bit elevated probably with resuscitation and the total carbon dioxide or bicarb is down. BUN and creatinine are both elevated for an 8-year-old. Albumin's low, CRP is way high and the blood gas shows hyperventilation and a marginal PO2 with a base deficit of 11 and a simultaneously measured lactate of 8.5. This is what her initial chest X-ray looks like. So I don't know if you are comprising your own differential diagnosis about what's going on here. But this was what the caretakers were originally thinking about. On the bottom is the excessive compulsive disorder. That's a long-term diagnosis. People were definitely interested or concerned about sepsis and septic shock in this patient with poor peripheral perfusion. So bacterial, perhaps viral, I think this was in the late fall, probably meets AR, not probably, meets ARDS criteria by pediatric guidelines, potential drug toxicity and that's where we were when this patient originally presented. So the initial things that were done, this patient was cannulated, blood cultures were taken, sepsis workup, urine, blood. The patient was started on ceftriaxone, had some volume resuscitation, needed to be started on a vasoactive inotropic agent. For kids, this is typically epinephrine, not norepinephrine first. Foley was placed, toxicology screen sent and the patient was intubated and initiated on mechanical ventilation and the pleural effusion was drained. So this is a follow-up X-ray and the ventilator settings. So 8 mils per kilogram, the PEEP was set at 10 with pressure support and peak inspiratory pressure to deliver this tidal volume of 8 was 35 and what's the last thing, 60% oxygen. So what happened next in the ICU in this patient with systemic inflammatory response was that urine output gradually decreased despite the fact that the peripheral perfusion actually improved and the patient was initiated on renal replacement therapy. There was a progression, not improvement in this picture of ARDS such that the patient actually required extracorporeal life support. This was several years ago, so at that time it was arteriovenous ECMO. The RRT allowed a daily even fluid balance but the patient still had, I would say, sort of a massive total hospitalization positive fluid balance. The C-reactive protein remained elevated and then in terms of unstable hemodynamics, addressing everything this patient required, several boluses, many boluses of calcium chloride to maintain a normal ionized calcium. Multiple blood cultures, patient still sick, remained sterile, the LDH was 35,000, that's high, amylase was 630, that's high, lipase was 450, that's high and the lactate just did not want to go down even with hemodynamic resuscitation, even with AV ECMO, this lactate remained elevated. Taking anybody anywhere? Well the patient was awake and awakened, had some sedation but was, could be awake enough to interact with her care providers and here is a point of care ultrasound. This is not actually from this patient but I don't know if you can see this but there is a arched curved structure there on top with the, pointed out by the arrows and it is inconsistent in its consistency, inhomogeneous and let me just orient you in a cross section here in the middle is the pancreas with the head and the tail sort of intact and this black region in the middle which is necrosis and the actual CAT scan again around the arrow shows this area of pancreatic, extensive pancreatic necrosis. So here are the causes of anybody's pancreatitis potentially. In this patient, you know, medications and anticonvulsants and oh, by the way, if you look, Depakote is right there on the top of the list of something that can cause a little bit or significant pancreatitis. So what happened next was the sepsis workup remained sterile. There's really no evidence of infection. The patient continued to be febrile. The white cell counts with left shift continued. The lactate did not normalize. The CRP stayed up. The patient required ongoing infusion of epinephrine and as I said, edema but daily even fluid balance achieved with RRT. The pleural effusion that was drained from the left reaccumulated and the patient continued with a distended abdomen edema and because of concern for abdominal compartment syndrome, a bladder pressure was measured and this was 18. In this setting of an increased bladder pressure, distended abdomen, I would say multiple organ dysfunction syndrome including early renal failure, the general surgeon finally after some convincing actually undertook this child to surgery and what was found was extensive pancreatic necrosis. Everything down there was all lumped together, duodenum, stomach, spleen. Spleen was taken out. Part of the duodenum was excised and primarily reanastomosed. So what happened next? Bladders remained sterile. The epinephrine was weaned. The lactate normalized. Like three days later, the patient came off ECMO. A few days later, the patient came off of the ventilator and like, I don't know, a few weeks later after that, the patient started urinating again and the continuous renal replacement therapy was discontinued. And when the patient was discharged from the ICU, her neurologic status was normal. The closing statement right there. Everything serves as not sepsis and at least for this case, this acute pancreatitis provided a, I would say, a perfect clinical mimic of sepsis and ultimately, I guess, source control of the pancreas and the pancreatitis is what fixed this patient. So thank you very much for staying and your attention. I'm happy to take any questions if you have any. All right, thanks for attending our session. I have a question actually. I take care of both adult and pediatric patients on trauma and there's a fair amount of literature about maintaining a spleen, right, in really young children and this, I was trying to remember if this was three or five year old, eight year old. So there are surgical techniques that allow us to preserve the spleen. They're painful for us surgeons and I would have to say I've only done it once in my career but it was very painful to do but we did save the spleen and I'm just wondering what your thoughts are on that. This case was several years ago and I don't remember if the splenic vasculature was comprised or something. I agree with you. In pediatrics trauma, it is completely unusual that a splenectomy is ever done and I'm sorry, I can't recall the exact reasons. I should have caught that. Good question. I don't know. Always preserve the spleen if we can. All right, well looks like that concludes our session. So thank you very much for staying and for listening to all of our cases and giving your feedback. Enjoy the rest of the afternoon.

case studies

complex injuries

cervical spine injury

quadriplegic

abdominal distension

feeding intolerance

healthy child

acute abdominal pain

multiple organ dysfunction syndrome

sepsis

acute pancreatitis

intensive care

multidisciplinary approach

barbiturate therapy

intracranial pressure