Welcome back. As promised, we are here again here with Dr. Liedman. You guys, some of you were at his talk on Wednesday going through angiograms and CT angiograms and MR angiograms. Today he's going to talk about the management of the unstable ICU patient. For those of you who haven't met him yet, let me just give you a quick skinny on him. He's a nationally recognized leader in cerebrovascular neurosurgery and care. He's uniquely trained in both traditional open and endovascular surgical techniques and he's the director of the cerebrovascular division at Drexel Neurosciences Institute. He's an associate professor in the Department of Neurosurgery at Drexel University College of Medicine. He's also the director of neurosurgical care for the Global Neurosciences Institute and the director of neurocritical care. Welcome to Dr. Liedman and he will talk about management of the unstable ICU patient. Thank you very much, Robin. It was a very both Wednesday and today a very nice introduction. I thank you very much. Good afternoon. Over the next hour I'm going to discuss the management of the critical care patient. I'm going to go over the basics, stabilizing a patient being admitted to the ICU, but I'm not going to go over the steps taken to code the patient. My goal, and hopefully I'll achieve my goal, is to go over reviewing and the assessment and stabilizing patient being admitted to the ICU. A critical illness is any disease process which causes physiologic instability or the potential for instability leading to death or disability within minutes to hours. A critically ill patient is one at immediate risk of death. The severity of this illness must be recognized early and appropriate measures taken promptly to assess, diagnose, and manage these illnesses. The ICU team, which the advanced practitioner is part of, needs to be able to provide appropriate care, specialized knowledge, skills, and the care delivery mechanism needed to support patients' needs. The patients are in such a situation they want continuous monitoring and potential treatment. The critically sick patients are often in a medically or surgically unstable state requiring this continuous monitoring that I mentioned. The team needs to be ready to deliver emergency life-saving and neuro-saving interventions. Speed and efficiency with delivering the essential treatment is imperative to prevent death or permanent disability, so prompt and protocolized treatment is necessary. That's very important, prompt and protocolized treatment. What do I mean by that? Well, let's say you're monitoring someone's intracranial pressures and they can they start to rise. There should be clear, concise algorithm to follow to reduce the ICP. Another example, a patient was a subarachnoid hemorrhage. I think Dr. Armano just talked about this in the previous talk. A patient at a subarachnoid hemorrhage underwent treatment and post hemorrhage day 6 to 7 to 8, they developed focal deficits. Again, there needs to be a very clear diagnostic and treatment algorithm to reduce the chance of permanent death. Urgent treatment of the life-threatening emergencies or neuro-emergencies such as herniation, the ICP problems I mentioned, hypotension, hypoxemia, etc. is the priority. In summary, the treatment, especially life-saving or neuro-saving treatment, needs to be initiated right away. Then one can start the analog portion that begins with a thorough history taking and knowing the diagnostic results that were ordered. This seems obvious, but it is not uncommon for health care providers not to ask all the needed questions and, surprisingly enough, not be aware of the results of labs or imaging studies they ordered. Patients being admitted to the neuro-ICU, patients that the advanced practitioner will be called to admit if indeed the advanced practitioner is the first line, are frequently suffering from stroke, either ischemic or hemorrhagic, head trauma, with or without associated intracranial pathology, extra axial bleeds, contusions, spinal cord injuries, patients in status epilepticus, acute neurologic disorders, or the post-operative patient. This is a typical neuro-ICU patient on a ventilator with a non-cardiac monitor. I'll talk about that in subsequent slides. An ICP monitor on a ventilator. The highest acuity patients and taking care of these patients, admitting them, discussing them, and then thinking about a treatment can be overwhelming. So that's what we're going to try to minimize, this overwhelming sense about these patients. The goal of the admitting neurosurgical team in the initial setting is to stabilize the patient. The best way to stabilize is to follow your A, B, C's and D's. A, airway, B, breathing, C, circulation, and D, disability or neuroassessment. First we go A and B. They often go hand-in-hand. So airway, you look. What do you look for? You look for signs of any airway obstruction, excessive secretions, blood, vomit. You look for foreign body. Do they require gentle suction? You listen. You want to listen for both normal and abnormal airway sounds, gurgling, snoring, grunting, hoarseness, wheezes, stridor, and then that segues into breathing. Breathing, you want to make sure the patient's not in distress. You want to look at the respiratory rate, their chest movement, auscultate the lungs, make sure they have bilateral symmetric breath sounds. You want to make sure they're not having paradoxical chest and abdominal movements, and you want to identify or understand the patient's using accessory muscles to respirate. A respiratory rate of greater than 30 breaths per minute or less than 8 breaths per minute is worrisome. It is important always to be aware of the patient's admitting diagnosis. Why are they being admitted to the ICU? So you can anticipate the likelihood of their deteriorating deterioration. I don't always obtain a blood gas. If the patient is very comfortable, satting well, especially on room air, there's no underlying pulmonary problems, I don't necessarily get a blood gas. But what the, and usually it is the mass practitioner, what we want to understand is, does the patient require intubation? And if they are to be intubated, then you should get a blood gas. Intubation or early intubation should be initiated if the patient's mental status is suppressed. So it's not always just a primary pulmonary problem, but if their mental status is suppressed so much they can't protect their airway, they indeed require intubation. So I just want to discuss some very basic physiology. Gas exchange in the lungs involves a transfer of oxygen from the atmosphere into the bloodstream and the removal of carbon dioxide from the bloodstream into the atmosphere. The site of gas exchange is the alveolar capillary membrane. At this membrane, gas is brought to and removed from the alveoli via the process of ventilation. So we talk about VQ, that's the V part, ventilation. And blood is brought to and removed from the alveolar capillary membrane into the systemic circulation via a process known as perfusion or Q. V, ventilation, Q is perfusion. The most common mechanism producing hypoxemia in respiratory disease is a mismatch of the VQ or VQ mismatch. Thus respiratory failure can occur if there's a problem with gas exchange and subsequent hypoxemia or alveolar hypoventilation resulting in hypercapnia or more likely a combination of both. Those of us who have spent enough time in the ICU have experienced a common scenario where gas exchange problems will lead to hypoventilation or hypoxia leads to hypercapnia. The patient, despite our efforts, remains hypoxic because there's a gas exchange problem and the patient works harder and harder to breathe. The respiratory rate starts to climb and the patient starts to use accessory muscles. The patient starts to tire out. They're hypoventilating and then you have a subsequent rise in PCO2. That's a very common scenario and it's obviously very concerning. I get very concerned when I see the PCO2 start to climb. Patients likely going to need early intubation. Now this is a gas that is concerning. PO2 of less than 50 millimeters of mercury and PACO2 of greater than 50. It's the 50-50 rule. Now not everybody with this gas requires intubation if they have a primary pulmonary problem, if they have COPD, etc. But if the patient does not have a pulmonary problem, they're a healthy person, then this is a concerning gas. Especially if the PACO2 starts to climb. That is a major concern of mine. When assessing the patient with arterial hypoxemia, it's not immediately necessary to determine the exact etiology of the problem. What is imperative is to rectify the hypoxia and potential hypercapnia. We start off by administering supplemental O2. After the patient's stable, meaning they're saturating well, breathing comfortably, then you can begin the evaluation process. And the initial evaluation doesn't have to be overly cerebral or overly academic. You first want to assess two things. Is the patient responding well to supplemental oxygen? If so, that's a good thing. And then you can move in a very slow, controlled fashion. Then you can determine if there is an AA gradient. Is there a pathologic difference between the alveolar oxygen pressure and the arterial oxygen pressure? If there is an abnormal AA gradient, then there is a problem. Gas exchange. And we have to then try to determine, once the patient's stable, try to determine where the problem occurs. If there is no pathologic AA gradient, the likely problem is hypoventilation issues. But I will tell you, I think a lot of that is again a lot of academic, a lot of this is what we teach people. But I strongly believe if you know the admitting diagnosis, you can anticipate the respiratory issues if they're secondary to either a gas exchange versus hypoventilation or a combination of both. So what do I mean by that? Okay, well, conditions that suppress one's ability to ventilate include neuromuscular problems like myasthenia gravis, patient has to suppress mental status, high cervical injury where the diaphragm isn't being innervated, so they're getting hyperventilated, or if they took some drugs that suppress ventilation. But the majority of patients admitted to the ICU who have progressive respiratory problems have a problem with their gas exchange, will have an AA gradient, and will have some type of a BQ mismatch. Now, truthfully, yes, this is the majority of patients, but these are the patients on more concerned about because hypoventilating, where you may be able to oxygenate, but their PCO2 starts to decline, and that's a dangerous mechanism, or that's a dangerous problem. These are the patients I tend to intubate pretty early. The hypoxic patients, those are not saturating well in Ramirez. So Ramirez is 21% oxygen. We will start with supplemental oxygen. Usually we start up with nasal cannula. With the nasal cannula, you can administer up to 46% oxygen. You then sometimes have to then progress to a face mask that's 60% oxygen, or a non-rebreather up to 100% oxygen. So we can deliver a lot of oxygen without requiring intubation. So in the initial assessment, and quite frankly throughout the ICU course, the ICU team needs to determine if the patient can maintain their airway, control secretions, and prevent aspiration, ventilate and oxygenate well, and remain clinically stable. And if not, either initially when the patient's admitted or any time during their critical care stay, the patient will likely need to be intubated. Then once we intubate and we stabilize the patient, we can now start the workup process. Is the gas exchange issue a primary problem with the lungs? Here you see consolidations in the dependent portion of the lung concerning for aspiration pneumonia. Here's a consolidation, any part of a lung, either community-acquired or hospital-acquired pneumonia. In this x-ray, before I put it up, I don't know if you can quiz yourselves, here's the visceral pleura, here's the parietal pleura. So the lung markings are quite collapsed. You don't see the lungs collapsed. That's a pneumothorax. So in this situation, the gas exchange was from a V. So there was a problem with the V of the lungs. Now let's say you get that chest x-ray and it's normal, and that you still have a clear gas exchange problem, and there's other signs of concern. Patient has acute chest pain, especially on inspiration. They have a cough. They have a cough. They have light head, they have a, they start to develop a tacky arrhythmia. And you, and as I said, the chest x-ray is normal. You get a CTA of the chest and you see thrombi within the vasculature of the lung. What does that represent? Shout it out. Right, pulmonary emboli. Or there's a problem with the Q. So gas exchange where there's a problem with the V, the lungs we talked about, now this is a problem with the perfusion. Components of the gas, I'm sure we're all aware of this, pH, pH 735 to 7.45. Partial pressure, oxygen, arterial, 75 to 100. Carbon dioxide, partial pressure, 35 to 45. Look at the bicarb, normal, and then you want to look at the O2 set. And then acidosis, if it's a respiratory alkalosis, the PCO2 will be less than 35, and the pH will be obviously greater than 74, 7.45. It's a respiratory acidosis, the PCO2 is climbing, and the pH is also, is dropping. And then metabolic alkalosis and acidosis. I'm going to skip over this. So again, when you're looking at the gas, someone's blood gas, it's not an absolute, these are absolute, must need intubation. But there are areas of concern is when the ratio of the PaO2 to the FiO2 is less than 200. So in a normal human being, we talked about the PaO2 is, the lower number normal is 75, and your FiO2 on Ramirez, 21%. So usually your, your, this ratio is anywhere from 370 to 470. So if it's less than 200, you start to get concerned. But then these are also some concerning, tachypnea, with an increasing PaCO2. Those are the concerns, and the, and we should start thinking about what's the next step. There are ways to administer non-invasive positive pressure, BiPAP or CPAP, but there are some contraindications to giving this type of oxygen. This is prior to intubating, another step in terms of advancing your supplemental oxygen. So if a patient is severely encephalopathic, they're inability to cooperate, protect their airway, high risk for aspiration, inability to clear secretions, upper airway obstruction or hemodynamic unstable, those are all contraindications to utilize non-invasive positive pressure. So first, stabilize the A's and B's, making sure the patient's comfortable, standing well, and they don't need intubation in the immediate setting. Then we can move on to C's. C's stand for circulation. You're assessing the pulse. When we're assessing the pulse, we want to be aware of the rate, but also the rhythm. Is the patient in a sinus rhythm or in a suprapentricular rhythm? And if they aren't in suprapentricular rhythm, are they rate controlled? That helps guide the next step. If what, do you have an idea of the patient's volume status? If the patient's in the sinus tachycardia and they're hypotensive, then they're likely volume depleted. Other signs of volume depletion is cold extremities, pale skin, poor capillary refill, poor urinary output. Also additional signs of hypovolemia. We obviously need to know the blood pressure, and it's important to determine on admission if the patient warrants an indwelling A-line for continuous blood pressure. And if you're going to start a vasopressor, you need to start a blood pressure. If the patient is a stroke patient and they're very blood pressure dependent, meaning you want to do permissive hypertension, I would advise putting in an A-line because that will give you immediate information. Once we've determined the patient needs volume resuscitation, we then say, do they need crystalloid or colloid? I will tell you that we, the vast majority of the time, because it's quick, we start off with a normal saline bolus because you don't need to get it from the pharmacy. The nurse can hang the bag immediately and then give a liter of, if that's all the needs, or more of a saline bolus. Do not give ringers lactate. Do not let your trauma colleagues give ringers lactate in the neurotrauma patient. You give normal saline and crystalloid. Then you can follow with colloid, either albumin or blood products. But it's important to act quickly. So if you're going to get blood products, you're likely going to wait for the lab values to come back. And it takes time for the lab values to come back and it takes time to get albumin. So crystalloid you initiate and then you can follow with colloid. Then you want to know right away, is the patient going into shock? What is shock? Well, shock is a life-threatening condition that occurs when the body is not getting enough blood supply. Lack of blood flow means the cells and organs do not get enough oxygen and nutrients to function properly. The patient is going into end organ failure. What are the types of shock? Septic shock from an overwhelming infection. Cardiogenic shock is a primary problem with the lungs. You'll probably see other evidence of fluid overload. Hypovolemia. There is too little blood volume. Anaphylactic shock from an allergic reaction to either, well, an allergic reaction to something. Or neurogenic shock, a spinal cord injury. But what's important is correcting the physiologic abnormality takes precedence of arriving at the accurate diagnosis. Although, it often goes hand in hand, meaning that you need to know the diagnosis to give the appropriate treatment. So obviously, there are certain things we need to obtain, such as an accurate history. Gives you an idea of whether there's some infection. Did the patient take any type of medicines that you'd be concerned about? An EKG, looking to make sure the patient doesn't have any acute cardiac problems that could lead to cardiogenic shock. A CBC to rule out blood loss. Infectious workup. Infectious workup, if the patient has, or you're concerned about a septic shock. And basic guidelines or parameters that would cause concern. Trauma patient, which I'm going to talk about a little detail. Systolic blood pressure less than or equal to 90. Amina or geopressure less than or equal to 60. A drop of the patient's blood pressure by greater than 40 millimeters of mercury from their baseline. And obviously, the concern is the patient is going to go into shock. And thus, they're going to have developed end organ failure. I just want to kind of real briefly talk about neurogenic shock. It's a devastating consequence of spinal cord injury, as I mentioned. It's also known as vasogenic shock. It's an injury to the cervical or high thoracic cord above T6. And this results in a sudden loss of sympathetic tone, which leads to an autonomic instability that manifests with hypotension, radiated arrhythmias, and temperature dysregulation. There are some basic diagnostic clues that can help one come up with an accurate diagnosis in the hypotensive patient and guide, subsequently guide your treatment. If the patient has a wide pulse pressure, means they have a diminished preload. And if they have the, as I mentioned, poor perfusion to the extremities, core extremities, pale, poor capillary refill, decreased urine output, then think of hypovolemia and think of a high. And they don't have to be in shock, but think of hypovolemia, diminished or volume. If the patient has a wide pulse pressure, diminished preload, but they have warm extremities, they have good capillary refill, patient is febrile, then think of septic shock or fever, septic shock. And obviously, we want to do more than just volume. We'll talk about that a little bit. If the patient has a decreased pulse pressure, so there's not necessarily a diminished preload, but they still are not getting the flow to the extremities. So they still have poor capillary refill. They have cold extremities. They have poor urine output. And there are other signs of fluid overload. They sound like they have their chest, when you auscultate the chest or get a chest x-ray, there's evidence of fluid overload. Think of cardiogenic shock. So basically, hypovolemic shock, septic shock, neurogenic shock, the first thing you do is you do volume resuscitation. You obviously don't want to do volume in a patient with cardiogenic shock, because that's only going to worsen their symptoms. So as I said, placing an A-line allows for continuous blood pressure monitoring. But we can get even more information utilizing the A-line. We can attach a non-invasive cardiac monitor to the A-line, which will give you very important clinical parameters that will also help guide you and aid in your diagnosis and subsequent treatment. So before I show, just quiz yourselves. Do you guys know what's normal cardiac output, cardiac index, systemic vascular resistance? But what I want to focus on is cardiac output, cardiac index, stroke volume, and stroke volume variance, because that's the data that we get with our non-invasive cardiac monitor. Normal cardiac output, 4 to 8 meters per minute. Normal cardiac index, 2.5 to 4 liter per minute per meter squared. Stroke volume, the amount of blood that's being ejected from the left ventricle on each systolic beat, 60 to 80 millimeters per beat. And stroke volume variance is less than 13%. So these are normal parameters. Remember these parameters. These are normal parameters. Now let's look at a patient. This is an actual patient that was once hypotensive, but we stabilized him. So these are all these numbers that you see. The bottom numbers, excuse me, are all the actual numbers of this patient. The stroke volume variance, well, I'm sorry, let's go to cardiac output, 4.6. It's 4 to 8, right? Cardiac index, 2.4, also within the normal range. Stroke volume, within the normal range, 79. And the stroke volume variance was less than 13%. Those are good numbers, and the patient was stable, so yay. But before we got them to good numbers and the patient was hypotensive, the patient initially had a cardiac output of 3, index of 1.5. The stroke volume was 45. So all the numbers were dropped. So why is that a problem? Well, the stroke volume variance was 18%, so it's above 13%. This is indicative of a dry patient. So we gave them, because we weren't, a patient wasn't an extremist, and the patient weren't based on blood volume or blood on the lab parameters, I'm sorry, we gave them blood products. And so we gave them that colloid. And the patient actually improved to the numbers that you see, and the patient's blood pressure improved as well. So getting back to, let me see if I talk about that. Actually, I can talk about it in my next slide. So I hope you guys as a group understand that's what we're, so we can use non-invasive cardiac monitors now. We don't necessarily have to put in a Swann-Ganz catheter. I don't remember the last time we've done that now, because we have non-invasive means to assess all the important parameters to identify what the etiology of the hypotension is, what the etiology is of the potential shock, so we can treat them appropriately. So we've stabilized our A's and our B's. We're attempting to stabilize the C's initially with volume expansion. And as I said, the majority of the shocks that you're going to experience, except for cardiogenic, you're going to give crystalloid, or you're going to give volume, excuse me, and you're going to start up with crystalloid. Do not give Ringer's lactate. Can't emphasize that enough. Ringer's lactate is hypoosmolar. It can exacerbate cerebral edema and other neurologic conditions, so you want normal saline. And then if we need to continue, we often will then switch to colloid. But in a septic patient, we have to do other things, such as start them on broad-spectrum antibiotics. And sometimes, volume replacement isn't adequate enough in certain types of shock, such as septic shock. So you need to progress to a vasopressor. As I said, if you're going to start with a vasopressor, you need to place an A-line. And in a septic shock, the vasopressor of choice is levophed, or norepinephrine. Why so? Because norepinephrine is battling the problem of septic shock, and that is your vasodilatation. So it increases your mean arterial pressure, primarily through vasoconstriction, without an effect on the heart rate, stroke volume, and cardigapolis. So it's sort of the ideal vasopressor in the septic patient. So I don't mean to be overly redundant, but important. We stabilized the A's, B's. We're good with the C's. So now we can move on to the D. D is disability of neuroassessment. And I certainly don't need to explain to this audience the need for a thorough neuro exam. Depending on the admitting problem, the patient will likely be, if it's a stroke, the patient won't be assigned an IHT. The patient won't be assigned an IH stroke scale. In the trauma patient, we're going to determine the level of consciousness by performing a Glasgow Coma score. You want to get a thorough neuro exam. Obviously, if the patient's unconscious, you want to get accurate brainstem reflexes. And it's important. And what we're trying to determine in the initial admitting state is the patient in extremis. That's the job of the initial admitting team. Is the patient in extremis? And if so, we need to do whatever we can to quickly get the patient out of this deteriorating state. So in the neuro trauma patient, it is important to get a very good general physical condition. Look for signs of skull-based fractures. Does the patient have a periorbital ecchymosis, indicative of what is called raccoon's eyes? This is indicative of a skull-based frontal fracture. Very important, because if there's evidence, if you have periorbital ecchymosis, as you all know, trauma patients get tubes in every orifice, including the nose. So you do not want to stop someone from putting an NG tube in a person that you suspect with a frontal fracture, because the NG tube can migrate intracranially. I had some x-rays. I don't know what I did with them, but I had x-rays actually showing that. Battle sign, or post-auricular ecchymosis, a skull-based fracture along the mastoid region. You want to palpate along the orbits if they don't have excessive edema, along the zygoma. And just make sure the patient doesn't have any type of orbital, or look for its fractures. You want to auscultate if you're concerned about any type of vascular injury. And you want to stabilize the spine. Up to 10% of patients who have some type of intracranial pathology or head trauma have a spine injury. And then, based on studies looking at the oxygen saturation, blood pressure parameters, and the outcome of trauma patients, we came up with these parameters. You want to maintain a blood pressure, systolic pressure of greater than 90, and O2 sat of greater than 90. It's a 90-90 rule. PO2 of greater than 60, and a perfusion pressure between 60 to 70. Now, it's tough to give a neuro talk, especially if I'm going to talk about trauma, without avoiding the Monroe Kelly doctrine. I'm sure you guys have heard this doctrine multiple times. The Monroe Kelly doctrine states that the intracranial volume is a fixed volume. And it's made up of brain, blood, and spinal fluid. And if there's an increase in one of these two, there has to be a subsequent decrease in the other to maintain a normal or a ICP that's not climbing. The modified Monroe Kelly doctrine is you add additional volume, a pathologic volume, a tumor, blood. And the more rapidly this volume expands or increases, the more likely the ICP is going to go up rather abruptly, because the brain doesn't have a chance to compensate. So we place an EVD in the trauma patient with severe head injury and abnormal CAT scan. Or if the patient has an abnormal CAT scan, and they're going to have a blunted exam, that's a very important point. And I've talked with my colleagues about this. If the patient has abnormal CAT scan, and they're going to have a blunted exam, and they're going to be paralyzed and sedated, I have a low threshold to put an EVD in, because you don't have an exam to follow. And ICP monitoring is helpful in early detection of intracranial mass lesions. Especially, as I said, if you have a blunted exam, you don't know if that subdural the patient has is expanding. It can limit the indiscriminate use of therapies to lower ICP, which can induce or result in secondary injury. You can actually treat the ICP by draining spinal fluid. So those are the advantages. And we use the absolute number, ICP number, that you're trying to be under. There's no absolute number. But in general, we do try to keep the ICPs lower than 20 to 25 millimeters of mercury. But the reason there's no absolute number is because we may be more or less aggressive with ICP management based on the patient's neuro exam. In the non-trauma setting, an EVD may be indicated in those patients who present with subarachnoid hemorrhage, intercerebral hemorrhage with or without interventricular extension, posterior fossil bleeds. So know the CAT scan. Again, it gets back to where I said, know the pathology. Why the patient's being admitted to the ICU? Because if you see these CAT scans and the patient's deteriorating, it's often from acute hydrocephalus. You better be aware of that because an emergent EVD is necessary to prevent death. I will argue that this patient actually needs to go to the OR. But the point being is that an emergent EVD is necessary. The goal in the neuropatient, and I mentioned this, I did mention secondary injury, is to prevent secondary injury by maintaining an adequate cerebral perfusion pressure. Local or global increase in intracranial pressure can and will result in a reduction in blood flow, subsequent blood volume. And the reduction can be so significant that the brain is not receiving enough nutrients to maintain its metabolic requirements. And that's the secondary injury is that the injury from the initial either trauma, cerebrospinal hemorrhage, et cetera, it's from the injury because perfusion is not getting to certain parts of the brain and thus it's not maintaining or not meeting the metabolic needs of the brain. Cerebral perfusion pressure is mean arterial pressure minus intracranial pressure. And you want to, and although we can't directly measure the CMRO2 requirements of the brain, the metabolic requirements of the brain, but we know that if we maintain a perfusion pressure between 60 to 70, we're adequately perfusing the brain to maintain its metabolic needs, avoiding the secondary injury. What are pathways you can do to reduce ICP? Well, some basic things in the beginning, especially in the trauma patient, seizure prophylaxis. Certainly with a seizure, elevate your ICP. Elevate the head of bed roughly 30 degrees. It maximizes venous outflow without interfering with arterial flow to the brain. Avoid jugular venous obstruction. If you're going to put a central line in, try to avoid the jugulars. Very gentle sedation, if need be, and maintaining adequate oxygen perfusion pressure, I should say, 60 to 70. More aggressive maneuvers. These are more aggressive maneuvers to ultimately get what we need to get, and that is repeat a head CT. Because what you want to do is, what are we trying to rule out? We're trying to rule out, if the patient has a space-occupying lesion, that rather than do all these maneuvers, the patient should be going right to the OR. And if the patient has a unilateral problem, not necessarily something you would evacuate, but it's causing ICP issues, I will indeed go to perform a decompressive hemicraniectomy much more aggressively. So it's important to understand the diagnosis to get a sense of why the patient may deteriorate. I've said that multiple times. It's obvious, but it's essential to know if the patient had an ischemic stroke, did they get TPA? Was there a large vessel occlusion? Did they undergo mechanical thrombolysis? In a hemorrhagic stroke, was it an aneurysmal subarachnoid hemorrhage? Is it a hypertensive bleed? So know where the blood is. Head trauma. And this seems obvious, but again, you need to know this. In a head trauma, does the patient have extraxial bleed or contusion? In the post-operative patient that's going to be spending time in your ICU, know the surgery. Know the side the operation was on. The reason it's so important is because there are different reasons for these patients to deteriorate. And it's the responsibility of the first line provider to right away rule in or rule out the worst case scenario. So again, we must think that the worst case scenario is occurring when the patient's decompensating. And once you stabilize your ABs and Cs, you then immediately need to obtain whatever imaging study is necessary, likely a non-contrast head CT, to rule in or rule out the worst case neurologic scenario. And again, this seems obvious, but I will tell you, and I'm sure many of you have horror stories where, and let's talk about the trauma patient. I don't mean to pick on my trauma colleagues, but let's talk about the trauma patient. A young guy comes in. He's kind of a jerky person. And because he was a jerky person, he was assaulted. He got his butt beat up and his head beat up. And he has a subdural. Not a big subdural, not something that warrants surgery, but something that we're aware of. The patient's admitted to the trauma ICU. And then throughout the night, the patient's getting more and more agitated. And I will tell you what happens, especially if that first line provider is not the neuro person, but the trauma person, they get sedatives. This, they will sedate to a point they'll intubate because they're just saying, well, he's a jerky guy. And he's just, his personality is manifesting, or he's going through drug or some type of alcohol withdrawal. But what they don't do is they don't think the worst case scenario is occurring, that maybe that subdural is expanding. And what has happened, and it's happened to me, is the next phone call you get is, the patient just blew their pupil. CAT scan shows that there was a massive subdural that if they had thought of the worst case scenario, obtained the CAT scan, we could have avoided the life-ending event. So think of that worst-case scenario, rule it out if the patient's in extremis. More challenging treatment plan is the management patients with bleeds, especially deep bleeds, that are not the result of an underlying treatable disease. For example, hypertensive bleed or a hemorrhagic immersion of ischemic stroke. And historically, our management, even if the patient wasn't really doing very well, is preventing the hemorrhage from expanding, either by controlling blood pressure or by reversing any type of coagulopathy the patient may be experiencing. And this study shows that when you control blood pressure in terms of maintaining systolic blood pressure less than 140, as opposed to the blood pressure rising, you can indeed reduce the chance of the hemorrhage expanding much more successfully. Just some ASA guidelines in terms of blood pressure management, but I don't really want to go into that. But now what's exciting is we now have the capability to evacuate these clots and get the patient out of extremis in a very minimally invasive manner. With image guidance and with the direct visualization of an endoscope, we can get directly into the clot and evacuate the hematoma under direct visualization. So the initial procedure was a two-man procedure. And what is happening is one person is running the endoscope while the other person is advancing this wand-like device, which has the capability to morselize the clot. So it vibrates to morselize the clot. It also irrigates and aspirates. You get right into the clot under image guidance, and then with the endoscope, you evacuate the clot. And as you can see, because we're using a regular channel scope, not that it's cumbersome, but it's certainly a little bit more difficult with a one-man procedure, because it's not so difficult to hold with just two hands. And then initially, pre-treatment, pretty decent-sized hemorrhage. You're already seeing effacement of the ipsilateral ventricle with paraphalocene herniation. Immediately post-op, clots gone, and the brain's well decompressed. And we didn't need to do, if you notice, the bones intact. We didn't do a hemicraniectomy. Pre-treatment, post-treatment, pre, post, and again, what you see is clot gone, mass effect gone, patient stable, and without any decompressive hemicraniectomy. But now, what we have is the Artemis I, which is the latest generation of this procedure. And what you can see is the endoscope, which is this gentleman's hand holding with just one hand, like you hold a pencil. And everything is contained within this endoscope. Much, much lower profile. Image guidance, the WAND system that's actually doing the irrigation, aspiration, morselize, and you have irrigation as well. So everything now is done through a one-person, because everything is contained in one easily held endoscope. The last thing I want to talk about is, as I mentioned, these patients are the highest acuity patients in the hospital. They often, as I showed you in my first or second, I forget, maybe fourth slide, the patients are intubated, they have the non-invasive cardiac monitor I mentioned, they have EVD, they're ventilated, and when you start to discuss and describe these patients, it is overwhelming. You don't know where to start. You don't even know how to start. So we've created a progress note, this is actually our ICU progress note, that really forces you to be systematic, that allows you to think about the patient in a very systematic fashion. So the first, the very beginning of the progress note is, what happened over the last 24 hours that we need to address right away? Are there any new radiologic studies? And then you go through the basic, this is nothing that fancy in terms of the vital signs and the labs, but then we have a problem list, but then what's really important, and I think this is what does make our progress notes a little bit different, is we then go by systems. So this is the assessment and plan part of our note, and this allows whoever's discussing the patient to do it in a very systematic fashion, where you can do, you say neurologic first, then you say cardiac and hemodynamic, and I know we talked about ABs and Cs, but we're neurosurgeons, so we do, we take, we say neuros first, and what we say is, we don't just say, okay, what is the, what's the exam? We actually talk about the plan, and we gather by the bedside, and it's a multidisciplinary rounds, where the neurosurgeon, if there's a fellow or resident, med students, but what's really important as part of our team, they're the most critical part of our teams, the advanced practitioner and the nurse taking care of the patient, and we go through and we talk about, again, neuro, what are the neuromeds, what are the problems, what is the plan for both, or in the immediate plan and the long-term plan from the neuro perspective, so let's talk about the subarachnoid hemorrhage patient again, so we say, okay, and we talk about this, we say, we have a Hunt-Hess grade, so we can anticipate the likelihood of a patient going into subsequent problems, we say, you know what, all right, is patient's post hemorrhage day six today, guys, okay, we need to know what the transcranial topos are, we need to know what the neuro exam is, because this patient had a lot of bleeding, a lot of blood in the brain, they were a smoker, African-American, they're a higher risk of vasospasm, so it allows us to anticipate the next problem, right, think of the worst-case scenario and make sure you rule it in and rule it out, then we move on to cardiac, and do the same thing, where are we keeping the blood pressures, are we doing permissive hypertension, are we concerned, are we keeping pressure on a lower blood pressure, do they have any acute cardiac events, what's the ejection fraction, lungs, are they intubated, is there any type of abnormal VEQ mismatch, chest x-rays are okay, not okay, etc., and then we move down, gastrointestinal, genitourinary, etc., as you can see, infection, now we do, we also, we do a, if we start antibiotics at 48 hours, we do an antibiotic timeout, or we make sure that we're putting patients on the right antibiotics, and we start to go from broad, broader coverages to, to more narrow coverages, based on what's happening with the infection, and then just in terms of what I want to identify, just go back, genitourinary, we also talk about, about Foley's, because we, we discuss if a patient has a Foley, every day we say, can we, can we take the Foley out, can we switch the Foley to a Texas catheter, or a Texas catheter, like in the female population, and then we talk about skin, so we don't, we don't want to miss a system, so again, what we do is, we take a, which can be a very chaotic situation, and we force ourselves to be very controlled, to talk about each of the systems, so we don't miss something, and we talk about DBT prophylaxis, etc., so that's the way, again, we take a very, a high-acuity patient that clearly can be overwhelming in terms of workup, talk about treatment, and then we make sure we control the patient. That's it. I hope I achieved my goal. Thank you. Is this your dog, first of all? I'm sorry? Is this your dog? Yeah, it is. Oh my god, I love it. Oh my god. I don't know if you can see. The, it's, we're big time Philadelphia Eagles fans, and this was, we were, my wife and I went to the Minnesota when they, when they went to the Super Bowl, and this was the outfit that we put on, but we put on our dog first, to take a picture. Oh my god, that's awesome. I love that Bulldog mug. Okay, that was great. That was a great overview, and we do have several questions, some I think that you kind of answered along the way, but let me get to several of these here. All right, so somebody was asking, I think, kind of generally speaking to people, but I thought I'd pose this to you as well. What's your EVD policy as far as kind of, you know, do the nurses clean the exit site every day? Do they put vasotracin on it? Do they just leave it alone? We, what we do is, we, no, we, the incision itself, we put Dermabond on the incision, so that protects the incision itself, and then we will cover it when, so the nurses do not. We don't, we, if we get concerned, we want to, with our advanced practitioners, we will monitor their cleaning of the EVD. They don't just indiscriminately clean it on their own, and they don't necessarily do it on a daily basis, and again, by putting Dermabond on the incision, it also allows us to not necessarily need addressing over the incision site. Got it, and then actually, I also had another side thing, so the documentation thing that you showed, do you guys not, you don't have electronic health record, or do you? No, that's a great, no, it's a great question. Right now, obviously, we're going to, when indeed we have electronic records, we're going to incorporate this in the records, but no, right now, we do not. That's a great question. Yeah, it's great to have a nice template like that for EMR, because it is, it's harder to make it look, you know, like a written note, so that's really helpful. Okay, so then somebody had a patient who had subarachnoid hemorrhage, had an EVD that was sporadically kind of dumping out, you know, 35, 40 cc's of CSF, normal ICPs, no neuro change, what would you do about something like that? What post hemorrhage day are they? I don't know, I don't know. Okay, because, so if, I'll answer this in somewhat a long-winded way, so if the patient's in a spasm period, although there's, I actually had an abstract, and then a paper came out that kind of disputed that CSF increases with increase in basal spasms, so I'm not really sure if that's accurate, but the point being is that if someone's dumping a fair bit of CSF, and they're in the peak spasm period, then I would monitor, but the reason that I need to ask more questions about that is because if they're dumping CSF, at what ICP are you draining? So if they're draining at, are you draining at 5, 10, 15, 20, where, at what level are you draining? Yeah, that was my first thought too, like where, where's the level of the drain, and is the patient coughing a lot, or was something, was it accidentally on the floor, or something like that? Right, no, that's exactly right, and, and there's, and the thing that I, I do, I tend not to leave the ICP, the EBD opened at, let's say 15, to drain at 15, and then, and then turn it to monitor. I do the other way around, I monitor it, and then if the ICP is continually climbing, and you either want to maintain a perfusion pressure, the patient is neurologically getting more lethargic, then we drain it. My point is, because what you just described, Robin, is if the patient, if you keep it just a level of 15, the patient coughs, sneezes, any valsalva, where physiologically our ICP climbs, they, they dump CSF. If the patient changes their position, they can dump CSF. I think there's a much greater chance and concern for inappropriately draining too much CSF if you just leave it open. Do you then just, like, if it goes to 20, or, you know, between, you know, over 20, for five minutes, or something, you drain, or if they have a neuro change? Okay, I do, what we do is, it depends on the initial admitting diagnosis, so if you're trying to maximize perfusion pressure, let's say that, again, let's talk about subarachnoid patient, then we will start off with a lower number, so we'll drain. If the patient has, begins with, if they start with ventriculomegaly, we may even drop it down to 10, and try to maintain a better perfusion pressure, and then, then slowly raise the threshold 10 to 15 to 20 over the ensuing days, depending on how the patient does, the transcranial dopplers, etc. Okay, all right, now I've got, so there's somebody who uses VBGs in their ICU instead of AVGs, how, you know, would you mind reviewing, kind of, you know, the results in regards to a VQ mismatch in that situation? I don't have that information here. Yeah, I know, we sometimes use venous blood gases as well, but tell me what you mean, what do you mean by going over the VQ mismatch? I'm not understanding what they mean by that. I guess I'm wondering if they're, kind of, saying, like, how to interpret a VBG, you know, compared to an AVG, in terms of, like, that kind of stuff. I don't have normal parameters for venous blood gas, I apologize. Shoot, I don't. I was just going back to see if I had that, too. Well, I'm trying to explain it in a way, in terms of the VQ mismatch, that's just a problem with gas exchange. So, you know, in terms of your normal parameters and non-normal parameters, which you're going to be aware of, if you have abnormal parameters on your blood gas, that means a venous or arterial, and it's a problem with oxygenation, then it's a gas exchange problem. It's a problem within this VQ region. I mean, the only time you're really going to not get a VQ mismatch, a gas exchange problem, is in this scenario, where, and you're going to be able to anticipate. So, I kind of skipped over, and I did talk about it, the AA gradient. I mean, yeah, certainly, if you want to get academic, and you calculate the AA gradient, that helps. But the vast majority of the time, your patients who are being admitted and are going into respiratory problems, you're going to know if there is a gas exchange problem versus a hypoventilation problem. Am I making sense? Does that make sense? Yeah, absolutely. I mean, I feel like, too, at least in the population that I see at our institution, so many times, the reason why a patient gets intubated is for lack of mental status and need for airway protection. It's not even necessarily that their gases look terrible. Yeah, that's right. You're right. Yeah. Okay. I can't agree with you more. All right. We talked about the LR thing. So, somebody's asking, which non-invasive cardiac output monitoring device do you prefer and why? Whatever the hospital has, because that's all they got for me. We use the FlowTrack. The FlowTrack is our non-invasive monitor, and it's not that I don't have stock in the Vigileo and our FlowTrack. It's just that's the non-invasive monitor they have, and that's the one that's more readily available. I mean, that's the one pretty much most people use, but it's not that I have an affinity towards one monitor and the other. I mean, I just need to know the parameters that it gives me. Yeah, and I was laughing when I was listening to this, because I mean, I was an MICU nurse and a neuro ICU nurse before I went back to school, and I used SWANs. So, I have an average. Oh, yeah, yeah, yeah. Yeah. Okay. I used to love the float SWANs. I know. Yeah, well, they're fun. Yeah, they were kind of fun. Okay. How about this one can be, we have, I guess, three more minutes here. So, somebody's asking how many patients, I'm guessing they're asking in the neuro ICU, is one PP managing at a time where you are? I'm not going to answer that. I'll have my, I don't know. I guess none of our APPs are on the line. Well, I'm going to answer. I'm going to be a bit cryptic with my answer and a little bit ambiguous. They take care of, our ICU is seven beds right now, our seven beds, but we often bleed in because we have a pretty high, our census is pretty high. We bleed into the other ICUs, and we're currently in the process of expanding our ICUs. So, we have a frontline APP, obviously, in-house. And during the day, we have three to four advanced practitioners in-house. But we also have always, always, always, always an attending, a fellow, and then, and then backups. So, you know, although they may be doing the initial assessment, there's constant communication with the fellow and the attending to discuss. But if it gets, if anything does get overwhelming, then the fellow or the attending drive in. And frequently, when someone's being admitted, the fellow or the attending or resident will be, will be there helping the admission. It doesn't really answer, but that's, that's sort of, that's the best way I'm going to answer that. It's kind of skating right past the answer, but that's okay. Okay, so it looks like we only have a minute left. Is that right, Ryan? Am I right about that? Maybe not. Okay, cool. So, that's okay. So, we will tie this up, and I will, I'm going to take screenshots of the rest of the questions. We have, I believe, a 30-minute break right now from 315 to 345 Central Time. We will return at 345 with Dr. Liebman and Dr. Armanda to talk about some cases that they have and kind of finish up some of these questions that you guys have posed. I hope you're enjoying this, and we will see you guys again soon. Thank you so much again, Dr. Liebman. Oh, my pleasure. Take care, everybody.

management

unstable ICU patients

assessment

stabilizing

ICU

critical care patients

continuous monitoring

treatment

early recognition