Transcript
Speaker: Welcome to Critical Matters, a sound critical care podcast covering a broad range of topics related to the practice of intensive care medicine.
Speaker: And now, your host, Dr. Sergio Zanotti.
Speaker: Today we have a very interesting topic which relates to neurological prognostication after cardiac arrest.
Speaker: And I'm very honored and pleased to have as our guest, Dr. Fred Rincon, who's Associate Professor of Neurology and Neurological Surgery at Thomas Jefferson University and a neurointensivist of the Division of Neurotrauma and Critical Care, Department of Neurological Surgery.
Speaker: Fred, I think, is not only a dear friend, but perhaps one of the most qualified people to talk about this topic.
Speaker: Fred has done extensive training and is board certified in internal medicine and critical care medicine through the American Board of Internal Medicine in neurology, vascular neurology, and neurocritical care.
Speaker: In addition, he has a master's in public health and bioethics and is a fellow of the American College of Physicians, the American College of Chest Physicians, and the American Heart Association and a member of several critical care and neurocritical care societies.
Speaker: I am very
Speaker: Honored and happy to have a good friend on the podcast today.
Speaker: Welcome, Fred.
Speaker: Thank you, Sergio.
Speaker: Thank you for having me here.
Speaker: So I think that this is obviously a topic that is dear to your heart, and you've seen both sides of the coin, both as your critical care internal medicine training, but also your neurology and neurocritical care training.
Speaker: And I think that ultimately, it's also an area that has evolved significantly in the last decade.
Speaker: So as all of us are aware, the outcomes of patients who suffer out of hospital and in hospital cardiac arrest are still devastating.
Speaker: And even though we call it cardiac arrest, the true issue is anoxic brain injury.
Speaker: And that's what ultimately determines how these patients who survive do in terms of returning to a meaningful life.
Speaker: So Fred, as we start exploring and diving into how do we most accurately
Speaker: predict or tell families what to expect from a neurological standpoint after a loved one has undergone or had a cardiac arrest.
Speaker: I would like to just ask you in general terms, where do you stand today in terms of targeted temper management and therapeutic hypothermia?
Speaker: What are you doing in your practice for a patient who has a V-fib arrest out of the hospital, is brought to the hospital, and after return circulation is not waking up or is comatose?
Speaker: Sergio, I think that I agree with you in everything that you mentioned before is a devastating condition and at the end of the day, what matters is how you would survive or how would the patient survive.
Speaker: At the end of the day, it's really how much brain injury the patient sustained.
Speaker: So when I deal with these patients in my practice, the first thing that I keep in mind is probably not to rush to conclusions too early in the onset of the disease.
Speaker: So the first message would be,
Speaker: wait, really don't try to prognosticate early on and the reason for that is because of the advances in resuscitation medicine that have not happened only in the intensive care unit or pre-hospital level.
Speaker: So the pre-hospital level we have better access to AED, CPR, bystander CPR because of all the campaigns that have happened in terms of
Speaker: bystander education.
Speaker: We have better technologies now.
Speaker: AEDs are primarily the ones that probably are saving a lot of lives.
Speaker: And then the access to the chain of survival that we all learned when we were taking our ACLS.
Speaker: So all those variables have contributed to a change in the outcome of this condition.
Speaker: So many patients are surviving now more after they arrive to the hospital after cardiac arrest.
Speaker: And the second thing are the advances in critical care, as you mentioned.
Speaker: Primarily,
Speaker: a neuroprotective strategies that were tested in clinical trials recently and that have demonstrated improvement in survival and functional outcome, primarily temperature management.
Speaker: So because of all of that, right, you have to consider that prior reports, prior studies that have shown different proportions of prognosis may have changed after all of the implementation of these technologies.
Speaker: Hypothermia and temperature management
Speaker: changed radically the way that we approach this and we have learned over the last 10 years after the clinical trials were reported and after we started implementing hypothermia post-cardiac arrest is that we probably need to be a little bit more conservative in terms of approaching neuro-prognosis.
Speaker: So that would be sort of like the first thing that I would emphasize to all of the intensives and all of the providers that deal with this condition
Speaker: today.
Speaker: Excellent.
Speaker: So I think that as a here very actionable and very powerful messages number one is
Speaker: Clearly, we have strategies now that help protect the brain and can mitigate the effects of anoxic brain injury after cardiac arrest.
Speaker: And that is, like you mentioned, the targeted temperature management.
Speaker: That will be maybe the topic of another podcast, diving into the specifics of where the literature stands there.
Speaker: But obviously, doing that for the right patient makes a difference.
Speaker: And I hear loud and clear your message, Fred, that especially because of this and because
Speaker: hypothermia or targeted temperature management has changed the natural course of anoxic brain injury after these types of insults, we have to be very careful how we utilize certain tools and when we utilize these tools to prognosticate neurological recovery.
Speaker: So with those two very, I think, strong messages, let's dive into some of the specific aspects and tools that we utilize or have available for establishing a neurological prognosis
Speaker: after a cardiac arrest, and then maybe at the end, discuss what a reasonable general approach would be based on the available literature and based on your opinion.
Speaker: So Fred, I would like to ask you, traditionally, we've always started with a physical exam.
Speaker: And tell me a little bit about what are physical findings that may be useful in terms of determining prognosis in patients who suffer a cardiac arrest and how you would use them.
Speaker: Yeah, so the first thing that I will look into is post-cardiac arrest to assess if the patient is a candidate for temperature management right.
Speaker: Is to see how good they are at post-cardiac arrest immediately after the resuscitation period because you know that one of the requirements is that the patient needs to remain in a comethode state in order to
Speaker: you know, be eligible for temperature management.
Speaker: So if the patient is waking up immediately after the cardiac arrest, starts to open the eyes and point commands and localizing, probably you have to reconsider how aggressive you want to be in terms of temperature management for that particular patient.
Speaker: For the patient that remains in a comatous state and that you are actually indicating the use of temperature management, then
Speaker: while you wait for the standard period, which is usually 24 hours, and then the rewarming period, the physical exam is the strongest predictor, believe it or not, of neurological recovery.
Speaker: This has been tested recently, Dave Greer, when he was at the university, at Yale University, I'm sorry.
Speaker: He really did the original studies done in the 1980s with a better cohort and in the area of hypothermia.
Speaker: What he found was that, for example, the pupillary reflexes and the motor exam were strong predictors of prognosis.
Speaker: That means that if you still have pupillary reflexes after rewarming, and if you are localizing, not having posturing or abnormal responses to painfully stimulation, and those are the ones that we call either flexion or extension posturing, if you don't have those and if you're localizing and you're doing spontaneous movements that look like meaningful,
Speaker: probably your prognosis is gonna be good.
Speaker: So those are the things that I am always looking when I'm examining these patients post-rewarming, and we will talk a little bit about that later, what's the right timing to do it.
Speaker: But the pupillary reflexes and the motor exam are the stronger predictors.
Speaker: So I think that if I get this right, Fred, clearly immediately after having returned to spontaneous circulation, before we do any interventions,
Speaker: If somebody's following commands, that tells you that probably is not the best candidate, but other findings in that immediate post-arrest situation are usually not very helpful.
Speaker: Correct?
Speaker: That's correct.
Speaker: And once we do the rewarming or we treat them with targeted temperature management for 24 hours and then we do the rewarming, that's when certain physical findings, like you said, the lack of pulmonary reaction or the response to motor stimuli can be useful.
Speaker: But as you said, there's also a timeframe in which the absence of these findings becomes more powerful.
Speaker: And I guess we'll touch about that a little bit later, but that is very, very important.
Speaker: I think again,
Speaker: We'll talk about other aspects or tools, but emphasizing what you just said, that the power of the physical exam, when the right findings are found at the right timing after rewarming, are still, I mean, very, very important for us to remember in our clinical practice.
Speaker: So quick comment on biochemical tests.
Speaker: Are there any biochemical tests that are in any views?
Speaker: I've always read about neurospecific enolase as one example, NSC, but to be honest, I don't use it in my practice.
Speaker: It's not available in my hospital.
Speaker: That's something that I think in a lot of the hospitals that we practice, we use routinely.
Speaker: Can you make some comments on that, Fred?
Speaker: Yes.
Speaker: So the biomarkers are sort of like the new key on the block, you can call it that way, in terms of neuroprognostication.
Speaker: They provide some power in terms of prognosis.
Speaker: And in my mind, the power when you be in conjunction with something else in what I call the multimodality neuro prognostication scheme.
Speaker: But biomarkers on their own, when you use it alone, don't provide that much of discrimination in terms of
Speaker: of prediction because there are many false positives.
Speaker: So you have to be careful when you're using biomarkers.
Speaker: It's important to emphasize that the recent cardiac arrest clinical trial by Nicholas Nielsen didn't use biomarkers for neuro prognostication.
Speaker: The only thing that they used actually was the clinical exam and electrophysiological testing for neuro prognostication.
Speaker: You have to be a little bit careful.
Speaker: They collected a lot of data, a lot of papers from that particular study that have shown that if you use any combination may guide you in terms of providing a likelihood of good or bad outcome.
Speaker: So I will be careful.
Speaker: The MOSES study one is the NSE.
Speaker: You mentioned it already, the neuronal specific analyze.
Speaker: and that has a discriminative power.
Speaker: There are some levels that can be used as cut-ups.
Speaker: I think the one that is generally accepted is 30 or 33 picograms per deciliter.
Speaker: And this is the one that when you have it, right, you can actually predict a poor outcome.
Speaker: I've been fooled before by this, and I could tell you that
Speaker: I became more humble in terms of how I interpret this stuff.
Speaker: So just to give you an example, I had a patient that had a level of 17, came in poor shape, we cooled him, and I signed out the patient to my colleague.
Speaker: I said, this guy's never going to recover.
Speaker: I gave my spiel to the family, and then I left, and then a week later, I came back to the intensive care unit, and the guy's watching TV.
Speaker: And I felt a little amazed about the outcome, but you have to be careful with this thing.
Speaker: You have to be a little bit more conservative and use it with other modalities.
Speaker: Excellent.
Speaker: And I think that it speaks to something that we'll probably readdress and a recurrent topic, which is that a lot of the testing done pre-hypothermia
Speaker: shows that these tools do not perform the same way once we apply hypothermia.
Speaker: So the cutoff of 33 picograms has been very publicized pre-hypothermia, but maybe it's not as predictive when you undergo temperature management post-cardic arrest.
Speaker: You're right.
Speaker: So I think that another area that I think is a lot of interest for us and something that our critical care colleagues do not manage, obviously, as frequently or as well as our neurocritical care or our neurology colleagues are the electrophysiological studies.
Speaker: And to that point specifically, the utilization of either somatosensory evoked potentials
Speaker: or more commonly in a lot of the hospitals where some critical care physicians practice is the use of EEG.
Speaker: Could you comment on both of these and how you see them?
Speaker: Yes, so electrophysiological studies, like you mentioned,
Speaker: evoked potentials, somatosensory evoked potentials on the EE are very powerful.
Speaker: But the timing is the most important thing.
Speaker: So very early on, they have very low sensitivity and you get a lot of false positives for the somatosensory evoked potentials.
Speaker: When using clinical trials, it seems that the best performance is usually after 72 hours post cardiac arrest and probably a little bit later after the re-warming is when I would start using them.
Speaker: I would start probably thinking about SSCPs and analyzing the EEG at around five, seven days post cardiac arrest, which is what we discussed before probably 72 hours after the re-warming.
Speaker: And the reason for this is that if you go into the literature, there are a lot of case reports where you get shut down of the SSCPs initially, right?
Speaker: But as you said before, hypothermia has changed that.
Speaker: So the way that I see it is that hypothermia is sort of like this neuroprotectant.
Speaker: It's sort of like shutting down the fire, right, that occurs initially with this reperfusion.
Speaker: And it's keeping the neurons in this sort of like sleeping mode, hibernating mode, and preserving them for survival.
Speaker: So if you get the SSCPs, you're not going to see anything.
Speaker: And SSCPs are just,
Speaker: a way to determining if there is a connection between a peripheral nerve, usually the median nerve, and the cerebral cortex.
Speaker: And the waveforms that you see indicate at what level you see the connection.
Speaker: The waveform that we usually follow is the N27, and that's usually an analysis of the
Speaker: function of the thalamocortical projection.
Speaker: So by not having that signal, you are assuming that there is a diffuse injury of thalamocortical projections that at the end of the day are the ones that regulate arousal and awakening.
Speaker: So that's how you use SDS, but as I mentioned before, if you do it too early, you're going to get a lot of false positives.
Speaker: In terms of EEG, it's a little bit more complex,
Speaker: even more powerful because now you have a way to look at the whole brain and the waveform activity.
Speaker: And the most important thing is really to look at the background or the rhythm of that EEG and see if there is reactivity when you are stimulating the patient.
Speaker: That's a powerful predictor of good outcome.
Speaker: If you see a change,
Speaker: which is consistent with the clinical, I mean during the clinical exam stimulation.
Speaker: So just to give you an example, so you have a patient that has a flat EEG or is diffusely slow, you start examining him, he starts opening the eyes, he starts responding to you, and then you see a pick up in the rhythm in the EEG, that's a good sign.
Speaker: So in that sense, this technology enables you, right, to take a look at the patient's
Speaker: And not just on a cross-sectional way, but actually in a dynamic way.
Speaker: You're examining and seeing what's going on in the brain.
Speaker: So that's why it's so powerful.
Speaker: So I guess, Fred, reiterating, it sounds like the SSEPs, when done in conjunction with other findings,
Speaker: at the right timing can add to a lot, especially when they're absent.
Speaker: And there's other signs that suggest severe anoxic damage, but they have to be done at 72 hours or later after re-warming.
Speaker: And it sounds like with the EEG, what is probably good or powerful is the ability to elicit reactivity in the background activity.
Speaker: And that probably requires a more involved EEG, not just sending a tech recorded EEG and then be reported by somebody later on, but more of a specific, the intensivist asking for an EEG for cardiac arrest, anoxic damage evaluation, looking to see if there's any reactivity to stimulize.
Speaker: Is that correct?
Speaker: Yes.
Speaker: And to tell you the truth, you know, I could tell you this even though I could get in trouble with my epilepsy colleagues, right?
Speaker: We always like that type of fact.
Speaker: But you don't need to be an epileptologist to look for reactivity.
Speaker: It's very simple.
Speaker: You can learn this in five minutes at one of the workshops, in one of the society meetings.
Speaker: If you see a workshop on an EG after cardiac arrest and you want to learn something about it, you could learn how to stimulate a patient and look at reactivity.
Speaker: It's a very simple process.
Speaker: It doesn't require a lot of analysis or training.
Speaker: So, since we're on the topic of EEG, I would like you to maybe once and for all clarify to all my colleagues the difference and the implications in that difference between a myoclonic jerk and a myoclonic status EEG pattern after cardiac arrest.
Speaker: Yeah, so myoclonic jerks are just muscular jerks and they're called myoclonic because they are usually originated in the muscle.
Speaker: Most of the myoclonals that you see in postpartic arrest patients do not originate or you cannot, you know, for whatever reason, you cannot pick them up originating from the cortex.
Speaker: So, you know, most of the myoclonals that you see are usually what we call subcortical.
Speaker: They originate in subcortical networks, even the spinal cord.
Speaker: And that's the main difference.
Speaker: It's called myoclonic.
Speaker: It's because of the pattern of the spike that you see in the EEG.
Speaker: It's usually a huge spike with very long amp, I'm sorry, big amplitude.
Speaker: And the difference between that and myoclonic status is that sometimes you can get those waveforms originating in the cortex, and they have that at the same amplitude, and they're big, right?
Speaker: But when you pick them up and they are consistent,
Speaker: and they evolve and you don't or you cannot treat them with conventional therapy.
Speaker: That's what we call the myoclonic status or like syndrome.
Speaker: And in the 1990s there were a couple of papers saying that if you had that, it was a game over postcardiocardia and everyone sort of like learn that and that's how I was taught for example in my
Speaker: residency that if I saw myoclonic status that was the end.
Speaker: But what you mentioned at the beginning hypothermia has changed, right, the natural course of this disease and now we have learned that if we treat aggressively, not just myoclonic status but any other type of status that you see post-cardiac arrest, patients can actually survive and do well.
Speaker: So the aggressiveness of the therapy for myoclonic or any other type of status
Speaker: should be in accordance with the aggressiveness of cooling.
Speaker: So if you are submitting somebody to cooling, right, and it's awakening, it's awakening, and now in the EEG, you're seeing my client status, you know, most of us would favor a trial of intervention before, you know, concluding that the outcome is going to be poor.
Speaker: So that's what I do in clinical practice.
Speaker: I'm aggressive, you know, treating these patterns in the EEG, and, you know,
Speaker: A couple of papers published recently have shown that if you treat them, that patients could do well.
Speaker: So my question also regarding the myoclonic jerks, I think that often clinicians see myoclonic activity externally, like the muscular jerks, and immediately say this patient has a horrible prognosis.
Speaker: And that has not been shown, right?
Speaker: On the other hand, if you find the myoclonic activity,
Speaker: status on the EEG, especially when it's refractory, that is associated with the worst prognosis.
Speaker: Is that correct?
Speaker: Well, the classic myoclonus that you see, you know, I don't think it's associated with that much of poor prognosis anymore after hypothermia.
Speaker: And if you're not seeing
Speaker: myoclonus or myoclonic status in the EEG even less.
Speaker: The problem is really the myoclonic status is the one that I would be concerned about because if you don't treat, right, then of course the patient is going to do poorly.
Speaker: So that's the problem with this issue, right, is that if you don't look for it, then you will never know.
Speaker: And in my mind, right, if your institution doesn't have access to continuous EEG,
Speaker: You should be able to either consider, you know, transmit a patient and see, you know, if another institution can deal with it because you're right.
Speaker: I don't think that's, you know, after hypothermia, I don't think it's associated with poor prognosis anymore.
Speaker: The most important thing is that if you diagnose it, you provide a trial of intervention.
Speaker: Excellent.
Speaker: And I think that moving along with other tools, obviously a very commonly utilized tool is neuroimaging, and either in the form of CT scans or MRIs, which as we all know from ordering them after severe anoxic injuries can sometimes be read as
Speaker: significant patterns that suggest anoxic damage, but we've also seen normal CTs or almost normal CTs in patients who never wake up.
Speaker: So what's the role of imaging in neuroprognostication after cardiac arrest?
Speaker: That's an excellent question, Sergio, and the data is even less convincing that it has enough discriminating power to
Speaker: to predict outcome on their own.
Speaker: So for imaging, we have conventional computerized tomography, CAT scans, and then we have magnetic resonance.
Speaker: So we have MRIs to sort of help us or aid us in terms of assessing the degree of brain injury.
Speaker: But to tell you the truth, right, when you use them as a single, you can call it biomarkers as well, because when you use them as a single biomarker, right,
Speaker: they don't have that much of discrimination.
Speaker: I've seen people that look very bad on MRI and then eventually they wake up and that tells you about the sensitivity and specificity of this testing.
Speaker: The timing is another very important thing.
Speaker: If you do it too early, you might not see a lot of damage and you may conclude that the patient
Speaker: has not sustained damage and the reason is because you probably did not wait enough time to pick it up.
Speaker: So I usually wait about five, seven days to even consider using a test unless I'm concerned about sero-ledema and intracranial hypertension.
Speaker: So there are some
Speaker: variables in the patient characteristics that may indicate which patients may be at higher risk of developing, for example, cerule edema.
Speaker: At the end of the day, the cause of death in these patients is neurological, is a neurological cause.
Speaker: It's usually cerule edema leading to herniation.
Speaker: So younger people, you know, prolonged return to spontaneous circulation are the ones that are probably at higher risk
Speaker: to develop significance really.
Speaker: But I usually wait for the MRI.
Speaker: The MRI is sort of like the one tool that I know researchers are concentrating on right now.
Speaker: And there are specific things on the MRI that they are looking for.
Speaker: you know the burden of anoxia the burden of diffusion weighted lesions for example volumetric analysis you know sort of like track recognition meaning tensor analysis in the MRI are the tools which are very advanced tools in MRI that they are using to determine promosives I think that those are more specific
Speaker: but I don't think they are ready for critical use.
Speaker: So, you know, you have to be careful with how you interpret that as well.
Speaker: So this is what I'm saying, using a multi-modality approach is a better way to go.
Speaker: Excellent.
Speaker: So I guess really it's just a piece of the puzzle, but you could have a normal
Speaker: or almost normal CT scan and never wake up.
Speaker: Or you could have some signs that suggest anoxic damage and still recover.
Speaker: So I think that not enough to just hang our hat on that imaging, but obviously it's something that very commonly patient families are requesting and they believe that the CT scan or the MRI will really give us a lot of information.
Speaker: So, go ahead.
Speaker: And it does.
Speaker: I mean, sometimes patients have combination of injuries.
Speaker: I mean, you know, sometimes patients have hemorrhages, you know, or something happens during the cardiac arrest that you don't know.
Speaker: Some people fall, and then eventually they have some additional injury.
Speaker: You know, people can have strokes or could have embolism, right, resuscitation that
Speaker: that if you see them in CAT scan or MRI can give you more ideas in terms of how to think about the prognosis form.
Speaker: Because if you have a cardiac arrest but then on top of that, you have bilateral MCA strokes for whatever reason,
Speaker: you know embolism or hyperperfusion because you were in shock for so many hours right then you know that adds to the prognosis you have to be a little bit more careful in terms of interpreting additional findings not just anoxia.
Speaker: Excellent.
Speaker: So I think that kind of as we're trying to close the loop, let's talk a little bit about the timing of neuroprognostication.
Speaker: And I think that you mentioned earlier, Fred, that immediately after a cardiac arrest, it's really hard to make any prognosis, right?
Speaker: If we decide we're going to treat these patients aggressively, we should undergo therapeutic hypothermia or targeted temperature management.
Speaker: complete the 24 hours at the specified target, rewarm them, and once they're back to normal thermia, let's call that time zero, what happens after that?
Speaker: How would you handle the timing of your neuroprognostication?
Speaker: Yeah, so this is a great question.
Speaker: So I usually put a paper from the University of Pennsylvania by Ben Avella and David Gajewski where they actually looked at
Speaker: the notes, right, that neurologists wrote in patients after cardiac arrest and you see all the sort of like super early or ultra early assessment of prognosis and, you know, when you read the paper they quote, for prognosis, you know, devastating disease,
Speaker: unlikely to record so I you know if if if the listeners want to remember only one thing after this podcast is that you really have to be more conservative in terms of prognosticating and don't
Speaker: rush to judgment, right, and write these comments in your notes so early because, I mean, more likely you will be wrong.
Speaker: And this is why I said at the beginning, you know, I've been humble before about this condition.
Speaker: So, you know, the clearest and more, the strongest evidence, right, that you have to wait to do an accurate assessment is the Nicholas Nielsen study that basically rewarm and then
Speaker: kept on neurothermia for 72 hours and then waited a period of almost 72 hours to assess for neurological prognosis.
Speaker: So that's like the best evidence and thus like the standard, right, is to wait at least 72 hours post rewarming to start considering any neurocognostication.
Speaker: And it's an important message that you need to convey to the families because families want to know upfront, right,
Speaker: What's the likelihood of survival?
Speaker: What's the likelihood of recovery?
Speaker: This patient is very hard to determine in the era of hypothermia if you have exposed the patient to cooling.
Speaker: So the message is probably wait 72 hours post-neuromathermia to start looking at all of these biomarkers.
Speaker: And by the way, they take a while to come back.
Speaker: So using an NSE, if you have availability like we do at my institution, it takes about 72 hours to come back.
Speaker: So it gives you a lot of time to see, you know, before you conclude anything, how the patient is doing on a clinical basis, right?
Speaker: And it enables you to get an MRI or SSCPs or a continuous EEG within that timeframe.
Speaker: So, yeah.
Speaker: And I think that along those lines, what I always say is that it,
Speaker: If you have a patient who clearly has advanced directives or comorbidities or situations that you truly believe are a horrible prognosis to begin with, I think it makes sense not to do critical care, period.
Speaker: So you wouldn't put them on a ventilator.
Speaker: You wouldn't take them to the cath lab.
Speaker: You wouldn't admit into the ICU.
Speaker: You wouldn't do the hypothermia.
Speaker: But short of that, if you're intubating people, calling cardiology, you should protect the brain.
Speaker: and you should give people a chance to recover.
Speaker: So it sounds like the most important take home message is that after the hypothermia, you've got to rewarm them.
Speaker: And from that rewarming, the clock starts, zero, wait 72 hours of good support, and then start implementing these tools.
Speaker: And as you gather information after the 72 hours of rewarming, you are probably in a better position to share with the family what is the most likely outcome based on that information.
Speaker: Is that correct?
Speaker: Yeah, so I agree.
Speaker: I think that's a great approach.
Speaker: I think that waiting, it's probably the best thing to do.
Speaker: And in your practice, Fred, what are the tools that you use on a regular basis in terms of your multimodality neuroevaluation for these patients?
Speaker: So as I said at the beginning, the clinical exam, right, that's very important.
Speaker: Second thing that I use is
Speaker: Continuous EEG.
Speaker: All of these patients in our institution are monitored by continuous EEG.
Speaker: And you would ask me why, and the reason is because if they're in a coma, right, there's no way of knowing what's going on in the brain.
Speaker: And by the way, the most critical part of the temperature management is the rewarming phase.
Speaker: And I know that you said you're going to have an additional podcast, and I think that for that podcast, you need to concentrate on the rewarming phase.
Speaker: With continuous EEG, you could see changes
Speaker: in the electrophysiology that could indicate, for example, worsening cerebral edema and risk of herniation.
Speaker: And that, in our protocol, right, indicates that you need to go back and recool the patient.
Speaker: So if you see changes in the amplitude of the EEG, for example, while you're re-warming, we will come back and keep the patient cool for an additional day until we can start the re-warming phase again.
Speaker: Those tools are so powerful, not just for prognosis but also for clinical management at the bedside.
Speaker: So that's the second tool that I use.
Speaker: The third tool is SSCPs.
Speaker: I do it usually 72 hours post-route warming.
Speaker: And then finally, the NLAs.
Speaker: I usually send the NLAs at the third day post-cardiac arrest.
Speaker: I don't do it immediately.
Speaker: I wait day number three and then I send the NLAs.
Speaker: And then finally, MRI, but more
Speaker: to give me an idea if there's any additional injury because I've seen bad MRIs that actually don't translate into a poor outcome, right?
Speaker: So what the MRI tells me is more of, you know, is the patient going to have a lot of cognitive impairment, for example, you know?
Speaker: Or did the patient have a dissection and now he has a stroke in the posterior circulation?
Speaker: Did dissection occur before, cardiac arrest, CPR, you know, that sort of thing.
Speaker: And does the patient need additional treatment for it?
Speaker: You name it aspirin or anicoagulation.
Speaker: So those four tools are the ones that I use in my clinical practice.
Speaker: Excellent.
Speaker: Well, I think that we definitely enjoyed talking with you, Fred, about a topic specifically about the neuroprognostication.
Speaker: I know that the Neurocritical Care Society and the American Academy of Neurology are working on the
Speaker: hypothermia or neuroprotective guidelines, and they'll be cooking up soon.
Speaker: So we'll probably have you back to talk in more details about targeted temperature management.
Speaker: But as we close, I would like to first thank you for your generosity with your time and your knowledge.
Speaker: It's always a pleasure to talk with you.
Speaker: And I'm sure that we'll talk again shortly.
Speaker: But I also, since in critical matters, we really try to cover all aspects of practicing critical care, would like to close with a couple of questions that are a little bit off the topic, but I think super relevant to what we do as physicians, to what we do as providers in the world of critical care.
Speaker: Would that be okay?
Speaker: Yes.
Speaker: So the first question I have for you and a lot of our friends and a lot of our listeners know that I'm an avid reader and always interesting and picking up new things to read or to gift.
Speaker: Is there a book or books that have influenced you the most or what book in particular have you gifted the most to others?
Speaker: So I have gifted a lot of books before and and and you know, so like a
Speaker: books that I've read when I was in high school and when I was younger.
Speaker: But one of the books that have actually influenced me a lot, and this is recently because I became a bioethicist recently, is Meditations by Marcus Aurelius.
Speaker: And it's like an excellent book if you're dealing with
Speaker: a lot of problems in life and critical care is just about problems, right?
Speaker: So, you know, I find it, you know, inspiring in terms of, you know, telling me
Speaker: how to react in critical conditions or in environments that have a lot of conflict, right?
Speaker: So if I were to gift a book to a friend or something, it would probably be Meditations from Marcus Aurelius.
Speaker: Excellent choice.
Speaker: And I think that it just speaks
Speaker: friends think alike it's one of my favorite books I have several copies in my house and who've stayed in my house as guests usually go with one of these some of them enjoy it some of them say not for me but I do agree with you I think that philosophy applies to what we do so powerfully is a great guide in terms of how to deal with adversity but more importantly
Speaker: which I think is important for critical care practitioners, it really talks about how to be humble and how to really focus on the things that we can control.
Speaker: And I think that that's a great, a great, a great book.
Speaker: Another question.
Speaker: Is there anything that or what do you believe to be true in medicine or in life that many people or most people around you don't believe in?
Speaker: Yeah.
Speaker: You know, I think that I've been humbled by my profession a lot and that when I became a physician, right, I became a physician to help and to restore, to prolong life.
Speaker: And I think most people believe, right, that we're immortal sometimes and that there is no end.
Speaker: And in my mind, I think we have to understand that
Speaker: There's always a beginning and there's always an end and both are physiological processes.
Speaker: Of course some have better impact in your mood and in your state of happiness, right?
Speaker: But I don't think a lot of people understand that there's an end to everything.
Speaker: Sometimes even colleagues, physicians, providers, understand that sometimes when the end is coming you have to probably
Speaker: stop what you're doing.
Speaker: And that's the part that I think is very hard to acknowledge, right?
Speaker: That life ends.
Speaker: Yep.
Speaker: I think that's a great point.
Speaker: I think that actually your friend Marcos Aurelius and the Stoics talked about memento mori, remember you will die.
Speaker: And I think that as a way of
Speaker: guiding what we do every day with the precious time we have, I think it's very valuable, but also something that we should share.
Speaker: And when we talk with our patients, I think is very, very valuable.
Speaker: So that's a great point.
Speaker: And I think that you're absolutely right.
Speaker: And the last question, Fred, is, is there anything in particular that you would want every intensivist in sound critical care to know?
Speaker: It's sort of like along the same lines that we've been discussing Sergio, is to understand, and I say this from an ethical perspective, you know, ethically and morally, it's okay to stop, it's okay to consider stopping life-sustaining therapies when you think that they are not doing any good and actually harming the patient.
Speaker: I think that as intensive as, you know, as I said, you know, one reason why I went to medicine
Speaker: was to help and prolong life and all that stuff and it was sort of like ingrained in my life.
Speaker: Then when I went into critical care, I suddenly realized that I was actually living in a life or death environment and sometimes I needed to make decisions to allow that normal process of death to happen.
Speaker: And you know, it takes a lot of courage to recognize when you need to stop something.
Speaker: But at the end of the day, you know,
Speaker: The intensivist is the skipper.
Speaker: The intensivist is the captain of that team.
Speaker: And in that sense, there's a lot of responsibility for a critical care doctor, right, to guide the team in a way that is in the best interest for the patient.
Speaker: And understanding that sometimes stopping is probably the best way to go.
Speaker: So I would like everyone to understand that concept as well.
Speaker: Most of us do it, and I'm glad.
Speaker: And if everyone that is listening understand it, then I'm happy.
Speaker: Excellent.
Speaker: Well, Fred, again, a pleasure, a treat for me to talk with you about these topics.
Speaker: We will have to revisit some of these topics and go deeper in some specifics regarding targeted temperature management.
Speaker: Always a pleasure.
Speaker: Thank you so much for your time and your generosity, and I look forward to talking with you again soon.
Speaker: Thank you, Sergio.
Speaker: Thank you.
Speaker: Thanks again for listening to Critical Matters.
Speaker: Make sure to subscribe to this podcast on iTunes or Google Play.
