All right, let's go ahead and get started. I want to welcome everybody to AAP virtual didactics today. My name is Sterling Herring I'm a PGY 3 at Vanderbilt Appreciate everybody joining us today. We're excited for today's lecture As always, I want to first recognize and appreciate folks that have been More directly affected by this COVID-19 Pandemic recognize that not all of us have been affected equally. So we appreciate those of you who have been personally or professionally affected by this pandemic So goals for this as always I know you're always looking forward to this kind of front matter on this lecture I know my co-resident Amos has a particularly appreciated all this so Goals of these lectures are to augment the didactic curricula that are Ongoing at all of your institutions to offload overstretched faculty We know there've been a lot of logistical challenges associated with this outbreak and kind of shifting folks around That has included pulling residents off schedule So we wanted to provide additional learning opportunities for off-schedule residents and develop further Digital learning opportunities to support physiatrists in general during the COVID-19 pandemic Housekeeping things as always we're gonna keep everybody video and audio muted. It's not personal. It's just about maintaining bandwidth and keeping Distractions to a minimum if you have any questions if you click on Participants you should see my name again. My name is Sterling Herring You should see my name up toward the top list somewhere You can click on that and send me via chat any questions and at appropriate times. I will I Will ask our presenter those questions if you have general questions suggestions concerns, there's an email there. You can find us on Twitter So without further ado We are excited for today's presenter today. Thank you for joining us Hey there There we go. Hi. Good afternoon, everyone. Thank you to join my name is Nikola Dragoilovich, and I'm one of the attending physicians at Tier Memorial Hermann and assistant professor in PM&R at the University of Texas Health Science Center at Houston. I'm gonna be sharing some experiences with you about Neurosurgical complications after traumatic brain injury and stroke I will be using poll everywhere a little bit throughout the presentation So if you guys have your cell phones, you'll see those opportunities to participate and I would certainly encourage that Wanted to let you guys know that I am a light hearted person And you know, we'll love to hear your feedback and questions at the end so please jot those down and save them for the end looking forward to it, but without further ado We're gonna be talking about common neurosurgical complications after brain injury and stroke really with an emphasis on patient presentations and imaging findings and I'm also hoping to highlight the Physiatric treatments that we can use to minimize their impact on people's functional recovery and you know, this lecture is Geared towards trainees, but I know that we have a variety of people in house So hopefully everyone can walk away with something good today First things first would love to see where everybody is from So if you in your mobile phone browser can put in poll eevee.com forward slash N D R A G O And start submitting responses. I would love to see where people are at and who's here So that we can snub our noses at those who aren't Can you say that again poll that poll eevee.com slash N D R A G O Ndrago I see someone is hanging out in the northern Atlantic Ocean. Very good. Looks like we got some people from Seattle Nevada, Texas coming through Ohio, California my home state California my home state Got some Michiganders in the house We got our New Yorkers, thanks for coming by We have people from Columbia Canada Salt Lake, Mexico, New Jersey, Milwaukee, Miami, Chile Miami Wow Excellent. So we have an international audience too. That's great Yeah, I'm seeing lots of lots of ones coming in still so Thank you so much. I'm glad that we have lots of people around and especially to our International participants. Thank you for coming The next question is just about level of training if you could let me know where you guys are at I will try to get a sense of Where people are coming in Okay, I think my survey is not working, unfortunately. But I suspect that we will probably have a mix of people. Sorry about those technical difficulties. We'll go ahead and move on to the good stuff. So first and foremost, I wanted to just play a little game that I call Name That Space. And something that I find perplexes me and the trainees often is how radiologists will term these spaces when you have intracranial hemorrhages or other findings. And oftentimes you will hear radiologists use the term extra axial. And that's essentially just meaning that it's outside the brain. So subarachnoid hemorrhages, subdural hemorrhages, including hygromas, epidural hemorrhages, subgallial collections, which are beneath the skin, but outside of the skull. These are all extra axial. They're essentially outside of the brain parenchyma. And sometimes radiologists will loop all of these together saying, oh, there is an increase in the extra axial collections. But it's important to try to get specifics from them about which one is bigger, which one is expanding, which one's not. Intraaxial spaces, think of cerebral contusions, intracerebral hemorrhages, or intraparenchymal hemorrhages along with intraventricular hemorrhages. So in the previous slide, we see a large epidural hemorrhage in slide A, subdural hemorrhage in B, and then a large intraparenchymal hemorrhage with intraventricular extension on C. And then on these two slides, you see subarachnoid hemorrhage filling in the supracellular cisterns, and it will commonly take the form of these highlighted areas, places where fissures in the brain should become hyperdense, because in a subarachnoid hemorrhage, blood is essentially sitting on the surface of the brain, and that blood is going to fill in those gaps where all the fissures and the sulci and the gyri are. And it shows up hyperdense on CT scan when it's acute. So we're gonna test our knowledge with some that I pulled out from a different textbook. Number one is a subarachnoid hemorrhage. Two is an intraventricular hemorrhage, likely coming from this number three intraparenchymal hemorrhage. Four and five are from the same patient, but interestingly, we have an epidural hemorrhage here with a little bit of air in it, pneumocephalus, and then a subdural hemorrhage on this side. And then number six, we have bifrontal hemorrhagic contusions, which you'll often see as a sequela of traumatic brain injury. When there's a frontal head strike, the interior poles of the frontal lobe will strike the front of the calvarial vault, and then you will get essentially bleeding bruises in the brain tissue, not always frank intraparenchymal hemorrhages like you see here. Okay, we got 100% on those ones. So then the neurosurgeon's favorite game is guess that herniation. So the brain sits in a closed box. There's only so much room for blood or swelling before you run the risk of different types of herniations. The most common type of herniation is a subthalasine herniation. And that's synonymous with what we're used to seeing like midline shifts. And what's essentially happening is like in this cartoon, there's an epidural hematoma that is giving local mass effect on the cerebral parenchyma. And because of that, medial brain tissues are going underneath the phalx, cerebri, so subthalasine below the phalx. Now, the brain has an innate ability to accommodate pressure changes slowly. But when there's a rapid bleed in a short amount of time, or a rapid accumulation, becomes difficult for the closed space to become accommodative of that. And that's when other more serious herniations might happen. So for example, the uncle herniation, where the medial inferior temporal lobe swings over the inferior part of the cranial vault over the, underneath the tentorium cerebelli, or what's called a trans-tentorial herniation because it's going through the tentorium cerebelli, usually results in characteristic imaging findings. And I have this phrase here, neurosurgeons love when you're down and out. So down and out is something that I want you guys to remember with uncle herniations because that's usually what happens to the eye. There's very characteristic findings with a cranial nerve three palsy that occurs in an uncle herniation. The eye will be inferiorly and outward deviated. They will have a blown pupil and you'll have a ptosis. And then those are characteristic signs of an intending uncle herniation. As it progresses, you can have central or downward herniation and you can get a different phenomenon called Kernighan's phenomenon. And I put this K to show you the area where it's happening. Kernighan's phenomenon is that when you have cerebral edema or a mass occupying space that's resulting in uncle and central herniations, it pushes this aspect of the midbrain and the cerebral peduncle, where the brainstem and the brain connect together, up against the tentorium cerebelli and this corner of the inferior calvarial vault. And what that does is it compresses the corticospinal tract on this side, resulting in hemiparesis or hemiplegia on the side of the bleed. So normally with a right-sided epidural, we would expect left-sided weakness. But if the swelling were to progress and you see Kernighan's phenomenon, you can then get hemiplegia or hemiparesis on the ipsilateral limb. And it's called a false localizing sign because it may confuse you as to what side the mass occupying space is actually on. So know that Kernighan's phenomenon exists in more serious times of herniation. With central or tonsillar herniations, you start to develop compression of the reticular activating system. So patients will become hypo-aroused, they will lose spontaneous ventilation. The corticospinal tract becomes further impaired, resulting in worsening pleasure and ultimately medullary compression can result in arrhythmias and cardiac arrests. So wanna be mindful of these different intracranial hemorrhage types and cerebral edema types so that we can avoid these scenarios. Now, a midline shift in and of itself isn't always dangerous. In fact, on an inpatient rehab unit, you may have patients with strokes or traumatic brain injuries who are admitted with midline shifts. But the stability of the midline shift, how quickly is it expanding or how quickly is it worsening, guides your treatment. If you have a patient who's been neurologically stable with a persistent midline shift of four millimeters, that's not as concerning as a patient who maybe is having neurological changes and the CT scan shows a midline shift change from four millimeters to eight millimeters. I would say in that case, that is a much more dangerous situation where worsening edema or worsening hemorrhage is occurring. But for patients who are clinically and neurologically stable, the midline shift in and of itself does not have to be worrisome as long as the patient is stable. Again, this principal accommodation and the rate of change is really important to keep in mind as we go through working with these patients. So I have to throw in some PM&R memes to keep your guys' attention, keep everyone going. Let's all remember that PM&R is super chill. So let's first talk about post-stroke hemorrhagic conversion. About 10% of patients with first ischemic stroke will experience hemorrhagic transformation. The primary risk factors are stroke size, increase in the NIH stroke score, hyperglycemia, renal disease, uncontrolled hypertension after stroke. If people had atrial fibrillation and they were on anticoagulation at the time of their stroke, that increases their risk for hemorrhagic conversion. And also people who received IV tPA and then got put on dual antiplatelet therapy for secondary stroke prophylaxis will have increased risks of hemorrhagic conversion. Know though that the data on the prevalence of hemorrhagic transformation in ischemic stroke varies wildly depending upon the stroke severity and the subtypes. So studies out there will list anywhere from 5% incidence up to 40% incidence of hemorrhagic transformation. And I think that's because a lot of the studies that we have available to us are in very heterogeneous populations. And in one group you may see a lot of hemorrhagic transformation, in another group you may not. But just be aware that around 10% of patients with first ischemic stroke will experience hemorrhagic transformation. My personal soapbox after having been a neuro rehab physiatrist at TIER for the last three to four years is that if you don't have a CT brain within the last seven days upon admission to inpatient rehab, it's good to get one. You need to know the neuroanatomy. And a lot of times the CT brain will show you previous existing conditions like evidence of prior lacunar strokes or have they already developed some hydrocephalus that was unappreciated at the previous facility. At TIER we often get referrals for patients from long-term acute care facilities or skilled nursing facilities where patients are not receiving regular intracranial imaging. And so I think we need to have a low threshold to scan and a high index for suspicion that there could be something going on even though the neuro exam seems stable with what was previously reported. Now, there's not a lot of guidelines about when to scan and to who during inpatient rehab time. And so I think the onus is on us to have that high index of suspicion and have a low threshold to scan so we know what we're working with and how best to help the patient. So I wanted to share with you the imaging and history of a recent patient of mine, a 58-year-old female, right-handed, history of hypertension and previous subcortical stroke in 2017 without any residual deficits, thankfully, who presented with recurrent right-sided weakness and aphasia, and that was as a result of both left ACA and MCA territory strokes. She underwent TPA and then actually had intra-arterial thrombectomy for the ACA thrombus, but following TPA had some subarachnoid hemorrhage. There was concern from the neurologist about possible cardioembolic etiology, and so she underwent a loop recorder place. Now, when she was admitted to inpatient rehab, she was about post-stroke, day eight, noted to have right facial weakness, expressive greater than receptive aphasia, flaccid right upper limb weakness, right upper limb sensory impairment and apraxia, and she had been started on a septoneur course for urinary tract infection. So very common presentation for a left ACA, MCA cortical-type stroke. And looking at her imaging, I would say that there isn't much here that seems out of the ordinary. In slide A, you see there is hypodense findings in the area of the MCA territory, extended some into the ACA territory, but on this side, I think you can appreciate that there's some cerebral edema here that's not present in the right hemisphere. And then as you go through the sequences, you will see this hypodense area associated with the MCA stroke, and maybe a little bit of mass effect on the lateral ventricles. Now, just as a matter of surveillance, I repeated her CT scan seven days later, so she had maintained complete neurologic stability. More out of curiosity than anything else, I actually performed the repeat CT scan. And upon the repeat CT scan one week later, there was actually worsening findings. So I think in slide D, compared to A, you can see that there's more, the area of the MCA stroke is showing up more. We see more hypodensity in that area than we did before. I think there's more cerebral edema in the left hemisphere. You can see there's some loss of sulci and gyri here in the left hemisphere that we had previously had seven days back, especially comparing to the right unaffected side, you see the effect of the cerebral edema. Now, in E and F, we see the development of some bright spots, almost punctate-type hemorrhagic conversion within the stroke bed. And with increased cerebral edema, we're getting some mass effect on the lateral ventricles. Lateral ventricles should be midline, but in her, they're actually shifted over. And I remember getting the report from the radiologist that they're shifted over about six millimeters. Now, again, her presentation was one of neurologic stability. It was more for surveillance than anything else. I wasn't seeing a lot of findings in the ACA territory, from the ACA territory being infarcted on her physical exam. And I was hoping that maybe a CT scan two weeks out from her initial stroke might show more findings in the ACA territory. And so I wasn't expecting to find that hemorrhagic conversion, but nonetheless, there it was. I'm glad we were able to identify it though, because speaking with neurology, they wanted to hold her secondary stroke prophylaxis. We instituted some neurologic checks and that process is underway and thankfully she's been stable. But that just goes to remind you that 10% of patients will get hemorrhagic stroke or I'm sorry, hemorrhagic conversion after an ischemic stroke and not always be symptomatic. So again, that threshold, that low threshold to scan high index of suspicion is important. So in terms of management, as we discussed, I think getting neurology back involved in the patient's care is really important because they're going to want to do, they're going to want to make changes to their secondary stroke and DVT prophylaxis in order to reduce the risk of bleeding. But that has to be weighed with the potential risk for recurrent stroke. I think we always need to be mindful of medications with adverse bleeding effects like NSAIDs or SSRIs that could contribute to the risk where hemorrhagic conversion is not uncommon to find patients with a coagulopathy that wasn't known about before. But know that your serologic examinations and imaging will be your guide. But again, the rate of bleeding and the rate of accommodation is really important. If there's a small amount of hemorrhagic transformation, the person stays neurologically stable, we're not seeing worsening midline shift, we're not seeing worsening bleeding, I don't think that's necessarily something that needs to halt the rehabilitation course. But if we're seeing rapid changes in the amount of bleeding, changes in the neurologic exam, obviously that represents a different situation. Zoolander's favorite movie of mine. We'll talk a little bit now about hydrocephalus. We're not talking about normal pressure hydrocephalus, we're not talking about the wet, wacky and wobbly patients. We're talking about patients who develop hydrocephalus as a result of stroke or traumatic brain injury. So I wanted to share with you the story about a former patient of mine named Nora. Now she's a 48 year old female who had hypertension, who initially presented with facial droop and left-sided weakness. And she initially had a subarachnoid hemorrhage with intraventricular extension due to rupture from the right internal carotid ophthalmic junction. She underwent coiling, but then despite coiling, she developed recurrent hemorrhages and had two burr hole craniotomies to evacuate that recurrent hemorrhage. But as a result of ongoing bleeding several days later, she would ultimately require decompressive hemotraniectomy. She underwent tracheostomy and PEG placement and was transferred to an LTAC for ventilator weaning and ongoing care. Once they were able to get her off mechanical ventilation and stabilize her infection, she was admitted to our freestanding inpatient rehab hospital. So upon admission, she was very hypo aroused, significantly reduced initiation, left facial weakness, left facet hemiplegia and a very dense left neglect. And when we look at her initial imaging, there's lots of things to be seen. She has undergone the decompressive, now day 36, this was day 36 from her stroke. And so she underwent decompressive hemotraniectomy. We see a large area of encephalomalacia in the right hemisphere, which you would expect with the right internal carotid injury. With the right internal carotid injury, you're going to impair blood flow to the ACA and MCA territories. And her CT imaging seems, you know, coincides with that. There's a lot of cerebral edema, not just in the right hemisphere, but in the left hemisphere as well. And as we walk through, you can see she's developing a extra axial fluid collection beneath the skin, but outside of the brain parenchyma. I think that was measured up to 1.8 centimeters at its largest at the time of admission. But then we see some accompanying expansion of the lateral ventricles and the third ventricle here, you know, suggestive of developing hydrocephalus, which is not surprising to me, given the fact that she had subarachnoid hemorrhage and intraventricular hemorrhage. Patients who have subarachnoid hemorrhage, intraventricular hemorrhage, are going to be at risk for hydrocephalus. Also, people who have large intraparenchymal hemorrhages and into the ventricular system, or that are sort of about the lateral ventricles, will be at risk because of the loss of structural stability of the periventricular tissues allows for a large amount of ventricular expansion. Other risk factors include meningitis or encephalitis, or a history of instrumentation. Patients with severe traumatic brain injury and diffuse axonal injury, especially grades two or higher, will be at risk for hydrocephalus as a result of injuries to the long white matter tracts in the periventricular area. Again, you lose that structural support next to the ventricular system that allows for sort of expansive accommodation. Now, I was called to the bedside because some 12 or 16 days later, rather, nursing staff was reporting that she had slower cognition and that she was having elevated systolic blood pressures, 160, 170, 180, which was out of the norm for her. So obviously, this sets off alarms. Why are we experiencing a cognitive change? Why is she suddenly hypertensive when her hypertension was previously well-controlled? So on intracranial imaging, we see the development of a new intraparenchymal hemorrhage over the parietal vertex. And I have these arrows to point to us, point out to us, rather, that we're seeing now expansion of the lateral ventricles and of the third ventricle bigger than the previous findings. And so within a matter of two weeks or so, not only had her hydrocephalus progressed, but she had recurrent bleeding. And so unfortunately, she required transfer out for urgent neurosurgical services. She ultimately required a VP shunt, ventricular peritoneal shunt, and then later cranioplasty to replace the skull defect. So when patients develop hydrocephalus, it's not typically this acute. Typically, you will see a slow and sort of insidious onset of a variety of neurologic signs. Oromotor perseverations, like persistent chewing or a worsening of dysphagia is very common. Patients will have cognitive and motor slowing, but more than anything, will have fluctuations in their performance. One day, they'll do great. The next day, they'll do not so great. Over the weekend, things were fine. Come back Monday, the person doesn't look as good again. And this sort of on and off type effect from one day to the next, and you're not really able to figure out, you know, infectious workup comes back normal. They're sleeping. They're tolerating tube feeds. And so you're seeing this sort of, you know, great day, bad day, great day, bad day, and a lot of fluctuations in between. Patients will often get worsening hypertonia or the infamous P word in rehab, the plateau, where a patient is progressing very well, and then all of a sudden their progress sort of peters out. It is much less common to see signs of increased intracranial pressure, it's very uncommon to see signs of increased intracranial pressure with hydrocephalus. Again, hydrocephalus typically develops slowly and insidiously over the matter of weeks to months after the event. It's very uncommon for it to develop so quickly as it did in Nora's case. On imaging, you'll see some characteristic finding. So on CT scan, you'll see periventricular lucency or ventricular dilatation. And so if we go back to Nora's, I think that you can certainly appreciate the ventricular dilatation, the periventricular lucencies has a good example right here about the anterior poles of the lateral ventricles, we see some changes there. And that's as a result of through the spinal fluid entering the brain parenchyma, and because of that edema, giving off signal changes different than the remainder of the brain parenchyma. If you're fortunate enough to be able to get MRI quickly, you will see T2 enhancement around the ventricles, indicating that transependymal flow of CSF. Cerebral spinal fluid is being, because of pressure is being pushed through the appendymal cells out into the brain parenchyma around the ventricular system, and we're getting interstitial edema and T2 will pick that up quickly. In terms of management, because these patients are having these fluctuations in their performance, it's really important to rule out the reversible causes. Got to rule out infections, seizures, medication adverse effects, among other things. A lot of times when you suspect hydrocephalus, neurosurgery may not always be apt to place a ventricular peritoneal or other type of shunt because of the risk of infection or bleeding complications, especially if it's close to the recent inciting event. So in these cases, or when evaluations sort of seem equivocal, a tap test or diagnostic lumbar puncture is helpful. Typically, someone will perform a lumbar puncture and then take off about 50 milliliters, 40 to 50 milliliters of cerebrospinal fluid, and then monitor the patient over the next six to 24 hours and look for any changes in their functional status and cognition. Now, if a tap test is positive, meaning that we saw changes in their cognition and arousal and therapy participation that were beneficial, we'll call that a positive test, and that really will help you win your case with a neurosurgeon, because a positive tap test will indicate to you that the patient will benefit from a ventricular shunt. A negative test does not rule out the potential benefit. So doing a tap test can be really helpful as long as it's positive, because it can help you sort of win the case with a neurosurgeon that they really do need the shunt, because the definitive treatment is ultimately a ventricular shunt placement. Emergently, if a shunt can't be placed, the neurosurgeons will place an external ventricular drain to drain that off, but ultimately ventricular shunting is the definitive treatment. But it's important to monitor for under or over shunting phenomena, or even hemorrhage along the catheter tract once the ventricular shunt is placed. And I wanted to highlight the case of another patient named Dean, a 50-year-old gentleman who had a fall with a severe TBI with diffused traumatic subarachnoid hemorrhage and had a right traumatic subdural hemorrhage, underwent decompressive hemicraniectomy. As you can see in A, B, and C, he admitted to us with left hemiparesis, dysphagia, behavioral lability, and dense cognitive impairment. Now on his imaging, we see the hallmark of a decompressive hemicraniectomy, that the right half of the covarium is off. We see a lot of cerebral edema here. We see effacement of the psoas and gyri in the right hemisphere, but then intact psoas and gyri in the left hemisphere. We see a significant amount of lateral ventricle and third ventricular expansion. And then these slit-like changes here, which was actually a very large subdural hygroma around the phallic cerebri that had developed as a result of his traumatic brain injury. Now, this is on his post-op day 94, that we see evidence of these changes. We see those periventricular lucencies again, indicating that we have a potential hydrocephalus case that we need to monitor. And so we monitored how he did, and he was making good gains, but he remained in PTA for a long post-traumatic amnesia for a long period of time. And while his left hemiparesis improved, he just had a real failure to progress from a cognitive standpoint. And ultimately underwent ventricular peritoneal shunt placed. As you can see in D, E, and F, you see the ventricular peritoneal shunt catheter in the left lateral ventricle, and then in the third ventricle here. And then he had a cranioplasty completed, but then has a fluid collection beneath the cranioplasty post-operatively. Now, one of the things that I wanted to highlight in his particular intracranial imaging was that a shunt can take off too much from the CSF space or it can take off not enough. If the shunt doesn't take off enough, the ventricles stay enlarged, and the shunt is not doing what we had intended it to do, right? Was to drain off some of the cerebrospinal fluid from the ventricular system in order to enhance cognitive function and improve recovery. Now, if they are over shunted, you drain the ventricular system too quickly. And just as we talked about the principle of accommodation regarding cerebral edema and bleeding changes previously, the same thing can happen with the ventricular system. And ideally, we are monitoring the evolution of the ventricular system after VP shunt place and hoping to see small changes. Rapid changes in the volume of the ventricular system is not well tolerated by patients, and they will almost certainly have a neurologic decline as a result of that. They can be over shunted, it drains too fast, and the ventricles become slit light, or they can be under shunted, meaning that you put the VP shunt in and it didn't really drain anything at all. Sometimes though, after cranioplasty, when they develop subdural hemorrhages or other bleeding complications, neurosurgeons will wanna be very judicious about the rate of drainage. Because if you keep the drainage at a rate relatively controlled rate, the pressure in the ventricular system will actually exert some sort of outward force up against the brain parenchyma here, and it sort of helped tamponade the expansion of postoperative fluid collections here. Now, if you over shunt and drain this too quickly, it allows for the more rapid accumulation. So almost like a vacuum or like a pulling effect, you pull off too much of that ventricular volume and you get expansion of postoperative fluid collection. So sometimes the neurosurgeons will use the presence of a VP shunt to their benefit to help control postoperative collections under a cranioplasty like this one, but that may result in a slower rate of drainage of the ventricular system. And so you may not get as rapid recovery of cognitive impairments as you were hoping for, but know that slower changes are always better tolerated than quick ones. Quick ones, in fact, usually require urgent neurosurgical evaluations. One of the last condition that I wanted to highlight is syndrome of the tryphine It has a couple different monikers trephination syndrome sunken flap syndrome sinking flap syndrome It's a known complication of decompressive hemicraniectomy weeks or months after the initial decompression That can result in a whole constellation of different neurologic signs and symptoms and usually when we notice it is because there's either an abrupt failure to continue along a path of improving rehabilitation or Initial gains and rehabilitation are quickly followed by a rapid decline So clinically what you will see is that Patients will have neuro worsening neurologic status when they're upright If you lay the patient supine Their neurologic exam improves you sit them up again. They have less cognition. They're hypo aroused They have may have worsening strength you lay them back down arousal improves speech improves command following improves You will see a visibly sunken hemicraniectomy flap like in this picture along with some scalp contracture scalp contraction over the edge of the craniectomy site And oftentimes after a decompressive hemicraniectomy there's so much swelling and cerebral edema or fluid collections that It doesn't become sunken in like this, you know They almost always present to inpatient rehab with sort of like a very full Head contour that that looks almost normal and then gradually over time as the edema improves It will start to take in a a more sunken appearance, but a rapid Sunken sinking in or a very extreme sinking in like we're seeing in this picture should you know alarm you to the existence of Of syndrome of the trophine in this particular case And it has some very characteristic intracranial imaging So I wanted to share with you the story of a patient a 39 year old female Who had a severe tbi in 2017? As a result of a motorcycle collision and then had a recurrent Motor vehicle accident with severe tbi again, unfortunately some three years later She had a traumatic right subdural hemorrhage and due to cerebral edema required decompressive hemicraniectomy Now she was admitted to our service. She had you know, extreme cognitive impairments She remained in post-traumatic amnesia had some mild left-sided weakness, but more than the weakness She was actually in coordinated but quite a bit of endosagnosia. She was you know, sort of blissfully naive to the fact of everything that had happened to her so This intracranial imaging was from post-op day five where we can see the you know signs of cerebral edema pneumocephalus and um extra axial fluid collections um at the site of the decompression along with some developing subdural hemorrhage here along the um along the line of the dura now Over the course of the next week during inpatient rehab. She was just having recalcitrant migraine symptoms No matter what we had thrown at her in terms of trying to get these migraine headaches under better control um, and and we noticed the You know emergence of you know, her hemicraniectomy site sinking in very quickly So on repeat imaging just some six days later you see that A lot of that edema that had maintained the normal cranial contour was gone. We see the Hemicraniectomy flap, you know almost looking as if it is nearly adhered to the surface of the brain and then the emergence of an interhemispheric and and left frontal subdural hemorrhage So Now neurologically she was actually improving but the migraine headaches were very severe and difficult to control So in terms of management when you have these patients Neurosurgery will often Not want to put the hemi will not want to perform cranioplasty right away You know at our local institutions neurosurgeons are often waiting two or three months to perform cranioplasties their Rationale being that they want to reduce the amount of edema At the surgical site so that when the cranioplasty is performed there is reduced risk of infection and wound breakdown and other complications So what do you do when you have a patient with trepanation signs and symptoms? that neurosurgery does not want to operate on immediately because we're having neurologic improvement despite you know, um other other symptoms so One of the easiest things to do is just to fluid resuscitate them But often these patients are requiring, you know, continuous IV fluid resuscitation In order to maintain their volume status and you know, not necessarily uvulaemia But even a little higher still as long as they can tolerate it which allows for a little bit of additional expansion of the soft tissues around the Around the hemicraniectomy site and and take some pressure off the sinking flap Oftentimes you'll be needing to perform therapies with the head of the bed at 30 degrees or less Again, these patients are exquisitely sensitive to positional changes in terms of their cognition and strength. So Sitting them up worsens their symptoms laying them down makes it better So if you can do therapies with the head of the bed at 30 degrees or less You're at least buying yourself some time in order to Monitor their symptom evolution before you can ultimately get them to definitive cranioplasty There's been a lot of studies about when is the optimal time The optimal time to perform cranioplasty and and the largest studies that we have to date Is a cohort of patients from the university of washington Where they noted that patients who had cranioplasty within 30 days of the initial hemicraniectomy Had reduced amounts of infection seizure and bone flap resorption but higher amounts of post-operative hydrocephalus Waiting longer like two or three months down the road longer still minimizes hydrocephalus, but um potentially increases seizure risk in this patient cohort and so Know that the time to cranioplasty Is something that sort of remains controversial and will often vary Geographically or from one institution to another so having open lines of communication with the neurosurgical services and and being on the lookout for signs of sinking flap syndrome is important and then knowing that you have the ability to You know use IV fluid resuscitation or more bed-based type therapy to sort of buy yourself some time until they're ready for definitive cranioplasty So I wanted to try to use the last 10 or 15 minutes we have or so to Open up to questions or get some discussion going especially since we have You know visitors from not just the united states, but internationally Um, so if you could I would love if you could just share one takeaway with us Thank you i'm watching for uh Comments and questions come in Um, can I ask a question real quick sure. All right, so To what extent do you incorporate Kind of ongoing surveillance imaging as a rule or does that only apply to certain? severities of injury certain patient types um, yeah, so I I think that there's certainly you know, sort of hallmarks or things that I that I I think about Um when i'm deciding, you know, how often to perform CT scans, I think there's no single rule that adequately fits the needs of patients um for You know patients who have had strokes or traumatic brain injuries with operative interventions with bleeding complications Then i'm certainly more apt to you know, do surveillance ct scans every you know Um 14 days or maybe you know every 21 days um To monitor when patients are on dual anti-platelets when they're on anti-coagulation um Those are things that sort of will make me want to scan them sooner rather than later If the initial ct scan shows some of those periventricular changes that make me think that they may be developing hydrocephalus or if they had subarachnoid hemorrhage with intraventricular extension and i'm thinking that they may develop hydrocephalus in the future because of that then I will be more apt to scan them And so I try to look for things that are bleeding risks and look for things that are sort of surgical risks That I see on you know, my initial evaluations and initial intracranial imaging and then use those to help guide me But unfortunately, there's no uniform rule um So that's why I think having that lower threshold to scan Is important now in a person who had a first ischemic stroke They're on aspirin and statin for secondary stroke prophylaxis and neurologically. They're doing really good I won't scan that person every seven days. I think that's that's you know, not necessary to do and just adds to You know their radiation exposure but if you're potentially surveilling for the development of hemorrhagic transformation or Hydrocephalus or there's an acute neurologic change that warrants, you know, ct scans. I think those are sort of the Decision-making things that guide me in one direction over another that's a bit of a long-winded explanation But unfortunately, there's no blanket rule No, but that's very helpful. I appreciate it kind of so it sounds like not only does it depend on the on the patient But also you're looking for very specific things. I think that's helpful Yeah, I I think so, you know, um keeping in mind medications that can can contribute to bleeding, um, You know getting good feedback from the therapist and the nurses about how patients are doing Um, you know many times we hear about changes from the therapist or from the nursing staff We don't see them with our own eyes the first time just because they spend so much more time with the patients than we do and so being able to You know trust them and and and have a sense of how the patient is doing at any given time it is important You know, I think will guide you more than anything else All right. Thanks another question that came in. Do we understand why oral motor preservation can be a symptom of hydrocephalus? I don't have a great answer to that question I will have to dig into that and look a little bit more is actually something that sort of um Was was shown to me by one of my mentors. Dr. Monica Verduzco Gutierrez um You know, I I very you know clearly remember as a resident and fellow Um, you know seeing patients rounding on patients and and I remember, you know, Dr. Verduzco Gutierrez saying You see how he's chewing like that. He is developing hydrocephalus Um, and I and I haven't found how to get in, you know, the neuroanatomy correlate Um, but I am going to look it up now, um and get back to you all about it because i'm actually very curious too But it's one of the most common signs and one of the things that I see most frequently is, you know changes in dysphagia and oral motor changes before the spasticity or cognitive or other changes show up Thank you for giving me more homework no, if you uh want to Send that over to me. I will put you in touch with the uh person who asked the question I think that's that that'll be interesting to see. Thank you. Yeah. Yeah. Thank you for that learning opportunity Um one more question here So And this is a great one. This is something that i've come across as well Um, so sometimes it can be difficult when you're looking at skin flap to say, you know, this one's okay This one, you know, it looks more like a sunken flap uh Syndrome, is this? Is it more progression or is it something you can walk in the room and say? Oh, yeah This is you know what I mean? Yeah. Yeah, absolutely and I think that's a great question and and I and I think one of the one of the things is to Keep looking at the hemicraniectomy site on a daily basis so that you have a sense of what it looks like from day to day um, because initially after hemi after decompressive hemicraniectomy the contour of the head will be very full and That's because there's a lot of swelling under the hemicraniectomy site Now usually over the course of you know, the intervening, you know, three four or five weeks It will gradually develop a sunken appearance Um, but it won't be as sunken in and as dramatic as as that picture was that I showed you In fact, what often happens is that it starts to cave in a little bit and then some of the swelling that was up At the at the top of the hemicraniectomy site starts to travel down the side of the face towards the zygoma into the cheeks and you know will often fill out the area around the eye or in front of the ear Or into the cheeks and the left side of the neck over the course of you know Three four or five weeks and so patients become very alarmed because they're seeing you know Swelling around their eye or around their face and they think something is happening, but that's actually the natural progression So, you know from when you look at a patient who has a full flap site If over the course of several weeks the flap site starts to sink in a little bit. That's very normal A rapid Sinking in or the sinking in within a week or two Of the initial decompressive hemicraniectomy is I think what tips me off to a trephination syndrome Um, and and so a slow evolution a slow sinking in is normal But if within two, you know, if within two weeks you're seeing you're seeing a really sunken in flap um that will that should give you pause and and and should you know have you contact the neurosurgeon because Normally the edema from the decompressive hemicraniectomy Will take weeks to resolve it shouldn't go away in 7 to 14 days Okay, thank you that makes a lot of sense Um, i'm not seeing any further questions at this point But if any more come in we can address them Um, I see you put up your email address your twitter handle there. So if anybody does have any questions that come up, please You know, I they can reach out to you directly Absolutely. Yeah, feel free to message me on twitter. I am a social media I am a social media Newbie, so please bear with me as I as I navigate these murky waters. I do not do it with as much You know aplomb as others do but feel free to email me or you know Send me interesting, you know patient patient presentations or cases on on on twitter, too Would love to hear from you guys Um, I really enjoyed being a part of this didactic series I think it's a lot of fun and a great opportunity for us to Share information with everyone as we go through these difficult times. So thank you all so much

Nikola Dragoilovich

virtual lecture

COVID-19 pandemic

learning opportunities

neurosurgical complications

intracranial hemorrhages

surveillance imaging

hydrocephalus

sinking flap syndrome