Hi again. So we are now up to talk two out of three. I know you guys get to spend a lot of time with me this morning or afternoon, wherever you are. We're going to switch gears a little bit and talk about traumatic brain injury. So from impact to recovery, mastering traumatic brain injury management. Same disclosure at the first talk, again, that relationship is done. Objectives are pretty straightforward for this one. We're going to describe the different characteristics and subcategories of severe TBI. You're going to appropriately identify and resuscitate patients with severe TBI. And I'm going to give you some tips and tricks along the way so that you guys can be superstars. It's actually a pretty important topic. About 80% of traumatic brain injury is considered mild. So that mortality is only about 1%. Mild, you want to think about all of your concussion patients. If you're a football fan, it's hard for me to even watch football anymore. I really do not think that TUA especially should be playing football anymore, but that's just my opinion. Moderate TBI has a mortality approaching about 20%. So mild, your GCS is about 14 to 15. Moderate, you're anywhere in the category from about 8 to 12. And severe TBI, so your GCS is less than 8, that mortality approaches 40%. It's really important for us to treat these traumatic brain injury patients emergently. Key takeaway that what you guys want to think of is nearly half of patients who die from a traumatic brain injury do so in the first two hours after injury. So that really highlights the role of all of you on this call about getting the initial diagnosis and the management correct. Two hours goes by in the blink of an eye, trust me. We can really make a difference for this population of patients. The most common causes of traumatic brain injury, false. There's a kind of a dichotomy of where you see them in very young children versus older adults. Motor vehicle crashes, motorcycles, bicycles, pedestrian struck, sports, recreation, work-related injuries, assault. Basically, all of these things on this list are never going away. This ensures your job security, but it also keeps us very busy, right? The elderly are always going to fall. Motor vehicle crashes are always going to happen. Then you do want to consider blast injuries in war zones specific to the military. Just a quick run through of the different types because I want to talk to you guys about the pearls of treatment more so. Epidural hematoma and subdural hematoma are two of the more common ones that we see. The subdural hematoma is caused by a tear of the bridging veins. It's the most common TBI that we see. It can happen up to 30%. Subdural means that the blood is collecting below the dura. The dural hematoma is an arterial injury. Usually it's some type of lateral head impact, like you're struck in the head with a baseball bat or you're involved in a car accident, and you get a tear of the middle meningeal artery or vein, usually the artery. In this case, it's epidural, so it's sitting on top of the dura, but you can see how both of these injuries can actually compress the brain. Your subdural hematoma is more of a convex shape. The epidural hematoma is more of your convex shape, and it gets stuck between the sutures. It does not cross the suture lines. Your subdural is more of a crescent or concave shape, and it will cross suture lines because it's below the dura. Traumatic subarachnoid hemorrhage. It's damage to the small arteries under the arachnoid matter. Just like ruptured aneurysm, traumatic subarachnoid hemorrhage can cause a decrease in mental status or increase in intracranial pressure. The amount of blood initially is important because it has prognostic value for your recovery. You want to think of cerebral contusions as bruising to the brain. The problem with these is that they can expand rapidly, especially if you're on any type of anticoagulants or if you have alcohol or intoxication on board. These can get associated with vasogenic edema, which can again increase your ICP. It can cause midline shift. It can cause worsening mental status and even herniation. It might not look that bad to start, but it can quickly progress to getting worse. Diffuse axonal injury and penetrating injury. Diffuse axonal injury or DAI, it often has a very benign CT appearance, so you're really just seeing these little dots of blood. Maybe your patient has a GCS of three and is intubated, but the CAT scan is not really showing you anything to get excited about. These result from severe acceleration, deceleration, and rotational forces. What it does is it stretches and disrupts the axons and that leads to neuronal death. This damage, when you're talking about diffuse axonal injury, it's widespread, but most importantly it's irreversible because it's damage to the neurons itself. It's a significant contributor to morbidity and mortality. You want to watch out for these patients. They can have secondary injuries from hypoxia and hypotension because again, it's damage to the actual neurons. The penetrating injuries, so what you're seeing here is you're seeing a bullet that went in the left side of the skull and actually transversed across both hemispheres. It's not as common in etiology as blunt traumatic injury, but it accounts for a disproportionate rate of mortality. We tend to see a higher rate of mortality for any type of penetrating injury versus blunt injury. You want to be careful here. Your big worry of secondary injury is infection. So DAI, you're worried about hypoxia, hypotension, penetrating injury, you're worried about infection. Yeah, and treatment is really to call the neurosurgery team as soon as possible. We talked about two hours being really important to impact mortality, but if most of you guys work at trauma centers, when you have your trauma survey, the surveyors look at surgeries that take longer than two hours to go from the emergency department to the operating room. Again, two hours goes by very quickly, so you now have motivation on two different reasons for why to get these patients treated quickly and appropriately. In order to really make a difference, you need to avoid hypoxia. Low hypoxia and hypercarbia can worsen outcomes, but even just one episode of hypoxia is significantly associated with a worse outcome. And this is really easy to do. All of your traumatic brain injury patients should be put on oxygen. Yes, in the emergency departments, there's this push towards getting away from oxygen if you don't need it, right? We've kind of figured out that it does maybe more harm than good if your pulse ox is okay, so we're not putting all of our chest pain patients or even our STEMI patients on oxygen anymore. But for this specific population, you need to keep their oxygen greater than 90%. When you're doing your ventilation parameters, you need to avoid hypercarbia, so you want to target a PaCO2 of 35 to 40. And you're considering placing a definitive airway if your GCS is less than 9, right? So GCS less than 8, intubate. Tips on intubation. If you want to be a superstar and keep your neurosurgical attendings happy and the ICU attendings happy, you want to use short-acting agents. Lidocaine, there's still a controversy over whether lidocaine is neuroprotective or not. My feeling is that I do use it in my daily practice because it certainly hasn't been shown to cause any harm. If anything, it has shown to be somewhat neuroprotective and decrease a cough reflex when we do our RSI intubations. Because if you can decrease a cough reflex, you can blunt any rises in ICP. Atomidate is a short-acting induxant agent, and succinylcholine is the shortest-acting paralytic that we have. So the half-life of succinylcholine is going to hang around for about 15 to 20 minutes, as opposed to rocuronium or vacuronium that's going to hang out for about 60 to 90 minutes depending on which agent you choose. And again, the neuro exam is really important. We can't have patients paralyzed for 60, 90, 120 minutes and not be able to monitor their exam. I can't tell you how many times I'm working in the emergency department when EMS rolls in with a traumatic brain injury, and they tell me that the patient had a GCS of 3 and was completely unresponsive, but they intubated with rocuronium or vacuronium plus ketamine plus Versed plus fentanyl. And I'm thinking to myself, I try not to give EMS a hard time, but I'm thinking in my head, well, which is it? Were they really unresponsive with a GCS of 3? Or did you really need to give Versed, fentanyl, ketamine, and rocuronium, and now I can't do any exam? There is a medication called Sugamidex. Hopefully you guys have heard of it and are maybe even using it. It is a specific binding agent for rocuronium, and it can produce rapid and complete reversal. It's got an interesting history. It was approved for use in Europe. Everything always gets approved for use in Europe and Asia. They have much less strict criteria than we do here in the United States. The FDA actually rejected it in 2008, but approved it in 2015, and we have been using it since. The problem with it is that it causes bradycardia, bronchospasm, and impaired hemostasis. And clearly when we're talking about this traumatic brain injury population, that's not a great side effect profile to have. So it's good to know about it, but you kind of want to weigh the risk benefit for using it. We talked about avoiding hypoxia and how to best intubate these patients so you can continue your neuro exam. You're going to keep the oxygen greater than 90%. When it comes to circulation, even one episode of systemic hypotension negatively impacts outcome in the setting of traumatic brain injury. This used to be easy where you remembered keep the pulse ox above 90 and keep the systolic blood pressure above 90. What we're figuring out though is that 90 is not high enough, that you really need to advocate to get that systolic blood pressure even higher to a great systolic blood pressure of greater than 110. And that makes sense because when you're treating hypotension, what you're trying to do is you're trying to bump up your math so that you can overcome an elevated ICP to still maintain cerebral perfusion pressure. It should always be isotonic solutions, normal saline or lactated ringers. An easy goal to remember is a map of 100. Clearly the blood pressure cuffs will measure it for you, but if you want to calculate it on your own, it's two times the diastolic plus the systolic divided by three. And again, if normal cerebral perfusion pressure is 50 to 70, and cerebral perfusion pressure is math minus ICP. So if your ICP, normal ICP should be about 15, right? Let's say that it's 30 now. You need to get that map up to 100, right? 100 minus 30, now you have your cerebral perfusion pressure at 70 where you need it to be. That's what you want to be thinking about when you're resuscitating these patients. For disability, when you're doing your focus neurologic exam, you want to be brief. You want to be focused. You specifically want to calculate a Glasgow Coma Scale. You want to do a pupillary exam and you want to do a motor function. So let's say you're in the trauma bay and there's 30 people in there and you need to get in there and do some type of neuro exam. You at least need to do those three things. Why? Because the facets of the motor component have the strongest correlation. Super secret neuro stuff from this talk, right? I told you it for the first talk. If a patient is paralyzed, you can still look like a superstar until you're attending. The patient's paralyzed with rocuronium that they just got 10 minutes ago, but you can still check their pupillary response to see if the pupils are reactive. Super important component because the presence of bilaterally dilated pupils and non-reactive pupils is associated with a poor outcome in over 70% of patients. So make sure that you are checking the pupils for all of your patients. We've already kind of touched on intracranial pressure. It's really important because our skulls are rigid, right? There's nowhere for the brain to go when it's compromised except to herniate downwards. You have to find that right balance of intracranial pressure with your mean arterial pressure or your systolic. Normal ICP is 15. With all of your traumatic brain injury patients, assume that it's elevated and be prepared to intervene. So intervene how? You can raise the head of the bed to 30, about 30 degrees. ICP is significantly lower in this position. So for your hemorrhagic, your traumatic brain injuries, head of the bed to 30 to lower ICP. You can use some analgesics and sedation. What this does is it reduces the metabolic demands of the injured brain. Again, short acting agents. So how can you be superstars? The shortest acting agents are Versed and Fentanyl. If you give patients Ativan or Valium, it's gonna hang around for hours. Valium might even hang around for days in an elderly patient. Fentanyl is much shorter acting than Morphine and Dilaudid. So there's no doubt that patients are going to need analgesia and sedation, but pick the right agent. Pick the shortest one. We talked about that you want to target the PCO2 to anywhere from 30 to 40. You just don't want patients to be hypercarbic. Other things that you can do to treat ICP medication-wise, you can give Manitol. These are your hyperosmotic agents. It's a powerful diuretic. You can give hypertonic saline. It's 100 milliliter bolus, which is thought in some camps to cause a more controlled diuresis with less electrolyte abnormality. So your hypertonic saline meaning 3% normal saline. You always have the basics right. You're gonna treat seizures. Traumatic brain injuries with blood in the brain definitely get seizure prophylaxis, or if they're actively seizing, you need to treat it. You're going to reverse any type of coagulopathy. The elderly are the most common population that present with these traumatic brain injuries. I feel like every other patient that I'm taking care of in the elderly population these days is on a pixaban, or rivaroxaban, or dabigatran, or still a good old warfarin is out there too. And then of course you have your antiplatelets of aspirin and clopidogrel. It's really important to address coagulopathy. Patients with pre-existing anticoagulant or antiplatelet use already have a poorer outcome in traumatic brain injury. You really want to try to reverse early. And another adding insult to injury here is that traumatic brain injury itself has a strong association with abnormalities throughout the coagulation cascade regardless if you're taking anticoagulants or platelets. So you already have a coagulation abnormality just from the traumatic brain injury itself, and anticoagulants and antiplatelets contribute to worsening. You want to watch out for a prolonged PT, prothombin time. That's the one that has been shown to be an independent risk factor for poor outcome after traumatic brain injury. I'm not going to go through this whole chart because this whole chart could literally be a whole talk in itself. If you guys want that for next year, we can talk about it. What I want to bring your attention to mostly is that dabigatrin or pradaxin does have a specific reversal agent. It's praxepine or ariduric cisimab. Rivaroxaban, apixaban, most of you are probably using Kcentra or four-factor prothrombin concentrates. There is a specific reversal agent that's available. It's Andexa. I would be interested to hear how many of you have it out there. It is not very available because it is a $25,000 to $50,000 drug. So if we thought that alteplase and tenecteplase drugs are expensive, they can't even hold a candle to andexanet alpha. Antiplatelets are always controversial. Antiplatelets tend to make neurosurgeons more scared than actual anticoagulants, though. These are the patients that are very oozy and very bleedy during procedures. I think that most neurosurgeons in this day and age, because there was the PATCH trial that said that giving platelets made outcomes worse, but it didn't specifically look at plavix. It looked at aspirin. So I think that most neurosurgeons, if you're going for a neurosurgical procedure and you're on an antiplatelet, especially clopidogrel, I do believe that they're going to give you DDABP or platelet transfusion. Breaking stuff for you guys. This was just presented. This was just in May of 2024, right? So May is only six months ago. This is finally the andexanet alpha trial, where it did compare head-to-head andexanet alpha versus usual care, which is your prothrombin complex concentrates like Kcentra. There was no doubt that it did decrease hematoma expansion volume, right? You can see the difference here in the percentages. The problem is that it did increase the risk of thrombotic events and ischemic stroke. Again, no doubt that it decreases hematoma expansion better than your PCCs, but it's definitely a challenge to find the balance between the two. Are you going to reverse hematoma expansion but at the expense of causing a thrombotic event or an ischemic stroke? Your options for surgery, ventriculostomy, or external ventricular drain. So these are things that can usually be done at the bedside or in the operating room. You do want to push for it to be an EVD. If you do a bolt only, now you can measure ICP, but if it's elevated, you can't do anything about it. So you might as well put in the external ventricular drain so that when you know the ICP is elevated, you can drain off some CSF and do something about it. Burr holes are an option, right? That would be a less minimally invasive type of brain surgery, if there's any type of minimally invasive brain surgery at all, where you're just drilling a couple holes to try to drain a subdural. Most often, these patients are getting craniotomies or craniectomy. The difference is in craniectomy, the neurosurgeon is going to remove the bone and they're going to leave it off for the brain to recover. With a craniotomy, we're going to put the bone back on. So you're going to take the bone off, you're going to do the procedure that you need to do, and then you're going to put the bone back on. So how do we put all of this together? This is actually my real case. I think that this was on a Saturday, and there's an 18-year-old male. He's a restrained front seat passenger with positive airbag deployment. His car flew off of a curve in the road and hit a tree. So it was morning. I think it was a little wet. There were some wet leaves on the road. He can't remember the accident and is agitated. Bystanders think that he did have some brief loss of consciousness. So EMS gets to the scene, and this is what they find. This is crazy. I had to get these pictures from EMS so that I could bring this to you guys. What you guys are seeing is this car split in half, okay? So this is the front of the car. The back of the car is actually facing the other way, and then look at the inside of the car here. All right, so you can see all of the airbag deployment. You can see the extensive damage to the inside of the car. Even though he was restrained, the force of this impact was so high that he actually got ejected. So this is probably going to be a pretty significant injury, but he is 18, and 18-year-olds tend to be more resilient. So remember the things that we're going to look at, right? We're going to look at a pulse ox greater than 90%. We're going to look at a systolic pressure greater than 90, preferably greater than 110, but you also have to be careful that your mean arterial pressure doesn't get too high so that you're not doing more harm than good that way either. And his blood pressure is 180 over 110 with a heart rate of 120. He opens his eyes to voice. He's confused, but he does follow simple commands. So if you open your eyes to voice, you lose one point. If you're confused, you lose one point, but he does follow simple commands, so his GCS is actually a 13. And because he's 18, there's no known meds or past medical history. Initial CAT scan shows a very small epidural hematoma right here. So the neurosurgeon actually did not want to do anything at this time because his GCS was 13, and this was a very small finding on CAT scan. But as most cases of epidural hematoma do, this continued to proceed. The patient deteriorated in the trauma bay. He became more agitated, less responsive, and now you're seeing the more classic epidural hematoma here. So what do we want to do for him now? We put him on oxygen right away because he was hypoxic. Remember to intubate with your short-acting agents, lidocaine, etomidate, substantial choline. Here we are actually going to lower his mean arterial pressure. You can still keep that number of 100 in mind, but a blood pressure of 180 over 110 is way too high for a traumatic brain injury. He's going to get seizure medication, and he's getting mannitol and Lasix, and he does end up now going to the emergency department for a burr hole and to tie off that middle meningeal artery bleeding. Thank goodness, even though the neurosurgeon did not want to take him, initially we were keeping a very close eye on him in the trauma bay. As soon as he started to deteriorate, we got him back in the CAT scanner, and because we did all of the things that you guys have learned today, he made a full recovery. So in summary for this talk for you guys, you're going to do vital signs prior to CAT scan. You've got to keep that oxygen greater than 90 and your systolic greater than 110, and it's really important to keep assessing and reassessing. If we had washed our hands of that 18-year-old patient and said, oh, neurosurgery says nothing to do, we might have had a much worse outcome. Get that trauma team and neurosurgery team involved as soon as possible. Remember you only have two hours. Two hours goes by super quick. We talked about appropriate drugs, right? Be a superstar, whether it's for intubation, sedation, analgesia, and then you guys learn some new tips about maybe how to discontinue or reverse anticoagulation. And if that wants to be a talk for next year, then we can talk about that. So I think I still have one minute to spare. I know that we're running a little bit behind because we started late, so I'll just leave it up to the moderators if we want to do questions or if we want to keep moving. Hi, Dr. Greenberg. I think we can try to maybe do a couple before somebody, maybe somebody will interrupt us, but it looks like there's a question about routinely using seizure prophylaxis, or is it dependent on the bleed size and location? So for all traumatic brain injury patients, we do put them on seizure medicine for at least a week. Okay. It's more your hemorrhagic stroke patients. If it's like a deep bleed in the thalamus where the neurosurgeons are getting away from seizure medication for all bleeds, but for traumatic brain injury patients, we are doing seizure prophylaxis for all of them. Great. Thank you. How about, Sarah says, our neurosurgeons are also encouraging keeping SBP less than 140. Is that still a good goal as well? Yeah. We can probably do a whole talk on just blood pressure management, and I'm actually going to talk to you guys about that in the next talk in regards to hemorrhagic stroke. Everybody's different. I think that you'll hear people say 160. I think you'll hear people say 140, and then you'll hear the other camp who talk in maps, and maybe they want it 70 to 90, or maybe they want it 80 to 100, and it depends on whether it's a full moon and whether Mercury is orbiting Venus. I think that 140 is probably a reasonable target. Just understand that there's still a lot of variability across all different sites. And then the last question is, do you think it's better to gear treatment towards ICP management or CPP? Ideally, both are within good parameters, I realize, but we have had cases where we've chased our tails trying to keep both in goal. Yeah. Yeah. So they both go hand in hand, right? Because we know that cerebral perfusion pressure depends on ICP. I think that clearly you need to monitor what that ICP is, and you're keeping in mind that that's going to have a direct effect on your cerebral perfusion pressure as well. In my opinion today, I would say if you have to choose between the two, that it would be ICP first. Wonderful. Thank you. That's all of our questions. So thank you so much. I appreciate your time. Great. Thank you.

traumatic brain injury

Glasgow Coma Scale

TBI management

seizure prophylaxis

neurosurgical intervention

brain injury types

treatment prioritization