The Role for ETV in Adult Hydrocephalus Free
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- Colleagues and friends, thank you for joining us for another session of the Virtual Operating Room from Neurosurgical Atlas. My name is Aaron Cohen. Our guest today is Dr. Mark Hamilton from University of Calgary. He's a professor of neurosurgery there, significant contribution to care of hydrocephalus. He's also the chairman of the adult hydrocephalus Clinical Research Network. We had two recent talks from him on normal pressure hydrocephalus as well as technical aspects of shunts. Today he's going to talk to us about the role of external third ventriculostomy in the management of hydrocephalus. Something that I'm very much interested in learning from as well, somewhat controversial, but at the same time a topic that deserves lots of attention. So Mark, thank you for being such a valuable contributor to this series and very much look forward to learning from you today.
- Thank you very much, Aaron. It's a real pleasure to be here and to talk about The Role for ETV in adult hydrocephalus. I'm going to sort of do some emphasis on the role, but talking about efficacy and safety, and then I'll go through some of the technical issues at the end. So I think it's important for people to have a background on why people should consider ETV in certain patients. So I always like to try and begin a talk about hydrocephalus, but a quick reminder about how common it is, and this is a systematic review that we published in 2018. And the important thing here is that it's very common, it's more common in adults than it is in children. The the information about the prevalence in young adults and middle aged adults is rather poor, but it's definitely an adult disease. And there's lots of other studies that demonstrate this. A pragmatic organization of adult hydrocephalus is really essential for understanding how to approach patients who have really different types of adult hydrocephalus. And this has very big relevance or important relevance to what we're gonna talk about ETV. So we set up a classification scheme where we use transitional. These are patients that were treated as children. Unrecognized congenital, so no treatment as a child. There are some more specific aspects of that definition. Acquired subarachnoid hemorrhage, trauma, infection, tumors. And then idiopathic normal-pressure hydrocephalus. Now the three that I've identified with colors and asterisks are the three that ETV plays a role in, an important role, whereas with INPH there's no proven benefit for ETV and INPH unless you have an elderly patient with a very clear cut obstructive hydrocephalus. So to give you some context for this, this is a paper we published back in 2019 the first 517 patients from the Adult Hydrocephalus Clinical Research Network registry. And this was the full definition. So unrecognized congenital, it has many names in the literature and this is one of the problems it's referred to as chronic hydrocephalus, arrested hydrocephalus. There's a long, long litany of names. So we tried to use something that was very descriptive. These are patients with imaging features or enlarged head circumference consistent with congenital hydrocephalus, but not treated before age 18 years. And again, looking at the current enrollment in our registry, we have just over 2,100 patients and about 354 of these are congenital, are unrecognized congenital patients. So coming back to this initial report. So at that time there were 137 patients with unrecognized congenital hydrocephalus. This is a distribution of the four types and you can, this is just looking at age and you can see that for sure this is a disease mostly presenting in the forties, fifties, and early sixties, usually in about the late fifties is the most common age. A transition is just makes sense. They're following out from pediatric experience. Acquired, distributed overall ages, and then by definition INPH over 60 or 65 years of age. Looking at those 137 patients, the most common etiologies were aqueductal stenosis and what sometimes is referred to as aqueductal pattern. I think that with high resolution imaging, which I'll show you later, these all end up being aqueductal stenosis that the resolution of the imaging just doesn't allow you to detect the web. But the pattern of hydrocephalus is very typical, and there's some other lesions here that are identified. So again, look, treatment status at the time of enrollment for these 517 patients, by definition, all the transition patients have had treatment. The unrecognized congenital patients, about two thirds have had treatment. In our experience in Calgary where I've seen probably about 500 of these patients, about a third don't have the criteria that we use to initially recommend treatment, and the other two thirds do. The distribution of the others is as one would expect based on the type and the age of the patients. Now if you look at some of the comorbidities in this group, and we're gonna again be focusing on the unrecognized congenital group. So the unrecognized, there are 137 patients again, very contrasting transition, acquired, into suspected INPH. This group is relatively healthy, very few comorbidities except for some, you know, things you expect in middle age, hypertension, whereas, a lot of the other comorbidities that occur in the elderly and in the transition group with spinal issues aren't as common. In fact, you know, about 41% of the patients actually had zero comorbidities. Now in our network we assess the patients using standard methodology. We use a 10-meter gait velocity. I use a video library as well, some of the members don't. We use counting the steps for 10-meters and the steps to turn 180 degrees. Use a Montreal Cognitive Assessment for cognition, Symbol Digit Modalities Test, Beck Depression Inventory 2, looking for depression overlay which can affect cognition and assessment, Lawton ADL and Overactive Bladder score. And there are some other things that have been added like quality of life and Tinetti Balance and Gait Scale. So this is just to look at some of the differences, again, between these patients in the different categories. The the top one here is MoCA and you can see that these patients tend to be on the whole when they present in the mid-range twenties, some people are normal, some people are worse off. The distribution and suspected INPH is a little more sloped and has a more variation in the scores. And then you see this difference between Symbol Digits Modalities scores and INPH, Gait Velocity and INPH. Gait velocity is not as big an issue in this population compared to INPH where gait is a predominant disorder. And the gait scale, the Boone Gait Scale, again, not as dramatic in this group. And the bladder issues not as dramatic in this group. Certainly they do occur, they're just not as dramatic in some of the other types of hydrocephalus. So again, what we're gonna be focusing on is the unrecognized congenital, not to dismiss acquired hydrocephalus, it's extremely important. There's just a simple example of a benign pineal cyst that had a bleed into it that produced obstructive hydrocephalus. And endoscopically this cyst was fenestrated and a third ventriculostomy was performed. And this is a year later and you could see the collapsed cyst. So there are lots of examples of acquired hydrocephalus where you can use endoscopic third ventriculostomy to treat their hydrocephalus. And the reason we're gonna focus on the unrecognized congenital is it gives us an opportunity to look at the role, the safety, and the efficacy in more detail. So this group, the unrecognized congenital has the best scores for function, the fewest comorbidities. So they're often presenting untreated. So it gives you an opportunity to assess them before and if you decide to treat after. And all that together gives you a really good opportunity to assess treatment effects and separate them from disease effects. So having somebody with a post-traumatic or tumor hydrocephalus, it's hard sometimes to separate out the differences between the underlying etiology and the hydrocephalus in terms of what is causing the most symptoms. So how do we, where do you find these patients? So what leads to identification of ventriculomegaly? Well, the most common presenting clinical issue, probably headache, it's very common and frequently totally unrelated to the hydrocephalus, but it leads to a CT scan and then an MRI scan. And for the reason that it's not related is the reason why it's not very responsive to treatment. Often the patients have an overlying headache issue and the hydrocephalus could potentially be aggravating that, but it is not usually the cause of headache unless there is high intracranial pressure. Some patients will present with seizure. And then there's a group that's identified incidentally after a CT or MRI for other reasons, traumatic brain injury, sometimes see patients having sinus CTs where they go back far enough they can see the ventricles look big. And so these are, I think, important to recognize because the natural history is complex for this patient group and it shouldn't be dismissed as chronic or arrested hydrocephalus. So I'm gonna look at these concepts with identifying three topics. So I'm gonna talk about hints from nature regarding the natural history. So how do you get from being born to being a 56 year old or a 60 year old with big ventricles, and then start to decline? When we look at these patients, I'll say that it's mostly about the cognitive function, that's the big issue. And then we're gonna talk about the best metrics for assessing patients with regard to treatment with an ETV. So for the first one, some hint from nature. One looks at the natural history. This is an example of something I identified when I was doing a lot of pediatric neurosurgery, the spontaneous third ventriculostomy. And it's an example of what can happen to allow the brain to reach a compensated state and the ventricles to stay large. So this one example is a four month old girl. She was sent because of an increasing head circumference, it was rapidly growing and then it just stabilized. She had a soft fontanel, no splaying of the sutures. So she had aqueductal stenosis. But without ever having surgery, had a defect in the floor with third ventricle. And on the face contrast image you can see a robust flow through that. So I refer to this as a spontaneous third ventriculostomy. She's did remarkably well. She had repeat MRI scans that confirmed persistence of the third ventriculostomy flow and I had followed her for 12 years and she had normal development and stable rate of head growth. So things happen in nature that allow us to get to be adults with this disorder. It is more likely that this occurs in very early childhood. Some of the patients will have bigger heads. So it may have occurred at a slightly later point. And of note, I'm just gonna show you some examples. This can also occur in the setting of acquired obstructive hydrocephalus. So back when I looked at a small series, you can see that there was one, the four month old I mentioned, but the rest were adults. And two of these were patients who had done okay with their disorder but required and had flow on their imaging but then required an expansion of their third ventriculostomy. So we had to go and expand upon what was already present to allow for treatment for additional treatment effect. And the last patient down here is a 69 year old patient who had a meningioma. So all of this emphasizes the need for long-term observation in this patient population. So what does this tell us? It tells us that, basically it helps us with our understanding why patients with obstructed hydrocephalus can stabilize. And I'm sure there are other solutions in nature, other points of CSF egress. And one of the concerns is that these are often not adequate in the long term. And why does that happen? Because brain physiology changes with the age. And so that's one of the things we're gonna look at in just a minute. Now ETV is a treatment modality that recapitulates what can happen spontaneously in nature. So we're doing surgically what we know happens spontaneously and is probably a reason why patients reach this point. So the second thing I'd like to talk about is the cognitive function. What do we know about unrecognized congenital hydrocephalus? So how do you sort of start approaching something that's this significant? This is, you know, enormous ventricles. This is somebody with aqueductal stenosis. Can we predict the natural history based on that MRI scan? In reality, ventricular size is unreliable in predicting increased ICP or the natural history in this patient group. There are other clinical exam features that are more reliable. A current cognitive assessment, so doing one at that time you see them is unreliable in necessarily predicting the natural history. So it's hard to determine what the speed of decline could be if they're doing it recently, well, or if they have a deficit, what the speed of decline would be. And what it can do is sometimes predict cognitive reserve. So this is an important concept that neuropsychologists use. So if you look at the memory test scores as an example on this axis, look at this as the point where dementia becomes obvious because as referenced by the scores, a normal person without hydrocephalus can go along and if something happens, they have a lot farther to go before they reach that threshold. Whereas the people with unrecognized congenital hydrocephalus probably were left with low reserve. And so at some point the, if something happens, it could be a trauma, it could be an infection, it could be just a change in brain physiology, they deteriorate at a more rapid rate because they reach the threshold faster. And so this is an important concept to remember. Sometimes with these patients, we'll hear that they've had a relatively minor head injury, but the cognitive effects were quite consequential. So I think cognitive decline is an important and the most common issue that I think we should be thinking about with these patients. And while it might seem obvious that treatment of hydrocephalus should result in improvements in cognitive function, this has not been given in the past and needs to be proven. And I'm gonna hopefully show you that it is effective. Can we predict a natural history, as I mentioned, that's difficult, but the best predictor of the need for treatment is evidence of cognitive decline. That the patient comes in and the family and the patient tell you that the patient, that they're having difficulty, that you know, they've had more trouble at work, more trouble in university, they're having more trouble with short-term memory, that's an important observation. If you already have a neurocognitive exam and you can repeat that and see a change, that's extremely valuable. So one of the challenges is identifying is there a cognitive threshold where treatment should be considered? And this is difficult. There is no randomized trial on this, there are no guidelines on this. The approach we've taken is that if the patient is declining and that's clear by either of the methods I mentioned or the patient has reached a point where their cognitive assessment is concerning enough that if they lose anymore, they're really gonna be incapacitated and have a real serious effect on their ability to function, that may be the time to intervene. Now the the opposite approach to this might be that you say that the natural history is so poor that everybody who's identified should be treated. I think most of us don't jump in to treat until we have evidence of a decline or we have evidence that they are at that concerning threshold. If you wanna really understand the effects of ETV, the best scenario is to examine, assess patients before and after treatment. And this is why I'm focusing on this patient population 'cause it presents the opportunity to do that. As I mentioned, this separates the underlying disease from potential surgical benefit or surgical damage. And the damage part is very important to, you know, to identify or to show doesn't exist. And sometimes a full assessment before treatment can be difficult. But this patient group offers a lot of opportunity for that. This was a paper that would be published in 2014. It was a series of patients who had third ventriculostomy where we were able to complete a comprehensive neuropsychology exam with neuropsychologists. Not the easiest thing to arrange when patients are declaim, but we were able to do this in 13 patients. The age range it showed that there were some children, but the majority were adults. And we had comprehensive neuropsychology testing the mean of about 16 months after the third ventriculostomy was performed, having the pre ETV data to look at. Where this show us, and this is using a reliable change approach, it showed us that you look at all these domains over here, all of these improved or they stopped getting worse. There was one patient who had a change in executive function. On the whole of what this is telling us is that ETV can improve or stabilize cognitive impairment for the vast majority of patients and that no patient was cognitively harmed using ETV to treat their hydrocephalus. So these are two important concepts. Does it work and is it harmful? And I think this helps set the stage for this. So the third approach or the third issue, is what are the best metrics for assessing treatment of ETV? Now traditionally what we've done is, and I'll show you a study that came from Calgary a number of years ago, the outcome measure we used was could we avoid a shunt and we should, you know, follow that along for at least a year to feel comfortable with that. That certainly has some bias and is a rather coarse measure. You can quantify or talk about patients' subjective improvements that with their, they say they're better, they're back to work, and you can look at your basic complication rate, course measurements, but important measurements because they do tell us some things. So this was a paper we published in 2016 looking at a sequential series of 163 adult patients and we included some with secondary ETVs and these are the patients with acquired hydrocephalus. So just note, this is not to forget them. I'm gonna show you these results because although there are more difficulties with this patient population using ETV, and these are people that usually have had a shunt before, that there is some benefit, significant benefit. So the mean age you could see was about 50 years and the mean duration of follow-up was 8.2 years in this patient population. So if you look at the green line, this is we call primary ETV, the blue line, the patients who had a shunt failure and we were able because of their underlying anatomy to perform an ETV. This group has a very high success rate in terms of avoiding a shunt. The patients who already had a shunt, you can get about 70% of them shunt free with some clear criteria on how to select those patients. So a good metric, I think one we'd all be satisfied with if we could avoid doing a shunt on a patient or another shunt revision. But is it good enough? Would the patients do better with a shunt? That's a question that people have raised on many occasions. Are the ventricles required to significantly decrease in size to demonstrate improvement? I'm gonna try and show you, and this is substantiated by evidence in the pediatric literature, that ETV is as, I think, as good as a shunt and the ventricles do not have to change in size to demonstrate improvement. So again, just remembering that we use objective measures, it's important to measure. So if you really wanted, see how we're doing with patients, use objective reproducible, standardized measures of gait, cognition, and use other scales as you feel necessary. So this is a paper that was published in 2022 from the HCRN and we're looking at the role of primary endoscopic third ventriculostomy in adults with chronic obstructive hydrocephalus. So we're looking for patients who were entered the registry where we could get both pre and post ETV gait and cognitive assessment. And because the registry is moving along, and we're enrolling patients, and we have patients who've been in longer than others as most registries would, we have patients who had sort of early follow up and late follow up. I'll show you the effects on gait velocity. So this is looking at the long-term follow up. The pre-gait velocity was 0.7 meters per second. The post-gait velocity at a long-term follow-up about a year later was 1.3 meters per second. That's a very significant clinical improvement. And then within patient change was about 0.4 meters per second. Show you the cognitive effects just using the MoCA. The pre-MoCA was in the long-term follow-up group was 23. The post-MoCA after the ETV and the long-term follow-up group was 26. And the within patient change was an increase of two in the MoCA. That's a clinically significant change in the MoCA. Although there is some variation in the literature on what is significant, it's somewhere between 1.86 and three to four. But this is I think a clinically significant result and we have now started the process of doing a follow-up to this, and we now have a much larger group of patients and more patients with longer follow up. So when you look at those changes that I just demonstrated, those cognitive gait changes are compatible with what we would expect with a shunt. And if you can think back to what we talked about with INPH, these are very, very consistent. And the treatment risk is significantly lower with an ETV than with the shunt, especially when there's very large ventricles. I think there's a major concern about the risk of over drainage in this patient population because of the large size ventricles and that is eliminated with a successful ETV. So that sort of brings us to, you know, why I think an ETV can be thought of as a safe and reliable way to treat patients who have obstructive hydrocephalus, adult patients with obstructive hydrocephalus, especially in this group where we've been able to demonstrate pre and post surgical results for cognition and gait, and with a very high degree of safety. I didn't show you the safety record or profile from the AHCRN paper, but it was extremely low and it was extremely low in our series when we published it. So now we're gonna just look at some of the technical aspects of ETV. I think starting with an approach to ETV is high resolution MRI imaging. MRI is extremely important for obvious reasons, but we really recommend that you get high resolution CISS or FIESTA Sagittal thin cut imaging, all the remaining imaging can be of value. Phase Contrast is mostly done in a qualitative fashion rather than quantitative in centers, but can be done quantitatively. And so this is, this sets the stage for looking at the anatomy is it a patient that's appropriate for and considering an endoscopic third ventriculostomy. So this is not what I would call high resolution imaging. This is, there's a lot of issues, we can barely see the floor here. These are massive ventricles. This is the T2-weighted T1. This is an example of high resolution imaging. These are both CISS imaging results and you can see a large third ventricle. You can see the lamina terminalis pushed forward, you can see the floor flattened, and the brainstem is sort of pushed forward to the clivus and you can see the blockage in the aqueduct here, and a constriction at this level as well. So the next question is, if so you've decided you've got good imaging, you're gonna do endoscopic third ventriculostomy, how do you do it? There are people who use rigid endoscopes and there are people who use flexible neuroendoscope. I think that there's a real important role for flexible neuroendoscopy. It's very accessible, it's inexpensive to set up, and it offers a lot of, excuse me, offers a lot of opportunity to do things that are a little more challenging with a rigid endoscope. What I'm gonna show you is based on my bias for using flexible neuroendoscopy, the imaging quality and the lighting quality have progressively increased. And we're now moving into a new generation of flexible endoscopes that have incredible resolution. So some people will use a Greenberg holder. I use a mayo stand and lay the flexible scope on the mayo stand. This is a bur hole that was fashioned. This is a peel away sheath. You'll see this in the video we're gonna show, this is the flexible scope being passed down the peel-away sheath into the ventricle. Again, the scope is situated on the mayo stand. This makes it just more convenient than trying to attach a Greenberg retractor, set up Greenberg holder. So now I'm going to show you a video. This was published in the recent Humans edition and it's a patient example and will illustrate the basics of the approach to selecting the patient and the endoscopic treatment of the patient in a few variations at the end.
- [Narrator] This video will provide an example of an endoscopic third ventriculostomy. The patient of record is a 54 year old male, otherwise healthy would notice difficulty performing as a teacher over a two year interval. The MoCA score was 26 out of 30, SDMT 30 out of 110, BDI 219, and gait velocity was normal. Imaging was completed, which included a high resolution CISS sagittal image demonstrating a web in the aqueduct and bowing of the floor of the anterior part of the third ventricle. The Axial T2 demonstrated ventriculomegaly. Surgery was offered to the patient and at the time of the OR the patient was positioned supine, the head slightly flexed, and Kocher's point was marked out. The position was confirmed with image guidance. Incision was marked and infiltrated with local anesthetic. The patient was prepped and draped in a standard fashion. The endoscope was placed on a mayo stand to allow ease of access and prepared for the surgery. The 12.5 French peel-away sheath with introducer was marked at a five centimeter depth for reference. The incision was opened and a bur hole was fashioned using a Midas Rex drill. The dur and underlying pier or monopolar coagulated and perforated in the center to allow access to the peel-away sheath which was passed using image guidance. The flexible scope was then passed down the peel-away sheath into the ventricle. Upon entering the ventricle, the Foramen of Monro could be visualized with the septum to the left. The choroid plexus and veins were also evident. Scope was passed into the third ventricle where the mammillary bodies were evident along with the thinned out anterior floor of the third ventricle. A probe was used to perforate and then opened to expand the whole anterior to the mammillary bodies and anterior to the basilar artery. The flexible scope was then passed down into the area anterior to the brainstem. There were some webs that were present, which were easily perforated to allow ease of CSF flow. While this is happening, the hole was gradually expanded with the use of the flexible scope. The third and sixth nerves were evident during the exploration of the space anterior to the brainstem. You just saw the sixth nerve. As the scope is pulled back through the membrane, the basilar artery and bifurcation are evident, and the hole in the floor of the third ventricle is evident. This is more than an adequate sized hole. The endoscope and peel-away sheath was removed and a Gelfoam plug in tissue gluer inserted. The wound is closed in a standard fashion. Postoperative day one MRI scan demonstrated evidence of the hole with good turbulent CSF flow and a change in the configuration of the floor of the third ventricle. Turbulent flow could also be seen on the Axial T2 image with a small bulb of air present. Clinical outcome at one year, the MoCA had improved to 29. The patient had resumed work without any new issues and the gait remained unchanged. We'll now describe some important intraoperative findings. One particular important issue is when the space between the brainstem and the basilar artery is very limited, the flexible scope adds eased to being able to explore this area with out the limitations imposed by the rigid scope. The dorsal cell can be evidenced just at the anterior edge of this opening. This is an example of a patient with multiple membranes. There is a set of membranes that have already been perforated. This is a membrane that's located halfway down the basilar artery. After successful perforation of the membranes, CSF flow is established to allow good access to the third ventricle. This is more easily accomplished with a flexible endoscope than with a rigid endoscope. In conclusion, careful patient selection is essential for endoscopic third ventriculostomy. It's really important to have quantitative measures of symptoms such as gait and cognitive function. High resolution imaging is required including CISS or FIESTA looking at the sagittal orientation looking for obstructions in the aqueduct. There is intraoperative variation that is present and one needs to be well aware of the anatomy and awareness of the potential risks and complications that are associated with this operation. Thank you.
- So that was a basic summary of the approach to doing a third ventriculostomy. There are so many different aspects that we could discuss. It's a operation that has a lot of nuances and there's definitely a role for the rigid endoscope. I just wanted to present my bias for using the flexible endoscope. I think it's a very, a good way for neurosurgeons to do endoscopic third ventriculostomy. Now I'm just gonna show you some examples of some imaging pre and post just to wrap up. This is the one I showed you already. And here's the pre-image of the aqueduct obstruction. And the post image, and you can see the turbulent flow and you can see the floor is actually no longer as flattened as it was here. Here's an example with a web at the bottom of the aqueduct. Not uncommon to see. And this is post, and you can see the space between the clivus and the brainstem has increased. The orientation of lamina terminalis has changed and you can see the defect here. And even the floor here doesn't look, the third doesn't look quite as pushed up. This is somebody who presented actually with high pressure hydrocephalus. This was an acquired variation and you can barely see the floor here on this image. You can see that everything looks tight up here with the lateral ventricle large, the third ventricle's very large. You can see that he is got, this person has a block right at the tip of the aqueduct. And after the third ventriculostomy, the floor is up, the anterior structures are forward, the roof is down. And you can see actually the better definition of what's going on in the aqueduct. The whole brainstem looks less compressed and the space in front of the brainstem has improved. This is an example of a patient with the bowing of the floor in the third ventricle, aqueductal stenosis. And post third ventriculostomy, the floor has come up. The brainstem again doesn't look as trapped. And this one, the space did not change as dramatically as some of the others. So that's basically, you know, an overview with some examples at the end to illustrate the versatility. I think anybody who wants to look after adult patients who have hydrocephalus should have experience with neuroendoscopy, 'cause I think it has a vital function in the management of a significant part of this patient population. Thank you.
- Great work, Mark. Very much enjoyed it. Nice overview of ETV. Something that I wanted to run by you if you can expand further. Is there any role for ETV in normal pressure hydrocephalus?
- At the end, the basic answer is no. There was some initial work that came out quite a long time ago that sort of started the speculation about this. There are two things that sort of confirm for sure in our minds that ETV doesn't have a role. It's also in a Kocher review was demonstrated during review of the literature not to have a role. There was a very nice study done with basic valves in Brazil. Fernando Pinto did it, it was a randomized trial, ETV and INPH versus shunt. And even with a non-program valve with a high incidence of over drainage, the shunted patients still did a lot better than the ETV patients. And so that was sort of very important. There's also an unpublished study that was presented as an abstract by Richard Edwards from Bristol and he was actually trying the equivalent of ETV CPC, choroid plexus coagulation that the pediatric network and other many others are using and studying. And he stopped that study. It was stopped because of adverse effects and failure to have any significant improvement. So again, basically no.
- Gotcha. And what is your threshold for using ETV if the prepontine cistern is really tight, if the basilar cap is just sitting there, there's not space. Where do you think the risk is significant?
- So I, my risk avoidance level or my avoidance of height basilar situations has changed a lot over the years as I've gotten more comfortable with it. If I can see a membrane, I think that's worth having a look at. If I could see a thinned out area, even if it's tiny, one of the things that happens as you, even if as you start to open it up, everything starts to settle back and the space actually gets bigger. I can also pass a flexible scope down with not, with very low risk of trauma. I've been down as far as the foramen magnum in patients who have a wide space. So it, I think it's worthwhile if you think that there's a point to access, to make a hole.
- So any small space, even a few millimeter, two or three millimeter in front of the basilar
- You think you're gonna give it a chance. And I agree with you. I think most surgeons put a lot of weight on this prepontine cistern space idea more than they should be. And that can really potentially deprive of some patients who would do well from ETV rev and getting a shunt. What is your threshold about redoing an ETV? And what are your considerations in doing so?
- So I think the issue of redo is, so assuming that you have imaging that demonstrates that you had a third ventriculostomy and it's actually closed. You had evidence of flow and there's no longer flow, it comes down to the etiology because like that has a big role in determining the risk of failure. So the unrecognized congenital population, they rarely ever close over. I think that'd be very rare unless something happens, you know, something that they bleed or something other, some other etiology. So those patients, if they fail to respond to ETV, it's a shunt. So then if you get the patients who have a subarachnoid hemorrhage infection, those are much higher risk for closure because I think there's more of an active inflammatory response and sometimes the cisterns aren't as good for the subarachnoid hemorrhage patients. The, I have a, I don't go back repeatedly unless I think there's a reasonable chance for anatomical correction. The group that's coming in for secondary ETVs is much more complex. You know, it depends on how good the third ventriculostomy was, why their shunt failed, how big their ventricles are. And I think the desire to go back in those is sort of a less than in the other patients.
- Agreed, agreed, very good. Well, Mark, I wanna thank you again, great lecture and really enjoyed some of your technical pearls. So thank you again and we look forward to having you with us in the near future.
- Thank you very much.
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