SCCM Resource Library-Year in Review: Neuroscience

Video Transcription

Thank you for the invitation to participate at the SCCM, and thank you, George, for organizing the yearly review.  My name is Jose Suarez, and I will speak to the Curing Coma Campaign. The actual logo of the Curing Coma Campaign, so what we're trying to do is we're trying  to promote recovery of consciousness through early intervention and long-term support. The outline of my talk, I'll start by defining what coma means, and then look at the coma  ecosystem, the cost of coma, and then we'll go over and try to answer some of the compelling questions about coma, and hopefully I'll give you a little bit about the background and  the history of the Curing Coma Campaign. So obviously, when it comes to the definition of coma, what we're referring to is a lack  of awareness of self with an inability to interact with and respond to one's internal and external environment.  So essentially, coma is a disorder of consciousness, so the person is not awake, the person is  not aware, the person is unresponsive, and there are many causes of coma, including traumatic brain injury, stroke, heart attack, severe infection, seizures, or drug overdose.  The coma ecosystem essentially includes many stakeholders, so not only patients, but also  families, physicians, nurses, therapists, hospital administration, and of course, government services as well that take care of patients.  Needless to say, coma is associated with a very high cost, both human cost and also society cost.  So for example, if you look at TBI, there are over 55,000 deaths a year in the U.S., and also there is a lot of withdrawal of life support that occurs in patients with coma.  There is a nihilistic approach to treatment of these patients, and as you can see, it costs a lot to society. It's estimated that the cost of coma exceeds $75 billion.  So obviously, there are compelling questions that families ask us every day that we take care of patients in coma. One of them is, will my loved one wake up?  And if so, when will my loved one wake up? And will they fully recover from the coma? These are the questions that we get, which we don't have any easy answers, because we  have a lot of gaps that we need to answer to in order to answer these compelling questions.  Whether it's a lack of knowledge of the biological basis of consciousness, that's a million-dollar  question, and this is being called the heart problem, you know, how do we define the biological underpinnings of consciousness?  There's a lot of variability when it comes to patient assessment. Patients are not that great at prognosticating, and the treatments are inconsistent, and patient  care is also inconsistent. So obviously, these are the needs when it comes to finding a cure for coma, right?  We need to identify the key insights into why science hasn't yet solved this problem.  We need to determine the scope of the research that is needed to address this problem, understand  what capabilities are currently available, identify the new capabilities that we may need, also scope out the resources required, break down the barriers that exist to address  this problem, define the risks and how they can be mitigated, and, of course, develop an action plan. Why has curing coma not yet been solved?  And obviously, there are many issues related to this here. One is because the problem had not been clearly defined before.  There was no ability to identify the type and location of the defects that these patients have, the lack of the appropriate diagnostic tools, and, of course, you know, researchers  have also worked in silos up until now. Now, with the Curing Coma Campaign, we're all coming together, right?  And the research team did not include everyone, so it did not always include patients, did not always include families or therapists or clergy or healthcare professionals.  There is obviously a lack of appropriate funding, and up until now, we did not have a champion or someone driving this.  So obviously, the Neurocritical Care Society took a bold initiative and launched, in 2019, the Curing Coma Campaign to try to address all this.  So everything started back in 2018, you know, when we had the fifth Neurocritical Care Research Conference that was set up in Boca Raton, Florida, and we were trying to look, trying  to define the future of Neurocritical Care Research, and we were really looking for a blue ocean. By that, we meant we wanted to swim in blue water.  So we didn't want to swim in red waters, you know, infested by sharks where everybody was competing for the same funding and for the same type of research.  We wanted to create something new. So we brought a bunch of scientists, you know, together, in total, there were 103 that met,  and then we tried to define the future, and then we came up with the idea that perhaps we should try to answer. So how is this problem being addressed at the moment?  So obviously, we wanted to have sort of a disciplined program management. We wanted to define technical tasks with specific milestones and deliverables, improve  the communication to keep all that, everybody that is interested in this area, to keep them well-informed, and of course, form some teams with complementary skills.  So we got together, and we tried to frame the initial scientific challenges. So we actually published this in a white paper in 2020.  The proceedings are our first Curing Coma Campaign Scientific Advisory Council. So what about the program management? How do we address this issue?  So obviously, we had to create committees. So we had six members that were part of the executive committee member, and I'm one of them.  Then we had to create scientific student committee members. We have 12, and then over 30 scientific advisory council members. And of course, we needed a program manager to help us.  So thank you, Connor Burton. So we have eight. I created eight mission control modules. So as you can see there on the slide, you know, there's several modules that have specific  tasks, you know, like engagement, community, collaborators, member sites, prospective data,  coma data science, expert, liaison, implementation science, and people that were going to help us also develop an investigative toolkit, right?  We all have objectives and milestones that have been established to make sure that everybody understood what they needed to do.  We have seven scientific advisory council working groups. As you can see, one of them is in charge of the deep dive science, common data elements,  prospective studies, patient care, existing data, rules of engagement, and funding. So we also have obviously all the technical tasks, you know, deliverables, and of course,  with the scientific tasks, you know, that a group of investigators that were charged with setting up the endotypes of coma, also helping us out with biomarkers, the proof  of concept of clinical trials, and finally, data analytics. So as you can see, this is a very complex, you know, tasks that need to be addressed.  And for that, we needed to create people to help us. So we also, with the early deliverable technical goals, of course, we're from the endotype,  we wanted to identify endotypes that will be amenable to treatment. That means going beyond the phenotype.  We wanted to cluster a group of patients that perhaps will respond to certain treatments and not others, right?  We also wanted to develop more of these biomarkers to correlate the endotypes with the clinical  outcomes, and also come up with more innovative proof of concept clinical trials for these patients. But of course, we also needed to create the infrastructure.  And for that, we needed to reach out to multiple societies over five continents. This problem, obviously, the care of the coma patient is also an important problem, right?  A problem to solve, because there is a lot of variance and a lot of variability. There is no, there is a lot of confounders, you know, that we obviously need to identify.  We also need to identify and prioritize targets for scientific discovery in key domains, right?  Like timing of the intervention, assessments, the technology, the clinical expertise that is needed, and also along the continuum of care, right?  Not only during the acute hospitalization, but also beyond. We needed to sort of tie everything in and not have people work in on one aspect of it.  So, for example, not just rehabilitation, but also what about acute intervention, that was also important. We also thought that it will be key to come up with common data elements.  And for this, we are actually partnering with NINDS, similar to the other NINDS projects for common data elements that we have worked with.  The idea behind this is that we want to make sure that we have common content standards  that will enable us to do clinical investigations, to systematically collect, analyze, and share data across the research community.  We wanted to make sure that regardless of where in the world these investigators are located, at least the language will be similar under this.  Obviously, we also needed a deep dive into the science of coma, you know, to essentially define the unmet science and trying to develop tools and how to dive into the science of  coma, right? So, obviously, we have five domains or five subgroups that are working into this.  As I mentioned before, classification of phenotypes, biological mechanism, prognostication, therapeutics, and precision medicine.  And obviously, we have set up gap analysis for those. We also thought that we needed to come up with a prospective study group that will help  us create a prospective site to attempt to define coma better and the gaps. And of course, we also needed to address and get the message across.  So, obviously, having the common data elements is a way to do it, right, reaching out to all the investigators to use a common language.  We also needed to publish several white papers, which we're doing right now. We have also set up the World Coma Day, and I'll show you, we'll have a slide for that.  Also, a website needed to be set up, and we needed to reach out to funding agencies. So, we have reached out to NIH.  We have secured funding from them to have this Curing Coma virtual symposium. Of course, it was in the middle of COVID. We have two meetings.  The first one is September of 2020, and then the follow-up meeting in May of 2021. We've also set up World Coma Day. We have picked March 22nd of every year to be World Coma Day.  So, we had a successful World Coma Day in 2021. Now, this will be the second World Coma Day in 2020. So, we also needed to form the problem, and I think we have. We have done this.  We have teaming agreements. We have a diversity, a group, we're very inclusive, so we're essentially moving forward with this.  We have rigorous, regular reviews of milestones, and we're adding expertise to fill the gaps. We have regular updates to the NCS and also NIH seeking funding.  So, this is essentially the take-home message. Much has been accomplished since the announcement of the Curing Coma campaign in October 2019  at the 17th NCS Annual Meeting in Vancouver. We have many field leaders and NCS members that are actually involved in propelling this colossal mission.  The goal of the campaign is to remain inclusive, like sort of the moonshot culture, adaptable, we learn as we go, and available, so the global platform for coma science.  And if you're interested in more information, you can find that in our website at curingcoma.org. That's where you'll find all the information.  And again, this is just a summary of the overall structure. As you can see, we have mission control with the steering committee. We have an advisory council.  We have working groups, and we have modules. Each one of those are actually have a specific task, and yes, there is some overlap specifically  with the prospective study groups because we have to include information from both the working groups.  So these are the members of the mission control, of which I'm a part of it. This is a big tag. There's a lot of investigators.  These are the leaders from the working groups, so you can see we're very diverse and inclusive and from different areas of the world.  And these are the modules, the lead participants in the modules that we have. The volunteers who are asking you to join the Curing Coma campaign, please visit www.curingcoma.org.  And if you have any questions, I'll be more than happy to answer them. Thank you very much for giving me the chance to talk to you about Curing Coma, and I think  we have a few minutes for questions. Thank you.  Good morning. My name is Eljam Tesoro. I'm a clinical pharmacist at the University of Illinois Health.  And a clinical associate professor at the College of Pharmacy at the University of Illinois at Chicago.  Today, I am presenting at the neuroscience section, Year in Review, and we'll review three articles specifically related to pharmacotherapy in neurocritically ill patients.  The objectives for this talk are to describe the potential role of milrinone in aneurysmal  subarachnoid hemorrhage, examine the safety and efficacy of 23.4% sodium chloride administered  peripherally, and compare nicardipine to clofidipine for blood pressure control in intracranial hemorrhage.  Cerebral vasospasm is a considerable complication in aneurysmal subarachnoid hemorrhage, leading to significant morbidity.  Endovascular therapies, such as intraarterial vasodilators and angioplasty, carry considerable  risks and may not be available everywhere. Milrinone, a phosphodiesterase-3 inhibitor with cerebral vasodilatory properties, has  been proposed as a treatment approach for vasospasm in conjunction with vasopressors. This single-center observational before-and-after study compared the combination of milrinone  with induced hypertension to induced hypertension alone in aneurysmal subarachnoid hemorrhage patients.  441 patients were prospectively followed on milrinone therapy and compared to historical control. Both groups received induced hypertension with vasopressors per local protocol.  Milrinone was initiated at a dose of 0.5 micrograms per kilogram per minute and titrated to a maximum dose of 1.5 micrograms per kilogram per minute.  There is no difference in age between the two groups, and most of the patients were women.  The majority of the patients were either Fischer 3 or 4, indicating a higher risk of cerebral vasospasm.  There is no difference in median ICU length of stay or hospital length of stay. There is no difference seen in 6-month mortality between the two groups.  Milrinone did seem to prevent a higher number of patients from requiring angioplasty versus the control group.  There were more patients with a good outcome, defined as a modified Rankin score of 0 or 1, which was statistically significant.  Milrinone seemed to have a lower 6-month functional disability and vasospasm-related brain infarctions with an adjusted odds ratio of 0.28 and 0.19, respectively.  Because of Milrinone's hypotensive effects, it was discontinued in about a third of patients. Despite this, Milrinone has some promise in improving clinical outcomes in aneurysmal  subarachnoid hemorrhage patients, especially if vasopressors can be used to mitigate systemic hypotension.  23.4% sodium chloride is used to treat cerebral edema, elevated intracranial pressures, and transcentorial herniation.  Due to its high osmolarity of over 8,000 milliosmoles per liter, it is recommended to be administered  via a central line to prevent thrombophlebitis, injection site pain, and tissue injury or necrosis if extravasated.  However, peripheral catheters are easy to insert and do not have the complications that are associated with central lines and allow for timely administration of emergent therapies  that may be lifesaving. This retrospective cohort study compared the safety and efficacy of 23.4% sodium chloride  given peripherally and centrally for the treatment of cerebral herniation and malignant ICP elevations.  90 patients received 23.4% centrally, and 51 patients received it peripherally. Most patients were admitted with traumatic brain injury or intracranial hemorrhage.  Each 30 mL dose of 23.4% sodium chloride was administered over 10 minutes as a slow IV push. In terms of safety, only two adverse events were reported, both in the peripheral group,  one extravasation, and one patient who complained of pain during administration. There was no differences in death rates between the two groups. Both agents were able to decrease  ICP in a similar fashion. The peripheral group had a higher drop in mean arterial pressure compared to the central group. And both groups had expected increases in serum sodium.  Both groups, interestingly, saw a drop in hemoglobin with the peripheral group seeing a statistically higher drop in hemoglobin when compared to the central group.  The etiology and implications of this finding are unknown. The results of this study indicate that 23.4% sodium chloride may be safely given peripherally in emergent situations.  Although promising, the safety of peripheral administration of scheduled doses of hypertonic saline still remains to be evaluated.  Clavidipine and nicardipine are two parenteral calcium channel blockers that can be used as continuous infusions when controlling blood pressure in neurocritically ill patients.  Previous studies examining these agents have been done in ischemic stroke patients, but this is the first study published that evaluated their use in intracranial hemorrhage.  Uncontrolled blood pressure in these patients can lead to hematoma expansion, re-bleeding, and poorer outcomes. This was a retrospective observational study  at a single hospital with the primary outcome of time to goal systolic blood pressure.  This table highlights some of the differences between clavidipine and nicardipine. Both are considered calcium channel blockers,  with clavidipine being our newer third generation calcium channel blocker and nicardipine being an older second generation calcium channel blocker.  Clavidipine has a shorter onset of action at two to four minutes, while nicardipine's onset of action is 10 minutes. Because of clavidipine's short half-life of about one minute,  it can be rapidly titrated to goal versus nicardipine, which has a half-life of eight hours. The standard concentration of clavidipine is 0.1 milligrams per ml, and this is  formulated as a lipid emulsion. Nicardipine's standard concentration is typically 0.5 milligrams per ml and can be diluted in either D5W or normal saline.  Clavidipine can be initiated at one to two milligrams per hour and then doubled every 90 seconds until near goal, then every five to 10 minutes up to a maximum rate  of 32 milligrams per hour. Nicardipine can start at five milligrams per hour and then titrate by 2.5 milligrams per hour every five minutes up to a maximum dose  of 15 milligrams per hour.  When looking at the primary outcome of minutes to systolic blood pressure goal, we can see that there was really no difference between the nicardipine group and clavidipine group  in the unmatched comparison. When the two groups were matched by propensity score, there still was no statistically significant difference  between the minutes to achieving systolic blood pressure goal. In terms of rebound hypertension, which was defined as a systolic blood pressure that  exceeded the goal within eight hours, there was a higher amount of rebound hypertension seen with clavidipine versus nicardipine, and this was statistically significant  and can be explained by clavidipine's lower half-life. The incidence of bradycardia was not seen to be statistically significantly different between the two groups.  However, when looking at the total volume of infusion that was given to patients, we see that nicardipine was associated with about 1.4 liters versus 300 cc's  for clavidipine, which is statistically significant. And this is very common, as we see nicardipine is associated with a very high fluid load, even when double concentrated.  Looking at cost in dollars, nicardipine was about $100 per patient versus $500 with clavidipine, and this was statistically significant.  In looking at some of the other outcomes from this study, we see that there was no difference in all-cause mortality, with a mortality rate of about 25%  seen in each of these groups. There was also no difference in hematoma expansion between the two agents. Both groups required additional antihypertensives  to attain their blood pressure goals. There was no difference in ICU length of stay or hospital length of stay seen in between the two agents.  So in summary, nicardipine and clavidipine both are able to attain blood pressure goals in intracerebral hemorrhage patients.  Nicardipine has the advantage of less rebound hypertension and a decreased cost, while clavidipine has the advantage of less fluid requirement.  The results of this study should be taken with caution as the study was underpowered.  To summarize this Neuroscience 2022 Pharmacotherapy Year in Review, milrinone may improve outcomes in aneurysmal subarachnoid hemorrhage patients if patients can tolerate it.  Peripherally administered 23.4% sodium chloride appears safe when given emergently and lowers intracranial pressure similarly to when given centrally.  And finally, clavidipine and nicardipine appear equivalent in attaining systolic blood pressure goals in intracranial hemorrhage patients.  Thank you for your attention in this session. If you'd like to contact me, you can use my email etesoro at uic.edu or follow me on Twitter at etnccrx.  Good morning. I'd like to take this opportunity to thank Dr. Lopez and the Society of Critical Care Medicine Annual Conference Planning Committee  for this opportunity to speak with you today regarding the research highlights in Neuroscience 2021. My name is Susan Yanker and I work as a lead nurse practitioner  in neurocritical care at the Ohio State University Wexner Medical Center  in Columbus, Ohio, United States. I have nothing to disclose except for I am the secretary of the Neurocritical Care Society and I serve as an ambassador  to the World Federation of Critical Care Nurses. The objectives of today's lecture are to provide an overview of select neurocritical care manuscripts.  It's just gonna be a scratch of the surface and give you a little bit of a flavor of what's occurred in 2021. The following is an overview of the search process  that I used in order to present the presentations that I am providing with you today. Short version is I tried to pick articles that might be of interest.  I'm gonna start with the patterns of benzodiazepine underdosing in the ESAT trial. The primary outcomes that were observed in this were drug dose route and setting  of first-line benzo use in status patients. The secondary outcome was to take a look at the association between that benzodosing against the primary outcome and seizure cessation.  The population of focus were ED patients that were refractory to adequate first-line benzodosing and were also enrolled in the ESAT trial.  Of the 460 patients that were included in this study, 1,170 benzodiazepine doses were given. The most frequently prescribed medication was lorazepam  and in all drug categories intravenous route was the most likely to have occurred. The emergency department was the most frequent setting where these drugs were administered  and adults were most commonly treated in this study. Of note, diazepam was more frequently administered prior to EMS.  The guidelines for recommended dosing were taken off of the European Federation of Neurological Society, the Neurocritical Care Society and the American Epilepsy Society.  The ESAT criteria for minimal adequate dosing included diazepam 10 milligrams, lorazepam 4 milligrams  and midazolam 10 milligrams with weight-based dosing for less than 32 kilograms.  This is a distribution of first dose for each drug and you can see in the fixed weight category in all of the diazepam, midazolam and lorazepam categories,  there was underdosing in each one of these areas. Additionally, in the weight-based dosing while there was improvement in getting to the appropriate dose,  underdosing still occurred.  In looking at the distribution of dosing in all benzodiazepine categories, the underdosing occurred more frequently and often in the midazolam and the lorazepam categories  with improvement in the diazepam category. There was a delay to adequate dosing of six minutes and up to 20 minutes and the median delay of onset of status  to first dose of benzo was 27 minutes and up to 49 minutes long.  Though not an international trial, it did include 57 United States sites. It was limited to ESAT enrolled patients which may have overestimated underdosing.  There was a planned educational underdosing intervention  after the first 200 ESAT patients were enrolled. This may or may not have impacted the results of this study. When patients are admitted to the emergency room,  it's not always clear if the patient is in status which may have resulted in some of the delays. But in conclusion, the study noted underdosing of benzodiazepine  and reflects the fact that we as providers may require more collaboration and education with our emergency department colleagues to try and help assist with timely intervention  related to status epilepticus.  In the next study, we'll review hypothermia versus normothermia in out-of-hospital cardiac arrest patients. This open label blinded assessment randomized control trial  looked at out-of-hospital cardiac arrest patients that were adults and had at least 20 minutes before ROSC was achieved. Patients were excluded if ROSC was greater than 180 minutes,  if the arrest was unwitnessed, and if asystole was the initial rhythm. The intervention included hypothermia of 33 degrees or target normothermia where no intervention was provided  unless the patient's temperature was greater than 37.8 degrees. Primary endpoints were death with secondary endpoints of modified Rankin scale.  Adverse effects that were also tracked included pneumonia, sepsis, bleeding, arrhythmia with hemodynamic compromise, as well as skin issues related to cooling devices.  Randomization occurred and patients were cooled for 28 hours after this. And at 96 hours post-randomization, a physician provided a neurologic assessment of the patient.  This is a figure that demonstrates the body temperature during the intervention period.  Of the 1,850 patients, you can see that the probability of survival was unchanged between the groups. And then looking at death at six months period of time  as it looks in subsets of patients between sex, age, time from ROSC, as well as initial rhythm and shock on admission, there were no differences between mortality at six months.  Looking at modified Rankin scale at six-month period of time, you can see there were also no differences between the groups.  Specifically looking at the serious adverse events in this study, the only one that was statistically significant was arrhythmia resulting in hemodynamic compromise.  The results of this study do show a difference from the 2002 trials looking at hypothermia. It is an international multi-site study. There was a degree of temperature overlap  during the time of the study period. Coronavirus did impact the modified Rankin scale evaluation. It ended up going into a binary look at this.  It went from good, which was zero to three, and poor, which is four to six because of the impact of visitation, as well as accessibility to patients.  While the staff were aware of the actual intervention, the physician assessors, as well as authors and statisticians were blinded. In conclusion, hypothermia did not decrease  the incidence of death or improved modified Rankin scale at six months. The final study I'd like to discuss with you is the BP-TARGET-C.  This was a multi-center randomized control trial in four academic medical centers in France. It involved adult patients with anterior circulation thrombus  that achieved TIKI2b or three revascularization. Patients were excluded if there was hemorrhage during the procedure, if there was a spontaneous blood pressure  of less than 130 post-procedure, and if the patients had a poor modified Rankin scale going in or if they had severe comorbidities such as malignancy.  The intervention included intensive blood pressure management to less than 128 or standard blood pressure management of 130 to 185.  This needed to be achieved after one hour of randomization and it needed to be maintained for 24 hours. Primary outcomes included radiographic  interpregnable hemorrhage at 24 and 36 hours, utilizing the classifications listed, the occurrence of hypotension. Secondary outcomes included modified Rankin scale  and all-cause mortality at three months. Feasibility was looking at whether or not the blood pressure can be maintained at less than 130 at 24 hours  and adverse effects such as ICH rates, hemicrane, mortality, and CVA worsening were also noted. So the intervention included non-invasive blood pressure cuff monitoring,  utilizing the following protocol. Nicardipine was recommended as a first-line medication. However, it was not required. If the spontaneous systolic blood pressure post-ETV  was less than 130, they did ultimately end up accepting that. It was a scan double-blinded independent radiologists that would review the images.  And if there were hyperdensities noted on the CAT scan at 24 and 36 hours, a follow-up scan at 72 hours was completed in order to ensure that interparenchymal hemorrhage  was present. At three months time, there was a telephone or in-person visit to take a look at modifying Rankin scores as well as serious event evaluation.  Patient characteristics were similar in both groups as well as the mean systolic blood pressure before ETV.  In looking specifically at the different groups, the all-cause mortality was without difference between the two groups. There was no difference between the symptomatic ICH  at 24 and 36 hours between groups. And there was also no difference between the modified Rankin scores between these two groups. This specifically takes a look at, again,  the mortality within three months that did not show any changes. And there was no difference between the hypotensive events between the intensive and normal-tensive groups.  They had a planned subgroup analysis that took a look at age, stroke location, and the administration of TPA. And again, there was no difference between those subgroups.  Between groups, you can see that 60% of the time, the patients were within the desired blood pressure range. In the intensive group, 83% of the patients received  an antihypertensive medication compared to 20% in the standard group. So in discussion, this was a randomized control trial  that was completed in France for academic medical centers. During the evaluation of blood pressures, non-invasive blood pressure monitoring was utilized.  And the frequency between different measures may have impacted the results. There was 30% crossover from the intensive and standard blood pressure goals.  Obviously, CAT scan is less sensitive for picking up on the interparenchymal hemorrhage. However, they tried to account for this by utilizing the follow-up CAT scan at 72 hours.  There was a very small range between what was considered intensive and standard. In conclusion, intensive blood pressure monitoring  less than 130 following ETB was not supported in this trial. It's the first randomized control trial looking at blood pressure control in ETB patients.  It does demonstrate that more work is needed, and we look forward to hearing more from the ENCHANTED2 and BEST2 trials on what that might look like.  Thank you very much for your time, and I can be reached at this email address should you have additional questions.

Video Summary

In a video presented at the SCCM 2022 conference, several research studies in the field of neurocritical care were highlighted. The first study focused on benzodiazepine underdosing in patients with status epilepticus. The study found that there was a significant underdosing of benzodiazepines, particularly in the midazolam and lorazepam categories, and a delay in the administration of these medications. This highlights the need for better education and collaboration between providers to improve timely intervention for status epilepticus. <br /><br />The second study compared hypothermia versus normothermia in out-of-hospital cardiac arrest patients. The study found that there was no difference in survival or neurological outcomes between the two groups. This contrasts with previous studies on hypothermia for cardiac arrest, suggesting that more research is needed in this area. <br /><br />The third study examined blood pressure management in patients with anterior circulation thrombus. The study found that intensive blood pressure management to less than 128 did not result in better outcomes compared to standard blood pressure management. There were no differences in mortality or neurological outcomes between the groups. <br /><br />Overall, these studies provide important insights into the management of status epilepticus, hypothermia for cardiac arrest, and blood pressure management in patients with anterior circulation thrombus. More research is needed in these areas to further optimize patient care.

Asset Subtitle

Professional Development and Education, Neuroscience, Quality and Patient Safety, 2022

Asset Caption

This session will highlight the latest research, lessons learned, and changes taking place in critical care neuroscience as they may apply to clinical practice. Topics covered include the Curing Coma Campaign and diversity and inclusion in neurocritical care.

Learning Objectives:
-Describe the Curing Coma Campaign initiative
-Illustrate diversity and inclusion initiatives in neurocritical care
-Appraise the latest research trials in the field of neurocritical care and how they may apply to clinical practice

Meta Tag

Content Type Presentation

Knowledge Area Professional Development and Education

Knowledge Area Neuroscience

Knowledge Area Quality and Patient Safety

Knowledge Level Foundational

Knowledge Level Intermediate

Knowledge Level Advanced

Membership Level Select

Tag Professional Development

Tag Coma

Tag Evidence Based Medicine

Year 2022

Keywords

neurocritical care

benzodiazepine underdosing

status epilepticus

hypothermia versus normothermia

out-of-hospital cardiac arrest

blood pressure management

anterior circulation thrombus

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