Hi, good evening, everyone. My name is Webster Crowley. I'm at Rush University and I'm really pleased to be introducing our webinar for tonight, which is ICU management during this COVID time. I think that all of us as neurosurgeons are eager to kind of contribute to the pandemic that's going on right now, but particularly I've heard a fair bit of anxiety surrounding us being put to use in things that we're not as comfortable with. So I'm really excited to hear from our experts tonight. We've got Dr. Alan Hoffer from Cleveland, Dr. Stephen Meyer from Detroit, and Dr. Howard Rena from New York City. So we'll start off with Dr. Alan Hoffer. He is Associate Professor of Neurosurgery and Neurology at Case Western Reserve in Cleveland, where he's the co-director of the Neurocritical Care Center. He's also the chair of the critical care committee for the AANS-CNS Joint Section on Neurotrauma and Critical Care. So Alan, take it away. Good evening. I'm Alan Hoffer. And as you just heard, I am the chair of the critical care committee for the AANS-CNS Joint Section on Neurotrauma and Critical Care. I'm a neurosurgeon and neurointensivist at University Hospital, Cleveland Medical Center. To begin with, I strongly recommend to everybody that they check out the AANS COVID-19 hub on the AANS website, which has tons of good resources about dealing with the COVID crisis, everything from medical care, from general critical care, including a full presentation of my slide deck, but also a lot of stuff about hospital management, socio-political issues, and other useful links. Also, please check out the neurotrauma section website at www.neurotraumasection.org. So, you know, as we've all seen this huge influx of COVID-19 patients, there are lots of places where neurosurgeons are being asked to participate in the care of critically ill patients, even those who don't have neurologic involvement. And so this is meant to be a basic guide to help neurosurgeons achieve this mission. I think lots of times that neurosurgeons are tapped to do this because of our ability to very closely monitor patients and to very swiftly and decisively treat patients who have acute issues. The presentation that I'm going to be giving tonight is based on our Mission Possible program at University Hospitals here, which is our protocols for dealing with the COVID crisis put together by one of our medical intensivists, Dr. Rana Hajal, who is kind of our field general. And you should please check with your home institutions to see if there are any variations in these protocols before implementing them in your own practice. So the COVID-19 virus is a newly emergent coronavirus related to the SARS virus that was first recognized in Wuhan, China. And when we look at patients who suffer the COVID-19 syndrome, they initially have an early infection, which may be asymptomatic. And this can last for even one to two weeks. And then as the host inflammatory response builds, we see the onset of symptoms and then sometimes progression to severe symptoms, hypoxia, and eventual respiratory failure, ARDS, as the inflammatory response builds. The most common presentation for hospitalization is a pneumonia. And here we have a chest CT showing the classic COVID bilateral pneumonia. But for lots of patients, and given the volumes of patients that we're seeing, it's not practical to take every single patient down for CT to evaluate them. But what we found is that point of care pulmonary ultrasound has many findings that correlate very well with the lung CT. And so in many places, emergency room ultrasound or other point of care ultrasound is used as the main diagnostic tool. Before we talk about specific diagnosis and treatment, I would like to encourage everybody to become familiar with your institution's policies regarding personal protective equipment. We certainly don't want any healthcare providers to have any more than absolutely necessary exposure to the virus for your own health, the health of your family. So our isolation protocols include negative pressure rooms, surgical masks when outside of the room, and N95 masks inside all of the rooms, and other means to minimize transmission between providers and patients and providers and each other. Again, you should please check with your home institutions regarding what your isolation protocols are. So there are lots of different reasons why COVID-19 patients end up in the ICU. Certainly probably most common is pneumonia with hypoxic respiratory failure. This can sometimes progress to acute respiratory distress syndrome. However, we're also seeing patients with sepsis, septic shock, and cardiac arrest a fair amount in our ICUs as well. So this is going to be sort of a very brief review of the pulmonary system and pulmonary pathophysiology. So the causes of respiratory symptoms, inflammation, or fluid within the alveoli can affect gas exchange. We also see issues with airway secretions, airway inadequacy, reactive airway disease, and these can culminate in clinically significant hypoxia. How do we deal with this? Well, we start out dealing with just simple supplemental oxygen therapy by nasal cannula. It's very important for patients to also have sometimes protective gear, a simple mask over their nasal cannula. And we usually start at six liters a minute of nasal flow and monitor their hypoxia. The next step is high flow nasal oxygen, which can be delivered at 20 to 30 liters per minute, an FiO2, an inhaled oxygen fraction of 50%, aiming for an oxygen saturation greater than 94%. And you can increase this up to about 40 liters. So, you know, these patients need to be monitored very closely. By the time a patient comes to the hospital and presents with hypoxia, they may be in a rapidly escalating phase of the disease. And so these patients need to be monitored very closely. And anybody who has significant increases in flow or in inspired oxygen should be reassessed for a more rapid escalation of care. Now, it's been very interesting as we have gone on in this COVID crisis. And, you know, one of the strange things about this COVID crisis is how rapidly it has progressed and the need to rapidly evolve our thinking. Initially, noninvasive ventilation, such as BiPAP, was really discouraged because of the concern for high risk of aerosolizing particles and exposing providers to them. But I think in our institution, we're starting to use this more and more, you just have to have a viral filter placed on the expiratory limb prior to starting up the circuit. And obviously, you want to minimize any chance of transfer, sorry, of particle disbursement. So we try not to transfer patients between units or down for testing on noninvasive ventilation. And again, these patients need to be closely monitored. More and more, though, you know, the initial recommendation from the surviving sepsis campaign was early intubation, rapid escalation. But we'll talk about some strategies that we're using to avoid intubation mechanical ventilation, which really commits the patient to a long ICU stay. So in non-intubated patients, we try and avoid nebulizing medication, again, to prevent the risk of spread of the virus. So we're using metered dose inhalers. In mechanically ventilated patients, nebulizers are usually tolerated because it's a closed circuit, although you can still use the metered dose inhaler with four puffs per dose or so. So as I said, the early recommendations for mechanical ventilation were that patients be intubated pretty early on in their course. Again, part of this was because they were patients who were rapidly escalating with their disease progression, but also to minimize some of the droplet spread. So, you know, the most common mode that we use is volume control ventilation. So this delivers a set volume to each breath for the patient. And the airway pressures, because it's a set volume, the airway pressures can vary with the respiratory mechanics of each individual. And so those have to be monitored. The goal of mechanical ventilation is to have an arterial oxygen content that is 55 to 80 or so. But, I'm sorry, and keep the saturations hopefully above 94. So what can we control with our ventilator? Well, we have the percent inspired oxygen, the respiratory rate, the tidal volume, and the positive end-expiratory pressure. And we'll remember that our ventilation, our ability to clear carbon dioxide is equal to the respiratory rate times the tidal volume. So when we initiate mechanical ventilation, based on the ARDSnet research for ARDS that's been done in the past, we base our tidal volume based on a predicted body weight calculation that's based on height. So here we have the calculation for males and females. We usually want to set the ventilator breath at roughly six to eight milliliters per kilogram of predicted body weight. And then what we're going to do is monitor some of the pressures to make sure that we are not causing any damage with the pressures that we're giving at those volumes. So below is the ARDSnet table that was published for treatment of ARDS. And the surviving sepsis campaign suggestion is to start with the high flow, the high PEEP at the bottom of the table. At our institution, we are actually starting with the low flow, but we have a pretty low threshold for increasing it to the high PEEP protocol if patients have low lung compliance and are requiring increased support. So we have to take into account the hemodynamic effects of positive pressure ventilation. So by increasing the intrathoracic pressure, we may be decreasing venous return to the heart, decreasing preload, and especially in patients who are hypovolemic, this can then affect your cardiac output and cause blood pressure drops. So we really need to make sure that patients are adequately resuscitated, but not over resuscitated in this condition. Certainly pulmonary edema can worsen the hypoxia. So we have to be very sensitive to that. All right. But the increased lung expansion can decrease the left ventricular afterload as well. So we have to keep that in mind. So monitoring the ventilator airway pressures is very important in dealing with patients with lung injuries. And the two pressures that we normally see on the ventilator are the peak pressure, which is the maximal airway pressure during any time in inspiration. So that's equal to the pressure necessary to overcome the resistance of the endotracheal tube, as well as the amount of pressure necessary to overcome the compliance of the thoracic cage. And then after the initial inspiration, then you have the plateau pressure. So that's the amount of pressure necessary to overcome the elastic recoil of the lung and thoracic cage. And we can measure the plateau pressure with an inspiratory hold maneuver. So here's an example of a waveform on a ventilator. And you can see at the beginning of the breath, we're pushing that air in, we have to overcome the resistance of the endotracheal tube. So that gives us our peak pressure. Once the volume of the breath is in and we're no longer actively flowing, we can do the inspiratory hold. And that gives us the plateau pressure. And the plateau pressure is important because that's what tells us when we cross the threshold to increased risk of pressure damage to the lung. So for plateau pressures greater than 30, that's our normal cutoff for what we consider safe for the lung. If the plateau pressures are higher than that, then we try to decrease the tidal volume as much as possible to try and decrease that pressure. There will be some acid-base management issues that we have to deal with, and we track those with arterial blood gas measurements that tell us the pH, the pressure of oxygen and carbon dioxide in the blood as well, the calculated bicarbonate level. If you need a measured bicarbonate level, we monitor that with the comprehensive metabolic panel. And then we have to keep in mind that the pH and carbon dioxide levels may be altered in patients with chronic conditions such as COPD or chronic kidney disease. And so we may need to adjust our treatment goals if necessary. Respiratory acidosis coming from hypoventilation and increase in carbon dioxide can be treated by increasing the minute ventilation. As we said, the minute ventilation is a calculation of the respiratory rate from the tidal volume. And if we want to avoid increasing our tidal volume because of concern of pressure injury, then we usually end up doing that by increasing the respiratory rate. Underventilation results in a metabolic alkalosis. A metabolic acidosis comes from a problem within the body such as a hypoperfusion causing a lactic acidosis, ketoacidosis, et cetera, or renal dysfunction, sometimes causing a non-anti-gap acidosis. We treat this by treating the underlying condition. Respiratory alkalosis, we can decrease the minute ventilation to allow the carbon dioxide to build up a little bit to correct our pH. And metabolic alkalosis, we commonly see from contraction alkalosis, depletion of intravascular volume requiring resuscitation, or sometimes from loss of acids such as gastric suctioning. And we can do some acid-based management, particularly the respiratory acidosis and alkalosis with the ventilator. With more of the metabolic problems, as I said, it's to treat the underlying cause. So once we get into severe lung injury, we look for evidence of acute respiratory distress syndrome. This is defined as worsening hypoxia within one week of a clinical insult, evidence of bilateral opacities. But there's no contribution of, or not fully explained by pulmonary edema, such as from pulmonary hypertension or from congestive heart failure. We break it down, we define it by what we call the PF ratio, which is the ratio of the partial pressure of oxygen, the PaO2 that we measure in blood gas, divided by the fraction of inhaled oxygen as a fraction of one. So for example, somebody is on 50% oxygen and the denominator in our equation is 0.5. So it's a fraction of one. So when we get to around 300 is where we start worrying about lung injury, 200 is where we get to ARDS. And then severe ARDS, severe lung injury is with a P to F ratio of less than 100. Now something that we have to be particularly careful of is barotrauma, which is the result of inflammation or fluid accumulation within the alveoli. And that makes the alveolus unable to expand. And when that happens, positive pressure is shunted away from these alveoli into healthy alveoli, resulting in overdistension and injury. Here's the American Thoracic Society's description of this, where the stiff alveolus can't accommodate the pressure. So it gets shunted into a healthy alveolus, which then becomes distended and can become damaged. So this is where the recommendation to keep the plateau pressure less than 30 comes in is to try to avoid that damage. So for patients requiring high oxygen with optimal PEEP, there's a few other maneuvers that we can try and do. The first of which is proning. So this is a therapy based on the fact that there are higher volumes of lung more posteriorly. And so when we flip patients prone, there is more volume of lung that can be aerated. So prone positioning is an option that can be really be done for up to 12 to 16 hours per day in severe ARDS. Contraindications include shock, acute bleeding. Interestingly, raised intracranial pressure is thought to be a contraindication, although there's not a lot of data behind this. And we're currently looking at coming out with a position statement from the joint section about what factors can be considered and when this can be considered for patients with neurological injuries. A few other contraindications to consider. And reasons you would immediately stop it if there's any evidence of endotracheal tube obstruction or any inadvertent extubation, hemodynamic changes that occur with proning. Those are reasons why you might have to be interrupted. So the proning technique, the patient is prepared to have one sheet under the patient. Enteral feedings are turned off, have emergency airway equipment on hand in case of inadvertent extubation. The patient should be sedated and paralyzed. A second sheet is placed over the first sheet and I'll skip to the graphic here. So you start with the sheet over the patient. There's a sheet under the patient. We then put three pillows over the chest, pelvis, and legs and put a third sheet on top of the patient. We roll all three sheets toward the middle until the patient really is tightly encased in these three sheets. And then we slide them to the side, disconnect the ventilator, flip them over, and then we remove the sheet that's on the back, reconnect the EKG leads then on the back of the patient, turn their head to one side with the arm up on that side in a swimmer's position and down on the other side. And the sides are turned every two hours or so. And then you have to monitor for hemodynamic instability, which can last five to 10 minutes after proning. So they may require increased fluid support or pressure support. There are some complications that you should look out for, nerve compression, pressure sores, as we said, changes in hemodynamic. State as well. Just a quick word as I talked about that there has been an evolution in how we're treating this. So we're actually starting to prone non-ventilated patients. Again, if you can prevent a patient from being intubated, there's potentially a huge benefit from that. So we've started, we've started proning non-ventilated patients to improve their oxygenation and hopefully prevent intubation, but you should check with your local institution for their protocol regarding this as well. You can also increase, you can do transient short increases in, in the pressure by switching the patient to CPAP with high pressures to try and recruit collapsed alveoli. And there are other rescue therapies, but you should definitely consult your pulmonologist regarding the need for airway pressure, release ventilation, other inhaled agents, and ECMO as well. The hemodynamic goals for COVID-19 are euvulemia. Again, we want to avoid hypervulemia and pulmonary edema from this. So there should be de-resuscitation within 24 to 48 hours after achieving stability, and point-of-care ultrasound of the inferior vena cava and cardiac output may be utilized to help with this. As I said, please, everybody take good care of themselves and use the appropriate protective equipment during ICU protocols, and remember your general critical care, good GI prophylaxis with either a H2 block or a proton pump inhibitor. DVT prophylaxis is very important. There have been reports of a prothrombotic state associated with COVID-19, so standard DVT prophylaxis may be inadequate, and your institution may have instruction on that. And good nutrition and glycemic control is important very well. So thank you, everybody, for listening. Please remember to follow your local protocols. Stay safe and healthy, and continue to follow along with the AANF on their COVID-19 information hub. Thank you. Great. Thank you. Thank you very much for that, Alan. While we switch over to our next speaker's slides, I want to ask any people who are watching, one, it sounds like there's some issues with the browser, so it may need to be in a browser such as Chrome if that's the problems that you're having. If you do have questions of the speakers, please enter them in the chat, and we should have time at the end for questions that we can relate to the speakers. So if we pull up Dr. Mayer's slides, I'll introduce Dr. Stefan Mayer. He's the professor and chairman of neurology at Henry Ford in Detroit. Prior to that, he was director of neurocritical care at Mount Sinai, and before that, even at New York Presbyterian Hospital and Columbia University. So we're really pleased to have him talk further on the ICU management, including some of the neurologic manifestations of COVID. Great. Thank you very much for the kind introduction. I want to thank the AANS for inviting me to speak to you briefly about a crash course. And what I'm going to try and do is I'm going to reiterate a lot of the points that Dr. Hofer made already. With some of my own personal spin, I want to kind of tell a little bit of the story, because this is really a remarkable chapter in history, certainly, and also I think it's going to have a lasting impact in terms of the way that we practice medicine, in particular emergency and critical care medicine, because things have been changing so fast that we've actually been relying more and more on channels such as social media to get the latest information out there. Not that what we get on social media is definitive, but at least it's able to alert people to, as people or different centers or sites have insights, when they get their wave of this patient population, they'll innovate and try something else. And so I'm going to kind of walk you through how this has played out over about the last five or six weeks. So, obviously, no relevant disclosures. So, certainly, we all recognize that this pandemic is an unprecedented event in human history. It's going to change human civilization in the same way the 9-11 changed the way that we think about security in the United States. This illness really has placed a spotlight fully on emergency and critical care medicine. Of course, it's all-important, and one of the things we're going to hear about from Dr. Rina is how do you continue to do the stuff we always do with the stroke, subarachnoid hemorrhage, trauma, and status in the setting of a pandemic, which is stressing our healthcare systems. One of the big take-home messages is that a crisis like this really demands an unprecedented degree of teamwork, flexibility, and ingenuity. You've heard the point that we all know, but a lot of our initial approach to managing the respiratory failure really was focused on, you know, well, what about us as the frontline people? You know, how do we protect ourselves? I'll talk about that, but, clearly, we have to remember, you know, that we have to, you know, get that oxygen mask, so to speak, on us first before we can help anyone else. We have to really take the process of PPE very seriously. There's a very carefully thought-out methodology for how to don and doc this equipment, and it literally can mean a matter of your own health, your own life, and the lives of the other professionals that you work with. This training, you've probably already undergone it, but it should involve detailed protocols. It should involve practice sessions with direct observation and critique, and pretty much anybody can go, and there's a lot of free videos available online on YouTube and such from the CDC and, obviously, other national agencies around the world. Disaster management is an established part of what we think about in emergency and critical care medicine. It's been thought through, and one organization, the U.S. Society for Critical Care Medicine, you know, offers this kind of graphic to sort of think about, well, how do we staff, you know, when we're dealing with unpredictable surges in patient population, like we are in New York and other cities in the U.S., where we really are the world epicenter, at least for now, and you can see the role here for, you know, physician recruits working closely with critical care nurses who are supervising step-down-and-floor nurses. So, again, it's time for everybody to just kind of figure out what can you do to lend a hand, how can you fit in, and there's a need for frictionless communication and teamwork. We all know about the clinical course of COVID-19. Again, coronavirus is the infectious agent. COVID-19, coronavirus disease 2019, is the disease entity, and we know, you heard from Dr. Hofer, that the typical syndrome, starting with the incubation, pre-symptomatic, the fever, the dry hacking, nonproductive coughs, sore throat, and then constitutional symptoms, a lot of headache, nausea, vomiting. Then shortness of breath hits at about a week, and then, as the respiratory illness, I mean, it can go on, you know, unremitted and kill you, but what we've seen is that sometimes people seem to be recovering, and their oxygenation is improving, and we're de-escalating the amount of ventilatory support, and then there's this crash that can occur, and it's often cardiovascular and circulatory collapse, so it's very unpredictable about which patients are going to get through it okay and which patients are going to crash, although we do know that, in addition to being older, for some reason, obesity, diabetes, and hypertension and cardiovascular disease seem to be the main risk factors for a more severe course, possibly a fatal course, and, again, changing so fast, we don't know exactly why that is, and there's other risk factors that we might have thought would put you in trouble. For instance, asthma and reactive airway disease and COPD doesn't seem to be as much of a problem as the obesity and diabetes. You should be aware that the diagnostic nasal swab, PCRs, are not perfect. It is well-established that there are a lot of people that come in with the exact profile of COVID-19, and the first or second nasal swab might be negative, so it still is a clinical diagnosis, and those patients still need to be treated as COVID-19, isolated and treated as such. There is a highly characteristic profile of laboratory abnormality shown on this slide, which you see again and again and again and again. Signs of chronic inflammation, in particular C-reactive protein, separates, the ferritin goes up. That always goes up with acute to chronic inflammatory states. There's lymphopenia, and sometimes combined with an increase in polymorphonuclear cells, which is also a poor prognostic sign. LFT abnormalities, CK elevations, LDH goes up. D-dimer goes up, and again, we know that there seems to be, in a lot of patients, a hypercoagulable state. Interleukin-6 levels can be measured. They go up as well. The albumin goes down, and anemia and low hemoglobin develop, so in certain patients of this profile, with that common clinical syndrome, if you see this and the swab is negative, it's probably still COVID-19. In terms of making the diagnosis, you've seen the chest CTs, the interstitial pneumonia, and Dr. Hofer made the point about the increasing rise of lung ultrasound. Lung ultrasound is so much easier to perform. It can be performed in the emergency department, in the ICUs. Most EM and ICU docs are very proficient at this bedside procedure, and what you see is this pattern of B-lines, not the old curly B-lines from chest X-rays, but as you sweep the transducer across the back, the interstitial edema shows these shining rays of light, and I'm sorry I wasn't able to show a video, but you get this kind of moving, shimmering effect. In addition, there's irregular pleural thickening. This is the pleura. It looks whiter than usual and has an irregular character to it, so simply wanding somebody with a lung ultrasound, you can make that diagnosis with a very high degree of confidence and not have to go through the whole rigmarole and the risks involved of doing a chest CT scan. In today's New York Times, a very prominent emergency medicine physician, Dr. James Levitan, wrote about his insights at Bellevue and basically made the point that what he noticed in the emergency department is a lot of people were coming in with non-COVID stuff, like they broke their arm, they fell, they had this problem, they had a syncope, and it turns out that they're COVID-19 anyway, positive, even though they don't have the respiratory symptoms or the characteristic early clinical symptoms, but what they do seem to have in common is this hypoxemia and oxygen desaturations. It seems to happen very early, and it can occur in people that are actually what we think of as asymptomatic or pre-symptomatic, so the point he makes in this op-ed today is that the easiest way to screen human beings with minimal expense, because pulse oximetry is everywhere, and you can even get it to another patient, is to just put a pulse ox. If somebody comes in and wants to be screened, and their stats are in the 80s, even if they're fine, you've got to assume they've got COVID-19, so I think we're getting a big reaction from this already. I think we're going to hear more and more about this simple way to screen in our emergency departments and even for outpatients. This early hypoxia, also, there seems to be a peculiar insensitivity that the emergency medicine physicians sit there and marvel and say, I can't believe this guy's stats are in the 70s, and he's not struggling to breathe. He seems to be meditating. He's on his cell phone having a conversation, and that's when people say there's something very strange about this disease that we don't understand. There are some theories circulating. We don't know what they are about what might lead to this tolerance or insensitivity to the hypoxia. Levitan and others think that it's simply early impaired gas exchange in the lung from surfactant deficiency, which lubricates the alveoli, and it's as simple as that. Others have promoted this theory that there may be some early neurotropic effect, citing the 30% frequency of anosmia and ajucia that we've already heard about, and maybe it's blunting normal brainstem autonomic responses. And there are other theories out there that the coronavirus might directly interfere with oxygen binding to hemoglobin in the same way that methemoglobinemia does. We don't know, but it is a fascinating aspect and important aspect of the illness. So these are just some early profiles of the patient clinical course in one of the early reports from Seattle. You see here the fever, the cough, the dyspnea, and then the bottom one, the red bar there, is when the guy gets intubated, and in short order, he crashes. He has cardiac injury, left ventricular dysfunction, goes into renal failure, develops a secondary sepsis syndrome, and dies. And so early on, the thinking was, when these people come in and desaturate, what we need to do is intubate them early and aggressively, RSI them, minimize the amount of viral droplet spread. And what the slide here is about the cardiac failure that is a characteristic in many of the fatal cases, maybe to myocarditis. But what we saw early on was a lot of enthusiasm for this early intubation strategy. And typically, we wait for people to get pretty sick, to keep the respiratory effort, work of breathing, desaturate pretty solidly. And these are sort of the existing protocols for how we escalate to mechanical ventilation. Going step by step, as shown here, and note here that proning has always been viewed as a kind of a late step. Once you're intubated and paralyzed, and your FiO2 and PEEP are up, if we still can't oxygenate you, then we're going to flip you and prone you. And that's really one of the main messages for this evening's webinar, is how that thinking has been turned on its head. So you've heard about the PF ratio. I don't really need to get back into that. It's the arterial PO2 divided by the FiO2 above 300. You know, normal should be 5600. And then, you know, below 100 is severe ARDS. 100 to 200 is moderate ARDS. 200 to 300 is mild ARDS. Again, as you heard before from Dr. Hofer. So, again, I want to emphasize how the story's been moving with what we call MedTwitter. It's been fascinating for me to follow this, and you see this post here from March 24th. And here's an intensivist saying, this is the breakthrough, you know, this is so helpful. We know we got to just skip the oxygen. We're going to go intubate these people right away. And then this report comes from Seattle. And in short order, in Italy and Seattle, they're reporting 60, up to 80% mortality rates in the people that get intubated. And the concern here is that with this disease, with intubation, they literally watch people crash within days of getting intubated, who simply have low SATs or looked okay. Next thing you know, they're in shock and renal failure. So the concern here is what we call ventilator-induced lung injury. You heard from Dr. Hofer, the volume trauma, the barotrauma, atelectra traumas when with each respiratory cycle, when the alveoli snap closed and snap open and snap closed and snap open. And we really use the PEEP to try to keep all the alveoli open as much as we can. And that's a technique we call open lung ventilation. And this is where ARBsNet comes from. This is why you're going to hear the minimized volume trauma, right? Tidal volumes of four to six mLs per kilogram. So for an average-sized person, we're talking 300 to 400 mL tidal volume, using volume cycles as the mode of choice. And then we follow the peak and plateau pressures, and then we make adjustments to keep the plateau pressure below 30, as you heard. Another concept you may hear about is driving pressure, which is the peak minus plateau, because it's been shown that when that number, when it's a very noncompliant system, when the driving pressure's above 14, that also seems to be a predictor in conventional ARDS of a poor outcome. So in this tweet here, you see somebody remarking, what started as a high-flow unit for us quickly turned into ARDS throughout our unit for my atrogenic lung injury after people are being intubated. And this led, a few days later, to this report again by AP New York Times. Some doctors are moving away from ventilators for virus patients. Again, this is the typical way we think, but what happened was people started sticking with the high flow, thinking we want to avoid intubating because people seem to be doing poorly, and at least it is protracted course. And so they were going, sticking with the high-flow ventilation. And again, like this is some of the protocol you heard about, the complex protocol of proning, you know, when somebody's been intubated, doing poorly, paralyzed, and everything else. So what about proning people early on? So proning again, why does it work? The answer seems to be that it redistributes alveolar inflation, it inflates the inferior and posterior basal segments of the lung that you can see being sucked in on those chest CTs. So here was a tweet that came across in early April, right, this ER guy saying, proning right here, right, browsing on a phone with that O2 sat. In an ER, on oxygen, high flow, using their iPhone, and their O2 sat is 54% on oxygen. And what we found was by flipping patients, even when they're awake on high levels of nasal cannula or high flow, here's another tweet that just came from earlier today, satting 60s on room air. This patient put on non-rebreather, satting 80s, put the patient on their stomach, now they're satting 95% while proned, while awake, talking to you, and again, wanting to make phone calls and surf the web on their phone. So I'm running out of time. I'm gonna hand it over to Dr. Rina again. Just a little bit more of the gospel. Avoid fluid overload in dealing with these severe lung injury patients. It aggravates the edema. And the last point I wanna make is you may think, well, look, you're either respiratory failure, COVID, or we're gonna have our strokes and our subarachnoid hemorrhages and what have you. I got on a conference call today with a bunch of neurointensivists working on various guidelines. And the conventional experience was that in the last few weeks in the high-intensity centers, about half the strokes that are coming in, half the intracerebral hemorrhages, half the subarachnoid hemorrhages are now COVID-19 positive. So there is a lot of overlap, again, related to coagulation disorders, largely hypercoagulable, but we don't really even know the full spectrum. This was a case in Michigan. We diagnosed in Henry Ford of a presumably invasive necrotizing encephalitis or reports of Guillain-Barre. And I just wanna end with this tweet, my favorite tweet on COVID so far. If you're a single-stranded RNA virus looking to survive in this big, bad universe, rule number one is surely not to pick a fight with the only double-stranded DNA-based organism that can sequence your genome and has eradicated more species than any other living thing. Thank you. That was great. Thank you. Thank you so much, Dr. Mayer. So we're gonna head now to Dr. Howard Rina. He's professor and vice chair of neurosurgery at the New York University. He's also director of NYU Center for Stroke and Neurovascular Disease. And obviously in the States, we all look to New York City for to learn from their experience with this. They're the epicenter. So we look forward to hearing his perspective. So thank you, Webster. And Alan and Stefan, amazing job in talking about the critical care of these patients. I have no relevant disclosures. I think the important, I'm gonna talk a little bit about how we maintain some semblance of a neurosurgical service at NYU and Bellevue while during the height of our surge. Now, many of you haven't come to the peak period of your cases. And so you can see this is a bad player and it's gonna affect, it affects everything that we do and it's gonna affect everything that we do for some time in the future. Remember in my discussion here, that this is my perspective. I'm a single individual at a specific institution in New York City and individuals at other places, even in the same city, my city, may have different experiences than that. So New York City or the city of New York, we are the most populous city in the United States. And we have a population of more than 8 million people, close to eight and a half million people. And if you use the tri-state area, we're close to 40 million people. And therein lies the rub, so to speak. Because of the population density, we were particularly at risk and not unlike some of the cities in Europe that were hit very hard. The city of New York has five counties or boroughs. They are, as you may or may not know, the Bronx, Brooklyn, Manhattan, Queens and Staten Island. There are over 800 languages spoken in New York City. And the last bit of information is important is that there are really only 62 acute care hospitals in the city of New York. And so when they were using the models to extrapolate how overrun we potentially could be and how the resources would be outstripped by the number of cases, that's why plans were made to convert our convention center, the Javits Center into a COVID hospital and to have the comfort ship set up from Norfolk also to take care of these patients. Now, without getting into too much detail about that, we actually have not at NYU or Bellevue been successful in getting very many patients either to the comfort or the Javits Center. They do accept COVID positive patients, but not really ventilator dependent patients. And that is also an issue. NYU Neurosurgery, just so you understand a little bit about our group. We work across three institutions, NYU Langone Health, which consists of what is the Tisch Hospital or our new Kimmel Pavilion. And I'll get into that a little bit more in a second. We have a hospital in Brooklyn, NYU Brooklyn. We have a hospital in Long Island, NYU Winthrop. And we have Langone Orthopedic Hospital. We also cover Bellevue Hospital and provide the neurosurgery care there. And the VA New York Harbor Health Care System Hospital or the Manhattan VA for short. We provide coverage. The Manhattan VA is essentially closed. Bellevue, as you know, is wide open and caring for hundreds of COVID patients as is Kimmel and Tisch. Now, the interesting thing about NYU and this was just our luck in timing is last year, essentially we opened a new hospital. And the significance of that is that our Kimmel Pavilion has 450 plus beds that are all negative pressure. And it has all new operating rooms that also can be converted to negative pressure. So immediately our new hospital was converted into a COVID hospital. And we opened up some portions of the closed Tisch Hospital to accommodate any non-COVID overflow. The Brooklyn and Winthrop campuses quickly filled with COVID patients. And the orthopedic hospital basically became a step-down hospital for patients that were recovering. The NYU system has treated over 5,000 patients with COVID. Currently the census have been declining. I think they've declined to less than 350 patients at Tisch Kimmel with approximately 130 or so that are intubated. Kimmel at one point had 500 patients that were COVID positive and close to 200 patients that were intubated. The whole system at its peak had over 1,300 patients that were COVID positive and close to 500 that were intubated. That's the entire system. So you can understand that during the peak surges of this, the system can be basically filled with these types of patients. And so the immediate issue is moving patients in for neurosurgery care. So based on the models that were being put out and discussions with the state, our administrator and our dean of the administration basically stopped all hospital visitors to the institution on March 4th. The governor then by March 15th ordered all elective surgeries postponed. And then basically by March 20th, shutdown was ending. Further restriction of activity on the 22nd of March to just emergency cases. All other scheduled cases were removed from the schedule. They weren't canceled, they were essentially postponed. So basically there was an emergency and urgent surgical cases. And those are basically that were cases where tissue was at risk, bleeding, obstruction, or where intervention would prevent a greater emergency. So basically we would then sort of prophylactically looking at our manpower and how to protect our personnel. As you know, and as Stephan mentioned and Alan, it's very important to protect the people that are providing care and protect the different services. So we immediately created skeleton crews for resident and fellow coverage for both neurosurgery and the neuro interventional services and sent everyone home. Anybody that was remotely symptomatic, remember we didn't have access to a lot of testing and maybe we should have been checking pulse oxys, but anyone that was remotely symptomatic was removed from any rotations and quarantined. Many residents volunteered to take care of patients on the COVID floors, but during the peak of the surge, by March 28th, we were asked to provide additional house staff to assist in coverage of the ICUs and COVID floors. We were very quickly after that asked to provide faculty to assist again in COVID ICU coverage. Senior faculty, especially faculty above the age of 65 or 70 or people that had other medical conditions that might put them at risk. If they were to contract COVID, we offered to exclude them from any of these services and then we maintained our neurosurgery coverage. So what has been done by neurosurgery during these, even during the peak periods? So the types of cases that we were able to do, and that we had to do, we've done several skull-based tumors where patients had progressive deficits that needed to be addressed immediately, herniation types of events or pending herniation types of events. Posterior fossa metastatic disease or large metastases. Traumatic spine injuries. A lot of people were told to shelter in place and people were exercising, riding bicycles. So we actually had several cases of jumped facets and spinal cord injury. Regular spine cases, however, with myelopathy or other symptoms, we didn't really see very much. We did have several shunt malfunctions. We did see a decent number of acute strokes in this. We definitely saw younger people with large clot burdens and with elevated D-dimers. So there's definitely a connection and we definitely saw this in the stroke population that we were seeing. Initially, we saw a very sharp decrease in the number of strokes and subarachnoid hemorrhages that were being transferred into the institution. And many of those may have made up patients that had expired at home. But as I said, we did see a different type of patient with stroke where there were large clot burdens. I opened up one patient myself last week with a fresh clot extending from the carotid bifurcation in the neck all the way up to the M2 level. We were able to open it up and the patient obviously was spurned upon and wound up having a decompressive craniectomy. We did have a ruptured dural AV fistula. We have giant aneurysm with cranial nerve deficits. We had several carotid endarterectomies with PIA or strokes presenting. We had post-stroke hemicraniotomies. And then at Bellevue, the usual trauma that we get but to a lesser degree, subdurals, epidurals and decompressive cranies for intracranial pressure. So there was a smattering of neurosurgery types of cases but as you can see, they were of the most critical nature. And we certainly had a decrease in the number of transfers for other types of neurosurgical conditions. So I think that's kind of where I am. I'm happy to take any questions. We have, I think, a few minutes left to answer some questions. That's great, Howard. Thank you so much. So I have a couple of questions I'll kind of pose to the panel. Maybe have Howard take this one first. Are you finding that the patients that you are, the neurosurgery patients you are treating are the ones that you normally would treat? Are you having to treat any of them differently than you otherwise would? You know, are subarachnoid hemorrhage patients having to leave the ICU earlier than you otherwise would? Or if you're more comfortable, you know, we heard stories from Italy of, you know, them just not performing mechanical thrombectomies, not performing aneurysm coilings during this time because of that. Now, obviously, I don't think the US has gotten to that point yet, but do you feel that your normal care to these patients, particularly in the ICU, has changed during this time because of the overwhelming? Yeah, I mean, I think, one, we're able to provide the most complex neurosurgical care at our centers. Even during the height for COVID-negative patients, we still had a buffer of another 50 to 100 rooms in the old hospital that we could, where we created quote-unquote COVID-negative ICUs and floors. That being said, everybody was COVID-positive. Anybody that was critically ill was COVID-positive, and they were very, very ill. And so I know Alan and Stefan were talking about the morbidity, but the intubated patients were quite ill, and many patients died. And so the stroke patients having COVID on top of it are in a really poor state. As far as subarachnoids, I have very close friends in Italy, and I was getting fairly regular updates from them. The Italian health system was completely overwhelmed, and I think that's why the early shelter-in-place orders went out, because they were afraid of all of the beds being consumed in a city like New York if a larger portion of the population got infected. And that's one of the concerns about how the reopening is gonna occur. Great, okay. And I've got a question maybe for Stefan, and maybe Alan can answer as well. We know that these patients tend to be hypercoagulable. If they're proned, if they're intubated and paralyzed, is there a role for checking on whether TCDs or intermittently waking up to make sure they're not developing clot? We talked to our intensivists, our cardiologists. They say they clot off every line that's ever been put in. And so do you worry that they're gonna develop a stroke or heart attack, things like that during this time? And again, is there a role for assessing them for that during this? Yeah, well, a couple. You already heard the point from Alan that you absolutely have to be doing compression, extremity compression, and DVP, chemoprophylaxis with your agent of choice, usually Lovenox or subcutaneous heparin. Probably wanna go at the higher dose. As far as wake-ups, we're all huge believers in wake-ups whenever you can. The problem is the two scenarios in critical care that are most common where wake-ups are dangerous is just ongoing ICP crisis, which, of course, we're all familiar with, and then you're on an FIR2 of 100% and barely hanging on because literally wake-ups in those types of people can really tip people over. But if somebody's on the mend or is intubated but is satting okay on a reasonable amount of PEEP, and even if FIR2 is 50, 60, 70, I'm a believer in wake-ups, and that's just assessive neurologically. It reduces the duration of ventilation. You can assess people better. Obviously, neurologically, you can progress faster to weaning and liberation from the ventilator. But a lot of this is so unknown. Other than that, we hope we wanna do the things that we can do. I could think of maybe doing screening lower-extremity ultrasounds to see if you find a DVT. There's almost no information out there yet about higher levels of full anticoagulation when people are clotting lines like that, which I've heard about as well, but this is all happening so fast. We do more, we try and screen. We have a higher risk for patients. We monitor, we check their D-dimers, and we based our DVT protocol based on that. I agree with Stefan that certainly we wanna try and wake people up when we can, definitely to kinda get a better idea about how quickly we can de-escalate them and get them breathing on their own. We said that getting these people off the ventilator as soon as you safely can is a benefit to the patient. It frees up beds for other patients, so it's good all around. I wanna, let me, if I can just jump in. I had to, with respect for Howard to get his talk in, but another very common issue that we've encountered and it's been corroborated by others is there's a lot of delirium and agitation. You, about 15% of the patients become, as it's quite, you know, in the setting of, in the throes of respiratory failure, you know, people become delirious, right? It's about 15, maybe up to 20%. But what's really interesting is when you start to do the wake-ups or you get people and you progress to that extubation, when you stop that sedation, some of the rates of agitation and delirium have been as high as 50, 60%. And what's interesting is a number of people have said, like, yeah, we all know people, you know, get delirious in ICUs, but I ain't seen nothing like this. So it's just another thing to be aware of if you're dealing with vented patients that often need prolonged infusions of what have you, propofol, fentanyl, or dexmedetomidine, that this is another feature of the illness. Great, thanks. Well, I guess we've kind of hit our time here, so we'll start to wind down. Stephane mentioned the role of social media in a lot of this, and I know there's a number of memes going around that always crack me up that try to convince people to shelter at home or stay at home or else a neurosurgeon might be intubating them. So hopefully most of you all listening are not pressed into that unless you, again, want to volunteer for that because you have the desire to do that. But I really appreciate the panel for helping us out here and hopefully preparing some people to do that if needed and then getting the perspectives from New York. We've got another webinar next week. Same time, this one will be how to triage surgical cases. And then there's the following week for re-emergent strategies. How do we kind of restart the normal or the new normal after this is done? So thank you all very much for coming and participating and listening. Really appreciate it.

ICU management

COVID-19 crisis

neurosurgeons

patient care

webinar

resources

disease progression

proning

emergency care

pandemic