All right, while we have a minute before we get started here, I'll go ahead and introduce our speakers. So my name is Dr. Mary Russell. I am an associate professor at University of Texas at Houston, and I am involved, also medical director of Tier Memorial Hermann in the Woodlands and vice chair for quality and compliance. I do a lot of rehabilitation consults with the trauma team and neurology and neurocritical care team. And so we put together this session today to try and kind of educate you a little bit on some neurocritical care fundamentals and a little bit about what you could be seeing with the management in terms of the ICU, as well as as a rehab physician, what you can contribute in terms of rehab assessments and rehab care that is more than just a disposition. So I have a really big shoes to fill after following Dr. Glaucoma Flecken. So hopefully you guys will find this a worthwhile session. I would like to introduce Dr. Rashi Krishnan. She's one of my wonderful colleagues at Memorial Hermann in the Woodlands, and she did her medical education at BJ Medical College in India, her residency and fellowship at University of Tennessee Health Science Center, and is board certified in psychiatry and neurology, as well as neurocritical care. And without further ado, Dr. Krishnan. Thank you, Dr. Russell, for the wonderful introduction. And thank you, AAPMNR, for inviting me as a guest speaker today. So I'll jump straight to my passion, which is neurocritical care diagnosis. Time is brain. This is the one thing that we're taught from the beginning of residencies, that time is brain in neurology. And that's why this time is very important to diagnose and treat all the neurocritical care and neurosurgical emergencies, because we know that when we treat them and diagnose them early on, that is a way to reduce the long-term morbidity, mortality, and improve the outcomes in our patients. The most common neurological conditions that we see in the neuro-ICU and that require neurocritical care expertise are acute ischemic strokes, intracerebral hemorrhage, aneurysmal subarachnoid hemorrhage, status epilepticus, and traumatic brain injury. I'll jump to a case. So here we have a 65-year-old male who presents to the ED with left face and arm weakness, inattention, and visual field neglect. The onset was witnessed from a family member, which was exactly 30 minutes prior to arrival. Past medical history of hypertension, hyperlipidemia. Home meds included simvastatin, lisinopril, and aspirin 81 milligram. Results on ED arrival, he was ephebrile, blood pressure was normal, 160 by 90, heart rate 96, respiratory rate 18, SATs were 98%, NIH stroke scale by the ED attending was 14, and blood glucose and acu-check was normal. The CT head on arrival in the ED, we see that he has normal age-related volume loss. I don't see any big major clots, hemorrhage, no subdurals, no contraindications for TNK administration. Then the next thing we do is a CTA, or CTA angiogram of a head and neck. On the left, you have the CTA of the head. If I may point out, you see an acute occlusion in the large vessel, which is in the right M1, which is the proximal MCA, which involves the entire right MCA territory. The right top is the rapid software, which we now use for CT perfusion to assess the amount of brain that is at stake to be lost if we don't treat it imminently. So the purple is the ischemic core, which means that's a core infarct, which is almost already dead, which is only 25 mils. But the rapid software also tells us that the perfusion lesion is the whole green area, which is close to 96 mils, which is the entire right MCA territory. So the mismatch volume here is 71, and the mismatch ratio is 3.8. What does this tell you? That if we don't treat it right now, there is almost 96 mils of brain tissue, which is at risk to have future infarction. So this patient underwent intravenous thrombolysis, received TNK, as well as intraarterial thrombectomy. The patient went straight to the cath lab for the thrombectomy. The clot was removed, and post-op, the left side weakness improved. The NIH stroke scale at 24-hour reduced from 13 to 2, which was only for dysarthria and facial droop. The patient continued to get better and was discharged to inpatient rehab. This is one of the most important and common examples that we see where treating them and diagnosing them early on and getting the right level of care can reduce significant disability. The 63-year-old male would have had a whole left-sided hemiplegia and hemiparesis requiring nursing home, or maybe a trachea and PEG tube placement. But the fact that we diagnosed early on and we treated that, that led him to just go home after some rehab placements within a NIH stroke scale of just 2, did not require any kind of disability or any future assistance. He was almost back to his baseline in three months. So I wanted to go over the absolute contraindications of TNK. TNK is tenecteplase, which is the intravenous thrombolysis. In general, the dose is 0.25 milligram per kilogram IV. It is given as a single bolus push over one to five minutes, and that's it. We're done there. The major contraindication, or the absolute contraindication that everyone needs to know are major head trauma, ischemic strokes, intracranial and spinal surgery in the last three months. History of ICH or intracranial neoplasm, any brain tumors, gliomas, any history, do not do a tenecteplase. Signs and symptoms of subarachnoid hemorrhage, like sudden onset thunderclap headache, even if you see the CT head is normal, then that might be a contraindication. History of endocarditis, because these patients usually have septic emboli going to the brain, and those bleed with tenecteplase, or aortic arch dissection. So when these patients come in with acute onset of hemiplegia, it's very important to make sure you have a chest x-ray, too, or the CTA head and neck is done, so that in the neck you can rule out an aortic arch dissection as well. GI malignancy or recent bleeding within the last 21 days, if the patient is on direct thrombin inhibitors, or direct factor X inhibitors, or warfarin with an INR of greater than 1.7. So even if on warfarin, but the INR is not greater than 1.7, then those patients do meet criteria for acute thrombosis. CT head, which if it shows severe hypotenuation, hypodensity, or involvement of greater than one-third of the cerebral hemisphere, or ICH. Of course, ICH is a contraindication, but if you already see a big hypodensity, that means the TNK window, which is up to four and a half hours, has passed, and they do not meet criteria for IV thrombosis. What happens if there is a side effect of TNK, which means that if you have a sudden onset of neurological deterioration in the first 24 hours after receiving tenecteplase, you try to get to the CT head as soon as possible. But basic things that need to be done first are you check vital signs every 15 minutes, check the pupils, because they could be herniating from the ICH, head of the bed up, obtain a non-contrast CT head, and notify your neurosurgeon colleagues on call. Get all the stat labs, including the DIC profile, PT, PTT, platelets, fibrinogen, and cryoprecipitate is given if you have the CT head, if confirmed hemorrhage. So cryodosing is ten units, that's standard. You just give it to them, and then repeat the fibrinogen level. If the fibrinogen level is still less than 200, then you repeat the cryodosing to make sure that the coagulopathy is corrected. I'll jump to the second case. Sixty-two-year-old male presents to the ED after pedestrian-struck accident. GCS is seven in the ED. No focal neurological deficits are seen. That means when you stun rub those patients, he's actually moving all four, but just GCS is seven. There is limited eye opening and no verbal response. The blood pressure on arrival is 115 by 62, heart rate is 95, SADS at 85%. He's intubated on arrival in the ED because of the low GCS and hypoxia. You get the CT head. The first CT, what do we see? We see bifrontal contusions and subdural hemorrhage, just overlying the both frontal lobes. There's a little bit of vasogenic edema around the contusions, a little mass effect over the ventricles, because as such, we don't see any big major lesion there. But what does this patient need? He needs an EVD. Why is that? Just for ICP monitoring. If you have to pinpoint why we need an ICP monitor, most common indication in the ED, if you have a traumatic brain injury and a GCS of eight or less, then those meet criteria to have an ICP monitor. We prefer to have an EVD because that not only helps us with ICP monitoring, but also helps in therapeutic drainage of the CSF if needed. So this patient gets an EVD in the ER, and the initial ICP measured is 29 millimeter versus mercury. So I put this case up just to discuss what and how we can treat and manage acute ICP in the ER as well as in the neuro ICU when they initially come. To understand what all tools we have as a neurointensivist or a treating physician in the neuro ICU to treat the ICP, you have to understand what is the basic of all these things. It's based on the Monroe-Kelley doctrine, which means that you have a closed skull and the volume in the skull is fixed. The CSF takes 150 mils, the blood takes the other 150 mils, and the brain tissue is 1,400 mils. Anytime this is a closed system, anytime one component increases or reduces, then you have to reduce the other two components so that you can control and manage the volume and the closed structure. So everything involved around this doctrine is how to treat the ICP. Suppose there's a clot hemorrhage or a big bleed in the brain, so the blood volume is increasing. So what do we do? We reduce the CSF volume, reduce the brain tissue volume. How do you reduce the CSF volume? It will be a CSF diversion by an EVD. How do you reduce the brain tissue edema would be by treating them with hyperosmotic agents like mannitol and hypertonic saline to reduce the cerebral edema. So everything revolves around this Monroe-Kelley doctrine. I'll go over in detail as to how we can have a tiered approach because everything now, we've tried to do a multimodality monitoring and everything in the ICU. So you go over step by step and how we can treat and treat the refractory ICP crisis. So the typical ICP for everyone, it's 7 to 15 millimeters of mercury and anything above 20 is considered pathological. The cerebral herniation syndrome in common to understand would be those five. The top one is the cingulate or sulfalazine herniation. This was the one our patient was at risk of and which had bifrontal contusions. So the cingulate lobe can go on from the left to the right to each side and cause herniation. Then you have the transcalvarial herniation, the uncle herniation where the uncus of the temporal lobe comes down and you have central herniation or transtentorial herniation. Upward cerebellar or transtentorial herniation happens in patients who have big cerebellar strokes and so instead of herniating downwards, they herniate upwards. And of course, we have downward cerebellar transcendental herniation too in these cases when they affect your spinal cord as well. So the ICP and the volume, it follows an exponential curve. In this curve, you see that in the beginning, it's just minor changes in the volume. The delta V does not cause that high increase in the ICP, but as time, if the volume curve keeps going up, if the delta V keeps increasing, at after a certain time, the compliance of the brain goes severely low and the ICP has an exponential rise. So elevated ICP by criteria is defined as anything about 22 millimeters of mercury for a sustained greater than five minutes. So if it is sustained for more than five minutes, that patient is considered to be in ICP crisis. To understand also, we have to know what cerebral perfusion pressure means. It means MAP minus the ICP. So normal cerebral perfusion is around 60 to 80. We always want to maintain that amount of perfusion into the brain so that you don't have ischemia as a result of controlling the ICP. So if your ICP is going high, suppose normal is 15, so the ICP is going around 25, 30. But if you drop the patient's blood pressure to a MAP of 60, which means like systolic, if it is like 90, you're trying to control the hemorrhage, you drop the blood pressure way too much, your MAP reduces. What will that do for the CPP? The CPP will severely drop. In acute setting, you control your ICP by controlling the MAP, but long-term, we have more risk of ischemia over hemorrhage, and so the ischemia is going to have more long-term morbidity and disability. So the art involves in controlling all the dynamics, the CPP, MAP, and ICP in the ICU so that we can control all the three tiers and then control your ICP and have better outcomes. So the tiered approach that I was talking to you all about managing the intracranial pressure involves Tier 0 standard measures 1, 2, and 3. Go over all these steps in detail with all of you. So Tier 0 involves assessing the ABCs, airway breathing circulation. Anyone who comes like our patient, GCS of less than 8, needs an airway. The technique for the airway is also very important in patients with brain because anything you change is going to cause increase in ICP. So I would ask for the most trained individual in the ED who would be intubating my patient. So that can be an anesthesiologist or an ED because I want one single attempt at 100% success rate. How can you achieve? Why is that important? Because if you all have seen the direct laryngoscope, it's a rigid device. And when you insert it in the trachea, the airway, that's going to cause increased intrathoracic pressure. And that increased intrathoracic pressure is going to just go and transduce to increasing the ICP even more. So you get the airway secured, but what do we have? The patient might have suffered cerebral herniation and brain death. So what do we achieve? Nothing. So that's why it's very important that the most trained individual intubates my patient and use paralytics, which means you have to have neuromuscular blockage. And so when you have neuromuscular blockage, the vocal cords are at ease. It means the single attempt would be my best attempt and successful attempt. Again, do sedate these patients too because of course, if you paralyze and not sedate and don't give adequate analgesia, the same thing, patient's going to be awake and yet ICP is going to be up. You want to reduce the cerebral metabolic activity to the minimum when you are targeting these things. These are very basic things, but very important in the long-term outcomes because the brain injury is happening every second when you're trying to mitigate these things. Once you intubate those patients, you need to minimize the noxious stimuli, like any tracheal suctioning. So that needs to be very minimal. Sedate them and give them adequate analgesia as well as sedation. We know fever is bad, but we are getting more and more away from hypothermia. Just focus on normal thermia. Head of the bed 30 degree up and head is mostly kept midline because all the venous drainage can be obstructed if you move the head left or right. So try to always keep patient's head has to be in the midline so that all the veins keep draining. So you see that everything is being focused on the same Monroe Kelly doctrine. I'm trying to reduce the blood volume so the veins drain down and the veins are draining down so head is in the midline so the ICP is going to be lowered. Of course, CT of the head. This is all in the tier zero approach. The tier one is when we, after doing all those things and we see that patient has elevated ICP still, we start working on hyperosmolar therapy. We have two gadgets. We have mannitol and the other one is hypertonic saline. Which one to pick? Which are my patients? Which works better for which patients? So if you have a common just IV, then I would go for mannitol because it can be given from a peripheral IV. Dosing is very simple, just one milligram per kilogram. So if you see an average weight patient around 50 to 60 kilograms, I would just go straight to 50 grams. If it's a big patient, then I would go to 100 grams. You don't have to do minute calculations because they're pre-mixed with pharmacy and they have either in numbers of 25, 50, 75, and 100. So just grab the 50 grams bag or 100 grams bag. So that can be given from a peripheral IV. It's given as a bolus and you're done. Hypertonic saline. When to pick? If you have a central line and you really want to work on the cerebral edema, then you pick 23.4. 23.4 is a high 174 around millicovalents of sodium in just a 30 cc small vial. It's given only through a central line. Only an MD can administer it. And it's given over one to five minutes. You can push it through a central line only. You give the 23.4 or if you have 3%, that can be given from a peripheral IV as well. But that 3% has a lot of volume. It's like you run it 50 cc's an hour. So you have a patient with congestive heart failure or has an EF of 20%, so you don't want to do fluid overload on those patients. So I would go to mannitol or I would go to 23.4 when I'm targeting my hypoosmolar therapy. So all these things is like in the short run and everything will work. But what we are trying to focus more in is in the long term outcomes. So even minor judgment decisions that we do, whether we're picking 3% boluses or we're picking 23.4, makes a big difference in the long term. So just by focusing on these minor details is very important. Of course, if I know that this patient needs to go to the OR, then I would try to do temporary hyperventilation, which means that I would hyperventilate the patient for a PCO2 range of 30 to 35. Why only temporary? Because if long term I do hyperventilation and the PCO2 keeps dropping, then these patients have rebound ICP crisis going on. So it only works in the small interim. So if I know a patient is going to go to the OR and going to have the skull cracked open, then yeah, I would do temporary hyperventilation on the ventilator. How does the hyperventilation work? PCO2, you drop the PCO2, which will cause vasoconstriction. When you cause vasoconstriction, the blood volume is going to go down and then the ICP will go down. Now if you have the EVD, I will try to do CSF drainage too from the EVD. And tier one does also involve surgical decompression as well. This is the first surgical decompression. So if you have a big intracranial hemorrhage or CTS showing post-tenecteplase bleed, then those patients also need to go for clot evacuation. So they would need to go to the OR or you have a big brain tumor or glioma causing several edema or ICP crisis, then they need to go to the OR to get that tumor off. So this would be, tier one would also involve some surgical decompression as well. Tier two essentially involves the same things but at a higher goals. So if I, in spite of doing all those things, my ICP is still elevated. Now I go up, keep going on the hyperosmolar therapy to achieve high sodium goals. I try to target 150 to 155 of sodium and not even, once you get to the goal, it's also important to keep it at the goal for at least until your ICP has stabilized. And even after, once your ICP is stabilized and the patient is going out of the ICU, you also want to slowly drop it. You don't want to suddenly drop the sodium from like 150 to 135 by giving an LR bolus or giving half normal saline fluids when they, even when they are like being downgraded and everything is neurologically stable. Because even with sudden, like even if they're stable, the sudden shifts in sodium can cause changes in the brain, brain milieu, and then that can cause like the symptoms to come back and then require a repeat scan and imaging as well. So you have to try to maintain the sodiums and slowly stabilize them and try to bring them to normal in future, but everything has to be slow. You optimize the sedation and analgesia. And then you have rescue decompressive craniotomy. The TBR literature shows that there are only two trials that was done for rescue decompressive craniotomy. One was rescue ICP and the other one was DECRA. Both those surgical trials, what showed that, of course, they reduced mortality significantly, but they also increased the morbidity and long-term requirements of nursing homes, tracheostomy, or PEG tube placements. So this surgery involves the maximum bone flap to be removed, bifrontal and biparietal, just to, this would be a rescue treatment for ICP crisis. We just let the brain swell out outwards. Of course, it is a little barbaric, but then, yeah, that did not show, it did show improvement of mortality, but the morbidity significantly goes up. Tier three approach for treatment of intracranial pressure would be the most aggressive steps and highest risk of adverse effects. Once we are talking about this tier for ICP crisis, then, of course, you try to take the family of the patient with you, keep them informed about everything, but if you're targeting sedation to pento-barb coma, then that's the time definitely to sit down, have a conversation, to let them know this is the most aggressive tier of management of ICP. Then that means you are committing to a tracheostomy or a PEG-2 placement, because this would need long-term care, and then we'll have to see how the outcomes are going from here. Sedation is targeted to ICP or birth suppression on the video EEG. We have EEG, but these patients definitely all the time need to be on video EEG. You target birth suppression, you bolus them with pento-barbitol, which reduces the cerebral metabolic rate to minimum, and they're almost like mimicking brain death criteria. So pupils will be blown, you'll have no cough, no gag reflex, the cerebral metabolic activity will be minimum. And then pento-barb infusion is usually continued to up to 96 hours. You target birth suppression in the EEG, no brainstem reflexes. Of course, you continue all the other, make sure all the other organ system are functioning effectively. And then once your ICP is treated and stabilized, that's when you start weaning the pento-barb and waking up the patients. At this time, you can also target hypocapnia up to 25 to 34 millimeters of mercury to try to see if that hypocapnia will reduce the cerebral metabolic activity. Moderate hypothermia targeting core temperature to up to 32 to 34 can be targeted when you're trying to do the most aggressive tier for refractory ICP crisis. I can't finish my talk without talking about neuroprognostication. So neuroprognostication, these days now, we are trying to do more and more tiered framework approach to predict the trajectory of the neurological outcomes and guiding the families. There's a recent paper that was published in September 2023 in Nature Medicine. This talks about multimodal assessment, improving the neuroprognostication and in unresponsive critically ill patients with brain injury. So how can we use all these multimodalities that we have in hand? So it requires a multidisciplinary team which involves neurologists, neurointensivists, neurophysiologists, neuroscientists and neuroradiologists. They all help together, come together, predict the outcomes of these patients with disorders of consciousness. We have a lot of tools, methods, scores. At the end, you have to treat your patient. So the tools that we have, we all know we have a GCS score, which is done at the time of admission and the time of immediate injury. Severe TBI, if you have a GCS of three to eight, they have higher mortality and likely poor outcomes. Moderate TBI patients, GCS nine to 12, have intermediate prognosis. Mild TBI, GCS 13 to 15, have good prognosis, but these post-concussive symptoms might persist in these patients. Pupillary light reflects, now we have the pupillometers to assess them as well, in which the reaction to pupil is a critical marker of the brainstem reflex because bilateral non-reactive blown pupils with an NPIS of zero bilaterally are poor prognostic indicators and indicate brainstem injury and acute brain herniation. But those brainstem herniation do reverse. So if you immediately detect them and treat them with hyperosmolar therapies and treat them with the head of the bed up and everything, then when you do the tiered approach, you can reverse the bilateral non-reactive pupils as well. Motor response and posturing. Decerebrate posturing indicates severe brain injury and poor outcomes. If you have no motor response, especially after 72 hours of acute brain injury with no sedation and no paralytics on board, that slightly tells that it's poor outcome in these patients. We have so many scores and all those patients would have acute brain injury. ICS score, it involves five criteria. The GCS, the ICH volume, the infertentorial location, whether it's cerebellar as well as cerebellar, the IVH, presence or absence, age, and total score. So you see that if the higher the ICS score, which predicts the 30-day mortality, if the ICS score is five, the 30-day mortality is almost 100%. You have scores for the aneurysmal subarachnoid hemorrhage to the Hunter-Ness grading scale. The higher the Hunter-Ness, the lower the survival rate. So the Hunt-Ness grading scale is five, which is coma or decerebrate posturing or flaccidity on motor examination. The survival rate on these patients is just 10%. Modalities, the number of modalities that you use in predicting these outcomes, the more the modalities, it reduces the uncertainty and the accuracy in predicting these outcomes increases. You have structural modalities available, which is CT, MRIs, serum biomarkers, which are neuron-specific NLAs and S100B. You also have functional markers, which are neurological exam, four score, GCS, EEG reactive as well as resting, somatosensory evoked potential, functional MRIs, transcranial magnetic stimulations, event-related potential, positron emission tomography, PET scans, as well as SPECT scan. So combining all the structural and functional modality, the more and more modalities you use, it reduces your uncertainty in predicting the outcome and improves your accuracy. Of course, you have to pay a lot of attention to the patient interest. Do those patients have an advanced directive, a living will of what their wishes are? The surrogates and family are the best people who help us decide in-depth understanding of the quality of life that these patients had before the injury and help in defining the specific goals of care. Not everything may be the right thing for the patient or maybe everything will be the right thing for the patient. Takeaway points from this multimodal assessment would be neuroprognostications in all patients with acute brain injury is a complex and now a nuanced process that benefits significantly from a multimodal approach. By integrating clinical assessments with advanced imaging, electrophysiological tests, SSEPs, EEGs, monitoring, biomarkers, clinicians can make better informed predictions about the neurological outcomes. No single tool offers complete certainty but the combination of all the modalities enhances your accuracy, allowing for better decision making, counseling, rehab, and family help. Ultimately, the use of multimodality tools in neuroprognostication provides a more comprehensive and personalized approach in patient setting in the Neurocritical Care ICU. Thank you. Thank you, Dr. Krishnan. And I'd like to introduce, so Dr. Matt Davis was supposed to be here and he sends his apologies. They had a family emergency. So fortunately, I have Dr. Marilyn Pacheco who's here to help us with the spinal cord section of this talk. And so she is Chief of Rehabilitation Services at the Heinz VA outside Chicago, Illinois. Hi, can everyone hear me? OK. So these slides are borrowed from Dr. Davis. That's my disclosure, I think. So body systems to consider for high tetra in the early acute phase. Not going to go over the bowel integumentary. Like most PMNR-trained residents and attendings, you guys know what to do with bowel and the skin. For bowels, just order, like, maybe suppository. Just because if you tell them to do digital stim in an acute care ICU setting, the nurses probably, or whoever's there, don't know how to do it. But if you just order regular suppository, not PRN, then you'll be fine. For the skin, it's all related to respiratory and getting them up, and then moving, positioning. And you know how to prevent pressure injury in a spinal cord injury patient. So cardiovascular, we're not going to go over autonomic dysreflexia also. So T6 and above, more common for autonomic dysreflexia. So much more for high tetraplegia, C1 to C4. Bradycardia, more common in high tetraplegia. It's very problematic during suctioning, because sometimes when you suction, they could even go to a systole, and then they call a code, and then cardiology gets involved, and then they get a pacemaker. So just make sure, like, maybe start teofilin. Usually it's about 100 BID, and that should save your patient from a pacemaker. Secretion management for respiratory part, these are usually, let's say, hypersecretory state. And then they have impaired cough, too. The hypersecretory state is because of the unopposed parasympathetic tone from the vagus nerve. This requires multimodal approaches. You have your pharmacologics usually use your orals and your nebulizers. You do the suctioning, but of course, be careful about the heart. And then there are different things, like you could do the mechanical insufflation, exhalation, and percussion vests. Mechanical insufflation and exhalation, for those are not familiar with, it's like it's a fast inhalation and then fast rapid exhalation. It's good for the bigger lung feel, like the, I'm losing my thought. But then in the other one for the percussion, it's usually better for the smaller bronchioles area. And then that's a vest that they wear, and then it gives this percussion. And then what basically it does is releases all the mucus, and then you could suction, and then that's better for them. However, of course, it's dependent upon your ICU respiratory therapist and the nurses in the ICU that you're with. Ventilator management. The question is usually, when do you win the patient? What's the tidal volume? What's the visceral capacity? And what's the negative inspiratory force? So to review a little bit of pulmonary, I'm not an expert, but tidal volume is when your regular breath, that's the volume. So you usually want the higher, around 15 milliliters per kilogram. And then for vital capacity, you want it to be about 10 to start winning. And vital capacity is when you inhale forcefully. So that's the vital capacity. And negative inspiratory force is a measure of the muscle strength. So when you inhale your muscles, you have a negative pressure in your chest wall, inside the chest wall, and that's the measure of the strength. So you want that about 20 to 30. The higher for the higher tetraplegia because you want the muscle to be stronger. What to monitor for winning success is all of these, and then plus their respiratory rate, their heart rate, and then, of course, their O2 saturation when you're weaning them. And if you're interested in a weaning protocol, come reach out to us for a weaning protocol for your area. For neurogenic bladder, the thing is there's spontaneous bladder voiding in patients. But just because they have spontaneous bladder voiding doesn't mean that it's safe for them. It can occur, and then it's low void, post-void residual. But it's not safe at those pressures, especially for ASIA A and ASIA B. So we know that they're in spinal shock. So please, you could leave the Foley catheter. At most, do a regular intermittent catheter. But leave the Foley catheter is what is preferred. And then most SCI docs, well, they're in spinal shock anyways. For ASIA C SCI, reflex voiding is complete, and it commonly occurs at safe pressures. But still, there's a substantial majority of the patients that's still occurring at high pressure. So it's not safe. So if it's high pressure, there's a risk of backflow to the kidneys. So this is Dr. Davis' study. They did a systematic review of bladder management for infection and infection risk. Because remember, in 2014, when no host like, remember, Catechor acquired UTI. We're not getting paid anymore in the hospital if the patient developed UTI while in the hospital. So he did this study. And the hypothesis that the indwelling catheters cause more UTIs, that intermittent catheterization is not supported by the scientific literature. Most studies failed to demonstrate significant difference in UTI. And studies with non-significant trends favoring intermittent catheterization were more susceptible to bias from confounding factors. Perceived risk of infection should not influence a patient's choice of catheter type. In SCI, high tetraplegia, acute, they're still in spinal shock. The bladder is still big. You could put the Foley catheter, and it's safe. Of course, you know. And then once they're out of their spinal shock, then you could consider intermittent catheterization. We'll get questions later. It's a short topic, so thank you. All right, thank you, Dr. Pacheco. So I'm going to talk a little bit about brain injury, kind of what I've done to build up consulting practice or consulting service at my institution, how I help in the neuro ICU and in the surgical ICUs, and then a little bit about kind of an innovative quality improvement project that we've done to help patients that are under-resourced or un-resourced and those with kind of poor social determinants of health. So I have nothing to disclose. I talked about already kind of a little bit of the objectives of this talk. So in the interest of time, I'm going to be moving on. Okay, and so, you know, Dr. Kennedy in his presidential address, you know, said, you know, what is our why? We all went into this so that we can take care of patients, so that we can work on, you know, establishing relationships with our patients and getting to know them and helping them and, you know, find meaning in that part. And why did we specifically go into PM&R? We went into PM&R because we have a passion for the field, an interest in the field, and we want to be able to help those specific populations. And so there is a lot of evidence for the benefits of physical medicine and rehabilitation consults and improving functional outcomes and reducing healthcare utilization. And that's been supported by several studies. So Robinson et al. in 2019 looked at the impact of introducing a physical medicine and rehabilitation consultation service in an academic burn center and found that the PM&R consults significantly reduced the length of stay in that population from 30 days to 24 days. Although it didn't affect acute care length of stay or functional independence measures, it did decrease that rehab length of stay, which, you know, is always something that's on the forefront of administrators' minds. And it also, you know, it eventually shortens the amount of time that patients need to get home. There was another study by Robinson as well that looked at an academic level one trauma center and found that early PM&R consultation within eight days of injury was associated with a markedly acute lower acute care length of stay, which was 12 versus 30 days, and fewer complications as well as reduced usage of benzodiazepines and antipsychotics. Now if anyone was in the talk this morning about managing agitation and kind of the swaying that they all tried to do, you know that benzodiazepines and antipsychotics are relatively contraindicated with any kind of brain injury, delirium, you know, confusional state. And Rapiti et al. also had a position paper on the PM&R professional practice for persons with spinal cord injury, and they emphasized that structured comprehensive rehabilitation programs that are led by PM&R physicians are effective in improving functional outcomes and reducing healthcare utilization, particularly in complex cases such as spinal cord injury. So we are so valuable to the acute care setting and, you know, we really do a lot, can do a lot more in terms of just making disposition recommendations. And Wepner et al. in 2021 showed that specialized PM&R consultation services such as brain injury medicine or continuity consult service, so continuing to follow those patients, has been associated with a shorter acute care length of stay, fewer unplanned acute care transfers once they get to rehabilitation, and an increased likelihood of patients emerging from a minimally conscious state during inpatient rehabilitation. And if anybody wants, I have the QR codes for the articles listed in the, on the slide there. So what have I done to build up the consult service at the institution that I'm at? So really it is going around and trying to really change the mindset. So you're there to try and help the patient, correct? So you want to try to get the patient to the most appropriate level of care as quickly as you can. You know, patients that are sitting around in acute care, they, especially older patients, can get delirium, can get confused, can get complications. And so we really want to try to move them to that next most appropriate level of care. And I would attend trauma rounds every day. This was initially established by one of my colleagues. He would go kind of intermittently, and then I would go to tabletop rounds every morning and really built relationships with the trauma team. So there's usually trauma, PTOT, speech, social work, pharmacy representation, dietician, respiratory therapist is also there. And if there's cases that I think, oh gosh, there's this severe TBI that's in there and they're having problems with trying to wean sedation, I'll ask if I can help. And so that can happen with brain injury, with spinal cord injuries, with any kind of polytrauma, amputations and such. And then I also attend neuro ICU rounds with Dr. Krishnan and her colleague. And so we'll do rounds around the unit on each patient and that usually involves critical care medicine, neuro critical care, PMNR, pharmacy, respiratory and dietician. And I'll also ask to be involved in cases that I feel like I can offer some assistance as well. That can be stroke, brain injury, Guillain-Barre, tumors, any kind of like central nervous system infection, seizures, anything like that. And really it's all about building relationships. Everything in life is about building relationships. And so making sure that you have good working relationships with the other services. Okay, and so what are the types of things? So of course, we always being PMNR physicians, we do evaluate for disposition and what we think in the amount of time that we have would be until they're likely ready for medical discharge, what we think the most appropriate level of care will be. One thing that I really had to change kind of a view on is if the patient's not appropriate, is there a way that I can make them appropriate for inpatient rehab? If it's a patient that is a stroke, say it's a left frontal stroke, and they're just not really waking up, they're not participating with therapy, can I add a little bit of an SSRI? Can I get that to perk them up a little bit, kind of get rid of that apathy or a little bit of a Mantadine or Provigil? Is there anything that I can do to try and to make them appropriate for intense rehabilitation setting? So medications for pain, if someone's really restless, not wanting to participate in therapy, can I help schedule their pain medicines? Maybe they have the stroke and they have some aphasia and they can't tell you that they're in pain. The medications for aphasia, there's Dinepazil that you can use for aphasia and then it takes a little bit of while to kick in, but down the road that can be helpful. Also kind of the acetylcholine supplementation is also beneficial. And then the biggest one is probably the workup for agitation. So you have a restless patient. I'll tell you my favorite scenario was a guy that came in to our unit. He was at a post-acute brain injury rehabilitation center and he had originally spent some time at Shepherd. And so this was 1,000 miles away from Atlanta and so we didn't have access to any records at that time or whatever. And he came in and had pulled out his PEG tube. And so he pulled out his PEG tube and GI came and saw him and they said, this guy needs to be on hospice. Like he's out of control, he's not doing anything, he's in the neuro ICU. He was actually in five point restraint. So he had arms, legs, lap and mittens on and managed to pull his EVD out. So this was before I talked to neurosurgery and I said, I think this guy might have hydrocephalus. So fortunately my training with Dr. Ivanhoe, that's always one of the things on my mind. And so I convinced neurosurgery to put an EVD in him. They actually had to put the bag on the floor because it was such low pressure hydrocephalus, but the guy just kind of perked up. And so they put a shunt in him. He actually was like min assist by the time he left from like a total assist, not following any commands, not doing anything. And then kind of went on to continue some rehabilitation. So really, if you're having agitation, first kind of look for the medical causes. So, you know, are they sleeping? Could it be seizures, subclinical seizures? That's also another thing. So I always kind of work with my neuro critical care, neurology friends, if that could be a potential. And then of course, hydrocephalus. I also work to make oral suggestions to work to get off drips. So, you know, if it's a lot of times we use a lot of Presidex, especially in the neuro ICU. And so sometimes scheduling, you know, even a little bit of like a gabapentin or some pain medicine, something like that can really help kind of get off some of the drips. And then of course, skin and wounds, bowel and bladder, and really try and work to get patients out of restraints. Now, when they're not in the ICU, sometimes I'll get consulted for a patient that isn't even really rehab appropriate, but they're having trouble getting them to the next level of care. And so I'll sometimes help with medication management just in that setting, if it's, you know, a dementia related or if it's, you know, stroke or brain injury related. And then I'm constantly in touch with the acute care teams, kind of discussing acute barriers and how we can start addressing them. So your drips, your lines, your drains, respiratory needs for rehab, the next level of care. So where I'm at, it's about 30 miles away from the medical center. And so I'll be in touch, like if we have a vent dependent spinal cord that we need to get down there. And also routes for nutritional needs, all of the typical rehab stuff that we would be looking at. And then I also give a lot of tips on why to hospitalists on why patients might need inpatient rehab over SNF. So for anyone who doesn't know, because I didn't know coming out of training, actually, it was a couple of years after training, there's a lot of differences between inpatient rehab and SNF level of care. So inpatient rehab, you know, obviously we all know that you have to have the three physician visits a week and you have to have that 24 hour nursing care as well as your therapies. So SNF, they have to be seen for that H and P within the first five to seven days. And then seen once a month by a physician for the first 90 days, and then like once every three months after that. So these patients that really it's the medical need that's holding them to inpatient rehab, if you can help kind of guide the hospitalists that way, that usually tends to be pretty helpful. And so I also work with the therapists. We'll work to get patients up, whether they're on the vent, whether they have an EVD in the neuro chair, ambulating, even if they're on the vent. The therapist had gotten this machine that is like a functional electrical stimulation machine. So even if they're laying in bed and you can't move them, they can still be working on that mass repetition and really kind of the prevention of atrophy. I'll work with speech on patients who like for example, we had a patient that was a very severe Guillain-Barre who was on the vent and was not funded and worked with speech to work on augmentative communication strategies. Our institution, the vents are not amenable to inline PMVs, but that would be an option as well in order to allow communication for patients. And then of course, I work very closely with case management on timely referrals and appropriateness. And so as we talked about spinal cord, we talked about kind of the critical care of brain injury. A lot of what I help with is the medical management or medical management of the brain condition trying to enhance recovery. And so going through this, you have your neurotransmitter systems. And so they all originate from different locations and the point of that is that nothing is an island in the brain, right? So just because you have this certain areas injured doesn't mean that another area can't also be affected. So you have your pathways that go there and a lot of what I'll do is to try and help with supplementation of those pathways that may be interrupted. And so managing agitation, there's kind of two schools of thought. One is to slow them down and the other is to speed them up. So the thing in the ICU is there's a lot of drains, a lot of lines, tubes, et cetera, and the goal is that you really need to kind of keep them safe. So as much as we can minimize any of those lines, I think that is great. Try to get them out of the ICU as quickly as possible for the ICU delirium. Limit neuroleptics. That can also, I mean, it's well established to, especially in TBI, to prolong the post-traumatic confusional state or post-traumatic amnesia. And then try and get them in a low-stimulation environment. Bowel and bladder, a lot of times if they're uncomfortable, if they have to pee, if they're feeling like they have to go to the bathroom, they'll be moving around. And then of course, good sleep. So this lovely picture is of my cat, Ellie. And so the thing is, is she looks really angry, right? She was yawning. So in that picture, I like to say that, you know, if you're tired, you can look really angry. So make sure that you're addressing sleep. And then for the school of thought of speeding up their thinking, I found this actually to be more helpful than sedating. And so you can use stimulants. You can use imantadine provigil, or modafinil, sorry. SSRIs like escitalopram, sertraline, denepazil, non-opioid pain medications in as low as dose possible. Oh, and I, Aricept is denepazil. And really try to find out what is causing their restlessness. So is it pain? Is it akesthesia? Is it just that period of inner restlessness, like especially after a TBI that they'll have? Do they have wounds developing? Do they have aphasia and they can't express themselves and that's why they're acting out? Do they have bathroom needs, seizures, hydrocephalus infection? So really kind of trying to look at the patient and I'll sit, you know, try and observe them in the room for a couple minutes before, or you know, a couple, like 30 seconds or something before I go in just to see if I can try to, try to see what I think is potentially being a cause. So the goals in the ICU and acute care. So the things that we can help with, again, sleep, pain, behavior, bowel and bladder, skin, educating on prognosis and rehabilitation course and expectations. You know, I think that's one of those things that if we can spend more time with our patients, you know, if the healthcare system allows and we can kind of continue to educate and everything, that that's a very fulfilling part of a consultation practice. Of course, removing barriers to discharge and preventing complications. And so I am extremely fortunate to work with a group of very passionate people who enjoy taking care of neurologic patients and one nurse, Christine Coates, she's a neurocritical care nurse practitioner, started this quality improvement project called BRAINS. And so what that stands for is bridging resources after inpatient neurologic stay. And so this is an ongoing QI project at Memorial Hermann the Woodlands. It's multi-disciplinary, we meet weekly and to be enrolled in our BRAINS program, you have to have a poor social determinant of health. So economic instability, low education, health literacy, limited access to healthcare. Where we're at, we draw from a lot of rural counties around the Houston area. So you could have transportation issues, immigration status, job status, or social support deficiencies. If you come in and you don't have, you live alone, that's someone that we might be having follow, that we're following in the program. The economic instability, that can be the unresourced or under-resourced individuals. And where we're at in Montgomery County doesn't have a lot of resources for those patients quite like Harris County that Houston is in. And so I will consult on each of those patients and follow along throughout their stay and try to remove barriers or try to make it as much like the inpatient rehab unit as we can knowing that we're not in the inpatient rehab unit. And so the therapists will try to see them every day. Of course, they are not getting three hours of therapy a day, but they'll really kind of work with nursing and with the other therapy disciplines on trying to work together to help in the functional mobility of the patient. And so we will meet weekly and have multidisciplinary difficult discharge rounds. And the goal is to improve the identified community resources for each patient and optimize patient care, standardize our discharge process. And our original aim was to reduce length of stay and reduce readmission rates for these patients. So a little bit about, so Texas Medical Center has two level one trauma centers in Texas Medical Center. So Memorial Hermann is one of those level one trauma centers. I'm about 30 miles north of there. And so this is a level two trauma center. We have 422 licensed beds, was named a comprehensive stroke center. There's a 24 bed acute neurospine unit, 12 bed neurovascular ICU and a 10 bed neuroscience ICU. And then we have a tier unit there that's 29 beds and outpatient rehab that's on site. And so for our program, we've had for fiscal year 23, we had a total of 83 patients. So a little bit about two to one males to females. The average age was 54 years. The average length of stay was 15.9 days. And the thing that was really profound for us is that the readmission rate was only 5%. And this is in patients that have at least one poor social determinant of health and have lack of funding or unfunding. And so when we originally started it, we were looking specifically at stroke patients and we kind of expanded to other neuropatient populations in this. So for the number of brain stroke patients for the year, we had 55, 25 were hemorrhagic, 30 were ischemic. There were again about two to one male to female. The average length of stay was 14.4 days. And that made up 67% or two thirds of all of our brains program patients. And that was 11% of all stroke patients at Memorial Hermann in the Woodlands. And so according to the American Heart Association, the national readmission rate for ischemic strokes without, you know, in all, so this includes funded, unfunded, everything, was 12%. And so for ours with the readmission rate being 5% for patients that are under resourced or non-resourced with poor social determinants of health, that's really a very significant finding. Okay, and that's about perfect. So we'll go ahead and take any questions that you all might have. Happy to answer any of them. We also have, like, an iPad question here. The first question is, what is the most common herniation type? Most common herniation type that we see is the cephalocene herniation, in which the cingulate gyrus pushes on the other side, when TBI, but in ischemic strokes, the most common herniation is uncle herniation, which involves a large portion of the MCA territory, and the uncus is the most common area to herniate downwards. Thank you. And then the next question is, you mentioned a patient after TBI that you suspected of hydrocephalus who ended up having normal or low-pressure hydrocephalus. Could you please specify what made you suspect this and how you frequently observe this phenomenon? I mean, I think the hydrocephalus queen is probably better suited to answer this question for me. But I think most post-TBI hydrocephalus is going to be normal or low-pressure hydrocephalus. How frequently do I see it? I mean, I feel like I'm looking for it a lot. So if they're presenting with that clinical picture, I can't really put a number to it. But I feel like it's more common than you would probably, most people would probably think. Dr. Ivanhoe? Do you have any? Sure. Yeah. Oh, you can come up here. This is nice of Mary Beth to have called me out, and I'm glad she brought up hydrocephalus. Hydrocephalus, I was taught by neurosurgeons, is a clinical diagnosis. So you look for either patients who are improving and then they get stuck, or you look for patients who are not improving and you should always look for hydrocephalus. It's very often sort of a conversation about ex vacuo. 20 years ago, they were trying to get rid of that term and I still hear it all the time. And if a patient was speaking, and maybe they've stopped speaking, you look for really subtle findings. And the only thing that's really helpful if you do a large volume tap is if you have an ambulatory patient who can then, whose gait improves. Well, how many of these patients are we measuring their gait? So you look for behavioral changes. You look for a lot of sort of frontal behaviors, apraxia. In a book chapter, I have a description of a patient, you know what I'm gonna do, who went up to the neurosurgeon when I consulted him and he just kept picking the lint off the neurosurgeon's sweater. That wasn't because he was trying to clean up the neurosurgeon. It was because he was perseverating and he couldn't stop. So that's a frontal behavior. Same thing can be true of apraxia. Sometimes, you know, you'll hear people say he's holding the food in his mouth. I've heard that a lot over the years, and that is apraxia, unable to trigger the swallow in front of a speech therapist. So we learn these terms, apraxia, perseveration, impersistence, whatever, but we don't necessarily correlate that with what we're actually seeing clinically. So I hope that it helped. Thank you. Yes, thank you so much. I think there were a couple more questions. There was one on can you speak to when to start neurostimulants and when you promote sleep in TBI patients? I think starting neurostimulants, we will start them if they have an EVD in. I think you can start, you know, some modafinil. I don't generally start Ritalin on that much, mostly because we're looking for the arousal at that point, or imantadine. And then promoting sleep. I think promoting sleep is making sure that they get good restful sleep at night is important kind of from the onset, because that's when you kind of get those most restorative effects. And then there was one question that the talk had great information on neuroprostication for TBI. What differs in neuroprostic, prostagne, no, sorry, neuroprognostication in acquired brain injury, Dr. Krishnan? So, in acquired brain injury, you mean ischemic stroke or intracerebral hemorrhages. In these cases, it's first thing is to understand, because the patient depends on what the population is, the pre-morbid Rankin scale that we always do, the modified Rankin scale when they present to us, which tells us what was the level of disability on presentation, were they able to do all the things on their own, or they needed assistance. The goal is to get to them. Of course, once you have an ischemia or a scarred brain, you're never going to go completely back to what you were. Because TBI, yeah, you know, you can plateau, and now we don't prognosticate up to two years. We have seen level of cognitive improvement even beyond two years. So, prognosis in TBI is completely different, whereas in ischemic stroke or ICH, once the brain is scarred, the level of improvement is low, but depends on how much you can improve. So, first thing that I do is I try to assess the pre-morbid Rankin scale as to what was the quality of life before the injury happened, and then try to assess what is the goal for the patient to get to. If the goal for the patient is get to, like, what, and once I ascertain what the family and the patient's expectations are, I try to help them gauge and understand to what level they can come to. So, it's like right and left MCA. It's completely different, you know. If you are left-handed, then the right MCA, the right side is your dominant side. So, mostly the motor response comes earlier, but the level of comprehension, the cognition, that takes the longest. So, for someone who was like a marathon runner, of course, for him to have an MCA ischemic stroke, he would be probably able to, like, walk and able to ambulate, and that quality of life might be acceptable for them. But for someone who is probably, like, someone who works in the lab and is a researcher, for that person, the cognition might be the most important thing, and that would be the last to come when you have the ischemic stroke in the MCA territory. So, I try to gauge and then prognosticate. Of course, you can never come back to what you were, but we try to see what we can best get to, and if that is an acceptable quality of life, we help the patients and the family to be. Another question for Dr. Krishnan, what are the risks of pushing mannitol in the tier one elevated ICP management? So mannitol is an osmotic diuretic, so of course it diureses. If your patient has ESRD or is aneuric, mannitol is not gonna work. So the first thing you need to know is, is the creatinine okay? Because it's the most common side effect of mannitol is AKI or kidney injury. When you are dealing with an acute herniation symptom, like I said, time is brain. So you got two kidneys, but you got one brain to save. So I'm okay with taking whatever the risk it takes to improve my brain outcome and I can take care of the kidneys later. So in brief, the most common side effect is kidney injury and if that patient has a viable kidney, then you can always get better from that. So there's no major contraindication or absolute contraindication unless you have an aneurea or ESRD. And Dr. Pacheco, at what point is it appropriate to start theophylline in high cervical spinal cord injury in the ICU? When you see bradycardia and they need to start suctioning as early as possible to start so that they don't code your patient when they're doing the suctioning. Yeah, I feel like in my clinical experience, the times when we've started talking about it in rounds has been when they're turning the patient and they brady down or when they're suctioning them and they're bradying down and they're calling rapids or they're calling codes, then that's usually about the time that we start talking about starting theophylline. And then there was another question, how much weight do physiatrists expertise and recommendations have on insurance coverage and approvals for patients? I think that's probably highly variable. I feel like Medicare Advantage programs, they don't seem to place that much weight. That might just be my own personal experience. But I do think that what we provide and what we say is highly valuable and that it's definitely worth fighting for patients to get the most appropriate level of care. I think it was in 2017, the AHA came out with guidelines that all stroke patients should be given the opportunity to get rehabilitation. And unfortunately, most stroke patients tend to be on the Medicare Advantage programs, which do tend to be a little bit more limiting in terms of their access to rehabilitation for those patients. And one more question, for the Brains Initiative, which social determinants of health were found most often throughout the project and which are the most challenging to find solutions to? So I think the most challenging is easy. I think those are going to be the patients who have limited family support. They also are unresourced and don't have any citizenship status. Those are gonna be the ones that are definitely the most challenging. And then the ones that were found most often, I would say are probably the under-resourced. So those are kind of easy to spot kind of from the onset when you look in the chart and you see the funding status. So that's probably what we see most often. Okay. If there's no other questions, thank you so much for your time and hopefully can walk away learning a little bit today. If you have any questions, we'll be up at the front.

neurocritical care

rehabilitation

stroke

intracranial pressure

thrombolysis

spinal cord injuries

physiatry

interdisciplinary collaboration

acute medical settings

BRAINS initiative

neurocritical emergencies