Welcome everybody to the second half of our general session at the AANS APP course. I really hope you guys are enjoying today. I know we had some great speakers this morning, and we've got a couple great speakers this afternoon as well. So on that note, I am going to introduce Dr. Armanda. He is a retired colonel from the US Army, is also director of the neuro, excuse me, of neuroendovascular surgery for medicine, MedStar Washington Hospital Center, and MedStar Georgetown University Hospital. He's surgical co-director for the neurointensive care unit and MedStar Washington. He's a professor of neurosurgery at Georgetown University, an associate professor and director of neurosurgery at the Uniformed Services University of the Health Sciences. His seminal work includes some really neat things, including detection and treatment of traumatic cerebral vasospasm, traumatic pseudoaneurysms, decompressive craniotomy for wartime trauma, craniofacial post-traumatic reconstruction, multimodal AVM treatments, and the design and deployment of the advanced neurointerventional operating room. So we're really excited to have him today. He is going to talk with us about cerebral vasospasm and the management of subarachnoid hemorrhage. Thank you so much for being here, Dr. Armanda. Robin, thank you very much for that introduction. So we're going to get underway here, and we're going to start with a case to get everybody's attention. And this is a case of a young man, 38 years old, sudden severe onset headache, and then lost consciousness, and was seen to be seizing, was picked up by EMS, was brought to an outside hospital. They obtained this scan. He's pretty groggy, lethargic, not following commands, and they call you with this image. And this is how the whole story usually starts. It's a sudden apoplectic event. The question then becomes, what do you want to do for this patient? What's the patient's test grade, and why is that important in the big picture of vasospasm and secondary brain injury? So we start out with looking at this particular CT scan and appreciating the subarachnoid hemorrhage that we see here. So the subarachnoid hemorrhage is pretty diffuse, but there is some asymmetry with blood, collected in the area of the sylvian fissure on the right side, as well as throughout the entire supercellar cisterns. And so when you see multiple cuts of blood like this, you know that this is at least a fissure grade 3. And if there's interventricular hemorrhage, a fissure grade 4. And with each fissure grade, there's a higher incidence of vasospasm. And more importantly, there's also a higher incidence of poor neurologic outcome. So what you see at the beginning can give you a foreboding of what's about to come. And then the question becomes, what's going to be your management plan of action for this patient? How do you want to take care of this patient? What's the priorities of intervention? Well, as with any emergency neurosurgical patient, you should think of your ABCs. Secure the airway, maintain breathing, ensure adequate circulation in that patient. And then the next should be, in fact, the role for ventriculostomy. Does this patient have evidence of hydrocephalus, placement of an early ventriculostomy, managing the ICP? Because that's going to be the most common acute causes for death and secondary injury at the very onset of this. And then as we proceed is, where is the source of the aneurysm or subarachnoid hemorrhage? And with that, how is the best way to treat this patient with interventional or microsurgical techniques? And so most of the focus of this particular lecture is really going to be on that of what I call as the counterattack. You can't stop that initial subarachnoid hemorrhage. You didn't have the ability to see this aneurysm before it ruptured. But now this patient is on your service and we're trying to prevent secondary insult. And so that secondary insult prevention starts with the ventriculostomy, starts with first getting the airway secured, adequate breathing circulation for this patient, avoiding hypotension, hypovolemia, hyperthermia is the part of what I call the five bad H's. The other things I would add to that would include the possibility of hyponatremia and hypotension. So again, avoid hypotension, hyponatremia, hypothermia, hypovolemia, and let's see, hydrocephalus as we talked about. So this is a nice little picture. This was Emma when she was about four and her goal was to get through her first little triathlon. And so she had to sort of think about what were her objectives to do to get through, get her mind in the right space to get through that triathlon. Because her real goal was really not the swim, the bike and the run. It was basically the moon bounce. This is now almost 15 years ago or so. So it's preparing your mind. And that's what Emma was about to do at this young stage of her life is preparing your mind. And so what you have to do is you have to prepare your mind for how you're going to take care of these patients in terms of anticipating the next step. Because if we're unprepared mentally, it becomes unexpected, unfamiliar terrain, and that's where patients get injured. So this is that patient's angiogram that demonstrates evidence of a discreet right MCA aneurysm, which goes with the area of the Sylvian Fisher hemorrhage that you saw. And in that you see evidence of basically a discreet small neck aneurysm and an irregular aneurysm measuring about six millimeters. And we were able to successfully coil a clue that. Well, at this point, you're all ready to declare mission accomplished, pat yourself on the back and say, we've got the job done. We can all go celebrate. But this is only the very first beginning of this patient's care and realize that in the course of the arc of this patient's illness, the second week is typically worse than the first week. In fact, this particular patient underwent four total treatments for his delayed cerebral vasospasm. Four separate trips back to the IR suite for treatments with both balloon angioplasty and verapamil treatment. And with that, it takes a concerted effort and team. Part of that team that we use is the transcranial Doppler monitoring and with our TCD technologists, who are very, very good and skilled at monitoring patients' transcranial Dopplers. So what you're seeing here is data from the 15th. This is after his two episodes of vasospasm. And he had what appeared to be improved TCDs with mean velocities that were less than 180. And then you see a big jump the next day, which is on the 16th with left side of velocities as high as 185 and the C1 velocities that were also somewhat increased as well. In addition, you see basal velocities shown down here. We'll talk a little bit about how those are gathered. And then radiographically, you're seeing evidence of vasospasm involving the posterior circulation. This is before treatment. And then this is after treatment with a combination of both intraarterial verapamil and angioplasty. Again, before and after treatment with combination of intraarterial vasodilators and angioplasty. But really, the ability to track these particular transcranial Dopplers from day to day, and in this case, we don't have much of an exam on the patient to follow, but the TCDs showed a dramatic change. And the dramatic change that we see here is basically an increase in the MCA velocities from 117 to 122 to high as 177 to 185. And that's a jump that's of significance. And so we look at jumps that usually are greater than 50 as being an important discriminator, especially 50 in one day, or asymmetry from one side to the other of greater than 50. And here, it's almost 100 difference from the MCA on the right side versus the MCA on the left side. Some of the agents that we used include verapamil and nacartopine. These other agents are less commonly used intraarterially. We'll talk about, you know, nemodipine orally as a prophylaxis, but in terms of intraarterial use, vasodil is used primarily in Japan. Historically, about a generation ago, we used to use papavirin, but we've moved away from papavirin. Papavirin is much more difficult to prepare. Papavirin is not as easy to administrate and can cause rises in ICP. So we started using papavirin in our shop here around the year 2000, so over 20 years ago. So this shows this particular patient's third treatment. And in this patient's third treatment, what we saw is that the vasospasm was affecting the more distal circulation. So if you look at the comparison before and after treatment with the use of intraarterial verapamil here, you see that the vessels look very thready pre-treatment on day 11 here. And then post-treatment, those vessels dilate up. The circulation time is actually much faster. We did some touch-up work with angioplasty involving the supraclinoid carotid artery here, as you can see here on the lateral film. But what was most distinct is to watch the cerebral circulation, see how rapidly the cerebral circulation improves after about 20 minutes post-verapamil injection. And this is intraarterial post-verapamil injection, a lateral film and an AP film. And you're filling the arterial tree much better. The whole arborized tree fills much quicker. And that area of thready irregularities that you saw out into the distal MCA and ACA have now completely resolved. So when we look at vasospasm in terms of angiographic vasospasm in this patient who was symptomatic, we classify as proximal vasospasm involving the proximal vessels, distal vasospasm involving the distal arborized tree, or diffuse involving both. We're actually able immediately after we treated this patient to repeat the TCDs to serve as a new baseline. And so the TCDs are performed at the bedside, in this case in the IR suite. This is a weekend, again with excellent tech and team. These are transcranial dopplers that are being performed. This is through the temporal window. Through the temporal window, they're visualizing the anterior circulation. And then retromastoid and towards the foramen magnum, they're going to be able to monitor the posterior circulation, the vertebral and basilar artery. So what's the implications of subarachnoid hemorrhage and vasospasm? So you think about in terms of stroke, it's not a very large number of patients with stroke. However, it's a very expensive cost of stroke because it usually affects younger patients. And they're usually left devastated in terms of the rest of their life, those who survive. So 30,000 cases of which angiographic vasospasm might be seen in up to 70%. But in terms of symptoms and clinical changes, that's only on the order of 20 to 30%. Of those who have symptoms, approximately 50% will have severe neurologic damage or mortality. So symptomatic vasospasm is a deadly disease. Patients who are young, female in particular, do very poorly with symptomatic vasospasm with this recurrent episodic spastic vessels that can occur typically from the second to third week. And some even present with acute vasospasm. Understand that vasospasm is the measurements of we're using here as a surrogate for delayed cerebral ischemia, but they're really very distinct entities, which we'll discuss in detail. We look at what's the cause for delayed cerebral ischemia that we can treat. So is it related to a secondary microcirculation problem or is it related to the macrocirculation? Is it related to seizures, metabolic problems, or fevers? Those are things that we'll talk in detail that we can address versus other things that we may not have as much control over, which may be the patient's underlying atherosclerotic disease. Ultimate recovery is going to basically depend on how well we prevent this secondary injury, how well we're able to basically improve the metabolic status of the brain in terms of blood flow, intracranial pressure, and allow subsequent healing. So when you look at the picture of subarachnoid hemorrhage, this is a very helpful diagram to understand that this sort of internal explosion in the brain, although it's a local event, it has systemic effects. So this local event, which is this rupture of the aneurysm then spilling blood into the subarachnoid space, creates a metabolic cascade of events that then lead to early brain injury, mechanical effects such as the hydrocephalus that we talked about, as well as global ischemia with decrease in blood flow, increased ICP, and microcirculatory problems, which are getting a lot more attention now because that seems to be associated with a lot of this late cerebral ischemia that we don't see large vessel stenosis with or vasospasm with. And with this pattern of early brain injury, you see problems associated with disruption of the blood-brain barrier, in particular if you look at what happens to the blood-brain barrier, it becomes very leaky. So what happens is that normal basement cell membrane starts breaking up, you get this apoptotic changes and cell death occurring to those endothelial layers and the basal layer, laminum, and as a result, you get an increase in edema, and that increase in edema you can see radiographically with low density or hyper densities that occur in the area of the white matter. With that, you also get activation of the platelets and that sets up this scenario for then microthrombosis. The systemic effects can be quite profound with cardiac dysfunction we'll talk about and neurogenic pulmonary edema. And so now the patients are having problems just oxygenating themselves as well as maintaining adequate mean arterial blood pressure. So these early events after subarachnoid hemorrhage, you want to intervene on rapidly. There's this systemic response to this increase in a sort of a neuroadrenergic response, which affects again like we mentioned the heart and the lungs. There's this accumulation of blood which is toxic in the subarachnoid space, it then breaks down into these other elements that then sets up the support layer that can then lead to vasospasm and delayed cerebral ischemia. This first 72 hours again sort of sets up this pattern of injury in terms of ICP, hydrocephalus being the predominant effects, and then the shock with neuroadrenergic response to the heart and lungs. And then in a delayed phenomenon, you'll see secondary triggers that then result in delayed deaths, delayed ischemia. So the early deaths with the sudden severe onset rupture of the aneurysm, we can't necessarily prevent those. Many of these patients will come in already in a comatose expired, irreversible state. However, if we can address their hydrocephalus, and if we can prevent the aneurysm from re-rupturing, it gives us a chance to prevent this secondary injury. The secondary injury typically occurs over the next 7 to 21 days, and with that, these delayed complications are sort of grouped in here. And most of these delayed complications involve this sort of combination of both delayed cerebral ischemia with or without vasospasm, as well as systemic complications, such as fever, pneumonia, associated electrolyte imbalances, of which hyponatremia is one of the primary ones. So there's the mechanical trauma from the subarachnoid hemorrhage, which then sets off this increased ICP, the mechanical trauma to the brain, but then it also sort of induces a vasoconstrictive response. And that sort of phylogenetically makes somewhat sense because the body is trying to stop the source of the bleeding, but it also creates this significant oxidative stress to the neurons in terms of now they're metabolically strained and they are set up to go into a period of potential apoptosis or programmed cell death. So just to emphasize, the reason why hydrocephalus treatment early is so important is because by treating the increased ICP, you're able to sort of improve CSF hydrostatic pressure, which will improve cerebral perfusion pressure, which will reduce ischemia. Failure to do this and delay in placement of a ventriculostomy can lead ongoing programmatic cell death and ongoing injury to the brain as the patient is either awaiting microsurgery for the aneurysm rupture or awaiting endovascular treatment. And realize when you treat patients either in the operating room or in the interventional suite, those patients are usually going to be supine, they're going to be flat, and that's going to be the period of which there's going to be the most increased period of intracranial pressure. This is a real injury that creates a massive sympathetic surge. You see it most profoundly in younger patients where their blood pressure will shoot up, you'll get significant cardiac wall abnormalities and flash pulmonary edema. So you'll have problems trying to oxygenate that patient as well as the common cardiac problems in terms of the effects on wall motion. You might have to put that patient prone in order to adequately ventilate that patient. And again, a prone patient, you want to be able to take care of their ICP. So this cushion response is usually a late phenomenon to increase ICP with increased blood pressure, decreased heart rate, irregular respirations, and that's usually a pre-death phenomenon. So we want to intervene way before that occurs. The hypothalamus usually has this vasopressin release, which then can cause other problems in terms of electrolyte abnormalities and vasoconstriction elsewhere in the body. So just to summarize again, it's a local event that has systemic effects. Those systemic effects include both the heart, the lungs, as well as effects in terms of electrolyte abnormalities and cerebral salt wasting, secondary brain edema. They also have effects in terms of affecting the cell membrane and the ability of the basal lamina to maintain adequate seal and prevent leaky membranes. So our focus at this point is now going to be primarily on the area of spasm of the vessels that can occur as a treatment option to prevent secondary injury. This is sort of a wonderful little graphic that illustrates the inflammatory components involved. You have the aneurysm rupture. It then creates basically an oxidative stress. There's an inhibition of nitric oxide, and as a result, there's a problem with inflammatory migration of white blood cells into the lamina, which then induces this stress in the vessels, causing vasoconstriction and a delayed phenomenon. And so our goal basically is to address those patients. Additionally, this is seen in the microcirculation, the vasoconstriction, which can prolong areas of circulation time, and that can lead to infarctions. Many times these infarctions can be in areas remote from where the conducting vessels, the large vessel vasoconstriction, may be seen. So you might see areas of infarction in the distal ACA or distal MCA, particularly the watershed areas, which are not necessarily related to the area of a particular vessel that's in large vessel spasm. They're hard to detect, these different areas of infarction, based on your exam alone, and you may need definitely imaging, serial CT or MRI imaging, to see areas of infarction. And it's thought because there's a hyperactivation of platelets leading to vasocollection of platelets and subsequent vasoconstriction and microthrombi. So another entity that adds to this impairment of neurologic recovery is cortical spreading depression and clustering of cortical spreading depression, which is basically this sort of tsunami that happens to the brain blood vessels as a result of this metabolic disruption to the neurons because of ischemia. With that, you get neuronal swelling, these electrical discharges that basically create a wave of microcirculation spasm and significant neurologic impairment. This is also very much correlated, cortical spreading depression, with patients who become hyperthermic. So another reason why we want to keep patients normal thermic during this time period. Many of these events are basically time course to follow the same time course that we see after an injury, after a trauma. So it's this sort of immunologic response to injury that basically leads to what we see is increase in vasospasm. In fact, if you look at somebody's fever curve, you can actually see a fever low that then precedes delayed vasospasm or delayed cerebral ischemia. With this, it's important to realize many of these patients have a collapse of their ability to maintain autoregulation. Their ability to maintain autoregulation has been impaired because the vessels are now in a dependent state where they depend upon increased circulation, increased mean arterial pressure to allow adequate cerebral perfusion and adequate delivery of red blood cells. They're unable to maintain their cerebral perfusion pressure through a wide range of blood pressures. On the other hand, some patients, especially younger patients, might be hyperdynamic and in their hyperdynamic standpoint may be driving the blood pressure up and also beyond that which is healthy for the brain and lead to increased ICP and decreased brain blood flow as a result. One way to detect outside of the use of transcranial Doppler's has been popularized and that's the use of CT scans and CTA scans. The combination of the CTA scan to look at vessel diameter. This is a bigger load of contrast though than what we typically use for many of our angiograms so it has to be judiciously used. Here's an example of how it's being used, the correlation between M1 and ICA stenosis as you can see on the angiogram. So this is MCA stenosis with vasospasm and you can see it here angiographically in these different zones. So this is like an ideal world, nice publication, but in real world you've got to be very judicious about putting patients through too many CTA scans and have a suspicion that's adequate. So I want to make a distinction here as I mentioned earlier between what we see angiographically as vasospasm which about 70% of patients get versus delayed cerebral ischemia which may or may not be related with these large vessel ischemia. You can have delayed ischemia in areas not affected by large vessel vasospasm. You can have delayed cerebral ischemia with no large vessel ischemia. So realize what we're trying to identify here is basically secondary insult. Not all angiographic vasospasm needs to be treated. In fact if a patient is asymptomatic we usually just watch that patient if they have increasing TCDs but a totally normal exam. We try to avoid hypotension, hypothermia, hypodilemia in those patients but we don't take them to the angiosuite for treatment. So what is vasospasm? By definition it's a narrowing of angiographic visible vessels after a subarachnoid hemorrhage and we usually measure that as mild, moderate, severe based on a matter of thirds. So one-third constriction, two-thirds constriction, near complete constriction being the definition of mild, moderate, and severe. The earliest can be upon presentation if a patient had had a previous sentinel hemorrhage and it presents to you vasospasm or they're going to be hyperacute in patients for three to four days after their initial rupture but typically doesn't peak until the second week, week seven, day seven to ten and usually is resolved by day 21. Now that is contrasted with what we call delayed cerebral ischemia. This is a clinical syndrome of neurologic deficits developing in about one-third of patients. It's a major cause of death and disability. It's just more than the consequence of vasospasm. It's actually cellular death related to events other than just ischemia that we can talk about. Ischemia is not necessarily occurring consistently in these areas displayed by the vessel undergoing spasm. So some of the things that can cause it include this early brain injury that we talked about earlier especially with the weakness of the basal laminar layer of the blood-brain barrier and leaky vessels. The entity known as cortical spreading depression that we touched on already where you have basically this cluster of cellular and electrical dysfunction within the brain that takes over the brain like a tsunami. This metabolic uncoupling where the demand of the cell goes up because of seizures and the blood supply is decreased or internally because the cell's metabolic engine has been disrupted because of mitochondrial dysfunction and cellular injury with electrolyte dysfunctions and cell membrane electrolyte control abnormalities. This is usually something that is primarily in the microcirculation with this loss of autoregulation. You can see edema and disruption blood-brain barrier. So there's a big picture. If we look at vasospasm you know majority of patients won't have symptomatic vasospasm. It's only a much smaller area that has vasospasm that's symptomatic and so this is of all patients with vasospasm versus patients without vasospasm comparison but those who actually have hypoperfusion with vasospasm is in the smaller diagram that you see here and those patients with delayed cerebral ischemia can include both populations. So both populations without evidence of large vessel vasospasm and vasospasm can make up this component and the patients who usually do poor are the patients within this part of the hypoperfusion diagram. So another way to look at this is that we can screen patients and evaluate them with transmural Doppler, CTA or digital subtraction angiography, find a narrow vessel but we can also screen these patients with CT or MRI seeing delayed infarcts and then some patients may manifest ischemic signs as well. So this overlap related to let's say large vessel vasospasm occurs sort of in this area with or without delayed infarcts in this area of the Venn diagram. Now other causes for neurologic deficits have to be evaluated and some of those causes are associated with a rebleed of the aneurysm, hydrocephalus, increased intracranial pressure, metabolic disruption like hyponatremia and other renal abnormalities or infectious causes, hypotension, hypoxia and seizures are also critical. So it's a time course event where you have this aneurysm rupture, you have secondary injury that's ongoing, you have neuronal dysfunction that may or may not be related to large vessel spasm or not. So you have to try to separate out is this in fact related to spasm of the vessel or is this related to another treatable effect which may be metabolic and or infectious or temperature irregulation to prevent tissue injury. So again you have this patient who presents to you has a worsening examination and you're in the process of sorting out what to do next. You take that patient for an angiogram, you take that patient for a head CT, you correct that patient's electrolytes, you try to get that patient a febrile at this point, does that patient benefit from continuous CEG, what should be your next step and that's all dictated based on what you see as a clinician at the bedside putting together your monitors and your patient's exam and imaging. So just to emphasize there is this separation between vessel spasm in general delayed cerebral ischemia and cerebral infarction. So ischemia can be reversible, infarction typically is not. We want to basically prevent delayed cerebral ischemia from progressing to an infarction with the use of appropriate interventions. So we have this sort of tiered approach in neurosurgery that we think of and this is something that we should start thinking of you know in all patients who have subarachnoid hemorrhage as I mentioned before. One of our first tiers of intervention includes that the ABCs followed by basically a ventriculostomy and then the role for induced hypertension, volume optimization with appropriate electrolytes to avoid hyponatremia and then identifying those patients that would best benefit from micro balloon angioplasty and intra-arterial vasodilators. The role for cardiac output augmentation was important for those patients who in fact have symptoms of vasospasm and then optimizing hemoglobin. The role for therapeutic hypothermia, intrathecal vasodilators, those are being you know somewhat debated. What we try to do is avoid fever for the most part. Whether a patient needs these other tier 2 or tier 3 interventions is to be debated. We typically don't go to aortic flow diversion or interaortic balloon pump unless the patient has significant cardiac abnormalities. We use hypertonic saline much earlier as a first and second line therapy early on in the patient's presentation however. So one of the cardiac abnormalities that we encounter in these patients with a subarachnoid hemorrhage and symptomatic vasospasm can be a tachysuppo abnormality. It's a wall motion abnormality that's been described where this wall motion basically leads to the impairment constriction. With this impairment constriction you see that basically you're getting ineffectual contraction of the heart and problems with their generation mean arterial pressure and systolic pressures. Other problems that can be associated with these patients includes that of neurogenic pulmonary edema and hyponatremia as significant secondary sources for brain swelling, injury, and hypoxia. So in our early treatment we talked about again prioritizing airway breathing circulation, maintaining adequate cerebral perfusion with placement of ventriculostomy, imaging to identify the aneurysm and treating the aneurysm, and then becoming very vigilant in surveying for evidence of vasospasm. And we use TCDs on a daily basis as well as patients neurologic examination. We avoid hypertension from the onset until the aneurysm is repaired and then we have permissive hypertension afterwards depending upon the needs of the patient. But the major things that we're trying to avoid as I mentioned earlier include hypotension, hyponatremia, electrode abnormalities such as hypomagazemia, problems associated with hypovolemia, hyperglycemia, fevers as being the essential ones. So in your group of patients you might have a low-risk patient who is a good exam that you can follow. Those patients you don't necessarily need to press or drive their pressures. You keep their fluid balance, IV balance in terms of preventing hypovolemia, but you don't need to necessarily be driving their blood pressure or volume status. Now you have another group of patients who are high-risk. They might have an exam you can follow or those that are high-risk who don't have an exam that you can follow. And it's these high-risk patients that do not have an exam that you can follow as well where we'll talk about the role for multimodal monitoring. It doesn't make sense to place a monitor on a patient who is awake, alert, following commands, but it certainly makes sense in a patient who's basically a tundid comatose or who has minimal exam and especially patients who are intubated. We'll go through some case examples to sort of walk through how we treat actual individual patients using TCD criteria and that's easier to follow than these boxes here. One of the things you have to separate out though is is the patient's exam deteriorated because of seizures or other neurologic events outside of ischemia. So in terms of guidelines, class 1 guidelines, oral nemotapine is one of our go-to agents that we use. It doesn't necessarily decrease large vessel vasospasm, but it does decrease the incidence of infarctions that are seen on follow-up. Not all patients can tolerate this. In fact, we have groups of patients who even with divided dose become hypotensive. So in those cases we tend to hold it and then attempt to re-administer it once their blood pressure is adequate. For patients with ruptured aneurysms, it's best that we evaluate them for both the role for endovascular first and neurosurgical clipping second. Why we say that is because the outcomes are better in these patients. We can treat them endovascularly and opposed to craniotomy where they will have brain retraction and a more prolonged procedure done with an endovascular approach. We shoot for uvulemia and normal circulating volume from the beginning. If the patient has evidence of radiographic delays through of ischemia or deficits, we try to elevate the patient's blood pressure and augmentation. In those patients, we typically will use a combination of hypertonic saline as well as pressors. There is no role for prophylactic hypervolemia or balloon angioplasty before they develop symptomatic vasospasm. It doesn't do the patient any good. In fact, it may add to neurogenic pulmonary edema with hypervolemia and with balloon angioplasty is significant risk in asymptomatic patients. We do, however, perform angioplasty and selective urinary-territorial vasovirilator therapy for patients who are developing symptoms or we have secondary evidence of ongoing brain injury or ischemia. So in terms of general care, we have frequent neuroexaminations. We elevate head of bed. We have strict eyes and nose and measurement of weight. We try to have an A-line in these patients, especially during the period that we're using blood pressure augmentation and ICP monitoring in the sickest patients. Daily H&H, chest x-ray, frequent EKGs to ensure they're not having any cardiac abnormalities, avoiding acidosis and hypoxia, rule out anemia, and hyponatremia. We tend to follow their sodiums very closely. The CT of the head is frequently obtained post-correlating after the aneurysm has been secured and then as we're managing the patients, hydrocephalus, and then also in a delayed fashion looking for evidence of delayed edema or delayed evidence of delayed cerebrovascular ischemia. So we typically don't use statins, albumin, or steroids in the majority of patients who are prolonged or acutely. We might use steroids in a short-term phase for maybe 24 to 72 hours. We do use IV nicartepine but more as a blood pressure control agent and not to treat vasospasm. There's been some interesting clinical work that has been done with the use of heparin infusions. We typically don't heparinize our patients except for those patients who are undergoing endovascular procedures but we don't prolong the heparinization post-coil on treatment of the aneurysm. The most important thing is a neurologic examination. Many times we have to forego the examination either for their lungs or because of ICP issues by identifying is that patient symptomatic because of problems with ACA, MCA, PCA, or vertebral basilar abnormalities and correlating changes in the examination becoming incredibly sensitive, especially for patients who don't have bone windows to allow transcranial Doppler. Multimodal monitoring, we try to pair together then our monitoring of patients with both transcranial Dopplers, ICP monitoring, brain tissue oxygen monitoring, as well as other forms of monitoring such as pupillometry to try to come up with what is the pattern, what is the mosaic of brain injury that this patient has. Back in the old days it was very difficult because we had multiple different separate monitors with multiple different separate probes. They were not very good at early detection. They were not very specific or sensitive. They were not continuous or highly spatially resolved because there's a focal area. We've gotten much better over time. We now have a monitor we're using here. I'm showing one of our PAs. Sarah put this in. This is back in 2014, I think. Now the PAs all put in these monitors for us. It's a plastic bolt. It has both brain tissue oxygen capability monitoring as well as brain temperature and ICP. We get a three for one. It gives us data about regional ischemia. This shows you, the next slide will show you a picture of it actually in place. The ventriculostomy goes in first and then this monitor goes in anterior to that, in this case, to monitor the anterior watershed. It becomes very helpful in this particular patient. You see a very low brain tissue oxygen, although ICP is normal, so we're able to augment, drive the patient's mean arterial pressure up and fluids up to help potentially underlying ischemia. Our go-to for vasospasm, though, has been transplanetal dopplers. This is a patient who has severe vasospasm. You hear that characteristic sound of vasospasm in this particular patient where there's basically, this is the posterior circulation, in this case, the vasoartery up to 104 mean velocities. Just back up for a second. This patient also had evidence of ischemia associated with Lycox. This is Lycox monitoring and also had elevated brain pressure. The brain oxygen dipped down, the brain pressure elevated up and above 20 in this particular case. A lot of that was also related to an episode of hypotension. This is, again, some hypotension, but a drop in the CPP because of this increasing ICP and concomitant drop in the patient's blood pressure. This is actually after the patient had undergone a decompressive craniectomy. The patient did not have vasospasm, but did have, in this particular picture up here, did have evidence of increased ICP. By doing a hemicraniectomy, we're able to see a marked improvement in brain oxygen and a reduction in the ICP. By following trends, we're able to see changes over time in terms of velocities. That's very important to characterize what the patient's status is in terms of risk for subsequent vasospasm. This shows severe vasospasm from the TCDs that were just done that you had seen. This is the left vertebral artery that's injected with vasospasm involving mainly the basal artery as a proximal source of spasm. There's also some spasm involved distally in the distal PCA, and that was treated concomitantly with the use of interarterial paraffin. This is a lateral projection of that particular patient showing, again, vasospasm involving the vertebral basal junction as well as the mid-basal portion. This is after both paraffin mill treatment as well as the use of lumen angioplasty. I have a series of cases that we can go into next, but I want to first see if there's any questions thus far what we talked about. We do have multiple questions here, actually. We have three minutes left, unfortunately, so we might just get to a couple of these and then have you do some cases when you come back for the Q&A, if that's okay. Okay, so one question. How often do you do TCDs? So we do TCDs on a daily basis to include weekends, holiday, usually once a day for most patients. We will repeat the TCDs after a patient undergoes treatment. So if a patient has TCDs at six in the morning, undergoes a treatment, we do get another set of baselines. Just out of curiosity, who does your TCDs? Do you have a dedicated team for that? That's right. We have a dedicated set of radiologic technologists who are ultrasound technologists who are all VASCR certified. There's a group of four of them. They're very, very good. They've been doing it here for about 10 years now, and it's very operator dependent. So we know them by first name basis, and it's very important to know who does the TCDs and if the technologists have changed from one day to the next. Yeah. Okay, great. This one's a little bit more involved, though. Skip that one till later. So how about patients who have aneurysmal subarachnoid hemorrhage and fever and kind of determining, you know, at what point do you say that their fevers are central versus infectious with their etiology? How many, like, you know, how many sets of cultures do you do over and over before you say, okay, fine, this is central kind of thing? Yeah. So we start out with a baseline set of cultures with the first fever, and then we treat, you know, appropriately. We also look at what their white count subarachnoid CRP is in some cases. We also test CSF for evidence of ventriculitis as well as part of that initial workup. And then many of these patients, that will be negative, and then we'll just implement, you know, basically a therapeutic normalthermia. So we try to start with normalthermia for all patients, but if they start spiking beyond that, then we go and get more aggressive with treatment, make sure we're not missing an infection, but we don't necessarily work them up every single time that they spike a fever. Got it. Okay. All right. I think that's all that we have time for right now. So what I will do, like I said, I'm going to screenshot these questions for the Q&A session, and then you can bring your cases too, and you and Dr. Leibman can kind of go back and forth, starting at 345 Central. That's 445 for me. Great. Perfect. Thank you so much, Dr. Armando. That was an awesome talk. I know it's definitely generated a lot of interest here, so we'll have a good discussion when you come back. You're welcome. Thanks, Rob. All right. See you soon. All right, everybody else, we're going to go to our next talk about management of the unstable ICU patient. I'll see you there in a minute.

cerebral vasospasm

subarachnoid hemorrhage

early intervention

secondary brain injury

angiographic vasospasm

delayed cerebral ischemia

systemic effects

cardiac dysfunction