Welcome to our live webcast, Neurogenic Lower Urinary Tract Dysfunction, and thank you for joining us. My name is Mike. I'll be the operator for the presentation today. Now, before we get started, I would like to take a moment to acquaint you with a few features of this web event technology. On the right-hand side of your screen, you see the Q&A window. To send a question, click in the text box and type your text. When you're finished, click the send button or push enter. All questions that you submit are only seen by today's presenters, and your questions will be responded to near the end of our presentation today. At the conclusion of today's program, we ask that you complete a brief post-event survey. Please take a moment to complete this survey, as it will help us plan future web events. We are joined today by our moderator, Lipitskaya, and our speaker, Stephen R. Krause, MD, FASC. So at this time, I'd like to turn things over to Lipitskaya to begin with some opening remarks. Welcome. Thank you so much, Mike. I'd like to welcome all of you to our next installment of our AUG's virtual forum web-based lecture series. This is a series of presentations by experts in our subspecialty from across the country focused on topics based on the CPMRS learning objectives, as well as relevant practice-related topics. The virtual format also provides AUG's members the opportunity to interact with the speakers in real time. The presentation will be then captured and made available for view at any time on the AUG's website. Upon completion of this program, you will be given an opportunity to provide some feedback, which we value greatly. For this evening's presentation, it's my pleasure to introduce Dr. Stephen Krause, the professor and interim chairman of the Department of Urology at the University of Texas Health Science Center at San Antonio, where he heads the Division of Female Urology, Neuro-Urology, and Voiding Dysfunction. His presentation today will be Neurogenic Lower Urinary Tract Dysfunction. Thank you, Dr. Krause, for being with us today. All right. Thank you for having me, and thanks for everyone joining in as I see people coming on. So I'm hoping that we can get through this, and I even have a case or two at the end if we get to the time. If not, they'll be on your materials, which you can download, I guess, on your own or have access to later. So let's get started. Start the clicker. Those are my disclosures. And the learning objectives are actually straight out of the FPMRS guide and similar to the FPMRS review course as well. So they're there for your review, but just to get moving, so why do we even care about neurogenic bladder? And saying someone has neurogenic bladder is kind of a very vague term. We use it a lot, but we really should be more specific. Someone who has neurogenic bladder is like saying someone has heart disease. I mean, it could be coronary disease, it could be cardiomyopathy, but we really can't correct that nomenclature problem, but we should do the best we can to really describe it more. So we really care about the neurogenic bladder because most important is that it can be detrimental to the upper tracts. In the olden days, people used to pretty much die and suffer from problems of the upper tracts, hydrophrosis, renal failure, hyaline nephritis, and serious febrile UTIs and sepsis. Symptoms or problems are that patients don't always have symptoms, but when they do, they may have incontinence. That's usually easy to tell, but they don't always have urgency symptoms because they don't have the sensation depending on the type of neurogenic bladder. They may think they're voiding well, but they actually may be in retention. There are social issues, especially when we have like our pediatric patients who become adults, a lot of times they've been living with a spondybifida type neurogenic bladder and then kind of get used to living in a diaper. When they move into adulthood, social issues like odor and trying to be more independent really become a factor, and that's where we may see these patients is they've been in the pediatric world being managed by the pediatric urologist, for example, and then graduate and now we've got an adult with a neurogenic bladder that needs to be kind of made contemporary. Recurrent UTIs, the different type, the ones that are more bacteria problems that don't necessarily need to be treated, but that's often an in-depth discussion with the patient to convince them that just because a provider finds bacteria in the urine doesn't mean you actually have to treat it. And then they are at risk for stones as well. This is a slide basically looking at why neurogenic bladder is such a serious concern. So you can see that the incidence of mortality with a spinal cord injury has dramatically gone down between World War I, World War II, Korean War, Vietnam War, ranging from 80 percent down to 5 percent. Now, if you look at the table below, prior to the early 1970s, the urinary tract system was the number one cause of death. Prior to 1972, urinary tract systems were, you know, again, renal failure, urosepsis and such were the main reason patients with spinal cord injury, neurogenic bladders would die. Now, it's down to number four and it's not necessarily that the other systems got worse. It's just that we do a better job now compared to before of managing neurogenic bladder. So when we want to look at this, the best way to go into it is this concept of storage and emptying. And this is the same format we use for assessing urodynamic abnormalities because, I mean, that's essentially what we're going to be doing here as well. But when we talk about urodynamics, we talk about, you know, looking at the storage phase, looking at the outlet phase, sorry, the emptying phase. And that's what we do for neurogenic bladder as well. For normal urinary, lower urinary tract function, during storage, you should have urine being stored under low pressure and that's part of the, that's the key because that's what protects kidneys. Sensations should be appropriate, not inappropriate, not absent either, but they should be appropriate. And then the outlet should remain closed so you don't have leakage. During the emptying phase, it should be volitional, meaning your brain tells it when to occur, not your bladder saying, go now because if not, you're going to have an accident. And it's a very coordinated event. The sphincter relaxes first and the bladder contraction occurs and the contraction should be strong enough and last long enough to allow for adequate emptying. And you shouldn't require abdominal straining and such to augment the void. It requires pretty much every component of the neurologic and muscle systems, skeletal muscle, smooth muscle, sympathetic system, parasympathetic somatic system, central cord, peripheral nerves, ascending, descending pathways, cortex, pons, I mean it's all in there. And the more components you have to it, the more complicated it can get and the more places it can run them up. So there's one or two slides. This is one of the two slides that I think are good slides to kind of go back to later on and for review. You can see a cartoon on the left-hand side and then the areas on the right. These are the major centers that are involved in micturition physiology and the sites of where pathology occur. And basically if you think of the bladder connecting to the sacral micturition center which is S2 to S4 and then you have ascending, descending pathways within the spinal cord itself going to the pons and then we've got input coming from the cortex going to the pons. The pons is actually a real key component. It is the switching center. It is the site that coordinates the bladder and the sphincter so they work together. If everything below the pons all the way down to the bladder are connected properly, you will have synergistic voiding, meaning the bladder, the sphincter relaxes first and then the bladder contracts. If there's no input coming from the cortex, pathologically maybe a stroke or maybe dementia or anything that affects the higher level above the level of pons, you will get a neurogenic bladder that is hyperactive or overactive but it should be relatively coordinated. On the other hand, if you have a lesion between the pons and the sacral micturition center such as a spinal cord injury, you run a risk of having the bladder and sphincter discoordinated and the term is dis-synergic, detrusor, sphincter, dis-synergic. So pons to the sacral micturition centers, all that's got to be intact for coordinated voiding to occur. We'll hit that a little bit more in a little bit. So the workup for the patient with the neurogenic bladder is obviously a good history, an exam. We'll go over elements of the exam that are a little more important in this population. What laboratories would you be getting, upper tract evaluation, lower tract evaluation and remember we'll go into that context of filling and emptying. So from a history perspective, you want to know what type of neurologic problem they have, how long it's been going on, do they have urinary symptoms because if they do, obviously we would like to address them but the problem is, remember, just because if they come and tell you they don't have urinary symptoms, that doesn't mean that everything is safe inside. You very well can have a patient who is asymptomatic and have hydronephrosis due to a high pressure storage bladder. So you can't rely on the symptoms but if you have symptoms, you definitely want to address them. How do they take care of their bladder, do they self-void, some of them will come in and doing intermittent cath already, some will have Foley catheter or suprapubic tube. If they are self-voiding, you want to know how often they void, do they ever measure their voided volumes, if they're doing intermittent cath, do they leak in between caths, how much they get out when they catheterize. If they have a Foley, you want to make sure they're changing it on a regular basis, minimum is four weeks, sooner if they have problems. So you can see urinary tract infection with a question mark because that just opens up a whole can of worms. They all think they've got UTIs and many of them do but they all think they have UTIs because someone told them that their urine was positive and they must have urinary tract infection. And we know better than that, we know that when they have a chronic catheter or if they're doing in and out cathing, they are going to have chronic bacteria because they're colonized. That does not necessarily mean they have urinary tract infection and just because they have a positive urine test and they have a low-grade fever, maybe it's UTI or maybe it's their upper respiratory infection that they have. The problem is that everyone, so your urine is positive and they just kind of leave it at that. A true urinary tract infection in this patient population is going to be someone who's got a positive urine culture and has urinary tract symptoms if they manifest with symptoms. So that's the problem. But they should have fevers and chills, hematuria, change in their voiding pattern. Are they needing to cath more often or if they're cathing every four hours, did all of a sudden they start to leak? If they're self-voiding, do they feel like they need to go more often? Just tell me you have a positive urine test and nothing else. I'm going to tell you that's nice. Don't treat the colonized urine, don't treat the bacteria because eventually you'll get resistant bacteria and when they do get a urinary tract infection, we'll be in trouble. You want to assess their hand function and dexterity because a lot of times we're going to be talking to them about doing in and out cathing. In some cases, it's the best management options for them, but if they have poor dexterity or poor hand function or can't get access to the urethra and to the pelvic area, then it may be the best recommendation for them, but it's not a reasonable recommendation. It's not realistic for them. But you do want to know if they have hand function because we have options that we can offer them maybe if they can't get down there and we'll go into that. We need to ask them about bowel function and do they have neurogenic bowel problems because nobody else will ask them that. That's the problem. Sometimes they may be plugged into a GI doc, but more often than not, they have just figured out what they need to do to barely get by, or they'll tell you they're wearing diapers because they don't know when they're going to have a fecal accident, and bowel programs are not hard. I don't have time to discuss it today, but it is not hard to put someone on spinal cord injury patients and get a simple bowel program with digital stimulation and a stool softener and that will usually have control of their bowel movements. You want to know if they get autonomic dysreflexia, and they may not even know what that term means, but you can kind of hone in on it. Do you get sweats, flushing, goosebumps, severe headaches? Does that tend to happen when your bladder is real full? Because chances are if it is, that's autonomic dysreflexia, and that can be a fairly serious problem. Basically, AD is when the autonomic nervous system responds to some sort of stimuli in a patient who's got a spinal cord injury, T6 or higher. So we're talking about patient population T6 or higher, and something causes a noxious stimuli to them. Most commonly, it's going to be bladder distention, but it could be bowel distention. It could be a broken foot, a broken toe, and some spinal cord patients may not know they have a lower extremity fracture, but basically their autonomic nervous system perceives it as a threat, and what does it do? It releases massive release of adrenaline. You get a very rapid rise in blood pressure due to the vasoconstriction. You'll then get a secondary rate of cardia, though sometimes you get a tachycardia from the adrenaline as well. They get diaphoretic. They often will know what's happening, and if they're reasonably educated, just removing the stimulus will take the problem away. So if it's bladder distention, just empty their bladder and it goes away, and again, sometimes they'll feel these symptoms. They'll actually get a prodromal before it comes. They'll get the goose bumps. They'll get facial flushing, goose bumps on the back of their neck, and they know it's coming. They better cath. If that happens and they tell you, yeah, when I cath, I get all better, then you know that you can at least handle the problem, but a lot of times you have to have some ways to manage their AD if they're brittle, they won't respond. Again, most common thing is to terminate the stimulus. If you're doing bladder distention during your dynamics, empty the bladder rapidly. Our rehab docs like to use the drugs that you see on the slide because they believe this is partially an autonomic nervous system problem, partially a pain response. So nifedipine sublingual, which technically is not supposed to be. I think it's off-label, but you can poke a hole in it and squirt it on your tongue. That's what our rehab docs like to do the most. Morphine, IM, because they feel this is a pain response, and then nitropaste. Some docs just use the nitropaste because in some clinics you can't get the morphine. And then nifedipine, the problem with it is that once it happens, your blood pressure goes down pretty quick, but then you get a headache from it and it doesn't come back right away, whereas the nitropaste, once their blood pressure stabilizes and the AD goes away, you can just wipe the paste off. And I have put patients in the ICU when they're really, really brittle to even just get them out of drip. Physical exams, so this is out of the American Spinal Cord Injury Association. It's complicated. You don't have to use it. The key points here are if you're seeing a patient who's a relatively fresh injury, you want to make sure that their spinal shock is worn off. And you can assess that by either looking to see if their reflex contractions are coming back, their reflexes like deep tendon reflex, they have lower extremity spasticity, mobile cavernosus reflex. All those things will tell you the spinal shock is worn off. The other thing you really need to do is you need to look at the urethral meatus, especially if it's a patient who has a chronic catheter. These patients are often insensate or have decreased sensation, so they don't feel the catheter. They don't feel when the catheter gets tugged on. And when the catheter starts ripping through the urethra and you get a urethral dilation where you can put two or three digits in, two or three fingers into the bladder through the urethra, they won't even feel it. Problem there is obviously the urethra gets damaged, they're incontinent, they can't hold the Foley catheter anymore. It's the classic patient who maybe starts out with a 16 French 5cc balloon, they're leaking around the catheter, so someone says, well, we should upsize your catheter. They put in an 18, they put in a 20, it works for a little while and then they upsize the balloon because they start leaking again. The next thing you know, a 24 French catheter with a 30cc balloon is easily coming out of the urethra. It won't retain it. That's something that's preventable, but we do a better job of looking at that. Imaging most commonly, it's a renal ultrasound and a KUB on an annual basis. Ultrasound initially they don't have hydro. KUB is a good screening tool for stones because these patients are at a higher risk for stones. They don't ambulate as much, they're not as mobile, so they demineralize and they have a higher risk of hypercalciuria, which then puts them at a higher risk for stones. We'll do nuclear scans, especially if we see hydro. Nuclear scans are one way to assess to make sure there's no obstruction present. It also gives us a split function and depending on the scan you do, you can even get a GFR, so that's a good test that we'll use, not infrequently. CT scan imaging, cross-sectional imaging, especially these days with stones, the stone guys like to do that more frequently. So not uncommonly we'll start with a renal ultrasound and KUB and if we see something concerning they'll go to a non-con CT to look for what stones are present. It's rare to get an IVP these days. Renal function assessment, again our rehab docs do it, so it's already done for me, but most of the time it's recommended you do not use a serum per annum because it's notoriously unreliable. It relies directly on muscle mass as part of the equation and for its formation and if you have patients with decreased muscle mass, you won't see, the serum cranium itself is unreliable. The best is to do a 24-hour cranium clearance or you can do, oh I'm blanking, it starts with a C, is it Cystat, I can look it up later, but it's a test that we don't use too often. Nephrology will use it, but 24-hour urine is a good way for us to start. You want to get either a voiding diary or if they're doing cathing, a catheterization diary, specifically if they measure their volume, to measure their volume so you know how much they get out with each void or with each catheterization and do they leak in between catheterization. Urodynamic evaluation, important cystoscopy, not necessarily needed unless there's an indication. So gross hematuria or any hematuria I guess for that matter, recurrent UTIs with an unknown etiology and such. Not uncommonly we'll do a VCUG or so we'll do fluoro at the time of the urodynamics and this way we can get the voiding study and see what the outlet looks like during voiding if there. So rationale for the urodynamic assessment again is a baseline assessment of their lower urinary tract once the spinal shock is worn off so we get an accurate assessment of what their bladder wants to do, bladder and outlet. You really want to identify those neurogenic bladders that are at risk for causing upper tract damage and other complications such as detrusor disinergia, DESD, detrusor external disinergia, or the noncompliant high pressure storage bladder. When we identify them we can put together a treatment plan, use urodynamics to make sure your treatment plan got better, made the bladder better because remember these patients won't say, oh, I know I'm better. They may have less leakage which is a good sign but you still need the urodynamics to prove the pressures have gone down. They're not going to be able to tell you that. And then you also use urodynamics for changing neurogenic platter. So for example, the patient had been doing well, the patient had been doing well for years and all of a sudden she's leaking a lot now, you'll use urodynamics to determine if there's a change in her neurogenic bladder and if there is, that could signify that there's a problem such as a tethered cord or other consequences of her neurologic issues. Okay, so moving in, different ways to classify neurogenic bladder. The one that we like to use is this failure to store, failure to empty problem. If it's a failure to store, is it a bladder problem or an outlet problem? If it's a failure to empty, is it a bladder problem or an outlet problem? So if it's a failure to store due to the bladder, we're talking about basically detrusor overactivity. If it's a known, if it's connected to a neurologic diagnosis such as MS or spinal cord injury or any relevant neurologic diagnosis, we call that neurogenic detrusor overactivity. If you read old text, you'll see they used to refer to that as detrusor hyperreflexia but now it's neurogenic DO. The other causes for bladder storage issues are impaired compliance, high pressures during storage can be seen, all these can be seen with spinal cord injury, you can see them in with MS as well, with Parkinson's and stroke, those are the common type entities I gave you. Failure to store due to an outlet problem, basically you have an incompetent outlet. This is basically glorified stress incontinence. But when it's neurogenic, it's going to be more associated with a sphincter deficiency or intrinsic sphincter deficiency. Some call it neurogenic stress incontinence or neurogenic sphincter dysfunction. You'll see this more likely with lower level injuries or lower level neurologic problems such as an L1 spinal cord injury or pelvic nerve injuries, spina bifida, peripheral nerves and injuries and stuff. The lower the level of the injury, the more likely you're going to have an incompetent outlet problem. Failure to empty due to the bladder means the bladder is not working so it will either be areflexic or hypotonic or hypotractile. You can see it with strokes. You can see it with MS. You can see it with strokes but that's kind of rare. And I mentioned earlier if you have a lesion above the level of the pons, usually everything is working. It's just an overdrive or hyper. So here I am telling you stroke is causing it to be hypo. It's not very common and typically if it's going to occur, it's going to occur in the acute phases of the stroke. Later on once the patient is stabilized, typically stroke bladders are going to be a hyperactive bladder. Failure to empty due to an outlet, basically there's obstruction present. In this case, detrusor sphincter disinterges, the one we talk, we worry about the most. Spinal cord injury and MS, typically where you'll see it. You can also get a slowly reacting sphincter due to Parkinson's. Remember Parkinson's, slow reaction of the skeletal muscle. The sphincter has skeletal muscle in it. So the bladder may be contracting and the skeletal muscle should have opened but it didn't open fast enough. So you get basically a sphincter bradykinesia. So there are a set of guidelines the AUA put out in regards to urodamic guidelines back in 2012 for neurogenic bladder. They're listed here but the bottom line is, first of all, if you notice the evidence is okay for PVR, it's not that great for the rest of them. PVR is a no-brainer because it's very little risk and it's important, especially if the patient thinks they're voiding on their own, you'll want to get a PVR to confirm or not. Regardless if they're doing voiding or in and out cathing, you want to get a CMG and a pressure flow study at least initially to show if their storage phase is safe and also tell you if their emptying phase is successful or not. If you're going to be following these patients, especially if you're initiating treatment and you have a patient who's at high risk for neurogenic bladder, then you really should be doing the CMG pressure flow study potentially on a regular basis. How often is the question of the year because no one really knows. There are guidelines on neurogenic bladder itself that are being worked on as we speak and hopefully we'll answer those questions but I suspect the data isn't going to be there but we'll hopefully come up with some reasonable statements. If you're doing a lot of these patients, the question is should you be doing your urodynamics with fluoro, fluoroscopy. I tend to see a lot of these patients so I have a fluoro machine in our clinic. If you don't and you're going to want to see a lot of patients with MS or spinal cord injury for example, then it might be worth considering it. On the other hand, you do not have to do it. I'd much rather have you do a good urodynamic study and not get the fluoro. Get the fluoro part another way, have them go to radiology and have them just get a PCUG and you put them together and you've got a reasonable assessment. If you are going to do a lot, maybe it's worth talking to your hospital or your group to see if it's worth investing in a fluoro unit. If you're going to be doing urodynamics, you should do your EMG to look at the syncter activity during the voiding. So those are the Reader's Digest version of the Neurogenic Bladder Guidelines. They're available online. I think AUA has them. I assume AUGS may link to them or have them as well, but you can certainly get them at the AUA and they're free for everybody. So the different types of neurodynamic patterns of neurogenic bladder, basically what type of neurogenic bladder are you going to see on the urodynamics? You may see a-reflexia, a-contractile or a-tonic, you may see overactivity, we've talked about that detrusor-sphincter dis-inertia where the bladder and sphincter are working against each other. And there's different versions of it. There's actually detrusor-external-sphincter dis-inertia, which is the more common one where the bladder is dis-coordinated with the external sphincter. But you can also get detrusor-internal-sphincter dis-inertia, where the bladder is basically dis-coordinated from the bladder neck. The bladder neck will close instead of open. And then again, we worry about hostile storage parameters, loss of compliance, and something called a high detrusor leak point pressure, which I'll get into. So a-reflexia, basically the bladder is not squeezing, or if it is squeezing, it's underactive or hyper-contractile. Oftentimes patients will have diminished contractions, they'll have increased capacity, and they'll have decreased sensations or no sensations at all. So that's a big floppy bladder, but the question is what's their compliance like? Sometimes it's real low or low pressure, so that's fine. But a lot of these a-reflexia patients, especially the spondybifida patients, they're at risk for impaired compliance. Impaired compliance means the bladder won't distend without the pressures rising. Normally, we want the pressures in the bladder to stay low as the bladder fills with more and more urine. The pressure should continue to stay low so that urine coming out of the kidneys can continue to drop into the bladder. On the other hand, if the pressures start going up in the bladder, because it's not as flexible and not as pliable as it should be, or if it's got a constant tonic squeeze to it, the urine can't get in because the pressure is too high. Basically we've shown, or people have shown, that you want to keep the storage pressures below 40. If they stay below 40, the risk to upper tract damage is less. If the pressures go over 40, that's a risk factor for upper tract damage. If they leak before 40, that's a good sign. It's bad for the patient because they're leaking, they're not going to be happy, but it's kind of like a pop-off valve. Let's say they leak and their detrusor pressure was 25. That means their detrusor leak point pressure is 25. We know that if the detrusor leak point pressure goes over 40, they're at risk for upper tract damage. Someone coming in with a DLPP of 25 is a good thing because their kidneys should be safe. They're not going to be happy because they're leaking all over the place, but it should be a safe situation. These patients, a lot of times, they'll be thought of to be like a floppy bladder, but you do really need to keep an eye on their upper tracts and monitor them closely. This is an example of detrusory reflexia. You can see the green line is the PDET line. It's relatively flat. This one has a little bit of loss of compliance. You can see it's starting off low here, and then it kind of has a slow, steady rise. We really only get to like 16 or so. It's really not that bad in terms of a compliance problem. I wouldn't be worried about its compliance, but it does slowly creep up. It never gets any higher than 16 or 17, but you don't see any real contractions at all. If you look at the volume, you can see here it's 738. First urge is kicking in here, which the number is not assigned, but we know that if this is from here to here is 738, that's about halfway, unless the pump got turned off, that's probably like 350 or so. I'll leave my little arrow there. So compliance, kind of reviewed this already, but it's the relationship with the bladder being able to accommodate higher and higher volumes of urine while keeping the bladder pressures low. You want to keep pressures low so that more and more urine can get in there. Basically it's a way to describe the bladder's ability to distend. The formula for it is delta volume over delta PDET. Most of us know the formula. Most of us never use the formula because the number we really, really want to see is we want to make sure that this trucer pressure never goes up to 40. McGuire has shown that if the trucer pressures go over 40 and there's no leaking or no popping off, then there's risk for upper tract damage. In females, typically pressures don't go past, they're usually in the 10 to 12 range, don't really go past 15 once in a while. This is an example of a non-compliant bladder. You can see in green the PDETs going up, up, up, up, up. That's not a slow bladder contraction, that is just resting, filling. That pressure's gone up to and over 100. That is dangerous. Now, this yellow is signifying that a leak occurred. You don't see a flow line, so you won't see that, but I'm telling you a leak occurred at this point. There it is, DE, which meant the trucer and leak point pressure just got cut off. If she leaked at a pressure of 66, that means her DLPP is 66. We mentioned earlier that if their DLPP is above 40, they're at risk for upper tract damage. Had she leaked with a detrusor leak point pressure of 25, that would have been protecting her kidneys, but in this case, she's not. This is another patient who came to me, live patient, actually just saw her not that long ago in the hospital, unfortunately. She came to us with recurrent urinary tract infections, and she had MS. When we examined her, she was in a diaper, she's like, I leak all the time, that doesn't bother me, it's these UTIs that are driving me nuts, so urodynamics. When we assessed her, she was really in what would look like overflow, but she was kind of in retention. You can see here, she's got a non-compliant bladder, no contractions occurring, pressure's going into the 50s and even higher, and her pressures are so high that you can see that she's actually refluxing up her right kidney. That's what happens when the compliance problems occur. In this case, not only are her pressures high, she popped off and blew out her right kidney. Her right kidney is basically a shell now, so it's massively distended with no real parenchym on it, it doesn't do her any good. She's living off of her left kidney. What her right kidney is doing for her is it's dissipating any of the pressures in here, it's basically sacrificed itself. Well, the best treatment for this is actually lower the pressures in here, and then things would get better. Moving on to overactivity, so you've probably seen this when you've done your urodynamics. There's different ways to describe the overactivity. This is from the ICS terminology. Phasic to tracer overactivity means the patient had an unstable contraction, which came up and it came back down. May or may not have been associated with leakage, but it didn't result in anything like stopping the test. So the patient may or may not have known they were having it, and it went away and the test continues. Terminal DO means they had an involuntary contraction that got so strong that either they voided or leaked, and the test had to stop. Neurogenic DO means they had unstable contractions with a relevant neurologic diagnosis. Idiopathic DO is regular DO with no known diagnosis. DOI, detrusor overactivity with incontinence. There is something called DHIC, which really should have been DOIC, but it's an old terminology that never got corrected when the nomenclature got readjusted back in 2002, I guess it was. But detrusor hyperactivity with impaired contractility means they're having unstable contractions, but each contraction is not strong enough or lasts long enough to allow for adequate emptying. So they may have a contraction, they may have a lot of contractions, it may even result in them leaking, but when you actually assess how well they empty, they don't empty well. They have over half a capacity still in their bladder. Problem with those patients is that if you wanna treat them and they stop leaking, you wanna put them on an anticholinergic or some sort of bladder medication, but they're already not emptying well and you could potentially make that worse. So that's something you have to be aware of. But that's something that we see in a neurogenic situation. You can get it with spinal cord, but you'll see it in MS and strokes and little ladies with strokes and such. This is a good example of someone who has bad detrusor overactivity. You can see phasic unstable contractions going up, down, up, down, up, down, and then they kinda peter out for a little while and then another one comes and basically the contraction just makes them pee. They can't stop it. Detrusor sphincter dyssynergia. Basically the definition of that is an involuntary contraction of the sphincter occurring at the same time as an involuntary contraction of the detrusor. They both have to be involuntary. You cannot have a voluntary detrusor contraction and have an involuntary sphincter contraction. If that happens, maybe it can happen, but that's not detrusor sphincter dyssynergia. Maybe that's dysfunctional voiding, but that is not detrusor sphincter dyssynergia. Detrusor sphincter dyssynergia is, everything's involuntary. The patients can't stop it. Typically gonna be, at spinal cord injuries, MS can happen as well. It's gonna be a lesion that is usually above the level, well, it's gotta be between the pons and the sacral matrician area, but typically it's gonna be a T6 or higher. The higher the level, the more likely you'll see it. The T6 seems to be a marker. I don't think anyone has actually looked at it to see it, but everyone in my world tends to say if they're a T6 or higher, they're at risk for DESD. I guess you're at risk no matter what. If your lesion's above the sacrum and below the pons, technically you're at risk no matter what, but the T6 is a good marker. These patients are at higher risk for elevated storage pressures. They're at risk for UTIs, hydro, reflux, renal deficiency, and such. This is a good example of the trusser-sphincter dyssynurgy. You can see the trusser relatively flat, and then boom, they have a contraction, and that contraction drops a little bit, and then comes back, and it never really relents at all. You can see the sphincter's going crazy throughout it, and then you can see pictures with 1,000 words here. You can see the bladder neck is there, and then the urethra's dilated, and then it just stops right there. What is the bladder seeing? So it's not that the pressure's got so high. It's just that they got so high, and they lasted for a long period of time. Someone had an intrusive pressure that got to 50, and it was during their voiding, and then it stopped. Still a little high for a female, but that's not gonna really hurt their kidneys. But in this case, this patient's holding 600 or 700 cc's, and about half of their maturation cycle is spent in these elevated storage pressure phase, which means half the time, their kidneys are doing elevated storage pressures. That's why they're at risk for upper tract damage. Okay, other ways to classify, there's some older terminology. This failure to store, failure to empty is what we like to use. There is the upper, lower motor neuron lesions, which probably makes some sense as well, but it's not as functional from a lower urinary tract dysfunction standpoint. There's the central vascular lesion, there's the central versus peripheral, and then anything goes means they have some lesion that we can't figure out. That's what urodynamic is for. So this is another cartoon slide that I think is a good one to use as a review. Basically, you can see on the left side, we've got all the anatomy stuff, and then in the middle, we've got all the neurologic diagnoses, and kind of relatively to the area where they would occur. And then you have, to the most right, you see the type of neurogenic dysfunction, neurogenic bladder dysfunction that you'll see. And again, so PONS is up high. Above the level of the PONS, anything here likely gonna cause the trucer overactivity, such as a stroke, Parkinson's, normal pressure hydrocephalus, trauma, traumatic brain injury, dementia, and such. Anything between the PONS and the sick maturation center, you're gonna get over, you're at risk for getting overactivity, and you may or may not get the trucer-shrinker disinergent. And then as you get lower and lower and lower, you're more likely to get a weakened bladder, and eventually get a hypotonic bladder, impaired contractility, maybe some compliance problems, and then you start worrying that the shrinker's not closing, and then they have that neurogenic stress and constant dementia. So just through some of the more common type of neurologic conditions, stroke, traumatic brain injury, it's above the level of the PONS. Most likely, you're gonna see loss of the inhibitory control that your brain has of avoiding. So basically, it's another way of saying they're gonna get neurogenic trucer overactivity. Most common, they're gonna be at risk for incontinence. We talked about them maybe having that trucer hyperactivity with impaired contractility. Now, here's the thing. These patients are usually sensate. So when they feel the sensations of urgency, what are they going to do? They're going to contract their sphincter, because they're gonna try and hold it. And people will often get confused and say, oh, they're having an unstable contraction, their sphincter's contracting too, so that must be the trucer-sphincter dyssynergia. That's not the trucer-sphincter dyssynergia. Number one, neuroanatomy-wise, it's not supposed to happen if your lesion is above the level of PONS. Number two, it always has to be involuntary. The way you can figure this one out is to do your urodynamics, you see it, the next time you tell, look, I'm gonna have you do this run again, I'm gonna fill you up, next time when you feel like you gotta go, don't let her hold it, just don't hold it, just let her rip. So if you get an urge, just go. And if you see the sphincter relax, you've just proven that they do not have dyssynergia, because you can't have voluntary dyssynergia. This is an example of someone who had a stroke. You can see just multiple unstable contractions, small capacity bladder, and then multiple small stable contractions resulting in leakage. The other thing I mentioned from the previous slide, or didn't mention, is initially these patients with strokes can again have areflexia, but it's temporary. So not uncommonly they'll ask you to see them and they're in retention. It may just be their stroke is resolving. Dysfunction with Parkinson's. So again, they're lesions above the level of PONS, so they'll have overactivity. They will have sensation, so they may get that pseudo-dyssynergia. They also may get an impaired or a slow relaxation of the sphincter, which will cause hesitancy symptoms, but that's gonna be more of a bradykinesia factor. And typically you may see the type of urodynamic abnormalities, detrusor overactivity, fairly common, overactivity with impaired contractility, or areflexia on occasion. Sometimes they're even normal. This is the best example of detrusor, sorry, sphincter bradykinesia I could find. So you can see this contraction. Sphincter's going loud. It's actually kind of loud after the contractions. Maybe she felt the contraction and now she's trying to stop it. Here you can see contraction occurred again, and we told her to go, but you can see the sphincter's still a little loud, but it is closing or slowing down here, which means it's trying to open, but by this time her contraction's halfway through already. Brain tumors, bottom line, so I would like to get the cases if we can, it's above the level of the pons, so you're gonna get overactivity again. Sphincter should work. You're still at risk for that pseudodyssynergia, but the sphincter should be from a neuroanatomic position. It should be synergistic. Hydrocephalus is gonna be overactivity again. Sometimes these patients present that triad, gait disturbance, dementia, urinary incontinence. This is one of the few times this is one of the few times where their bladder function may actually improve if they get their normal fresh hydrocephalus treated. So we send them to the nurse, I should say it this way, this is one of the few times when we send them to the neurosurgeon and their actual bladder may get better. Most of the time when we see neurogenic bladder, they go to the neurosurgeon afterwards, it's too late. But in this case, if they get a shunt, all of a sudden their leakage may get better. This is an example of a patient actually, oh, this is a patient of mine. I did a sling on this lady a year or so ago and she was doing well for the first few months and then she comes back almost a year later and she says, I've got horrible leakage again, I've got urgency frequency, I've got urgent conduct and I'm thinking my sling is too tight. So I put her through the workup and she does look like she's got involuntary contractions there and they look like they're a little high pressure. But then she tells me, oh, oh, by the way, they just diagnosed me with normal pressure hydrocephalus. And I'm thinking, really? Why couldn't have told me that first? Because I probably wouldn't have done the serodynamic study on you. I don't think the sling was too tight. It was normal pressure hydrocephalus because she had done so well for the whole year prior. Dementia, again, most commonly gonna be to choose for overactivity. But because there's the potential for a cognitive impairment these patients may also have a functional leakage. They can't move or get to the bathroom in a timely fashion. So that's a functional incontinence, but more from a neurodynamic standpoint, it's gonna be an overactive picture. Just another uridamic. So it's terminal to choose for overactivity. Spinal cord injury, that's what I wanted to get to. Again, these patients will go through different phases during the spinal shock, which is the initial phase. They're pretty much just gonna have an araphylactic bladder, which means nothing to us. Because in a month or two, the spinal shock wore off and whatever flaccid bladder they had will change and then they could potentially have a dangerous bladder. So you wanna wait till they're in this stable phase. And again, once they're stable phases, how do you know it's occurred? Well, if you wait two or three months, it's gonna be there. But if you're not sure, you wanna see that their reflexes have returned, that their spasticity's come back. You wanna identify these patients early if they're at risk for upper tract damage. So you wanna get them on as quickly as, ideally as soon as the spinal shock has worn off. It is important to remember, you should not treat spinal cord patients just because, oh, I know they have a T2 injury, so I know what to expect there. Because it's not always the same neurogenic bladder pattern with every level. They may be variants, they may be identical, they may not be. So you don't wanna treat just on supposition. There was this old terminology we called the balanced bladder. Don't do it. It basically means I don't think they leak, so we're okay. But that's not safe because in between voiding or in between cathing, they may have high pressures. And remember, the enemy of the upper tracts, the kidneys, is elevated storage pressures. This is a study that was done by Kaplan that looked at the different types of spinal cord levels, spinal cord injury levels, and the different types of neurogenic bladder you'll see. And you do see a pattern. Red is the tracer sphincter dyssynergia, and you can see from lower level to higher levels, its incidence goes up, that makes sense. You can see hyperreflexia or overactivity, old term, also going up, makes sense. You can see the areflexic or weak bladders 18%, even lower here, but then it bumps up here. That would make sense. As I go lower, they expect to see the incidence of areflexia go up. But I don't know what happens here. It's like everything's all equal. And still, I've got some dyssynergia over here, and I've got some areflexia up there, which shouldn't be. But it's not all or none, and that's important to know. That's why you do the urodynamics. MS, this one's a little more interesting, because you can get plaques in the cortex, you can get plaques in the cord, anywhere. Typically more common with females than males. Most patients with MS at some point will present with urinary symptoms, frequency, urgency, urgent contents, and such. In fact, I remember reading somewhere that maybe 20% of the time, patients will actually present with a urinary symptom, and they actually may have the MS, or MS is their real problem, but they don't show other symptoms of MS yet. Bladder may be the first cause. These are the different neurogenic bladder patterns you'll see here. Overactivity's gonna be the most common, 67%, but you can still get the true disfigured dyssynergia, 25%. Some weak bladder, impaired contractility, 20%. And in about half or more, we'll have a changing urodynamic pattern, which is again, goes with the disease process. Tethered cord, basically, tethered cord, basically, some best way to describe it is the cord is either pulled down or during a growth spurt is not allowed to grow. Typically, my world will see spina bifida children who go through their growth spurt, but their cord is scarred in place from their spina bifida or from the surgery that they had, so that when they go through their growth spurt, their cord is pulled upon. Causes mitochondrial anoxia and anoxial injury is the main reason for the neurogenic lesions that were neurologic deficits that we'll see. You get bladder and bowel dysfunction, and this is the kind of patient who may have been sitting just fine for a while, their bladder was stable, and all of a sudden they start leaking again, they're 16, that patient may have had a growth spurt and have tethered cord. You can also get it in adulthood, not that you're gonna grow in adulthood, but you can get an extrinsic compression of it, or you can get syrinxes or cysts within the spinal cord that can cause it to tether and to even pull on. Tethered cord is one where if you pick up on it, because the patient, like I said, had a changing neurogenic pattern, you do the aerodynamics and you see something different than you'd seen before, this is one where you do wanna send them to the neurosurgeon. Now, it's unlikely that the neurosurgeon is gonna make them better, but it is possible that they're gonna stabilize it and prevent it from getting worse, and that's the key thing. So I leave it up to the neurosurgeon, sometimes they'll operate and untether them to prevent their other neurologic deficits from getting worse and their bladder from getting worse. Sometimes they won't, sometimes they'll just leave them be and monitor them, but it's out of my pay scheme. But you do wanna bring these patients to their attention because you may be the first person they see because of it. Spina bifida, again, I wanna move a little quicker. Spina bifida, you guys probably have seen it during the OB parts of your training. Basically, you have a deficit at the neurostructural level so that the cord itself isn't covered properly and you get protrusions to different degrees. You can get a whole multitude of different neurogenic bladder patterns. You commonly get aryflexia, but you very, very well may get a non-compliant bladder, and these are the patients that are problematic. And they also may, because it's a lower-level lesion, they may have an open or an incompetent bladder outlet. So they've got stress incontinence, they've got an atonic bladder, and they've got non-compliant bladder. These are dangerous patients because you think, oh, they're leaking, so they're probably just leaking all over, but they still have high storage pressures and they're at risk for upper tract damage, hydronephrosis and such. So they're wet, but they're in real danger. Usually, the pediatric urologist will be handling these patients as children. They'll evaluate them at the appropriate time to see if they have a dangerous bladder or not. And then if they don't, then they usually will let them be until they're reaching potty training years, and then they'll use the neurogenic bladder dysfunctions to figure out which way to go for potty training. It may be doing in-and-out casting. More often than not, that is it. A lot of times if these patients have hostile bladders, they'll get augmented at an earlier age, especially if meds are not working, and then they'll come to you after that. Pelvic plexus injury, see the various surgeries that are associated with potential for pelvic plexus injury, and also pelvic fracture, anything that can cause the peripheral nerves to the lower uterine tract area to be damaged and such. Pelvic plexus is a very complicated plexus. It can have sympathetic, parasympathetic, somatic, depending on what part of the plexus was injured, you can get loss of sympathetic tone. That may give you an incompetent outlet. You can get loss of the parasympathetic component, so you may get loss of compliance, loss of contractility. You may get injury of the pudendal or the somatic aspect, so you get an open sphincter or a locked sphincter. You may get a praxial injury where the plexus was perhaps damaged by stretching on it, which is not necessarily a permanent finding, which is the reason why I wouldn't jump to anything permanent on these patients. I'd want to stabilize them. Meds if they have high pressures, but not do anything that's unresolved, that you can't return from. But remember, these patients, if there are noncompliant bladders, they're at risk. Diabetes classically is known as a diabetic systemopathy, weak, floppy bladder, but a lot of times these patients will initially present with overactivity. They may not come to you because of it. That may not be what drives them in. What drives them into the office is the retention part or the emptying part, and then you find they have that classic diabetic systopathy. Some people believe that the classic diabetic systopathy bladder is the end-stage bladder, and it first goes through this overactive phase first. You can see the different types of neurogenic bladder you'll see with females with diabetes, 44% with diabetic systopathy, 31% with overactivity, 12% with urgent continence, 12% with stress incontinence, and again, oftentimes this won't show up for many years before you see it. So treatment. So the treatment plan, the goals here are to protect the kidneys, protect the upper tracts, secondarily alleviate symptoms such as incontinence. The good news is that if you do a good job of keeping the pressures low to protect the kidneys, usually it also takes care of the leakage problems too. Urodynamics often will dictate how you treat these patients, because again, it's not like the non-neurogenic patient where we don't need urodynamics to dictate where they need a sling. These patients, urodynamics is key to telling us what direction to go to. So if we have a failure to store problem, such as a bladder problem, failure to store due to the bladder, that's gonna be overactivity or loss of compliance. If we have a failure to store due to an outlet problem, sphincter problem, it's an incompetent outlet, neurogenic stress incontinence. If we have failure to empty due to a bladder problem, it's gonna be either an underactive or an atonic bladder. If we have failure to empty due to an outlet problem, it's gonna be an obstruction, such as detrusor sphincter dysinergia. So if we, so we're gonna go over pharmacologic treatments and then the others. If you have a failure to store due to a bladder problem, such as overactivity or loss of compliance, primary treatments are usually anticholinergics. Botulinum toxin injection can be used, mainly if they have detrusor overactivity. That's what it's on label for. There are studies and there are people have tried using Botox for noncompliant bladders. My experience is it does help, just not as dramatically as it does for the overactivity. But it may help and oftentimes I'll do it in conjunction with an anticholinergic. There has been some people talking about using beta-3 agonist for this as well. Most, there are some studies, there's small anecdotal type stuff. Hopefully that'll get better with time. In my anecdotal experience, it actually is fairly impressive. I've had patients who were getting Botox on a routine basis and heard about the beta-3, tried a beta-3 and decided they didn't wanna go back to Botox. Failure to store due to an outlet problem, means they have stress gonads. There is no real pharmacologic agent treatment for that. Failure to empty due to an underactive bladder. In theory, Bethanacol or Uricoline would be a parasympathetic agonist, make the bladder contract. But in theory only, it's really not successful. Any patient, anyone who says they've used it and says their patients got better, especially in a female, more likely than not, they've just learned to strain void. And they can void by straining and you'd think it's the Bethanacol, but it's probably not. Failure to empty due to a sphincter problem, which is again, detritus or dyssynergia. Botulinum toxin injection for men exists. There really is no treatment for women. If you inject the sphincter with Botox, you can open the sphincter, which is your goal, but then they're gonna be leaking. With men, we can use an external condom catheter. For women, you have to use a collection device of some kind, they don't usually work too well. If you don't empty well, the other options, intermittent catheterization is the best way if they can do it, but again, patient has to have good dexterity for it and has to be able to get access to the urethra. Tube drainage is a foliar suprapubic tube. It's their options, I don't like them, but sometimes you have no choice. If you're going to do a suprapubic tube, keep an eye on the outlet, because if you had an obliterated outlet and you put an SP tube in from above, they still may just leak from below. You may need to do something from below to close them off, either a primary closure. I like to do occlusive slings. I don't use mesh for these cases. I would be using an autologous fascial sling that is meant to be tight to occlude the urethra so they don't leak that way, they only drain through their SP tube. Synchrotomy in men is an option, not option for female. An incontinent diversion, basically an ileal conduit, which is what we do mostly. Ileal vesicostomy, we don't do very often, but they take a loop of bowel, you plug the ureters into it and have it drain to an external bag. In ileal vesicostomy, you take your conduit, but you don't plug them into the ureters, you leave the ureters attached to the bladder, you take the conduit and you plug it into the bladder, and then the bladder fills up and then it drains through the ileum. In theory, it's a great idea, because you don't have to deal with ureters, but what tends to happen is the bladder stops squeezing and then it just fills up and then you have a teapot. The bladder has to fill first before the urine comes into the conduit. Conid diversion, a catheterizable pouch. This is an option for a patient who has some hand dexterity, but maybe limited, can maybe be able to hold the catheter with one hand, but not be able to use her other hand. We give her a fixed stoma on her abdominal wall, she very well may be able to catheterize herself. That in combination with an augment can make a fairly good quality of life. Neuroprosthesis is not the one we talk about for sacral nerve stimulation, like the inner stem. That is, this is a device called a Brinley, not commonly done. In and out catheting, easy, low pressure. You gotta make sure these patients have low pressures in between the catheterizations. So if you've got someone doing CIC, you need to make sure their pressures are low in between. Indwelling catheterizations, it's easy, simple. A lot of times when people start on it, they don't want to switch out because it is so easy. Problem is, is that they're at risk for chronic infections, stone formation, tissue erosion, hypospadias, ripping of the urethra. Neoplasia, I used to not think it was such a big deal. I did a conduit on someone, we left their bladder intact because they had an eroded outlet. We didn't think it was gonna ever fill up with anything. And that was about five, eight years ago. And then about two months ago, she presented with squamous cell of the bladder because she'd had a chronic catheter in for all those years prior to it. This is an example of something I just saw today. And this is not an uncommon thing. This is the vagina. This is the vaginal canal. This is the anterior vaginal wall. This is her urethra. I'm saying it like you see my arrow and I realized you don't, so I'm gonna do that again. This is the vagina. That's the anterior vaginal wall. That's her urethra. You should not be able to see into the bladder. That's bladder neck, bladder mucosa. That's a bad day. In anal catheter, like I said, it's the best option when possible if the patient has the dexterity to do it. Wanna be able to make sure the pressures in the bladder are low in between the caths. So you need your dynamics to prove that. Again, these patients can, if they have high storage pressures and they're cathing, they may not leak, but they may be transmitting those pressures up so they get hydrochlorosis and reflux. If they weren't cathing and you start cathing, that hydrochlorosis and reflux can be resolved just by having them empty more often. They're at risk for false passages and strictures, more so for a male than a female. Urethra than female, less likely for those things to happen. These patients will become colonized. They're at risk for being told they have UTIs when they don't really have it. Men, we do see occasionally episodes of epididymitis. We don't typically see any type of GYN infections to ovarian abscess. That doesn't tend to happen. But we need to make sure these patients have reasonable dexterity. Almost done. Value to storage into the bladder. Botox injections will relax the bladder. Augmentation cystoplasty, make the bladder bigger with a loop of intestine patch, with or without a catheterizable stoma. Failure to store due to the outlet means they have an incompetent outlet. This patient, the patient I would do a fascial sling on, I would not use mesh because they're either doing or they'll be at risk for doing in and out cathing for the rest of their life. Urethra closures, so that slide I showed you earlier, one could attempt to put a fascial sling in and tighten it up real tight. Probably won't work because it's so badly damaged. She would probably be better off with a bladder neck closure or abandon it and just give her a conduit. The Brindleys, the one I told you about, we don't really do. Failure to empty the outlet is for men. We don't talk about it. Diversion options, conduit. Chimney, not too common. Reservoir or what's called the Indiana pouch, is what I like to do. This is an augmentation. Basically, you can see the intestines been taken out of the GI tract, still got its mesentery. We open and size it along its anti-mesentery border, fold it into a couple different directions, and then you get a patch. This is it being folded. It's shaped, I keep using my arrow thinking it's there. This is the intestine. It's been detubularized, and then it's been folded into a U-shape, and then we sew it in a different orientation along the middle of the U, so that now it's just a flat plate and it cannot peristalsis. The term is detubularizing it. In theory, here's the bladder. It's been filleted open. We take this intestinal pouch, sew it onto the bladder, bring it all the way down, and make a new wall for the bladder. This is what it looks like in real life. You can see here, Foley catheter. The bladder's been filleted open. This is the intestinal pouch. We're going to sew from here. We're going to bring this edge to this edge. We're going to bring this edge to this edge, and we're going to take the top of the bladder here, and we're going to sew it to the top of the intestinal segment here, and when we're done, we'll have a new sphere that is maybe three quarters bladder, a quarter intestine, or maybe some degree of it, maybe a half and half. This is that Indiana, or the pouch with the catheterizable stoma. Basically, what we do is we take the right colon, we detubularize it, we make it into a pouch, we take the ileum and taper it so it's real small, narrow lumen. This gets patched to the bladder. This gets brought out to either the belly button or the right lower quadrant, so it's a small little stoma, usually about the size of a dime, and they catheterize themselves through there. This is ideal for the high-level quad who may have some level of hand function but can't use two hands or can't get down there, but you can catheterize this guy because it's mature to her abdominal wall. She doesn't have to pull her shirt up. She doesn't have to get out of the wheelchair. Easy for her to do. And on that note, seven minutes over, sorry. We did start a little late. So, we know we're running. We probably won't be able to get to the case, but I know that there's one question, so guys, chime in with questions if you want. I'll answer the ones we got. I'll read it off. I noticed P urethra is not measured during my urodynamics. Doesn't it add value, especially for detrusor sphincter dyssynergia? Also, where do you place the EMG patches? Do you use needle or patches? That's a great question. So, P urethra, yeah, you could measure EMG. You can measure sphincter function with the P urethra. It's a little more complicated because it's different than what you're using for urethral closure pressures. This urethral catheter, the urethral islet, has to stay in the exact same position during the entire micturition cycle, including when the contraction occurs. But if you, and that's kind of labor intensive, but if you do that, you will see a rise in pressure when the sphincter's contracting, and it should line up with the EMG. Most of the people who do a lot of this stuff will do fluoro, and you'll see it occurring with the fluoro. Probably more reliable than the urethra, I wouldn't fault you for using it if you could do it. But again, this is not a UPP pressure. This is one where you basically have to make sure that catheter doesn't move. So, the urethral islet is gonna be at the level of the sphincter, and it can't move at all during the study. Remember, when you're doing a UPP, you start with the catheter in the bladder, and then you pull it into the urethra, you'll see the rise in pressure there, and then you're done. That takes about five seconds. Now, this has gotta stay there for the entire test. Other questions? And again, just with a reminder, if you do have a question, with a couple of minutes that we have remaining, Q&A located on the right-hand side of your screen. If you'd like to submit a question, please type your question in the small text box at the bottom. When you're finished, click the Send button or push Enter. Perhaps Dr. Krause will give everyone just a moment or two longer to see if there are any additional questions from our attendees. Yep. I give him credit for hanging in this long. Well, thank you, Dr. Krause, for your fantastic presentation. Thank you to you all, as well, to cutting out your time on your busy day to participate in this virtual forum with our speaker and with each other. Upon completion of this program, you will be prompted to provide feedback. Please do share your thoughts and impressions with us. And so we are looking to our next program on July 12th, when we will be talking about perspectives on the Quality Payment Program. Until then, be well and see you next month.

neurogenic lower urinary tract dysfunction

bladder function assessment

diagnostic tests

treatment options

upper tract damage

regular monitoring

urodynamic studies

bladder dysfunctions

pharmacologic treatments

surgical options