So good evening, we're glad you could join us today. In this talk, we will explore common challenges faced by neurorehab physiatrists being consulted in the ICU patients recovering from brain injuries, spinal cord injuries, and stroke. This session is co-hosted by the CNS Brain Injury Medicine Fellowship and SCI member communities. My name is Dan Zhou, I'm Chief Resident at JFK Johnson Rehabilitation Institute, and I'll be going on to do a Brain Injury Medicine Fellowship at Spalding Rehabilitation Hospital. I will also be the moderator for this session. So now I'll take the time to introduce our three amazing speakers. So starting our session is Dr. Kian Nasuri. He received his Bachelor of Science in Physiology and Neuroscience from the University of California, San Diego. Dr. Nasuri then attended the Arizona College of Osteopathic Medicine of Midwestern University. He went on to complete his residency at the Shirley Ryan Ability Lab under Northwestern University, where he is currently completing his Brain Injury Medicine Fellowship. During this time, he was heavily involved in medical student and resident education, for which he was inducted into the Feinberg Academy of Medical Educators. After fellowship, he will remain at the Shirley Ryan Ability Lab as an inpatient brain injury attending physician, working with patients with moderate to severe brain injury, including those in disorders of consciousness. Dr. Nasuri will begin our session by discussing pertinent ICU issues for patients with brain injury and stroke. Following that, we will have Dr. Krista Noramili. Dr. Noramili received her BA in Biochemistry from Rice University in Houston, Texas, and then earned her medical degree from the University of Cincinnati College of Medicine. She then completed her PM&R residency at the Spaulding Rehabilitation Hospital under Harvard Medical School. During residency, she received various accolades, including Administrative Chief of Resident, Harvard Business School Leadership Program graduate, and the Emanuel J. Lipson Award for a significant contribution to Spaulding Rehabilitation. Currently, Dr. Noramili is the Spinal Cord Injury Medicine Fellow at Shirley Ryan Ability Lab under McGaugh Medical Center of Northwestern University. Her academic contributions include numerous publications and presentations with a focus on healthcare disparities, women's health, and enhancing access to care for individuals with spinal cord injuries. Upon graduation, Dr. Noramili will be joining Fraser Rehabilitation Institute under the University of Louisville as an Assistant Professor of Spinal Cord Injury Medicine. Today, she will be discussing considerations in the ICU for patients with spinal cord injuries. Dr. Noramili and Dr. Nasuri will take us through a dual diagnosis case as part of their talks. And our final speaker will be Dr. Matthew Peterbaugh. Dr. Peterbaugh attended medical school at the Rocky Vista University College of Osteopathic Medicine, and then completed his internship at St. Joseph Mercy Oakland in Pontiac, Michigan. He then served as a flight surgeon for the United States Air Force for five years. After his active duty service, he completed his PMR residency at the University of Minnesota while continuing his service as a flight surgeon in the Minnesota Air National Guard. Dr. Peterbaugh further specialized in brain injury medicine through a fellowship at the University of Minnesota. Throughout his career, Dr. Peterbaugh has received numerous awards as an educator and authored numerous publications on traumatic brain injury. Presently, he serves as the Brain Injury Medicine Physiatrist at the Department of Physical Medicine Rehabilitation at Hennepin Healthcare in Minneapolis, Minnesota, where he also holds the position of Traumatic Brain Injury Fellowship Site Director. Today, Dr. Peterbaugh will be sharing insights into facilitating communication for neurorehabilitation consultations in the ICU. All right, so that wraps up the introductions. We also have time at the end for Q&A. You can also submit your questions via the chat, which I'll be monitoring, and then we can go over later. So without further ado, I will turn it over to our speakers, starting with Dr. Nasuri and Dr. Nora Mealy. Thanks for that intro, Dan. So kind of like Dan said earlier, we'll just be reviewing PM&R's role, specifically in the ICU, dealing with these kind of various neurologic diagnoses, including stroke, traumatic brain injury, and spinal cord injury. Krista's actually gonna be driving for me, so I'll be kind of be saying next to kind of like move on to the slides. But so just kind of like in brief, so I'll initially start kind of with stroke and TBI. Krista will move into spinal cord injury, and then Matt will finally kind of go into a little bit of a discussion in terms of facilitating some of those kind of interdisciplinary discussions with the various team members in the ICU. So in terms of just our objectives for this lecture, we just kind of want to make sure that everyone has a general understanding of some of the neurologic sequelae that result as a result of these CNS injuries. And then we're gonna identify some kind of key management and points of intervention that we specifically as PM&R providers can recommend for these patients. And then finally, again, reviewing kind of our specific role within this kind of advanced acute care setting and how to kind of like properly facilitate conversations and make sure that our recommendations are actually going through with these patients. So we have no financial professional disclosures at this time. So we'll start with a case that Krista and I actually had the opportunity to kind of co-manage during our fellowship year. And I just kind of want you all to like, as we kind of present some of the components of this case, just kind of like marinate on it, and then just think about the various kind of recommendations that we'll go through and see how you would kind of apply some of those concepts to the patient that we're presenting. But so essentially you're the PM&R doctor that's been consulted on a 52 year old male who's now in the ICU after he sustained a 25 foot fall. So in terms of initial injuries, he had pretty significant traumatic brain injury with bilateral posterior cerebral artery strokes, as well as a cervical spinal cord injury. His hospital course thus far was significant for a cervical spine fixation and non-operative management of his TBI. He did have some complications, including PA arrest for which he had a pacemaker placed, completed antibiotics for pneumonia, also had his tracheostomy for which he still remains on the ventilator. This injury actually did occur outside of the United States. So he was recently transferred back to the US. On admission, he did have this like lip twitching episode that was concerning for seizures. So they did get continuous EEG, which showed diffuse encephalopathy, no kind of evidence for seizures, as well as kind of sleep-wake state changes, but no kind of specific end-to-sleep transients. And there's ultimately a plan for a C-spine revision. Those are his current medications. And then in terms of his physical exam, so just kind of in general, like some pertinent positives, he has a hard cervical collar. He has an NG tube. He does have a pacemaker that's functioning like with a regular rate, which you're noting the pacemaker spikes on the monitor. In terms of his neurologic exam, he's pretty much flaccid in his portion. He's opened his eyes to a trap squeeze, but no kind of like evidence of tracking to visual stimuli, no blink response, and no kind of like localization to any sort of like auditory stimuli. So starting with kind of starting with stroke and brain injury, and a lot of these recommendations do have kind of decent overlap with each other. So for the most part, I'll just be kind of talking about some entities that are pretty much kind of like uniform, or at least can be like translated between the two. But the number one kind of thing I wanted to discuss was this concept of early mobility, which is kind of slowly gaining traction as like an emerging clinical practice. Right now, it's pretty kind of in its early stages where it's very kind of like loosely defined whether or not it's better to kind of like be active versus passive, and there's no actual standardized protocols or doses. But for the most part, based on some of the research studies that have been performed, generally kind of we ideally would want some sort of like out of bed activity that's initiated in this early acute phase within the first 48 hours that could include sitting, standing, or walking. Again, this promotes neuroplasticity as well as reducing some of those immobility related complications. It is a relatively low risk intervention, but we do need a lot of kind of like ancillary support if we are to kind of like mobilize these patients, especially in the setting of the ICU, just thinking about the various tubes and lines as well as devices that these patients are attached to. But if we're able to do it successfully, it has been shown to improve patient outcome where these patients have shown higher mobility as well as daily activity scores during this kind of critical period. Next, so the first clinical entity that I'm gonna be talking about is hypertonia and kind of spasticity, which fall under this category of upper motor neuron sign, which essentially is the result of damage to neurons responsible for the creation and coordination of movement. It's very common after CNS injury can include weakness, clonus, co-contraction, hyperreflexia and dystonia. But in terms of like differentiating kind of hypertonia versus spasticity, just remembering that hypertonia is essentially that loss of descending inhibition to the motor pathways leading to excessive muscle tone, where spasticity is that velocity dependent resistance to stretch. However, in terms of the consequences, it can overlap between the two, wherein the patients can have loss of function, weakness, pain, decreased inactivity, contractors and just kind of like overall improper positioning that can make performing ADLs very difficult for them. So if we're thinking, Chris, the next slide. So if we're thinking about kind of the progression of spasticity after an acute neurologic event, it generally occurs over this one to six to one, this one to six week period where you'll initially kind of have flaccidity, which will kind of develop into our like synergy patterns. And then finally at its peak, you'll develop marked spasticity. This is kind of the point that we want to prevent the complications gone on and kind of targets for our interventions. Because ultimately, if we were to kind of follow the appropriate progression of recovery, we do want our patients to be able to kind of like be able to perform isolated and coordinated movement. So really making sure that we're addressing it as it's kind of peaking is key. So we can kind of subdivide management into two various categories, kind of starting with non-pharmacologic versus pharmacologic. I will say like for me, when I'm generally providing recommendations for patients in the ICU, I have a tendency to kind of hedge more so on these non-pharmacologic interventions that we'll generally recommend just because of the amount of like medical issues that may be going on at this time. So again, generally recommending proper positioning, making sure the body is in a balanced symmetric position to avoid exacerbating ongoing tone. I'll also recommend that our therapists kind of initiate some sort of stretching program that they can incorporate family and caregivers with. And especially if the patient is able to performing some of those active movements themselves for multiple repetitions per day, if they're able to. If needed and your patient is kind of in this setting for a more prolonged period of time, you can make orthotic recommendations that have certain like heating or cooling properties that can kind of like affect or like modulate the tone. But like a simple intervention is just, can be as simple as like asking them to like wrap a hand towel on the patient's hand to kind of prevent some of the fisting that like some of our patients may develop. But if we're finding ourselves where the tone is kind of like becoming kind of unmanageable, that's generally when we move on to some of those pharmacologic recommendations. Some oral medications that are generally my initial go-tos are Baclofen as well as Dantrium, especially specifically in the traumatic brain injury population. When we think about antispasmodic medications kind of like as a whole, they're generally like very sedating. And one of the kind of key goals for patients with a traumatic brain injury is promotion of consciousness. So I'll tend to kind of like recommend Dantrium, but like, to be honest, I'm not kind of very aggressive with pharmacologic management, at least in this early acute period. However, for patients kind of that are in the ICU for more prolonged periods of time that are kind of developing like spastic quadriparesis, can consider evaluation for an intrathecal Baclofen pump. Again, there has been research that it can help kind of like mitigate some of the kind of post-TBI issues such as paroxysmal sympathetic hyperactivity, which I'll be talking about later in this talk, as well as helping facilitate emergence from a disorder of consciousness. There have also been kind of various studies that have looked at kind of like its utility in like post-stroke spastic hypertonia, specifically hemiplegia, where a Baclofen pump actually did, kind of was able to treat the spastic limb without affecting the unaffected side. But also we do have to keep in mind that not all of these patients necessarily make it to the acute inpatient rehabilitation setting and can be lost to follow-ups. So I'll also gently like recommend that if our patient isn't being kind of admitted to like an acute inpatient rehab setting, that they do have some sort of like outpatient referral to establish with a physiatrist so that there could be consideration for botulinum injections at some point. Next, the next clinical entity that I'll be discussing is paroxysmal sympathetic hyperactivity, commonly known as neurostorming or storming, but essentially what these are, discrete episodes of hypertension, tachycardia, tachypnea, diaphoresis, fever, and dystonia or posturing. It was actually first described in 1929 as diencephalic autonomic seizures. And kind of like the thought process behind this was that elevated intracranial pressures as a result of kind of like a CNS insult did cause like epileptiform discharges from the thalamic neurons that resulted in kind of this clinical syndrome. It's been known through kind of like various names, such as again, paroxysmal sympathetic storms, midbrain dysregulatory syndrome, paroxysmal autonomic instability with dystonia or PAID syndrome. Again, there's no general consensus regarding its nomenclature, diagnosis, or even like the evidence-based management. And the actual pathophysiology is generally unclear at this time. But what we do know is that it's essentially this kind of disconnection syndrome where you have this exaggerated stress response due to sympathetic and parasympathetic dissociation. And it is a relatively common occurrence in CNS injury, including traumatic brain injury, hypoxic ischemic brain injury, and stroke, and can actually occur in roughly like 15 to 30% of severe TBI. So not kind of like an insignificant number. So when we're thinking about diagnosis, I think one of the kind of key things to remember about this is that it's a diagnosis that is a very kind of great mimicker of other clinical entities that could include neuroleptic malignant syndrome, central fevers, malignant hyperthermia, or just kind of like a general like infection. So back in 2004, a physician named Blackman proposed kind of like certain clinical criteria to more specifically delineate this as a diagnosis, wherein kind of in order to kind of appropriately diagnose that a patient had to have some sort of severe brain injury and essentially be at a Rancho Los Inigos level of four or lower, have a temperature of at least 38.5, a respiratory rate of 140 breaths per minute, heart rate greater than 130, had some sort of agitation, diaphoresis, and dystonia. And these had to occur in like kind of a cyclical pattern where at least they'd have one cycle of this per day for at least three days with kind of ruling out other conditions, which essentially firmly established this diagnosis as a diagnosis of exclusion. Kind of now in relatively like more modern times, we have various kind of like assessment tools, such as the Paroxysmal Sympathetic Hyperactivity Scale Assessment Measure that can kind of more appropriately like identify as well as stratify kind of these storming episodes, wherein you have that kind of clinical feature scale where you can essentially grade it in terms of the actual kind of like grade of the clinical symptoms that are taking effect, and then kind of compiling that with a diagnosis likelihood tool, which would essentially kind of tell you whether or not this is likely storming or not. It's useful again, because it allows you to kind of like stratify when these discrete episodes are happening, which can have implications in terms of the management that you're recommending. So, but when we're thinking about management of this, so again, since this is a diagnosis of exclusion, making sure that you are initiating a broad workup when these episodes do happen, and you want to kind of like definitively rule it in as a diagnosis of exclusion. So I'll generally recommend kind of like a global workup for kind of evaluation of various kind of like entities. And if I'm able to identify an alternative cause, I'll make sure that I'll treat that first. I did have a patient that was having kind of these intermittent kind of like hypertensive and storming episodes like in the rehabilitation setting. And when we did our workup, it ended up that he just had like a kidney stone. So we gave him like aggressive fluids and those symptoms actually kind of like decreased in frequency. So it can be just as simple as that. But once you do kind of like identify some of the triggers, you want to make sure you're treating that as well as providing supportive management. So that could include minimizing external stimuli, clustering care, maintaining temperature, repositioning, and then giving fluids, initiating cooling measures and making sure they're regulated in terms of their bowel and bladder. And then finally, if these are just kind of occurring, if they're occurring and kind of like out of the control of some more of these kind of non-pharmacologic interventions, that's when I'll generally kind of recommend either sympathetic blockade, which is usually propanolol that'll start at kind of like 10 milligrams DID. You can also consider clonidine, but these patients also happen to be on IV drip. So kind of you can titrate some of those infusions. You can also consider like various neuromodulatory agents. Bromocriptine is also a really good one to use because you have that dual capability of providing some level of neurostimulation, but then also providing kind of like recommendations for tone management, as well as kind of pain management too. The next is post-traumatic seizures, which are abnormal and sudden bursts of uncontrolled electrical activity in the brain. Again, you can stratify this into various types that include vocal versus generalized, simple versus complex, and again, immediate, which is usually within the first 24 hours, early, which is, again, a little bit more specific to when we're thinking about brain injury-specific recommendations, and then late seizures, which is generally after that seven-day period. Temkin in 1990 kind of did publish that landmark study that did look at phenytoin administration over a seven-day period that did show it was useful for prevention of early seizures, but actually showed that there was no evidence that it prevented late post-traumatic seizures. Now we've kind of, or a lot of the teams have extrapolated kind of that to Keppra just because it is a cleaner medication. So we'll generally provide seven days of prophylaxis, but if there is a concern, again, obtaining an EEG and initiating appropriate kind of like medication management if there are occurring seizures. Next is agitation, which is a very common behavioral issue after traumatic brain injury that we have a lot of experience kind of dealing with, but essentially this is a state of psychomotor disturbance characterized by an increase in motor and psychological activity. Again, why it's significant is because it can kind of cause harm to the patient as well as their family and staff, lead to decreased participation, potentially functioning as a barrier to rehabilitation and leading to overall increased length of acute care stay. Within the rehabilitation setting, we have our own assessment tools of quantifying agitation, such as the agitated behavioral scale, but in the ICU, the scale that they're using is the Richmond agitation and sedation scale where they're typically targeting a RAS goal of zero to negative two. Again, it's useful because it gives us ability to quantify agitation, which again, drives management. And then depending on their score, it can also lead them to perform the confusion assessment measure in the ICU, which is essentially a way that they can also quantify if delirium is co-occurring. But similarly to hypertonia, I kind of stratify management to pharmacologic versus, or to non-pharmacologic versus pharmacologic. Again, having a tendency to lead to non-pharmacologic interventions first and then initiating pharmacologic interventions. So number one, assessing the patient and ruling out and treating other causes, but in terms of environmental measures that you consider, just minimizing nighttime interruptions to promote kind of that sleep-wake, maintaining a general low stim environment, which may be a challenge in the acute care setting, but thinking about ways that we can reduce noise, cluster care as appropriate, reducing the number of providers present, mobilizing the patient in a safe way if we're able to, kind of frequently reorienting the patient, providing a sitter if needed. And then in kind of the case of impending harm, consideration of restraints if we need to. Then with pharmacologic, again, I think the hallmark of, and the foundation of recovery after brain injury is making sure that patients are getting appropriate sleep. So generally my kind of initial recommendations will be more geared toward making sure that patients are more regulated and kind of sleeping well. So I do have like a low threshold for initiating medications for sleep, but in cases where it's kind of acting as a kind of, it's kind of acting as a barrier throughout the day, I'll generally recommend propranolol because there have been kind of studies that have shown that scheduled propranolol has been shown to decrease restraint use, as well as the intensity of the agitated episodes. At our facility, we are biased towards trazodone just because of its cleaner side effect profile compared to various other antipsychotics and antiepileptics, but also knowing that those are within your wheelhouse to use. With regard to the various antipsychotics, generally there's kind of no real kind of like clinical guidelines of which one is better than the other. It's just kind of whichever neurotransmitter target that you're looking for. And if you need a PO agent versus an IM agent, and then also considering that various antiepileptic medications can function as kind of mood stabilizer medications, but I'm a lot less kind of gung ho about initiating this in the ICU setting, just because a lot of the hematologic implications of these medications, such as the platelet dysfunction that can result with Depakote use, as well as the agranulocytosis that can result with Tegretol. And then remembering that men, well, in an ideal world recommending against Taldol, but some of our providers may be a little bit biased to those recommend, or some of our other colleagues may be a little bit biased to that medication, but remembering that use of that medication does put our patients at increased risk of neuroleptic malignant syndrome, because they are already in a dopamine depleted state and can lead to pretty significant worst functional outcomes. Then with regard to recommendations for Trach and PEG, kind of universally for both stroke and TBI, PEG placement is usually within the first two weeks of either stroke or TBI. Specifically in stroke, we have a kind of more tendency to favor kind of these interventions if there are strokes affecting the reticular activating system, as well as respiratory or swallowing centers, and dysphagia can occur in roughly 30 to 80% of patients with an acute stroke. The data is a little bit mixed between stroke and TBI, versus kind of tracheostomy placement, where early versus late tracheostomy just kind of has shown like neutral results for stroke patients, but in the traumatic brain injury population, early tracheostomy has been associated with improved neurologic outcome, as well as reduced length of stay in acute care. I also just want to clarify that we're generally recommending against nasogastric tube placement in traumatic brain injury patients, just because of the frequent co-occurrence of facial fractures, as well as like issues with agitation, because if they do pull it out, they, again, that may be a reason to kind of, that we may have to transfer them back to an acute care hospital, once they are in our setting in acute rehab. And then finally, just addressing neurostimulation. So I included this picture that was published in Recovery of Disorders of Consciousness by Dr. Ed Lowe at MassGen Hospital, because I think it really kind of beautifully captures kind of the various categories that our patients can fall in when they kind of fall under that umbrella of a disorder of consciousness, which is that state of prolonged altered level of consciousness, wherein specifically arousal and awareness are affected. When we think about the pathophysiology about this, it's essentially a broad withdrawal of excitatory synaptic activity across the global cerebral cortex, with specifically loss or reduced input to thalamic neurons, as well as the neocortex, which is termed disfacilitation. Again, it has a high rate of occurrence in patients with traumatic brain injury, hypoxic ischemic brain injury, and ischemic and hemorrhagic stroke. So when we're thinking about what we can provide as PM and R providers, again, I think because of our experience in our training, working with these patients, we're very kind of competent at accurately stratifying these patients, which ultimately informs the plan of care and ultimate disposition. There was a track TBI study done by Dr. McCrea in 2021, that did kind of state that we should avoid early prognostic generalizations of patients in a disorder of consciousness, because it did look at a cohort of patients that were identified as unresponsive, wakeful, or vegetative kind of initially in that kind of early two week period after TBI. And roughly 75% of those patients did kind of regain consciousness at the one year mark, and then 25% of those patients regained orientation. So again, while these patients may look kind of severe in their initial presentation, they do have capacity for pretty significant functional outcome at the one year mark. But generally, we're also recommending obtaining an MRI brain without contrast when able to give us a better idea of the kind of the types of damage that has taken place, because again, it can kind of drive our anticipatory guidance of some of the behaviors that our patients may display later on, as well as considering EEG to evaluate sleep architecture, as well as evaluation if any sort of like seizures are taking place. And then when we're performing our clinician assessment, again, performing a comprehensive physical exam, potentially incorporating a GCS score so that we have a more objective way of trending patient's recovery, as well as kind of having therapy co-administer validated skills, such as the coma recovery skill to make sure that we have like the most accurate diagnosis possible at that time. And then finally, when we're thinking about potential like medication recommendations, again, number one thing I think that's most important is assessing barriers to consciousness. So having a critical review of the patient's current medications, lab values, neuroimaging, and treating those causes that may potentially be acting as a barrier for our patients to emerge. Next, making sure that we have appropriate sleep-wake regulation. As I stated earlier, this is the foundation of recovery after brain injury. So making sure that our patients are sleeping well at night so that we can promote like neuroplasticity. And then finally, if we do think medications are appropriate, there's various agents that we can use. Again, I think the most kind of commonly used medication is imantadine because it is the only medication that does have a randomized control trial backing its use. However, that's more specific within the subacute kind of traumatic brain injury population. But again, we can kind of extrapolate those results to patients in the ICU setting if we're targeting wakefulness specifically considering modafinil and then if storming is a component considering bromocriptine. And then finally, I just want to review some emerging concepts that include cognitive motor dissonance or covert consciousness, which is this relatively new clinical entity that's gaining more and more traction. It can occur in roughly 15% of acute DOC. So a relatively small kind of subset of patients, but kind of the general principle behind this is that these are patients that are, that have, they're capable of having volitional thought, but they're incapable of kind of like executing any sort of like motoric action. So we'll identify these patients with task-based functional MRI or EEG. Next, we can also consider, and this is like a relatively new frontier of like neuromodulation, especially if we're thinking about helping patients emerge that can include median nerve stimulation, noninvasive anal nerve stimulation, low intensity focused ultrasound, hyperbaric oxygen and affected sensory stimuli. And then finally, I think there's emerging interest in the field of neuroprotection, pharmacologic neuroprotection where we're preventing that excitotoxic secondary cascade that's responsible for some more of the kind of chronic deficits that we see after TBI. And if we're really kind of like addressing and preventing this initial cascade from occurring, we can prevent some of those later complications. So now I'm going to pass it on to Krista. We'll be talking about some of the spinal cord injury considerations. Okay, thank you so much. I hope everyone can hear me. So yes, I'm going to move forward on the spinal cord injury considerations. And my hope is that as I move through some of these aspects to spinal cord injury management within the ICU, you can continue the framework of the patient, the case presentation that Keon started with and consider like what additional things you might've suggested and or what continued management might be considered for a patient you might've interacted with within the ICU. So first I just wanted to discuss some of the discrete presentations that you can see with the patient with the spinal cord injury when they're first coming into the ICU. And I wanted to discuss the differences between this presentation of neurogenic shock and that sort of hyper acute presentation of spinal cord injury and spinal shock. And so when we're considering neurogenic shock, which is on the left, this is most common within patients who have cervical injuries and it's because of the dysregulation or really just the sudden lack of sympathetic innervation to the spinal cord and the nerves, which leads to a superimposed or very large parasympathetic overdrive within the body. So in these patients, you're getting this arterial vasodilation. They are super hypotensive. That you can also have reduced cardiac contractility, which then favors bradycardia. And then similarly, these patients can have thermodysregulation. They also can be hypothermic on presentation. And because of this profound sort of neurogenic shock picture due to the parasympathetic hyperactivity or basically lack of sympathetic activity, it can also mask the presentation of sort of like hypovolemic shock or other forms of shock that may also be contributing to the picture. So similarly, if you had a patient with hypervolemic shock, you would expect their heart rate to go up, but because of this neurogenic picture, they don't have the ability to do that. So when you're considering a patient coming in or specifically one in the ICU where they might be having trouble regulating the blood pressure, you could consider the mechanism of injury and whether there's a component of hypovolemic shock that's going untreated. Similarly with this, this does resolve within the first few weeks. And so it is really within that hyperacute period following the spinal cord injury. And when we're considering spinal shock, this is actually a completely different phenomenon where you actually have depression of that reflex arc really below the level of the injury. So with these patients, we're focusing on a slightly different neurological picture where they have this flaccid paralysis, loss of deep tendon reflexes or primitive reflexes. They also lose a lot of their tone, which means that they have a reflexic or a loss of tone in their bowel and bladder. But similarly, but depending on where the level of the lesion is, you can see some cardiac arrhythmias or profound hypotension that develops. So separately, different from neurogenic shock, there's no real agreed upon timeframe for how long spinal shock lasts. So there are some patients who will be in spinal shock throughout their ICU stay. And if you are experienced, since you have a patient who is in spinal shock, you want to think about the bowel and bladder and some of the recommendations you might make based on this flaccid presentation. In general, we, and there's also no sort of agreed upon definition as terms of when is the end of spinal shock. Some physicians think it's when you start to see the return of reflexes. Some say it's when you have, you've regained all of the reflexes. But overall, in general, we find that it is, spinal shock ends around three weeks or so. And that also, like I said, that tends to be throughout the predominance of a patient's ICU course. In terms of the acute management as well, this is slightly older data, but there has been this conversation about whether there is any use for neuroprotective agents in terms of protecting or leading to long-term motor recovery or neuro recovery in patients with spinal cord injuries. And a lot of the data has looked into steroids and whether there is any benefit to utilization of steroids within that hyperacute period following spinal cord injury. And so the studies that we reference are three major studies that came out of the National Acute Spinal Cord Injury Study. So it's studies one, two, and three that basically looked as to whether there is any true benefit for utilization of steroids in terms of motor recovery or motor protection, neuro recovery in these patients. So the first study, what it was looking at was whether there was a difference. It compared basically high dose and low dose methylprednisone in patients with acute spinal cord injury and presenting within the first 48 hours, excuse me. And within that study, they actually saw that there was no difference in terms of neuro recovery or in terms of neuro protection, maintaining their neurological status in either group. But a downfall or negative of that study is there was not a placebo group in the study. So some might've said that, well, maybe all of the patients are getting better because there is no placebo group and it doesn't necessarily matter the dose of the steroids. And so if we looked at the studies of two and three, they actually looked at, there was a placebo group within these studies and it looked at basically if there was a benefit to a certain amount of steroids within the hyperacute period within the first 23 hours of following spinal cord injury. So in the NASCIS, I was trying to not mess that up. They actually found that there was no difference in neuro recovery at one year when they looked at patients who had steroids and those who did not. But they did know that some patients who received high dose methylprednisone within the first eight hours after their injury did seem to have some improvement in their motor recovery compared to placebo at one year. But the caveat in that study is that they did note that the effect seemed to be marginal and there was concern for significant medical complications with the utilization of high dose steroids. And then finally, in the third study, they wanted to tease out whether there was really a difference between kind of high dose steroids in the first two days or the first 24 hours following spinal cord injury and whether it differed based on dose. And so again, they did find that there was better neurologic outcomes for patients who received steroids within the first eight hours of injuries, of the injury, excuse me, but there was significant medical complications with patients who received these steroids, including severe pneumonia, sepsis, and infection. And so overall, the consensus was that the risk really outweighs the benefit in terms of utilization of steroids in that hyperacute period for the goal of promoting neuro-recovery or neuro-protection in acute spinal cord injury. So it's something that we do not recommend and is not utilized in terms of the ICU or acute presentation following spinal cord injury. Similar, in addition to that, we think about the acute management of blood pressure. So as I stated, these patients, whether it's due to neurogenic shock or sometimes the spinal shock that we see in our patients, there is this period of hypoperfusion. And if it's not managed appropriately, it can lead to secondary injury in our patients. So whether that's a secondary hypoxic brain injury, or sometimes there can be a worsening or progression of the spinal cord injury due to hypoperfusion of the spinal cord. And so it's very important that we maintain a blood pressure goal within that early period following spinal cord injury. Right now, the data supports maintaining a MAP pressure of at least 85 within the first seven days. There's very little support that states that maintaining a blood, that MAP goal beyond the first seven days really provides a benefit in terms of the prevention of a secondary injury. So in terms of our recommendations within the ICU, we really like to focus in within the first seven days of treatment. In terms of utilization of medications, fluids and vasopressors are, the support of utilizing them is there. I just wanted to take a brief minute and talk about within spinal cord injury itself, we really don't have any data to support any other agents in terms of providing a neuroprotective quality in the acute phase following spinal cord injury. There've been multiple studies, most of them within Europe that have looked at various drugs. For the sake of time, I'm not going to go into all of them, but there have been various studies from the 1990s, the 2000s to even recently. And thus far, we have not seen a drug that has panned out in terms of having a true benefit from the standpoint of motor or neuro recovery or neuroprotection after someone sustains a spinal cord injury. And then with the remaining time that I have, I'm going to focus in on some of the like organ system specific implications within acute spinal cord injury or considerations within the ICU. So starting with the cardiac implications, depending on the level of the injury, you can see these presentation of bradyarrhythmias or bradycardia. And this is likely due to the parasympathetic overdrive or really the lack of sympathetic innervation, depending on the level of the lesion. A lot of the innervation to the heart in terms of the parasympathetic capabilities is innervated through cranial nerve. So they're largely intact following a spinal cord injury. And a lot of the sympathetic tone comes from those high thoracic nerve roots. And so if you have a higher injury that can lead to dysregulation and then the presentation of these bradyarrhythmias or bradycardia. So patients can have this bradycardia or bradyarrhythmia, sorry, excuse me, bradyarrhythmia at baseline, but it is also something that can be provoked in terms of a noxious stimuli. So within the ICU, it's not uncommon to see that patients will flip into an arrhythmia when they're having suctioning, when they are receiving breathing treatments, when they're being rolled or repositioned. And it usually resolves when that noxious stimuli is removed. When we're considering this management, we just have to be aware of what some of the triggers might be. Similarly, there are medications or procedures that we can do. But as the patient comes out of spinal shock, usually the bradyarrhythmias or bradycardia improve to the point where you don't need long-term intervention. So when we're thinking about management for bradyarrhythmias or arrhythmias in general, we're tending to think more in terms of situational management, whether that through atropine, which is a quick-on medication. Like if they're going to be suctioned and you know that's something that triggers their cardiarrhythmia, you can pre-treat with atropine to try and mitigate some of those effects. If you have a patient who is having these cardiarrhythmias frequently, there's also transcutaneous casing that can be used and usually comes off as the patient gets farther out from their initial injury. Finally, some patients do require pacemaker placement. So in terms of this case, he did actually go into PEA arrest following his initial injury. And so that would be an indication for a pacemaker placement. But in general, it's fairly rare and we don't recommend placement because like I said, as you get farther out from the injury, the cardiarrhythmias do resolve, really by the time the patient is just a couple of weeks out and sometimes still within the ICU. In terms of the pulmonary implications, similarly, it can depend on the level of the lesion. And so I broke it up into some of the autonomic dysregulation that you might see and then some of the dysregulation that you might see based on some of the de-innervation of the somatic muscles for respiration. So again, if you have dysregulation of that sympathetic and parasympathetic tone, the lungs tend to favor sort of bronchial constriction because we're thinking about that parasympathetic, that rest and digest. And similarly, it favors alveoli relaxation. Also within the ICU, because of that sympathetic overtone, I apologize if you can hear my daughter from the background, but you can see the parasympathetic overtone, which can also lead to an increased production in terms of the secretions within the lung. And all of these things together can lead to basically tight airways with relaxed alveoli, which favors atelectasis and mucus plugging. And then similarly, on top of that, you add on the fact that they are making more secretions. So within that ICU period, patients are at a much higher risk for pneumonias, mucus plugging, and even pulmonary edema because of that relaxation of the pulmonary arteries or the vasodilation of the arteries within the respiratory system. Similarly, in terms of the somatic de-innervation, so a lot of the muscles that drive respiration are, there's muscles that drive respiration. So if you have any of these muscles affected, it can lead to more of a hypoventilation presentation for a patient. So that can present itself as decreased lung volumes, whether the diaphragm is involved, it might actually lead to the patient not being able to breathe on their own. Similarly, if you're lacking some of the somatic control to the abdominal wall or chest intercostal muscles, it can lead to ineffective puffs or difficulty clearing secretions. And then there's also what we call paradoxical respiration, which is where instead of the chest wall going out with inspiration and the abdominal wall coming in, you actually have the reverse where the chest wall comes in and the abdominal wall goes out, which also favors collapsed lungs when they're breathing. So I'm just highlighting a few that shows that like following acute spinal cord injury, the respiratory risks are fairly high. When we're managing it, so there's been quite a few studies that have actually looked at that patients with spinal cord injury seem to have improvement in their respiratory status with slightly higher lung volumes in terms of tidal volumes compared to other patients within the ICU. And so there've been various studies that have talked about various numbers, but in general, it has been found that if we can slightly increase the tidal volume for ventilated patients, there is a decreased risk of ventilator-associated pneumonia and also if the patient is able to wean leads to faster weaning. Similarly, if you do have a patient, whether they are ventilated or not, the use of mechanical insufflator, exsufflator to actually allow for expansion of the chest wall and expansion of the alveoli and then also sucking out some of the secretions, there's still the form of quad cough or like pulmonary PT to allow some of those secretions to come up and deep suctioning. Similarly, in terms of medication management, there's the normal bronchodilators and there's also medications that you can use to both thicken or manage secretions. I just wanted to highlight that we don't use, at least in my practice, we don't utilize glycopyrrolate fairly much anymore because it is a medication that can also like paradoxically thicken the secretions. And so if you're already having a difficult time getting the secretions out or managing them, then causing them to be thick can kind of make it more difficult for management. Very quickly, I did wanna talk about early tracheostomy placement in spinal cord injury patients. So there's not a study that looked at spinal cord injury exclusively, but it did look at spinal cord injury patients as a group of a severely or critically ill ICU patients. And even though, so within that group, they looked at whether there was a benefit to early tracheostomy patient or patients who are critically ill. And it did find that early tracheostomy placement led to reduced length of stay and decreased duration of mechanical ventilation. So they were able to decannulate on their own much faster. And so in general, because of these studies, we do recommend early tracheostomy placement for patients with acute spinal cord injury who are going to need, whether they're going to be ventilator dependent or have to be slowly weaned from the vent. And in general, the optimal timeframe is seven to 14 days. And so in general, we use the timeframe of 10 days, at 10 days out from injury as being, as it occurring within that timeframe for being the optimal timeframe for placement of trach. Quickly, with the remaining time I have, I did wanna talk about some of the GI and GU implications. So I do not, I did wanna take a minute to talk about dysphagia and how common that is, especially within patients who have a concomitant brain injury. If they had any instrumentation or surgery of the anterior neck as a result of their spinal cord injury, many of our patients end up in collars or even just like prolonged intubation or tracheostomy can put patients at an increased risk of dysphagia. So we want to make sure that we are evaluating for this in our patients, because that also does increase their risk of pneumonias or worsen their respiratory status, which is already at risk in the acute phase of spinal cord injury. Similarly, there is an increased ulcer risk. And that is because the increase of gastric secretions due to that increased parasympathetic effect following acute spinal cord injury. So we generally do recommend that as long as they're not necessarily using a PEG tube for feeds, that you do empirically use a PPI or an H2 agonist for at least four weeks of treatment following spinal cord injury. There is some data to note that if there is prolonged PPI use greater than four weeks, that does increase the risk of C. diff. So as long as there's no other indication for utilization of one of these medications, we do like to limit it to four weeks. In terms of like lower bowel management and in the ICU, a lot of it does sort of depend on how the spinal cord injury is classified and if the patient is out of spinal shock. So as I stated before, if the patient is still in spinal shock, they're going to have a lack of rectal tone or some of those reflexes that we can utilize for a bowel program, and therefore they will be ineffective. So if we're thinking about the utilization of digital stimulation or the utilization of a suppository, those medications work largely through the utilization of the rectocolic reflex, where you have irritation of the rectum that then leads to a reflexive evacuation of the colon and a patient within spinal shock, those are rendered ineffective. So in general, if you have a patient where you're concerned that they're still in spinal shock, we still largely manage them as an areflexic bowel, meaning you might have to utilize manual disimpaction and then continuing to use a motility agent in terms of SENA or another medication like that because the intrinsic plexus is still intact and that's where that medication works to increase peristalsis. Otherwise, depending on the injury, if you can continue with an areflexic bowel program if needed, or if there's evidence of a reflexic or upper motor neuron bowel program, you can utilize some of those positional and medications within the bowel program to allow for evacuation within the bowel. In terms of bladder management, very quickly, we generally recommend continued use of a Foley while the patient is within the ICU. That's because it allows us for adequate measurement of the Is and Os. These patients tend to be getting a lot of fluids and maintaining appropriate bladder pressures and bladder volumes with the amount of fluids or medications that these patients are getting is really difficult. And then similarly, a Foley can manage a bladder effectively whether the patient's still in spinal shock or they have an upper motor neuron or lower motor neuron bowel, sorry, bladder. So in general, we do recommend maintaining the Foley when it is indicated to remove the Foley, whether that's still within the ICU or not. My general rule of thumb is watching their urine output for 24 hours and hoping for a urine output of less than 2,400 CCs. So if we think about it, if we are capping a patient at most every four hours, if our goal is to have around 500 or so CCs in the bladder every four hours, that those numbers kind of add up in terms of being a safe amount of urine that can stay in the bladder. So once I see evidence that there's two liters or so of urine in 24 hours, that's an indication that we can consider switching to intermittent capping. Finally, I did wanna talk about skin protection and DVT risk. So very briefly, pressure injuries are a major concern within the ICU and ensuring that patients don't develop contractures or maintain an adequate or appropriate positioning of their arms and legs is very important. So I just wanted to emphasize Q2 turning, making sure the patient is up to bed as often as they can. Kian talked about early mobility and the benefits of that. And then just ensuring that we are using proper equipment, whether that's Prefos or green soft boot or the big fluffy boots to keep the heels off the bed to minimize pressure. Sometimes you can use a putty pillow or wedges to just ensure appropriate turning. And then if you do have a patient who is going to be up in the chair, ensuring that they're sitting on a cushion that's appropriate for them and has appropriate fit. And then finally, in terms of DVT risk, so about 50% of SEI patients within the ICU will develop a blood clot or a DVT if they are not on prophylaxis. And 92% of them will develop a blood clot if they're not on prophylaxis within the first three months. And so I just state that to document how important it is that these patients end up on empiric DVT prophylaxis. We also have data to support that the highest risk for DVT is within that first 72 hour to 14 day period. And so if we're thinking about management, there's various forms. So there is the mechanical compression or SEDs is how they're called in our hospital where you do have compression of the leg vasculature to improve blood return back to the heart. In general, our data supports that these are inefficient or insufficient as a monotherapy for prevention of DVTs. And really there isn't a study that shows that they are really effective in general, but it's thought to be a low risk medium or a low risk intervention as long as there's no evidence of active DVT. For patients with a spinal cord injury, the question is what medication would be best for chemoprophylaxis? And just very quickly, the data supports Lovinox being somewhat superior to unfractionated Eprin. And that is from the standpoint of in the studies, they noted that patients who were on Lovinox had lower risk of developing pulmonary embolism and also were noted to have lower risk of major bleed. And so if we're going to pick between the two of them, it's thought that Lovinox is slightly safer within our patient population. Similarly, there have been studies that have looked at whether 30 milligrams VID versus 40 milligrams daily is better. In general, the studies we have right now note that they're equivalent, but in my general practice and those who I've trained under, given the highest risk is within those first two weeks, if able, we prefer to do the 30 milligrams VID within the first two weeks and then transition to the 40 milligrams daily for the duration of what the patient needs in terms of their DVT prophylaxis. So with that, that's the end of my portion. And I am going to turn it over to Matt, who's gonna touch on how to make some of these recommendations in a multidisciplinary approach when you're working with other clinicians in the ICU. So I'll stop sharing my screen. All right, just give me a moment to switch over to the presenter mode. And let's see if I got this. All right. Can you guys see the screen okay? All right. Does it have the Zoom stuff on it? Nope. Okay, good. All right. So today, I'll try and be as brief as possible so that we can save time for questions. Again, what we're going to be talking about from my portion is trying to figure out what kind of barriers may be present to doing a PM&R consult in the ICU. So again, let's go back to that case study. We have that 52-year-old gentleman. He had a fall. He's still in the ICU. You follow up three days later, and you notice not one of your treatments have been started. So what do you do? You can always rewrite the note in bold, highlight, italicize all your recommendations again. You can angrily wander around the ICU muttering, they never listened to me. You can work at a different hospital. There's that. Or you can refuse to take any other patients to acute rehab. But let's find a better way than doing that. So today, what I'm going to be talking to you is how to facilitate that ICU culture. I'm primarily going to be speaking about my experience working to increase our ICU consults in my large safety net hospital in a large municipal region. So there's three strategies that I use to help increase our ICU consults for PM&R. It's been a slow process, but it's been doing very well. I've gotten a lot of really good feedback so far. So first off is knowing the culture. What is life like in the ICU? Are consultants allowed to put in orders? Who's the teams that are running? Who are those teams that are running as primary in there? Do you have neurosurgery that's a primary? Is it a trauma team? Do you actually have a dedicated SICU primary team, etc. Also knowing your arguments for your treatments, would be the other thing that I really talk a lot about. What is the evidence for imantadine that you're going to be talking about with the brain injury patients? So first off, when I started here, it was really rare that physiatrists was consulted in the ICU. Aside from maybe those mandatory stroke consults as a stroke center, we really only got invited up into the ICU just for disposition questions. That just seemed like very limited use of our skill and resources. The idea that PM&R could help with things like agitation management was really not a thought. It was particularly thought of that we could muddy the prognosis if we're consulted too soon. Oh no, we're talking about rehab when the patient may have a poor prognosis. I do recall being told a story about a prior PM&R doc that had walked into an ICU room and told the family that the patient would be getting better soon. They'd be coming to rehab and three days later, they had deceased. So there was a lot of trepidation about PM&R that I didn't necessarily understand when I first started and then it cleared up. There was also a lot of people who didn't recognize any early benefit to PM&R. They're just like, well, you're just going to tell me that my patients are going to rehab or not. One of the other things I noticed about the culture is that it's very much a multidisciplinary as opposed to interdisciplinary approach that you've got lots of great consultants and multiple attending teams, but not a lot of people are talking to each other. Even on the rounds, you could see like four different teams rounding at the same time but not talking to each other. There's also noted personality conflicts. I mean, I don't know which hospital you go to that doesn't have personality conflicts within their staff, but that could definitely limit your treatment options as people might have a poor opinion of somebody else and maybe not do the best thing for that patient. We hope that's not the case, but it can happen. Typically for agitation management and all of our patients, psychiatry was typically consulted. Boy, did they love haloperidol. It's been a lot of fun trying to break that habit. The next argument I usually say is trying to know your team. There's that great Sun Tzu quote about if you know your enemy and know yourself, you need not fear results in 100 battles. Well, not only do you need to understand what you're capable of bringing, but you need to know where the team is at. Do they have residents on there? Is there a lot of APPs who are doing a lot of the day-to-day decision? What's your relationship with the other attendings? Are you able to teach your nurses? Finding out who your allies are. I found out that we've got some great therapists in the ICU, but they may not be familiar with a lot of the things that even rehab or PM&R can bring to that early ICU stay. Your other care teams such as palliative medicine or psychiatry can be great partners with to help educate and maybe turn that tide to see, hey, how can we interface and do a lot of the recommendations you just heard about? Other thing that I really wanted to talk about is orders versus collaboration. There's oftentimes that people would write orders, but nobody follows it through. It's because the other teams aren't necessarily engaged. They may not understand the thought process behind those orders. There was a lot of breakdown in communication across teams. Knowing the argument for PM&R. This is one of the areas that's very important to be educated on. There's a lot of limited and I want to almost say bad evidence. It's not necessarily like horrible, but it's limiting, right? There's evidence to suggest in a retrospective study that early imantadine use is more harmful because it prolongs their DOC and increases medication use such as antipsychotics and opiates. There was a comparison that recently got published about imantadine versus modafinil versus something that they called standard of care, which was fairly ill-defined. But it was a retrospective study where even the authors themselves concluded that we may have not picked the right patient population to compare this to. But this is stuff that's in the literature. This is stuff that the other teams were coming back and saying, well, no, of course we don't want to do it because of these reasons. There's also a lack of PM&R rehabilitation. And many of the clinical practice guidelines that are used in the ICU. The Brain Trauma Foundation actually does not mention rehabilitation or PM&R. And that's the one that's predominantly used by neurosurgeons for moderate to severe TBI. Aspen does not actually have a guideline for trauma. It goes under their acute care critical illness. The American College of Surgeons, they actually do mention PM&R within the spine injury guidance, probably because ACRM helped co-write that. But it's also another evidence that we're very limited in these conversations. And so because of that, we're not able to really kind of interface with people. So why PM&R in the ICU? Well, there is evidence suggested. So the first one is that PM&R consult within seven days did decrease length of stay overall. It also decreased benzodiazepine and antipsychotic use. So those are two hats that definitely can be helpful. Furthermore, there is evidence that suggests a brain injury medicine specific consult within seven days reduced length of stay by six days. You also reduce the bounce backs. You had improved emergence from DOC. And if you did consult within two days, you reduced the acute care stay as well. So there is some really good evidence to say, hey, getting us involved early can be helpful. You also want to know your arguments. So just as my fellow presenters really talked about what kind of recommendations there are, knowing the clinical practice guidelines is very, very, very helpful. And I've been able to use those to kind of understand and tell people, hey, this is how we should be practicing autonomic dysreflexia. See, the PVA has this whole guideline on this. Or, you know, hey, early discussions about amputation should probably be done before you amputate the limb, et cetera. I really like using the Canadian, formerly the Ontario Neurotrauma Guidelines. And it's not quite as expansive for ICU, but it does give you some more information that you can take to your team to help build. So these are some great resources that I've used to help build my practice. So putting all this into practice. So the first thing that I did was I coordinated with my team. There's three, now four of us physicians, physiatrists. And so what I ended up doing was I built templates to ensure consistency. So we have a order set for moderate severe TBI, for SCI, for amputation, for stroke, to really kind of help us be on the same page there. And they're more of an expansive guideline. And so that way, each provider can trim down what they think might not necessarily be there, but at least gives each person a starting point for, hey, we probably need to address this. Building relationships. This was the biggest factor of all. I regularly met with our neurosurgery and neurology teams. I also was part of our SCI management working group as they were re-updating their SCI criteria. And by being part of that, I was able to add in a little bit more influence and to get us consulted within 48 hours of spinal cord injury. I'm a huge educator guy. I really love talking to people and educating, and I love cross-pollination. So I've been lecturing to trauma residents, the palliative care, psychiatry, neurosurgery, internal medicine, family medicine. I'm basically going in there and really talking about things. And I've got a lot of things about, you know, early consults, TBI management, and things like that, that has been very, very helpful for these other teams and has improved my working relationship with them. I also built in face-to-face time. You know, I, yes, I'll go and see these patients at SICU, but I'll stop in their office or I'll go track down the residents and have that face-to-face time. And being able to, if I can't round with the SICU. I really like doing this, especially if I'm wanting to talk to them about, hey, what do you think about Amanda Dean? And really trying to build up some collaboration with them and also get them to do the orders with me if that's appropriate. So, progress so far. Pros, I've built some really great alliance, especially with our APP staff within our SICU. After just conversations with them, they feel much more confident in TBI agitation. They are able to help advance our TBI patients faster, more direction with trial avoid in SCI patients, especially we got a new neurogenic bladder protocol, and that's been extremely helpful for our ICU nursing. Also, just this idea of helping with neurostorming and autonomic dysreflexia, bringing that to their attention, because there's episodes that were occurring that they were not recognizing. We're now auto-consulted for SCI, as I said. We are taking more patients from the ICU to our acute rehab. And less haloperidol. Cons, there's still been a hesitancy towards certain orders, especially for agitation management. That's been a very hard barrier, and there's a lot of preconceived notions that have been really working on trying to break down or try and interface with. Limited adoption with early recommendations. So, even though I'll have a lot of recommendations, it's very slow to bite into that. And to be fair, there's a lot of other acute care issues that are going on. So, trying to be working with them and helping to educate and facilitate them helps to improve that communication. I've also found it's been difficult to maintain consistent follow-up. So, that's one of the things I always want to just make sure I mention to my colleagues, is that trying to get in there, you know, two times, hopefully three a week to assess some of these patients is very helpful. So, you can keep building that face-to-face and keep helping to progress their medications and treatments. In the future, we really want to have rehab auto-consulted for our trauma patients and trying to help increasing our staff to help follow up with consults as well. Finally, helpful hints. You can build critical care time. Talk to your facility about this, but this has been something I've been able to do. It does have to be on the floor, and it does have to be directly influencing the length of stay. So, anytime I'm doing agitation management with a patient, that definitely has been counting. And so, you get some pretty decent RVUs out of that. I really like the approach of collaboration. So, working with the team going, instead of wandering in there and go, hey, you need to do this, having them say, hey, what do you think about starting imantadine? Or, I'm pretty certain agitation is going to come. They're starting to be in this MCS state. How do we, this is how we might want to approach with this. And trying to get the low-hanging fruit, such as early labs, like zinc and other things, or DVT screening, can be very helpful, especially as you build your relationships. I also really try and identify when families are present. So, asking nursing. So, that way I can come around, answer a lot of the questions, and provide them a general arching viewpoint of what may be going on, to provide a lot more family education. All right. I'm sorry. I tried to push through as fast as I could. If you have any questions, here are my emails. All right. Thank you to our wonderful speakers. We'll open it up to just one or two questions, if anyone has any. But there's nothing in the chat right now. So, you can unmute yourself and ask. I think I see a question about elaborating on zinc. If you look at the Ontario Neurotrauma Guidelines, there is a recommendation for assessing zinc early on. I believe the real assessment is just trying to get in the door. If people are deficient, there's evidence to suggest replacement early on in their stay helps to reduce overall outcomes, or improve overall outcomes. All right. If not anymore, I think that concludes our session. Thank you, everybody, for joining. Definitely hope you enjoyed our talk. These were great, great talks. I definitely enjoyed them. So, yeah, hope you guys, you know, learn something and have a great rest of your evenings. Again, I think some people put in some kind of... Yeah, there's a couple of questions. All right. Yeah, I'll try to address like the one about prognosis kind of like quickly. So I like speaking from like brain injuries kind of like specifically. So there's actually kind of like in terms of this study that I had cited, and if you do review the ACRM guidelines, when we're thinking about like disorder of consciousness, we actually shouldn't be having any definitive conversations regarding prognosis in terms of patients in a disorder of consciousness. So I tend or I generally like won't kind of recommend like favoring having kind of like those like in-depth kind of like family meetings unless a patient is in kind of like a coma and approaching like that four-week mark, because there has been literature that's shown that once kind of if patients like remain in a coma, like past the four-week mark, generally the global prognosis is pretty kind of universally poor at that point. But there are various like online calculators. I think Impact has an online calculator where you can enter patient-specific data that can give you a generalized idea of where you can potentially expect a patient like outcome, like I think like at the six-month mark. But again, you have to be a little bit cautious in terms of using that just to kind of like avoid giving kind of patients as well as families any kind of like definitive idea of where That Impact calculator specifically says not for clinical use, only for research. I'd say from the standpoint of spinal cord injury, I also just err on the side of not saying anything definitive, especially for a lot of these patients when they're acutely in the ICU, they're still within spinal shock. And I find that in terms of spinal cord injury, traumatic spinal cord injury, we're using the INSCE or the AIS assessment to help with prognosis. And the benefit of that really only comes into play when a patient is at a spinal shock. So you can really assess their rectal tone. So again, I do get a general idea of like where their level might be, because that might help from vent weaning or other conversations that might come up. But anything definitive, I try to delay until like we can have a more in-depth examination. In terms of how I talk about guidelines, when I write a note, I've been made fun of, but I do write fairly lengthy notes when I'm consulted in the ICU and I have referenced papers before. I just like to document in the chart. So I do both. I have a very, if I can, I try to get as much face time with the team, like Matt was saying, and have these conversations in person. But I always like to have that reference in the chart as well. Yeah, I would say my typical template does not have the specific guidelines written, but I will pull them out if there's been a little bit of sparring about something. And I will always, when I'm educating people, especially face-to-face, I'm specifically referencing which guideline I'm pulling from. I was told we can go to 825, so we still have time for some questions. There's another one. Do you want that? Or do you want me to take that one? Yeah, I can take that one. So just in terms of if I am leading toward antipsychotics, I will say a lot of it is due to institutional preference and what people have grown with. So generally, I do personally, I have a tendency to favor Risperdal a little bit more. I feel like it kind of helps control some more of that kind of motoric disinhibition pathways. However, out of the three of them, it is the strongest antidopaminergic one. So that is something to be aware of. Steroquel tends to be a little bit more antihistaminergic. It also has a shorter half-life. So you might need to use more frequent doses of that medication as opposed to Risperdal versus Olanzapine, which is perhaps the most long-lasting out of the three. It also comes in that IM form that you can use off the cuff in episodes of combative, severe agitation. So that's when that would be useful. So it's pretty patient-specific, at least for me. But in general, I don't, like in terms of like one kind of like over the other, I think for the most part, if you're not using Haldol, like pretty much any of those medications are better. Yeah, I'll dovetail off that one. So I would say that my, our ICU likes Seroquel first. And so that's been one of the things, and you're right, it's usually been a TID. So like 50-50-100 or something like that is how they'll do a dosing schedule. And, but when I start seeing people more being more sleepy or I'm trying to awaken them or we're starting to get a little bit more like agitation that just isn't seeming to fit right, I'm usually recommending Risperdal back. Risperdal just doesn't have as much of that anticholinergic effect. It does help kind of lead that out. So as a cleaner drug, you kind of limit a little bit some of this additional delirium-esque picture that might be complicating your TBI delirium. Olanzapine, as it is available IM, it is also commonly used IV in the ICU. And so there's been numerous papers to describe that it's effective in an IV situation as well. Not FDA approved, but that is something that is clinically done, and it's commonly done here. I see a question that says, from the standpoint of the ASIA exam, when do you recommend performing first and interval examination? So a lot of the data does say that there is benefit to perform and see within the first 72 hours following spinal cord injury. I think that I try to follow a similar pathway to get a general idea of what I think I might be, their level might be, but I tend to not say anything definitive until I do see evidence that they're out of spinal shock. So when I'm seeing patients in the ICU, I'm reevaluating fairly frequently. I'm looking for some of those more subtle or first signs of out of spinal shock. So I know there's talk back and forth in terms of the usefulness of anal wink or bubble cavernosis reflex or things like that. But I do think that, especially within the ICU, some of those things do have utility. Similarly, some of these patients, you can't really turn given some of the surgical implications that they might have. So in general, I try to get a general idea pretty early on. And then usually if these patients are coming to acute rehab, we do one within the first 72 hours of them getting to acute rehab. Then I try to do one again within 72 hours of discharge. After that, the recommendations are doing one at one year following spinal cord injury. And then you could also evaluate if there's any signs of significant motor return in between. Yeah, I'd say one of the early challenges is sedation in SCI patients and just you might blow past that 72 hours just because they aren't able to participate in the exam yet. All right, any other questions? All right, there's one more for TBI DVT prophylaxis. Yeah, so in general, I don't think like, at least in comparison to like spinal cord injury, there isn't kind of like any kind of clear kind of guidance whether or not like if there's like a set time period of kind of like how long you should like prophylactically like anticoagulate like a patient after traumatic brain injury. We do know that patients are in this more like hypercoagulable state as a result of the brain injury. So generally, we will kind of like recommend at least kind of using some sort of like Lovenox kind of like prophylaxis um kind of like with the caveat where kind of like depending on like the extent and level of breed there may or may not be kind of like worsening or kind of like a worsening evolution of the bleed. I will say that like a lot of the times when that kind of like discussion is being made of whether or not to kind of like hold like anticoagulation or prophylactic anticoagulation or not there it's a very kind of like clear kind of communication with the um with the ICU teams and by the time um that our patients do come over to like the acute rehab setting they're kind of like out of that period where you'll kind of like expect further progression of their bleed which tends to resolve within the first like three three to four days after the event. But I think that's a really just kind of like good question in terms of whether or not um kind of we should be kind of like recommending that versus not but I think that's more of like just kind of an interdisciplinary or an interdisciplinary conversation with um some of our kind of like surgical colleagues that we're frequently co-managing these patients with. Alright, so it's past 8.25. I want to thank all the speakers again. We're staying a little later too to answer questions. Thank you all for the good questions from the audience. And yeah, thank you all for joining us today. All right, have a good one, everyone.

neurorehabilitation physiatrists

ICU patients

brain injuries

spinal cord injuries

strokes

early mobility

hypertonia management

seizures

agitation management

trach placement

PEG placement

spinal shock