Good afternoon, everyone. My name is Jong Lee. I'm the moderator for this session. Thank you very much for staying till the end to attend our burn session. This is titled Acute Burn Care for Non-Burn Clinicians. And before we start, we're going to have a few housekeeping stuff. In case of fires, there are obviously exits on the back, and there's one on the corner. But luckily, we have burn specialists for this session. So if you end up getting burned, we got specialists who can take care of you. But hopefully, there is no fire and no burns. And then if you can silence your phone for the session. And we have three outstanding speakers for this session. And what we're going to do is we're going to have everyone speak first. And we'll have a question and answer session at the end. So there are about 486,000 burn injuries requiring some form of medical treatment per year. And about 40,000 require some form of hospital admissions. And about 30,000 are admitted to burn centers. And about 10,000 are admitted to non-burn centers. So if you, at some point, you may end up seeing burn patients if they have big enough burns in your ICUs, whether it may be MICU or surgical ICUs. But most times, it won't be a problem because you can transfer patients to a burn center. But if the burn center happens to have no availability, then you know, you may have to take care of these patients for a while. And especially if you have a, you know, disaster situation, you know, then what do you do if the burn, there is not enough burn beds available. So our first speaker, Dr. James Jang, will talk about treatment options when no burn beds are available. Dr. Jang is the chairman of the American Burn Association Disaster Subcommittee and an attending surgeon at Nason Spear Regional Burn Treatment Center in Philadelphia. Dr. Jang. Thank you, Dr. Lee. I'm really flattered that you, we got the invite. I'm actually representing the American Burn Association in a form of fashion today. I, along with many other people, have been working diligently on the mass casualty situation for burns. Let's do a clicker. It's not this guy. And a lot of the stuff I'm going to be presenting right now, it's going to, it's a little frightening. He said to just use the mouse. Oh, this guy? Okay. It's a little frightening, but it's really important because whether you like it or not, in a big mass casualty situation which the United States and federal government are preparing for, we the burn community are not going to be the burn doctors. It's actually going to be you guys, the critical care doctors, the trauma surgeons, and the general surgeons. So, there actually is a real reason why you want to learn some of this stuff. So, under what circumstances are there going to be no burn beds? Not in everyday care. I mean, the burn care in this country is pretty well regionalized and organized so that any of you on any given day can get yourself a burn bed. You call your local burn unit, and if they don't have a bed, they're going to get you a bed through the consortium within your region. Apocalyptic situations are different. And the federal government has been working with the burn community over the past 10 years, 15 years, to get ready for an apocalyptic situation. Ever since 9-11 occurred, the federal government has been really focusing on this stuff. And it used to be they told us, what are you guys going to do for 200 burns at one time, or 2,000 burns? And then they said, you know, the top-end scenario is going to be 20,000 burns, right, if there's a suitcase bomb. Well, about a year and a half ago, they came to us and they basically said, hold it. With the stuff going on with North Korea and then great power competition, you need to go up another order of magnitude. What are you guys going to do to cogently deal with 200,000 Americans that are potentially survivable after a strike? And they're taking it to the degree of seriousness that we've exercised this with the federal government. About two or three years ago, there was an exercise called Operation Gotham Shield. And I actually was at Mount Sinai for three years. And during this exercise, Gotham Shield, I was still working in Manhattan. And, you know, they told me that, I know you're the disaster chair of the ABA Disaster Committee, but you've just been vaporized. And so you don't get to play. And what the exercise was was a small one, a 10KT suitcase bomb that was detonated at the Lincoln Tunnel coming into Manhattan. And this is the plume that the Lawrence Livermore Laboratory in California said that would be the radiation fallout from the typical prevailing winds in the New York City area. And, you know, so that top-end scenario is about 20,000. Can you guys imagine 20,000 flash burns that are not dead instantly, that are not dead from trauma, but they have major surface burns? What are we as a country and a healthcare system supposed to do? And now, if you take 10KT and you make it more like 150KT, which is what we'd expect from a North Korean nuclear strike on Seattle or San Francisco or LA or San Diego, now, you know, you're talking about 200,000 Americans that are burned alive, have the wherewithal to live, but how the heck are you gonna make that happen? And so that's what we're talking about, okay? And that's why the people in this room are actually gonna be the burn care providers in the 2,000, 200,000, 20,000 casualty, because we are a small community, the burn care community, and we can't scale up. It's economically impossible. We're regionalized with the burn care community to five regions, the West, the Great Lakes, the Midwest, the South, and the Northeast. The red dots are ABA-verified burn centers. The black dots are non-verified burn centers. About 1,800 to 2,000 burn beds extant in the country. About 300 burn surgeons, about 3,000 burn nurses, right? And on any given day, the occupancy rate in those 1,800 beds is about 80%. So the buck does stop here in this room, at this meeting, with your trauma brethren, with your general surgery brethren, because if we've only got 300 burn surgeons and 3,000 burn nurses, and you've got 20,000 injuries, it doesn't take a lot of mathematics to figure out that the critical care people and the general surgeons and the trauma surgeons are gonna have to know some more than basic burn care. And there's a real problem, because burn knowledge is really, really, really waning. Tina Palmieri, who's gonna be giving one of the two speaks following mine, is a recent past president of the American Burn Association, and she, during her tenure as president of the ABA, made disaster preparedness a huge part of her scope of work during that year. She also is probably the only author who was on versions one, two, and three of the triage tables that the American Burn Association has sanctioned, and what I'm gonna show you in this talk is version three. This is actually a fairly mature set of triage tables, not a single triage table, but a family of triage tables that are graduated, that degrade gracefully, given enough situational awareness about what we're dealing with in terms of the magnitude. This triage table is pretty much everyday care, right? The white areas are basically ambulatory care. The gray areas are care is going to be deferred until beds are available, and that's the very elderly and the very large burns, so that's pretty much what expectant care is now in day in and day out, non-crisis situations, and the orange, the yellow areas are basically get to a burn unit. It also represents our plan for about 50 to 200 burn injuries. Did anybody hear about the volcano that went off in New Zealand? Anybody know how many burns there were? There were about 30 significant burns that required hospitalization, and you know it was a big to do. It basically wiped out their capacity in New Zealand. I've got good friends at Middlemore in Auckland at the National Burn Center, and I was getting feeds by text message all the time as to their evolution for about 30 big burns, right? So we're talking about 50 to 200 here, which we're gonna try to fold into everyday care. Anybody know about the Taiwan incident in 2015? There was a 500 burn casualty event in Taipei, color dust explosion, 500 young adults, you know, 40, 50, 60, 80% burns. It's bigger than this, so if we get something north of what New Zealand was, and more like what Taipei was, about 500 injuries, we're not gonna be able to meet everyday standard of care. So if we can't meet everyday standard of care with our 1,800 burn beds and our, with the 80% occupancy rate, with the 300 burn surgeons, 3,000 burn nurses, and you guys then become the burn doctors and burn nurses, burn care providers, along with the trauma guys and the general surgeons, your goal, your goal of care is time smearing, okay? You want a time smear. You don't want people to die because they don't have the basic needs. You want to time smear their needs so that we can get them through the system and the system can ramp up somehow to accommodate these 2,000, 20,000, 200,000 potentially survivable Americans with big burns. So focus on that. The goal is time smearing. And we work a lot with the federal government, HHS ASPR, Assistant Secretary for Preparedness and Readiness, and I plagiarized this from ASPR. It's a very nice graph. It basically talks about the initial care of burns and mass casualty and then the definitive care. And if you look over the initial care, the red part, that's where you guys need to step in in a mass casualty because we're gonna be overwhelmed. And what you want to do is you want to buttress us, be the backstop to expand gigantically that initial care and time smear towards the blue, towards the right of the screen so that we can save as many lives as possible, okay? That's the mission. So here's 100 to 500 major burns. And this is, you see the table now is starting to change from everyday care. The expected areas, the ones that we're gonna delay getting to burn care are now getting larger. The older, the big burns. The area that's going to existing burn beds is smaller and we're letting bigger, bigger injuries now be outpatient care, right? Very logical, right? We want to degrade gracefully. And this is table number two in a graceful degradation. But 500 injuries is like what happened to Taiwan. It totally filled the whole country. They did an incredible job. The federal government and the ABA went to visit and learn lessons from them. And they were pretty amazing actually. And so what are the things that you guys are gonna be called to do in a Taiwan sized incident when we're starting to fail everyday standard of care? You guys are actually incredibly well versed at three of the four things that you need to do to time smear. Number one, you know better than anybody about how to control airways, right? Angioedema, anybody here deal with angioedema? Ever seen it in your career? This is nothing but a case of angioedema. You know what to do, okay? So the first thing that's going to get you in these burn victims is airway loss. You guys know that better than we do. Just think of it as a bad angioedema case. The next thing you gotta do, this is the one that you're not familiar with, but we're ramping up telemedicine so that we're gonna hold your hand and we're gonna be a telepresence. One of the things that might have to happen is if there is a limb that has circumferential full thickness leathery burns, they're gonna lose that limb because it's basically an arterial tourniquet. And what you gotta do is you gotta take a bow of your electrocautery and release that tourniquet. This is something that you guys are not prepared to do, but we're prepared to be there as a telepresence. And that telepresence capability is sincerely ramping up as we speak so that we can be there for you to get you through this only one thing out of four that are critical that you guys are probably not prepared to do now. The next thing is you guys need to do a quality burn shock resuscitation. Now everybody's afraid of this, but you need not be afraid of it, all right? Tina Palmieri, past president of the ABA is gonna give you the full Monty discussion about burn shock. I'm gonna give you the military DOD quick and dirty approach, right? And that's the ISR rule of 10 or what I call the Chung formula. Kevin Chung is a well known burns person who is also very active in SCCM. He's the chair of medicine at USUHS. One of his most important publications is this paper where he codifies what the standard operating procedure is for the military these past 10 years, right? I call it the Chung formula, it's the ISR rule of 10s and it's really easy, guys. 10% burn, 100 cc's an hour of lactated ringers. 20% burn, 200 cc's per hour of lactated ringers. 30% burn, what? What do you give for 30%? 300, 40%, what do you give? 400 an hour, right? 99%, how much do you give an hour? A liter an hour. Guys, notice, you never go over a liter an hour. And the reason why the military adopted this is because early on in the Iraqi and Afghan OIF, OEF war, soldiers were coming back and having to have their bellies open in a C-17 over the Atlantic and they uniformly died. They basically floated away on chrysalloid and they all died, right? So the main problem now in burn resuscitation is not under resuscitation. We've been hearing that since I was like in diapers, like you need a lot of fluid. The main problem right now with burn shock resuscitation is over resuscitation and that's why I'm telling you this Chung formula is fabulous because you never go over a liter and it's just basically 10%, 100 CC, 20%, 20 CC, It doesn't, no calculation required. It just gets you into the ballpark and then you try to get them to pee 30, 50 CCs an hour. It's, I mean, that's what we do every day in ICU, right? We check the kidneys, we check the folate. Hey, is he peeing 30, 50 an hour? That's not unique to burns. That's unique to any sort of critical care. Am I right here? Can I have a yes? Can I have an amen? Is that what we do, right? All righty, and then here's the other thing. You guys are pros at rescue ventilation and not all these guys are gonna need rescue ventilation. You guys are pros at ventilator management. I mean, this is the Professional Society of Pulmonary Medicine. The only caveat that I would have you know is that if you practice ARDSnet while you're time smearing to help us out, it might not work. It might not work. Small tidal volumes, you know, small rapid tidal volumes might not work. And there's a review paper that talks about how burn care ventilation is different from rescue ventilation in the general ICU population. So, you know, the small tidal volumes might not work. You probably might wanna auto-download this article, right? Okay? But you guys are experts at rescue ventilation. You guys are experts at managing lungs. So, don't worry about that. So, the summary is three out of the four critical things that need to happen for you guys to help us time smear. You guys know because you're pros already. Now, who here has used sylvedim before? It's a hot mess. And not only is it a hot mess, but the shelf life is not very good. It's very labor intensive. And at the very minimum, you gotta change it every 24 hours, right? When we and the federal government got together, we said, the hell with that, we're not doing that. And so, anybody know what the strategic national stockpile is? Anybody here know what it is? It's a cash that the federal government puts together to buttress the materiel that we in American healthcare can call upon in a mass casualty situation. And we've participated with the CDC and HHS to revamp the strategic national stockpile and you will no longer find sylvedim, thank God, in the SNS. You're gonna find this stuff. It's called Silvalon. It's basically an ACE wrap or a Curlex that's impregnated with silver. And the nice thing about it is you put it on and you leave it on for a week. You leave it on for a week. So there's no pain, there's no dressing change, there's no nursing care. You just roll it on like a Curlex roll, you leave it on for a week and it wards off burn wound sepsis for a week. Remember what I said? Your job number one is time smear. You see how this plays into time smear? This is the king of time smear. You roll it on and you leave it on for a week, right? It's like manna from heaven. All right, now if you start getting into even uglier and uglier scenarios, now let's say we've exceeded 2,000 injuries. 2,000 injuries is basically a kinetic explosion at the local ballpark. Let's say it's something hairier than that now. You're starting to get 5,000, 10,000 injuries, et cetera, et cetera. How many Foley's do you think there are in the state of Florida? Do you think there's 5,000 Foley's in the state of Florida? Yes, no, maybe? How many Angiocats do you think there are in the state of Florida? Are there 5,000? Are there 10,000? Yes, no, maybe? I don't know, right? But can you imagine a scenario where you don't have the ability to start an IV? Do you think there's 20,000 bags of lactated ringers in the state of Florida right now? Maybe not, maybe not, right? So the other thing that all of you, I would beseech you to download, because in a crisis situation, the internet may not be up, are these series of austere guidelines for burn care. A lot of people worked on this. And actually, again, Dr. Palmieri was the reason that this quartet of guidelines exists. It basically, please download these articles, they're free. They're unrestricted download on the ABA website. It's basically, it's gonna tell you what to do if you're starting to get more than two, three, five, 10, 20, 50,000 burns, right? What do you do if you don't have IV fluids? What do you do if you don't have Foley's? What do you do, right? Well, if you don't have IV fluids, if you don't have Angiocats, if you don't have Foley's to measure 30 to 50 cc of urine an hour, you're gonna go to the guidelines and you're gonna see all these recipes on how to orally resuscitate burns. You can start with Gatorade. You can start with coconut milk. You can start with congee. You can start with iced tea. And it'll tell you what to add to these fluids and how you can orally resuscitate patients who have been burned. That's a game changer, guys. If you've got 5,000 burns and you're gonna watch them die because you don't have IVs or IV fluids, think about it, right? You want to download this article. You want to know how to orally resuscitate, right? And so this is just more. Actually, these tables, this family of tables have been exercised last year with the federal government and Massachusetts and Mass General. We actually had a big mass casualty event and we actually used these actionable tables and used these tables based on situational awareness to call out the triage and redistribution and secondary triage of the mock burn victims. And so this is the zombie apocalypse situation. Basically, almost everybody's expectant. Only the most survivable patients, young, small burns are at burn centers. If that's scary, let me scare you even deeper. A lot of work is being done with the federal government now and the Radiation Injury Treatment Network to deal with combined trauma, thermal flash burns and radiation, acute radiation syndrome, right? And this is the federal government zen diagram for what you're gonna be dealing with with a nuclear strike. These are the Radiation Injury Treatment Network centers. They don't all perfectly overlap with the burn centers. We're in the process, as we speak, of writing a mutual guideline for care of burn plus radiation injury and we're gonna publish that. So again, you've got a cookbook and you've got some basic rules of the road and what to do come the North Korean missile strike and the radiation and the burns, right? Somebody's gotta think of this. It's pretty scary and that somebody is us in this room. And finally, the critical care transport, that's something that we're working on very hard. There's an ongoing, raging discussion as to whether you bring the patients out from the epicenter and or you bring the burn care teams into the epicenter. I think the solution is gonna be a combination of both. And there's a lot of partners working on this. Last slide. There is a fundamental knowledge gap in this country in American healthcare about how to take care of burns. Lay that at the feet of the fact that burn care was taken out of the general surgery training syllabus about 20 years ago and basically watered down to near nothing in the plastic surgery training syllabus. And old farts like me are dying off left and right. So the fund of knowledge is diminishing in how to take care of burns when in a kinetic injury explosion, 15 to 25% of all explosions are not gonna be just trauma but they're gonna have life-threatening burns. To address this fundamental lack of knowledge in this country, we're really starting to push ABLS onto our brethren like critical care, like trauma, like general surgery. And at the East meeting that was here just last month, we put on the first joint ABA, Eastern Association of Surgery Trauma, ABLS course. We're also here at this meeting to try to see if we can't have a same frequency with SCCM leadership to see if in the future we can diffuse this waning knowledge to this very important group of people at this meeting. And I think I'm out of things to say. A month from now, the national meeting is gonna be here. If you guys have any interest in burns, it's a good meeting. Thank you for your attention. Thank you, Dr. Jiang. One of the first things you think of when talking about burn patients is probably resuscitation. We all know how to resuscitate. But burn resuscitation is a little bit different. It's like having resuscitation on steroids. And you tend to give a whole lot of fluids and then it lasts 24 hours, maybe longer. So our next speaker, Dr. Tina Palmieri, will speak about initial resuscitation of burn patients. Dr. Palmieri is a professor of surgery and the director of Firefighters Burn Institute Regional Burn Center at UC Davis. And she's also the assistant chief of burns at Shriners Hospital at Northern California. Dr. Palmieri. All right, it's always hard to follow Dr. Jiang. He's just his own kind of guy. So, but we're gonna do it. And today, I'm gonna hit rubber hits road. This is resuscitation 101 with a few twists for intensivists in the audience, because as everybody knows, a cardiac patient in the ICU is different than a pulmonary patient is different than a neurosurgical patient. There are subtleties to resuscitation. We all have commonalities. We all have differences. So we're gonna do some big commonalities and some differences. And I have some disclosures, you know, disasters in my blood, Northern California wildfires, triage officer. Okay, and burns and disasters are hand in hand. So today, we're gonna learn about that. Today, we're gonna talk about the basics of management priorities. You know these. I'm gonna give you a little twist after I tell you what you already know. And some fluid resuscitation issues, and then how to apply it to a patient. There's nothing that makes burn resuscitation more real than a case. This is an actual case. A 32-year-old gentleman and his two-year-old son are trying to fix the propane heater. You can just see the little dude is hanging behind his father when it blows up. So they're both brought to the hospital after being trapped for 10 minutes in the garage. They both have burns over the entire head, both arms, chest, and back. So what are you going to do? Where do you start? And you're like, jeez Louise, please don't do this to me. Of course you know this. Airway, breathing, circulation. Forget the wound. Forget the fact that the janitor, everybody and their brother who's in the hallway of the hospital runs into the room to see the wounds. You're the person who directs everybody to, hey, we're focusing. Airway, breathing, circulation. Very common. So we go on, and they're awake, they're confused, and they're breathing about 30 times per minute. Their oxygen saturation is 100%. Why are they altered mentally? There's no signs of trauma. How should you treat them? And what, by the way, is inhalation injury? Actually, inhalation injury is not one thing. It is three things at the very least. There's type one, which is the gaseous component. Type two, upper airway obstruction. And type three is what everybody thinks about when they think about inhalation, but it's actually the injury to the parenchyma. Type one, hypoxia, is actually the leading cause of death at the scene of a fire. Oxygen is consumed by the fire in the room, and people die from it in that room. The second gaseous type is carbon monoxide. And again, as they're trapped in that room, carbon monoxide is generated, and it literally has 250 times the affinity to hemoglobin that oxygen does. What it basically does is it knocks oxygen off of hemoglobin and deprives it from the tissue, deprives it from the lungs. It shifts the oxygen-hemoglobin dissociation curve to the left so oxygen doesn't get delivered. It also affects the cytochrome oxidase enzyme system. That's the enzyme system that allows all of your bodily functions to work. Without that system, you cannot generate a response to injury. So in severe inhalation, that becomes a problem. How do you identify it? Progressive neurologic dysfunction. As carbon monoxide levels rise, people become more confused. The classic is the gentleman who goes in and out of his house to rescue first his kids, then his dog, and then he's going back in for the cat because everyone knows the cat hides the hardest, right? And he can't find the cat, but suddenly he can't remember where the door is. He runs around, literally, in the middle of his living room in circles until he becomes unconscious. That's progressive mental deterioration. Classic carbon monoxide toxicity. We're in Disney, so you got to show a Disney character. Red nose, red cheeks. Almost no burn patient shows up with red nose and red cheeks. Why? Because they're hypoxic and have elevated carboxyhemoglobin levels. They do not use colour. You really do have to measure carboxyhemoglobin levels. There's only one type of pulse oximeter that actually can distinguish oxygenated hemoglobin from carboxyhemoglobin, and most of us don't have them in our ICU. So keep that patient on 100% oxygen until you get a blood gas with co-oxymetry to determine if carbon monoxide toxicity exists. The good news is that you can actually treat carbon monoxide toxicity with 100% oxygen. Literally overpower carbon monoxide, knock it off the hemoglobin molecule and replace it. Now, the hyperbaric chamber sounds like a great thing. Has anyone here ever sent a critically ill patient into a hyperbaric chamber? Suction doesn't happen. Anything metal can be a problem. Diabetics tend to have the seizure thing when they go into hyperbaric chambers. You cannot get to the patient in a hyperbaric chamber. So generally, burn patients are not recommended if with major burns for a hyperbaric chamber. Pure inhalation, carboxyhemoglobin toxicity, yes, but burn patients, no. So back to our patients. You're smart, you put everybody on 100% oxygen because you're an intensivist, you know what you're doing. The carboxyhemoglobin is 15% in the father, 25% in the child. The child develops stridor but not dad, why? Type two, airway obstruction. This is the one that in the United States frequently occurs within four hours. If you go to a country that lacks resuscitation algorithms, it occurs later because they don't get the resuscitation fluids. What happens is that air in a burning room gets extremely hot, over 150 degrees centigrade, and that causes injury to the upper pharynx. Actually, your upper pharynx diminishes the heat. It dissipates the heat. Think about it like when, have you ever cleaned a room with ammonia and you accidentally get a whiff of it? You inhale, and your glottis closes. You limit the injury to above the glottis. The same thing happens with the heat injury. The other thing to remember is that most people don't sit there and stare at the burning thing. They turn to run away. So patients tend to have one side or the other more burned, and that causes anatomic distortions. Burn patients can be among the most difficult to intubate. The top child, you can see, this is, it's a deep, partial thickness burn. That airway comes out. It's surgical or death. The lower patient, nobody would argue, that's a fourth-degree burn. Intubation is our classic ICU intubation criteria. Obviously, respiratory distress, deep burns. A massive burn, well, what is that? If it's a prolonged transport, anything much above 40 to 50%. This is non-disaster. In a disaster, we'd be talking other things. You'd have to kind of do it until you got your tube. Children and adults also differ, and this is why the child develops stridor. Not only is everything shorter in a child, it's smaller. Their vocal cords are more anterior, and to intubate a child, it's more of a right angle than in an adult. Now, the good news is kids have baby teeth, so you don't have to worry quite as much about their teeth. They do have large tonsils, and that can definitely get in the way. An edema has a much bigger effect, the radius to the fourth. The other anatomic consideration is that the cricoid space is the smallest space in a child. So a cricothyroidomy is relatively contraindicated in a young child. So we get everybody intubated, because you are good, you can get those tubes in, and you see soot coming out. You're like, uh-oh, we're in the soot now. Type III respiratory injury, that to the pulmonary parenchyma. It's more serious than the heat alone. It's due to airway closure and atelectasis. And the body burn actually potentiates this injury with causing an increase in fluid requirement of approximately 20 to 30%. More fluid with lung injury. This is a difference in burn injury. If you under-resuscitate a burn, you will magnify the lung injury. Make sure you give the appropriate amount of fluid. These are the changes in the upper airway. Burn patients with inhalation injury actually damage the cilia. They get surfactant deactivation. And this is why Dr. Jiang was hinting that the ideal tidal volume for a burn patient is not really known. Sometimes they need that bigger tidal volume, sometimes they don't. You have to be an intensivist and think it through. There's tissue hypoxia, there's shunting, there's VQ mismatch, and there's cast formations. How do you identify this? History, history, history. If you are lighting your barbecue and you put a little too much propane on and it flashes your face, and you come in the next day wearing sunglasses because your eyebrows are gone, right? If you had gone to an emergency room, there's a 50-50 chance someone would have intubated you if they hadn't heard your history. But you are fine. A brief exposure to flame will not generate something that needs an intubation. However, that prolonged exposure is the issue. Look for that elevated carboxyhemoglobin. Bronchoscopy and pharyngoscopy can be very telling. Caveat, if you are going to use bronchoscopy to evaluate somebody's airway, be prepared with an endotracheal tube on the bronchoscope so that if you see impending airway obstruction from edema, you can do something. Because the bronchoscope itself will cause enough edema in some patients to tip them over the edge. Treatment is aggressive pulmonary toilet, adequate resuscitation. PEEP is a wonderful thing in burn patients. Determining optimal PEEP can be very helpful. Humidification of your circuit in your ventilator to keep those secretions from drying. If a burn patient pulmonary secretions get dry, they turn into cement and can obstruct your tube. And changing an endotracheal tube when you have a child or an adult whose head is huge is a real feat. Bronchodilators and our next speaker will be talking about that and bronchoscopy to clear debris. Tips, these are pro tips. Secure the tube. As people become, and monitor that tube even with x-rays at times because as the patient becomes edematous, it pulls the tube out. Especially with oral intubation, the tongue gets very big and the tube pulls out. A child this size can flip his head around and pull his tube right out. Notice there's no tape. Tape won't stick on this. This is a halter system that works extremely well in both patients with edema as well as burn patients. It's literally trach tie in respiratory tubing. And it's tied once around below the ear and one above, just like you would a bridle. And it's good in two directions. It's an outstanding way to keep a tube in somebody who is a bit recalcitrant. Use the right size tube. Do not use a smaller tube because you think, oh, they have an airway injury. Use the tube that's appropriate for that person's age. Keep things clear, keep things humid. Back to the case. You got the airway. This is the ICU thing. Now, how are you gonna address the circulatory issues? What is fluid resuscitation? When do you resuscitate a burn patient? Something most people never talk about. At least 20% in adults and 15% burn in children. Now, those size burns need resuscitation. Smaller burns, sicker people, that old 90-year-old lady who's got a 10% burn, she may need a resuscitation because her norm is dehydration. IVs can go anywhere. Just make sure they don't have a compartment syndrome. So why do burns need fluid? Because basically they develop leaky capillaries and they develop hypovolemic shock because all their intravascular fluid leaches into their subcutaneous space. That's why they look swollen. Think of it as you sprain your ankle. Your ankle swells. You burn your skin, everything swells. Other caveat is that burn resuscitation is not static. Burn patients actually lose variable amounts of fluid as those capillaries leak. And over time it decreases. And this is a classic diagram. This is actually the original diagram in Dr. Baxter's paper when he developed the Parkland formula. No, this is what the Parkland formula estimates you need. This is what the patient actually needed. Underestimates in the beginning, overestimates in the end. So the actual important thing is to adjust your fluids. Many things increase your fluid requirements. Obviously the burn size, the burn depth, age. Children require more fluid than adults do. They have a bigger body surface area per unit volume. Delayed resuscitation increases it. If you start someone on a propofol drip, you might as well just double your fluids because that's what's going to happen. That continuous vasodilation causes an increase in fluid requirements. Fasciotomies, escharotomies open the doorway to fluids. Electrical and alcohol and drugs, I'd like to say in California we never see anybody with drugs. But I would be lying because it's 30% of my population. And that is all age groups. Metamphetamine is being used by 70 and 80-year-olds. So Dr. Jiang introduced a formula. And I'm here to tell you there's at least 20 different burn formulas. Now when we have 20 ways to do something in medicine, that generally means they don't work in everybody. So my main thing is, I don't care if you remember which formula you remember. Remember one, the Dr. Chung's formula, 10, 20, if that's what you remember, go for it. The key is adjusting your fluid after you start. The reason these formulas were invented is because nobody has the courage to start someone at 1, 2 and 3 liters an hour and say, I'm going to start 3 liters an hour in somebody and I'm going to keep it going for 8 hours. Nobody would do that without something to back them up. That's where these formulas really came from. Parkland formula is one of the most common formulas that's used. Like I said, I don't care which one you use. The places where formulas fall apart is in the very young and the very old. This is where you have to be very careful after you start fluids is to really monitor them. Lactated ringers is the fluid of choice for burn resuscitation. If you use saline, you run the risk of hyperchloremic metabolic acidosis because of the sheer volume of salt you would be giving people. Think about 30 to 40 liters of IV fluid in a 24-hour period. If you give it all the saline, you will generate a metabolic acidosis. The formula is just a starting point and you should adjust the fluids. We're going to talk about this 30 to 50 mils in adults and 1 mil per kg in children. How do you figure out how big the burn is? Your palm is 1% of you, including your fingers. You can figure it out on any patient if you cannot remember the Rule of Nines by putting your hand up to the patient's hand, give them a high five and see how close your hand is to theirs and then palm it out. It's the easiest way to do it. You don't have to remember is it 9 or 18 on the arm or back or front. Your palm and the patient's palm is 1% of them. And only count what's at least blistered. So what's at least blistered or obvious third-degree burn. So if we calculate burn size in our patients, dad actually has a smaller surface area than son. And that is because children have bigger heads. So if your 12-year-old tells you that he's smarter than you, his head is bigger, you can give him that. So how do you monitor burn resuscitation? Key difference between burns and other things. Burns patients are hypermetabolic when you get in that 20, 30, 40 and above range. They will be tachycardic. You can give them the entire cadre of fluid in your unit and they will still be tachycardic. You cannot use heart rate to titrate burn resuscitation. You cannot use heart rate to titrate your fluids for burn resuscitation. You have to use something else. Otherwise you will over resuscitate. Urine is one way to do this. And we already talked about the monitoring. Old burn nurse rule of thumb taught to me many, many years ago is you decrease in increments of 10% or increase in increments of 10%. The biggest problem we have, as Dr. Jiang alluded to, is fluid creep. Too much of a thing is bad. If you over resuscitate a burn, you can get pulmonary edema, pleural fluid. I've had to put chest tubes in patients because of that issue. Pericardial effusions, abdominal and chest compartment syndrome, extremity compartment syndrome, intraocular hypertension leading to blindness has actually been reported not infrequently from burn over resuscitation. So how do we minimize that over resuscitation? Well one, follow the formula more closely. Number two is more accurately determine the formula variables. And three is measure something else. This is a classic burn resuscitation. If you look at over resuscitation, this is the 0.5. This is the goal for urine output. This is the actual urine output. We have a problem, right. It was above the goal the whole time. So what if we have a computerized resuscitation, which it does exist. This is one of the closed-loop resuscitation formulas using technically artificial intelligence that tells you how to adjust your fluid rates based on urine output. Now this is great, but it only works if urine output is truly a measure of resuscitation. And you are ICU people because I am not even going to try and tell you that urine output is a great measure of resuscitation because it's not the best. We all know that hyperglycemia and many other things influence urine output. So there have been people looking in the ICU world at can we use some of our advanced hemodynamic monitoring. Generally this meta-analysis suggests that dynamic hemodynamic monitoring may improve our resuscitation. However, don't forget your goal is oxygen delivery to the tissue. The static hemodynamic parameters are not helpful and lead to over resuscitation. So what you want is continuous variables. And I recommend use several factors. Use that with lactate, base deficit, urine output. Do what intensivists do. You look at everything and make a decision sequentially based on all those things. This is from a paper. I actually love this diagram. Of course I had to modify it because I'm a burn surgeon. I cannot accept anything as it was written. But this was a very nicely done paper and this is a nice algorithm that combines urine output with some of the more advanced techniques that we have in the ICU as an algorithm for how to treat and burn resuscitation. And it takes you all the way through. One tip that we frequently will use in burns is if we are lagging behind in resuscitation, albumin can be helpful. So suddenly father and son, their extremities become cold and cool and tight. So what do you have to assess? Compartment syndromes are a reality in burns. Sometimes it's fluid over resuscitation, but not always. So don't kick yourself if it happens. It does happen in people with severe burns. It can involve the extremities, the chest or the abdomen. Now the fancy way is to measure compartment pressures. How many people in here have actually measured compartment pressure? Right. So not too many. If you have to, and you're not... this is Palmieri's rule. You know how when you buy a peach, right, if you're going to eat it right away it's got to be kind of soft and mushy? That's an extremity that's cool. You don't have compartment syndrome. If that peach is so hard, you remember how if you get a peach it's like, oh, this is not quite ready. I'm going to hold off. That is someone you're worried about compartment syndrome, okay? Everybody knows food. Not everybody knows compartment syndrome. But that is the poor man's way of saying, ooh, I'm worried about compartment syndrome. And then you can measure it. Now the way you can measure it, you all have art lines in your ICUs. Put a needle on the art line and you can put it right in the compartment. Or get your favorite best friend surgeon to help you out. Because if they won't help you out with this, you've got a bigger problem. Okay. Normally compartment syndrome takes about 6-8 hours. In delayed resuscitation it will take longer. Don't wait for the pulse. Don't wait for the Doppler signal to go away. You've missed the boat. And the patient will also tell you if they're awake. If they're awake and alert, and burn patients scarily are very awake after a burn injury. If they have severe, unrelenting pain in the limb, look at it. Look at the urine. If the urine is red, you either have a compartment syndrome or you have a deep burn that extends into the muscle or an electrical burn. One of those three things are likely to be happening. Chest escharotomy again, that happens to 6-8 hours. What your respiratory therapist will say is we're having progressive diminution in our airway volumes with increasing pressures needed to get the same tidal volume. It's either a pneumothorax, a chest compartment syndrome or an airway obstruction. And you know how to do two of those three. Just look at the chest and see if it looks like it's firm. And again, the peach thing works here too. Again, you need to do something. Abdominal compartment syndrome is something to think about and burns over 60%. That's the predominant issue. And it's usually in people who need more resuscitation than you expect. And that chest X-ray is a classic. You get a chest X-ray and see how the diaphragm is halfway into the chest? That is advanced compartment syndrome. You missed it. It was going on for a few hours before then. But once you see that, you can relieve it. Now for the surgeons in the audience, you're like, oh my God, that's one of those silos. We use wound vacs now for this. I hate to tell you this, but if you put a wound vac on a wet burn abdomen and you roll the patient, you will be very unhappy. Your intra-abdominal contents will end up in the bed. So that's why in a burn patient you can't get a wound vac to stick. There's nothing to stick it to. And if somebody ever finds a way to do that, you're going to be very good. So burn fluid management pitfalls. The first one is under or overestimating burn size. In the U.S. we are off by an average of 20%. So when I get a phone call with a burn of 20%, it's anywhere from 0 to 40, sometimes even farther. Incorrect weight. Let's face it. How many people get weight in the emergency room? Not a whole lot. People start the fluids. And they start them wide open because it's a burn and you want to give them fluid and they forget. And all of a sudden there's 8 liters that have gone in. I'm sure you've never seen that in other conditions. People are afraid to turn the fluids down when that patient's making like 32 milliliters an hour of urine. It's like, oh, but I want to make sure they're good 2 hours in a row. You missed an opportunity to drop the fluids. And inadequate resuscitation. So what do you do? You're an intensivist. You've done all the things you're supposed to do. There's still no urine. You're like, is this like a real Foley or did you give me the imitation one that's blocked up? If you're at twice your resuscitation volume and you are still having low urine output, first of all, recheck your IV lines. Because if someone put in a very short catheter, they can actually come out of the vascular treat. You want to make sure they're all in the right place. Check the Foley. Make sure it's not obstructed. If you've given someone a drip, intravenous infusion of propofol or any of those things, turn them off. Because they're increasing your intravascular space. Turn them off. Your patient will do fine. You can give them hourly pushes. Get them stabilized and then think about it again. The paper that was presented, that is one of the top papers about limiting sedation is really important for burn patients. Albumin and FFP are colloids that can be your best friend. There's actually a randomized prospective trial on both of these substances going on in burns right now. Many burn surgeons use albumin and FFP as early rescue, giving some boluses in that regard. Look for abdominal compartment syndrome. Because if the abdomen is tight, the patient will get compression on their kidneys and they will not be producing urine. And the last one, and this is the hardest one, this is the one that makes no sense to many people. If the patient is becoming more acidotic, not responding to your fluids, not responding to your pressures, you see that your resuscitation is runaway resuscitation and the patient's not getting better, you have to operate. This is the patient who you have to take them to the operating room and remove the burn. If you remove the inciting cause, the inflammatory response stops and now it can turn your entire patient around. This is one of the gutsiest calls you can make in the ICU. You have to decide. Because if you're wrong, they die. If you're right, they survive. It's a tough one. So how long do you use any of our formulas? What's your goal? And then what do you do with the burn? After that Parkland formula, how do you know where your endpoint is? We haven't told you, have we? Your endpoint is actually the point at which you reach the patient's normal fluid loss through their wounds plus their normal IV maintenance rate. So the average adult in this room, your normal IV maintenance rate is what, 100-125 milliliters an hour. This formula here, and that's your normal 24-hour fluid requirement. To calculate how much fluid you lose through the burn, this is the part that you lose through the wound, 25 plus your burn size times your body surface area. That's your hourly fluid loss through the burn wound itself. So that is your endpoint for your resuscitation. You don't go below that. And for children, note that children, that maintenance is just a little bit higher than for the adults. Temperature management issues, a normal temperature in a large burn is 38.5. If a burn patient is 37, there's something wrong. That is not normal thermic for a burn patient. They should be warmer. And with respect to wounds, you can put anything you want on them. Silvalon that the military has in their cache is fine. The one caveat, wash it before you put the dressing on. I cannot overemphasize, it's such a simple thing but people forget, burns are not sterile when they come in. Burns are contaminated. They must be washed and then put the dressing on. It's not a popular thing to do if you're the person who has to do it and you've never done it before. But they have to be washed, get off that bacterial burden, and then put the dressings on. And early enteral nutrition, absolutely key. Because if a burn patient loses their nutritional reserve, they will not heal the wound. And this is about the only thing in critical care where if that wound doesn't heal, the patient dies. This is one of the few times where the wound determines survivability. So in conclusion, burn resuscitation is kind of simple for most of intensivists because you're already doing all this stuff. I just talked to you about a few little tips and tricks that you can use to get yourself through some of the tough times. And some of them are hard to swallow because they do go against what normal people's grain. You want to monitor your airway, your circulation, and understand the basics and the differences in physiology. And this is a little dude on the right that you saw before, this is him. He really, with the right care, was able to survive. And I thank you for the privilege of the podium. So you may also see inhalation injury in your hospital, especially if somebody comes in with pure inhalation injury with no external burns. So they may end up in your medical ICU or surgical ICU. So third speaker, Dr. Pan-Li Engpakta, will discuss treatment options for inhalation injury. Dr. Engpakta is Professor of Anesthesiology and Director of Translational Intensive Care Unit at University of Texas Medical Branch in Galveston. His research focuses on inhalation injury in large animal models. Dr. Engpakta. Thank you, Dr. Lee, for such a nice introduction. And thank you, everybody, for staying for this late. And I also like to thank Dr. Padméry for such a nice introduction to the beta physiology of the lung injury. That makes my job a lot easier. So everybody knows that smoking inhalation injury can be classified as pulmonary and non-pulmonary organ injuries. And today, actually, I will focus on the therapeutic options based on the beta physiologic changes in lower airways. Wait. Okay. I think it's going to take some time to. Okay. So there is no consensus on the diagnostics and also severity criteria of the smoking inhalation injury exist. This is why there are no specific therapies available for treatment of smoking inhalation injury. And then treatment of the smoking inhalation actually differs among the hospitals and burn centers. But I show in here just an example of the therapeutic approach provided at Shriners Hospital in Galveston, Texas. But most hospitals use nebulizer tapering, albuterol, and anesthesia stain. So beta physiology of smoking inhalation injury is very, very complex. Of course, I am not going to go through all this pathway. But I just wanted to emphasize the critical role of the airway changes in beta physiology of lung injury after smoking inhalation, such as coagulopathy, bronchospasm, excessive mucus secretion, airway epithelial injury, and also, most importantly, airway hyperemia and the airway mucosal edema. So airway dysfunction can be characterized mainly by three factors, such as bronchospasm, airway obstruction with massive airway obstructive cast containing a lot of inflammatory cells, and also, most importantly, airway hyperemia and airway mucosal tissue edema. So in this slide, I just want to show you that current status of treatment of smoking inhalation injury. And I kind of talked about the nebulized albuterol is used to antagonize the bronchospasm. And anesthesia stain is nebulized to reduce the excessive mucus secretion. And heparin is nebulized to prevent some clot formations. However, the very, very strong critical factors that potentially contribute to the airway dysfunction, such as airway inflammation, airway epithelial cell damage, and also the delayed repair, and all the foreign fibrin cast, and also airway hyperemia and airway mucosal edema are neglected. There is no therapy focusing on those critical factors. And unfortunately, those important factors are kind of ignored now and understudied. So that's why I just wanted to focus now a little bit on the pathophysiology of lower airways and talk about some therapeutic options. So first, let's talk about a little bit on the airway mucosal edema and some therapeutic options. So of course, you know that the bronchial circulation drains into the pulmonary circulation. It's about 1% of the cardiac output. So it doesn't really affect the pulmonary transvascular fluid flux. However, smoke inhalation increases the airway blood flow almost 20-fold. This is the huge flux of the volume of the fluid through the parenchymal circulation that may cause the lung edema. So that's the problem of the increased airway blood flow after smoke inhalation injury. So in this slide, I want to show you the increase in pulmonary transvascular fluid flux, which is actually, you may say, edema. The index of the edema formation is increased about 6 to 7-fold after smoke inhalation injury. So it's a huge increase in pulmonary transvascular fluid flux, actually leading to the lung edema as evidenced by here, by the CT scan, and also by measuring the extravascular lung fluid. So the question is that it seems that you can see the very nice association of the extremely increased airway blood flow and also very strong, severe lung edema after smoke inhalation injury. But the question is that, is there any link between those two pathologies? And then another question is, if there is a link, if this increased airway blood flow actually cause or contribute the lung edema after smoke inhalation injury. So to answer this very important question, we actually ablated bronchocirculation in the sheep exposed to the smoke inhalation injury. As you can see here, if you ablate the bronchocirculation, like shown in here, that airway blood flow abolished. But very interestingly, this bronchocirculation ablation actually almost completely inhibited the lung lymph flow, which is index of the pulmonary transvascular fluid flux leading to the lung edema formation. It's almost completely inhibited, meaning that increased airway blood flow indeed causes, if you will, and or contributes, significantly contributes to the formation of the edema in the lung tissue after smoke inhalation injury. So in this slide, I just wanted to show that also the ablation of the bronchocirculation significantly improved pulmonary function in this case, improved oxygenation, and improved PTF ratio, and decreased the pulmonary shunt fractions. So in this slide, I want to show a very interesting result. Here I just want to show you that augmented airway blood flow not only brings huge amount of the fluid to the parenchymal tissue after smoke injury, thus causing the lung edema, but this augmented airway blood flow may actually flux inflammatory mediators to the lung parenchyma, thus exacerbating the tissue injury. So this is a very interesting concept that should be really studied in the future studies. So now, just in brief summary, that increased airway blood flow causes the pulmonary dysfunction by the variety of the ways. It increased the mucosal edema, lumen narrowing, and hypoxia. But it also caused the lung edema and also tissue injury by fluxing huge amount of fluids to the lung parenchyma and also the inflammatory mediators. So as I showed you, that ablation of the bronchocirculation actually takes care of all those pathologies, but it's not feasible to ablate or ligate the bronchial artery in a human. So what we should do? So we think that nebulized epinephrine can be the ideal candidate for treatment of the smoking-conditioning injury because of its dual effects. Epinephrine may reduce the airway, epinephrine, and mucosal edema by its alpha-1 effect. And at the same time, it may actually antagonize the bronchospasm, which is the frequent complication of the smoking-conditioning injury, as Dr. Palmieri mentioned. So as you know, that epinephrine is very cheap and readily available and also FDA-approved drug. So I think that epinephrine is a very ideal candidate for treatment of the smoking-conditioning injury. So in this slide, strikingly, nebulized epinephrine completely inhibited airway blood flow as you can see here in trachea and lower airways. This is exactly the bronchial artery ligation-like syndrome, like effect. So meaning that nebulized epinephrine can act as ablation of the bronchial circulation. So more importantly, nebulized epinephrine almost completely deblocked the area of mucosal edema, reduced lung edema almost completely, and also attenuated lung tissue edema, suggesting that nebulized epinephrine can be a very nice and efficient therapeutic option for smoking-conditioning injury. So in this slide, I just wanted to show some systemic effects of the nebulized epinephrine. It actually reduced the whole-body fluid retention and also improved, in some extent, the urinary output. But the exact mechanisms behind the salutary effects of nebulized epinephrine remains unknown. But we think that this might be related to the epinephrine's effect, which is independent on its adrenergic agonist effect. This may be something else. So as you can see here, we measured a very important endothelial adhesion molecule called E-catecholine. And we measured that epinephrine... only epinephrine actually preserved the V-catecholine, but not the albuterol and phenylephrine, suggesting that epinephrine may have some beneficial effect on the microvascular hyperpermeability, independent on its... the adrenergic agonist effect. Of course, this has to be tested in future studies. So in this study, I just wanted to show that nebulized epinephrine nicely reduced airway pressures behaved by its beta-2 agonist effect, and also improved the pulmonary gas exchange. So finally, we completed some clinical... very small pilot clinical studies with nebulized epinephrine. And we showed that actually nebulized epinephrine was safe in burn patients with smog inhalation injury. So now, a few words on the airway obstruction. So airway obstruction can be life-threatening. You can see here that massive airway obstructive cast, both in sheep and humans, with the smog inhalation injury. And what this massive obstruction causes is that it causes atyptosis and also causes hypoxia, which actually may lead to the immediate death. So again, the same occurred to... of course, many, many factors are involved in pathophysiology of the airway cast formations. But in my opinion, the fibrin is very important. Actually, the fibrin clot actually solidifies the content of the airway secretions, makes them very hard to remove, even by very aggressive airway toilet. So the question is, how are we going to manage this coagulopathy, and how are we going to prevent this airway clot formation after smog injury? So of course, everybody knows that burn and the smog cause very, very severe imbalance in coagulation. You can see here that burn and smog inhalation almost depletes the most important endogenous anticoagulant, anthracterin, and this is in sheep with burn and smog inhalation injury. But this happens... same thing happens in humans. So I just want to remind you here is that heparin and anthracterin are very weak anticoagulants when they're separated. When heparin binds to the anthracterin, anthracterin's anticoagulant effect is increased dramatically. But I'm going to talk to this a little bit later. But at the same time, in burn and smog injury, the fibrinolytic system is impaired. As you can see here, that massive fibrin deposition in the airway, and also the clots in the microvasculature of the lung, evidenced by the histology and also CT. So how we prevent this coagulopathy and also this fibrin clot after smog and clotting injury? So there are two ways. One is to use anticoagulants to prevent fibrin clots. And the other way is to use fibrinolytics to lyse all of the formed fibrin clots. So in this slide, I just want to show you the effect of combined therapy with nebulized heparin and intravenously administered antithrombin. As you can see here, this combined therapy significantly reduced airway obstruction, significantly reduced the peak airway pressures, reduced the lung edema. So it's very effective. And I just want to remind you again that heparin actually potentiates antithrombin's anticoagulant effect. But unfortunately, heparin inhibits antithrombin's anti-inflammatory effect. So when heparin binds to the antithrombin, antithrombin is not anti-inflammatory. So then to avoid this problem, we nebulized heparin to have local airway effect against the coagulopathy. And same time, we administered antithrombin intravenously to have systemic anti-inflammatory effect of antithrombin. So as you can see here, this combined therapy significantly inhibited some of the inflammatory mediators, such as excessive nitric oxide and VGF, suggesting that antithrombin or this combined therapy is indeed anti-inflammatory in burn and smoke injury. So in another study, actually, we confirmed, again, the SHIP study, we confirmed that antithrombin actually inhibits neutrophil activation, reduces the circulatory numbers of the neutrophils, and most importantly, also, the antithrombin prevents the migration of the neutrophils through the lung endothelial barrier. So then another thing is that also antithrombin significantly inhibited reactive nitrogen species, confirming, again, anti-inflammatory effect of the antithrombin in burn and smoke injury. So there are quite few studies actually showing the beneficial effects of the antithrombin in reducing morbidity and mortality of the burn patients. So actually, the Dr. Karol Wernethaus showed that antithrombin does not cause or does not augment bleeding during the sclerotomy of the burn patients, so meaning that antithrombin is safe to use in burn patients without fear of the increased bleeding. So how we deal with other deformed fibrin clots? So in this case, we nebulized the tissue plasmidin activator, which actually lights the fibrin through promoting the plasming. As you can see here, this TPA, tissue plasmidin activator, significantly improved the pulmonary gas exchange and reduced the lung edema. So a few words about the bronchospasm now. So as mentioned, albuterol is used as a standard therapy in burn centers. And albuterol is also an FDA-approved drug. And back more than 10 years ago, Dr. Palmieri actually reported that continuous nebulization of albuterol significantly reduces the airway pressure, reduces airway obstruction, and improves lung compliance and also improves the pulmonary gas exchange. I just wanted to emphasize here that in this case, that albuterol was nebulized continuously. So of course, everybody knows that the recent clinical trial on use of albuterol for patients with acute lung injury, but unfortunately, this trial was stopped because of the inefficiency. I just want to note here is that albuterol was nebulized for these patients intermittently, not continuously. So in this slide, I just wanted to show you the superior effects of the nebulized epinephrine versus nebulized albuterol and also phenylephrine. So as you can see here, the nebulized epinephrine more efficiently reduces peak airway pressures, more efficiently improved the pulmonary gas exchange, and more efficiently reduced the pulmonary edema compared to the phenylephrine and albuterol. So exact mechanism is not known, but I think that those salutary effects of the nebulized epinephrine is attributable to its dual effect, the alpha-1 and beta-2 agonist effect. So I think that, but I also want to emphasize in here that albuterol was nebulized intermittently here, not continuously, just too much that epinephrine, because epinephrine was nebulized intermittently. So now, finally, a few words about cellular therapy. In a few years back, actually, we showed beneficial effects of the human bone marrow-derived mesenchymal stem cells on acute lung injury induced by pneumonia and smog inhalation. In that time, we actually used different dose of the mesenchymal stem cells, and 200 million cells were very effective in ameliorating acute lung injury in the SHIP model. Very recently, we also showed the efficacy of the ovarian adipose-derived mesenchymal stem cells on the lung injury induced by smog inhalation. And as you can see here, these mesenchymal stem cells significantly reduced lung edema, also significantly reduced the endothelial permeability to not only water, also to the protein. So it's very effective therapy. And then in this slide, I just want to show that the mesenchymal stem cells actually improve the pulmonary gas exchange. But most importantly, those cells were migrating to the alveoli and kind of replacing the injured epithelial cells in the lung tissue. So it's very important. So in this slide, I just wanted to... it's very complex that I cannot explain all this, but I just want to show you that if the concomitant skin bone actually reduces the efficacy of the intravenously administered stem cells, because the injured skin, they were expressing more chemokines to attract the stem cells from the lung. So that's why the efficacy of the stem cells on the lung was reduced. So if the burden is present, especially the big burden is present, then I think that it's a good idea to increase those of the mesenchymal stem cells to administer the IV. So finally, in summary, I think that nebulized epinephrine is a very good candidate for treatment of smog-inducing injury because of its dual effect on both alveolar mucosal edema and also bronchospasm. So if albuterol is used, remember that albuterol should be used as a continuous nebulization. And then also that combined therapy with nebulized heparin in intravenously administered antithrombic could be also a very good candidate for treatment of smog-inducing injury because it takes care of both coagulopathy and also inflammation. So finally, the cellular therapy, the stem cell therapy, should be also applied. But of course, the more basic science studies are needed to understand the mechanistic aspects of the mesenchymal stem cells in smog-inducing injury. And nevertheless, I think that the pilot clinical studies needed to investigate the efficacy and safety of those therapeutic approaches, they're being very, very effective in basic science. Thank you very much for your attention. Thank you. Thank you, Dr. Angpaktok. I know it's past 5 o'clock. If you guys have any questions, we can certainly have a question and answer session. If not, you guys can come and we'll stay here so you can come talk to our speakers. But I'd like to thank the speakers for their excellent talks and thanks everyone for staying till the end. Thank you.

acute burn care

non-burn clinicians

burn patients

mass casualty situations

telemedicine

inhalation injuries

carbon monoxide toxicity

intubating burn patients

burn resuscitation

fluid balance

complications