Okay, we can go ahead and get started. Welcome to the Augs Fellows webinar series. I'm Dr. Peter Rosi, the moderator for today's webinar. I am currently a third year urogynecology fellow at Louisiana State University in New Orleans. Today's webinar is titled Functional Anatomy of the Lower Urinary System. Our speaker is Dr. Christian Winners. Introduction for Dr. Winners, he earned his medical degree from Louisiana State University Medical Center in New Orleans and completed LSU Ochsner Urology Residency. He then served as a fellow in female urology, avoiding dysfunction at the Cleveland Clinic in 1995. Dr. Winners is currently the H. Eusis Riley Professor of Urology and Chairman of the Department of Urology, Vice Chancellor of Clinical Affairs and CEO of LSU Health at Louisiana State University Health Sciences Center in New Orleans. He is board certified in urology, FPMRS, and a past president of the American Board of Urology. Dr. Winners has served as president of the Society of Urodynamics and Female Pelvic Medicine and Urogenital Reconstruction, SUFU, and the Louisiana State Urological Society. He served on the American Urological Association AUA Stress Urinary Incontinence Guidelines Panel and chair of the AUA Urodynamics Guidelines. He has published over 100 peer-reviewed manuscripts and text chapters. Dr. Winners was recognized as National Teacher of the Year by the AUA in 2009 and was awarded the Christina Mantis Award for Mentorship of Women in Urology and as Continence Care Champion by the National Foundation for Continence in 2016. He was given the Distinguished Service Award by the AUA in 2020 for teaching and mentorship in female urology, avoiding dysfunction. We are honored to have Dr. Winners with us today to share his knowledge as an expert in the field. Before we begin, I'd like to review some housekeeping items. The presentation will run approximately 45 minutes. The last 15 minutes of the webinar will be dedicated to Q&A. This webinar will be recorded and live-streamed. A recording of the webinar will be made available in the AUG's e-learning portal. Please use the Q&A feature of the Zoom webinar to ask any of the speakers questions. We will answer them at the end of the presentation. And please use the chat feature if you have any technical issues. AUG staff will be monitoring the chat and can assist. Thank you. Thanks, Peter. I appreciate it. And welcome, everybody. I know it's, again, a little bit late, at least where I am, and it's a little bit of a dry topic to start with tonight. But I look forward to the opportunity of going over functional anatomy of the lower urinary tract. And I will say, but some of this is basically how I learned it because it is a complex topic. So some of it may be simplified in some areas, but it allows me to translate it and try to teach it to each one of you. And then I'll kind of go through some overview of the end of some of the treatment principles. We really can't get into every aspect of treatment, but we'll try to touch on it to kind of give you some familiarity of how we can coordinate and correlate some of the things we see in urodynamics and then also in our evaluation in the actual treatment. So I do think it's important to understand when we start talking about patients who have neurogenic lower tract disorders, that the goals of bladder management are a little bit different than some of the other conditions that we treat. First is that we do have an obligation to make sure that we preserve normal upper urinary tract integrity. These patients are unique because in some instances, if left alone, they can start to develop issues involving the upper tracts. They are obviously more prone to urinary tract infections, so we need to work on that. I think it's important to think about and distinguish between UTIs and asymptomatic bacteria in that population because certainly we don't want to over-treat as well. We're also incumbent upon us to create a system that basically provides physiologically normal upper urinary tract transport of urine into the bladder, which we'll touch on quite a bit in this talk. In addition to that, we want a patient to be confident and then to be able to empty the bladder as efficiently as they can. We'll talk about all of these principles as we go through the corpus of this lecture. I think it's hard to start focusing on abnormal without knowing some things regarding the normal. What I will do is go over some of the relevant neuroanatomy, what I've seen on exams, what I've read in books, and actually what I've written some questions about. First we'll start with the idea of the concept of the entire nicturition cycle. I think it could be easily broken down into urine storage and urine emptying or avoiding. For us, urine storage is largely a sympathetic, if you will, a driven phenomenon. What happens is there's a network of nerves in the pelvis and all this is coordinated through the circuitry of the spinal cord and the brainstem as well as the brain. The brain, the cortical centers, the cerebellum, and the upper brain centers are largely inhibitory on the entire urinary process. Many times, because it's not an appropriate place for us to toilet, the brain is turning off, if you will, the urinary emptying reflex and activating the storage reflex. That is actually coordinated in the brainstem, in the pons, in an area known as the pontine nicturition center. That's an area of complex centers within the pons. It's not just one unit, but it's a number of different areas of the pons that regulate emptying and voiding of the bladder. Basically the pontine nicturition center is largely under inhibitory control by the upper brain and promoting storage. What it does is it activates two neural structures. One, it activates the sympathetic nervous system through spinal cord segments T10 to L2. Basically, largely traveling by way of the hypogastric nerve, this stimulation stimulates beta receptors in the bladder body, therefore promoting bladder relaxation. It also stimulates alpha receptors in the bladder neck and proximal urethra. Those alpha receptors, when stimulated with the release of norepinephrine, actually contract the proximal urethra in the bladder neck, leading to intrinsic urethral closure and, if you will, passive continence. In addition to that, there's a somatic nerve emanating from sacral segments S2 to S4 from onus nucleus in the spinal cord, and the pedendal nerve derives from that, and it releases nicotine at the level of the somatic striated muscles of the pelvic floor and external sphincter. This muscle actually will contract both tonically, meaning it increases its activity during filling, and then also voluntarily, if you will, or reflexively during a cough, where it actually increases closure of the pelvic floor, and that's how we maintain confidence during stress. This controls the striated muscle of the pelvic floor. So, as you can see, both of these actions promote urine storage. As the afferent activity from the bladder travels through the brain and basically is delivering very strong signals that the bladder is full, and then the brain processes that you're in an appropriate place to toilet, the inhibitory center of the upper brain turns off. It basically activates the pontimicturician center, if you will, to start the voiding reflex. The first part of the voiding reflex is to turn off the sympathetic nervous system and to turn off bonus nucleus. So, the previous stimulation is turned off. So, you may see on an exam, what is the first thing that occurs during voiding? It's actually pelvic floor urethra relaxation. So, the relaxation of the outlet is the first thing that happens during the initiation of voiding. As that is done, it then turns on the parasympathetic nervous system, which originates from the sacral segments S2 to S4 in the sacral spine, traveling predominantly through the pelvic nerve, and it releases acetylcholine at the bladder body. This stimulates the muscarinic receptors of the bladder, and that elicits a bladder contraction. So, what has happened? We've turned off the sympathetic, relaxing the sphincter by way of relaxing the alpha receptors. We've turned off bonus nucleus, relaxing the sphincter. We've decreased the beta inhibition of the bladder of the sympathetic nervous system, and we've activated the cholinergic system to provide the bladder to empty. So, therefore, the bladder is emptying in an open outlet of the bladder. So, those two graphics look like distinct nerves, the hypogastric nerve and the pelvic nerve. Well, this is really the reality of what the pelvic plexus looks like. As you can see here, it's like a ball of yarn. It's like a crosstalk. So, we already know that some of the hypogastric sympathetic fibers travel in the pelvic nerve. That's already a known fact, and more than likely that some of the pelvic nerve fibers travel as well in some of the terminal hypogastrics as well, although that's less known. My point is there is a crosstalk, and that's important in both in bladder dysfunction and also extremely important in pelvic pain, which is a topic for another day. So, let's review urine storage. So, we have bladder distention, which is initiating the pelvic hypogastric reflex, which is the sympathetic nervous system, and that's done by the afferent signaling along the pelvic nerve, basically, which activates the sympathetic fibers by sending input to the spinal cord up into the pontine maturation center. Eventually, what it does, in addition to activating the sympathetic nervous system, it decreases the parasympathetic nervous system, basically turning off any potential for a bladder contraction. So, again, as I mentioned before, the fibers release noradrenaline, which basically promotes bladder relaxation by stimulating the beta receptors and also by contracting the proximal urethra. Remember, there's also that guarding reflex by the pedendal nerve, which increases as the bladder fills because of that afferent signaling and also has a dynamic reflex during clavival salvo, which many of us know as one of the mechanisms to maintain confidence during stress, even in our female patients undergoing midurethral slings. And then the system turns itself off and flips the switch, if you will, to empty the bladder. So those stretch receptors in the bladder eventually fire enough that they've given that signal to the brain stem, which enough to process that and turn off, or when the inhibition of the cortical brain turns off, meaning you're in an appropriate place to toilet, it flips the switch, turns off the sympathetic, turns off the pedendal, and then it essentially allows activation of the parasympathetic nerve to the bladder internal sphincter. So the first action is the internal sphincter and the external sphincter turned off, and then the bladder contracts without obstruction from the outlet. So that's how it works in a coordinated fashion, coordinated in the brainstem by something known as the pontine maturation center. So essentially, if you can break it down simplistically, which it probably really isn't, but as a way to learn it, if you will, breaking it down simplistically, there's three neural pathways which regulate lower urinary tract function. First, remember, and before you even start to think about those pathways, remember the quarterback is what I call it, the pontine maturation center in the brainstem. That coordinates everything, okay? So then the first center is going to be suprapontine, which is going to be cortical cerebellar, providing that input into the brainstem to coordinate this activity as we've described. The second is going to be the suprasacral spinal cord. This is a very, very important neural pathway because this is one of the biggest areas of significant dysfunction in injury. So this is below the level of the coordination, but still both the afferent and afferent arcs to the bladder are intact, which means everything can still be stimulated. That's important to remember. The third segment is the sacral cord. So those are the nerves going directly to and from the bladder. And if those get injured, then things become areflexic. They don't work. And the most common thing there is more flaccidity and loss of sensation, okay, which can be a lower risk bladder because in many instances, low pressure. So then when you start to put this all together, you can actually start to then think about what lower tract urinary abnormality may be suggested by the level of neural injury. So what do I mean by that? So if I look at a suprapontine lesion, okay, which is that in the green, what do I have? That suprapontine lesion has done what? It's knocked out all the inhibition that I've been describing, but it's left the quarterback intact, if you will, or the coordination of the pontine maturation center. And so therefore, I have a lack of inhibition, but I have sphincteric and bladder coordination. So what happens is this is basically involuntary voids across an open, a normally opening sphincteric complex. So therefore, there's no significant pressure abnormality. So this is a low risk bladder really, other than the fact that this person is going to have incontinence, and it's going to be mainly about managing those symptoms. When we think about the second level, the suprasacral area in yellow, this is a bit different because what's happened? We've lost the inhibition, we've lost the coordination. So now I've got sphincter and bladder, both without any inhibition, acting independently of each other in an uncoordinated fashion and excitable, meaning those nerves through whatever noxious stimulus or Ed Baron stimulus that they're going to have now, both the sphincter can be activated, the bladder can be activated, each one can activate each other because there's no inhibition, and so it becomes wholly uncoordinated. And these are the types of bladders that develop the bladder contracting against the sphincter, and over time that can become a significant problem. The third level is sacral. And again, many times in the sacral cord, you've knocked out, if you will, the nerves that are going directly to and from the bladder, so therefore you left many instances what we call a reflexia, nothing's happening. The bladder is just storing urine, and it doesn't rise in pressure, the patient has no sensation, and over time that process could just repeat itself. The one caveat that I'd like to leave The one caveat that I'd like to leave with you guys about sacral levels of injury is that they're more commonly associated with peripheral nerve injury, which can result in denervation, which can also create a poorly compliant bladder, so all of these patients still need to be evaluated. So when I start talking about evaluation, I ask first, what is the neurologic lesion? Because, for instance, if I go back, if I go back, I can pretty much say a stroke in the upper brain, if you will, or brain tumor is going to be largely associated with incontinence, but without any significant aberrations in pressure, and it's coordinated, so it's a little bit less of a risk other than dealing with the symptoms of that patient. If I have a patient with transverse myelitis, spinal cord tumor, spinal cord injury, I'm dealing with an uninhibited, excitable bladder and sphincter that are totally out of whack, totally out of coordination, and I'll show you some examples of how the bladder pressure paradoxically rises when the sphincter does, and left unchecked over time, that can create significant dysfunction of the urinary system, okay? These patients are more at risk, okay? So by knowing this pathophysiology, I can predict someone with a spinal cord pathology above the level of the sacral cord is going to have a significant issue potentially if left unchecked. And then lastly, the sacral cord, let's think about cardioquina syndrome. What happens? Many of those paid bladders are reflexic, okay? And sometimes the sphincters are even incompetent, and so these patients will leak or they certainly won't empty, okay? But they usually don't develop upper tract abnormalities either. So that's what I mean by understanding what is the neurogenic lesion and what might be the expected issues. Do I think the upper tracts could be at risk? And then at what stage are they? Are they early or late? Because that's important, as I'll show you in a moment. How is the patient managing his or her bladder currently? Are there any medications that may affect bladder function? Have they any previous urologic or gynecologic procedures that may be pertinent? And of course, in any one of these patients, if they have a neurogenic dysfunction of the bladder, they're going to have usually a neurogenic dysfunction of bowel, and they may also have a sexual history, and we should never, ever forget that to manage our entire patient. In addition to that, I'm going to ask, is the patient able to catheterize themselves if needed? Are they currently incontinent? Are they currently having problems with infection? Once again, we've got to ask about asymptomatic bacteria really characterize what these infections really are. Have they had hospital admissions for pyelonephritis or stones? Have they had any previous stones? So it's a pretty multidisciplinary significant history. And then I think most importantly, I want to know what my patient knows about his or her disease. What is the care network around them? And actually, what are their goals and expectations? Because part of my job is to give them prognostic information and really try to tell them what it really is that we can or can't do for them, so we can all agree on the most appropriate goals and expectations for this particular patient. So when we look at patients who have neurogenic bladder disorders or neurogenic lower tract dysfunction, the basic evaluation essentially is a urinalysis, a blood test to assess renal function and a post-void residual. That would be the basic evaluation. And for someone who comes into my office, for instance, with a stroke or a brain tumor and they're just having incontinence and they're not having any other significant history, that may be all that I do, okay? Because I know that they're not at risk and their renal function is normal. So I'm gonna empirically treat their symptoms. But also understand upper tract imaging in the form of an ultrasound is readily available. And so I don't really fault many individuals for leaning toward that because it's so easy to do. And then urodynamics as indicated. And these would be clearly for patients at risk. So anyone with a suprasacral injury, and then also if any of these other basic evaluation functions are abnormal, you would certainly need to consider doing urodynamics. So I know many of you may know how to do urodynamics, so I'm gonna gloss through this a little bit, but there are some nuances about this that I should show you. But as you know, urodynamics is a complex study. It consists of a urinal flow, which measures the velocity of the urine as it leaves the body or the velocity of urine flow. It's a subtractive systometry to measure both the bladder pressure during emptying, as well as during filling. And then it's of course, adding EMG in the neurologically impaired patient. And then also you'll see some examples of how we integrate fluoroscopy to this. So as you can see here in this particular graphic, we all know that if we place a catheter in the bladder, we're measuring the vesicle pressure. And the vesicle pressure basically represents the abdominal pressure, which is extra-luminal, pressing on the outside of the bladder, and the intra-luminal detrusor pressure. So then we place the second catheter in the rectum, or it could be in another orifice if needed, but the rectum is most common. That measures the abdominal pressure. And so therefore the computer gives us a continued subtracted pressure of the bladder or the detrusor pressure. So this is what a normal urodynamic study would look like without fluoro. And as you can see here, this is more of a study that UroFlow, for whatever reason, is not showing here. But if you look at it, you can see that we're zero to atmosphere. And you can see as the patient fills, they're asked to cough and valsalva. There are several times. You can notice they're having fairly normal sensory events, and then they ultimately void. And as you look at the bladder, one can see the bladder pressure stays very, very stable. There's no involuntary rises in bladder pressure. The compliance, which we'll talk about in a moment, is also normal. And then there's reasonable contractility. This is about 30 centimeters of water when the patient wants to void. This is a fairly normal study, mainly focusing on storage. Look at this difference though when we're doing the urodynamics. Notice in a very similar lab, different patient, similar circumstances, zero to atmosphere. Notice as we start to fill, even at a very, very low volume, okay? This patient has an involuntary contraction of the bladder. You can see the leak on the uroflow, and you can see the leak basically reported by us. And you can see that it happens. We turn it off. We let the bladder pressure come back down. Happens again. This term, and I'm sorry, I'm gonna apologize. It's not detrusor instability anymore. It's actually detrusor overactivity. So detrusor overactivity is the urodynamic observation of an involuntary contraction of the bladder, okay? So this is what we all think contributes to urge incompetence as a symptom, okay? Because the bladder involuntarily contracts and the patient leaks urine, okay? And as an example of that. So we're gonna talk a little bit about video urodynamics, particularly for my at-risk patients or those with significant dysfunction emptying. I'm gonna be doing a video urodynamic study. So we've already talked about the complex system metrogram a bit. We've talked about who can measure the sensation, but we're gonna really focus on what is compliance? What are leak point pressures, okay? We already talked about detrusor overactivity. So we're gonna focus on these three issues during storage. And then I mentioned a little bit about EMG and fluoroscopy and how it relates to these patients. So let's start with the concept of compliance. Compliance, fortunately, is one of the most reliable and reproducible urodynamic measurements. If you have the catheter, if both catheters in the right place and the machine is recording appropriately, you will be able to measure compliance very accurately. This is important because in my opinion, it's one of the most important urodynamic measurements that we do, okay? Compliance is defined as the change in urine volume per the change in pressure. So basically it's simply measured by dividing the volume change over the change in detrusor pressure. So most commonly, the volume change for us is gonna be we're at zero volume and it's just a metric capacity. And then we just measure the change in pressure that occurred in that period of time, okay? And so for most of us, we may see patients that look like this. For the most part, the bladder is fairly compliant. And I'm back to that other study that I showed you earlier. So when we look at it, we say, okay, over this 495 CCs that were instilled in this patient, there was about a three centimeter change in pressure, okay? So therefore the compliance is 165 milliliters per centimeter of water. So this bladder fills very readily to a reasonable high volume without rises in pressure, which is a good thing. That's what the bladder is supposed to do. It's a unique ability of the bladder to accommodate and that's precisely what it's supposed to do. However, if you look at this patient, a little bit different. One can clearly see it without having to show it to you, but look at the filling curve of this bladder, okay? And as you can see, over the 400 CCs of bladder filling in this individual, the pressure change was 62 centimeters of water, okay? There was a 62 centimeter water pressure change over 400 milliliters. So that calculation is 6.5 milliliters per centimeter of water. That's a vastly different storage characteristic of the bladder, okay? That means that the urine in this bladder is being stored at abnormally high pressures, which then has some implications on upper urinary tract dynamics. It's got to flow into the bladder. And if the pressure becomes too high, it impedes its flow. It may even promote reflux, which promotes other problems as well. So the normal number for compliance, which you don't really see on an exam, is about 12 to 15 milliliters per centimeter of water. But what I will tell you, if I'm doing a study on somebody and the urine storage is sitting in the 25 to 30 range, I'm checking things out to make sure things are adding up. That's probably abnormally high urine storage, and you need to go back and make sure you're recording things correctly and or you've got a good history, make sure there's no other confounding factors because persistent storage pressures over 25 to 30, I think is what triggers me to start worrying. Let's talk a little bit about leak point pressures. This commonly appears on examinations as well. So there's two types of leak point pressures when doing urinamics. The first one, which is much, much more rare, is a detrusor leak point pressure. That's actually a measurement in neurogenic bladder for the most part. So for cases of stress incontinence or OEB, without a significant neurogenic pathology, you're really not gonna see this that often. But what basically this is, it's the lowest detrusor pressure at which urine leakage occurs in the absence of either a bladder contraction or increased abdominal pressure. So basically we're just measuring that, that patient's just basically laying there, and we're measuring the bladder as it fills. Patient's not doing anything, and the patient's not urinating. And then all of a sudden the compliance becomes abnormal, the bladder will leak, okay? And if that pressure goes up and it goes really, really high, at the point of leakage, that's the detrusor leak point pressure. That's important because there's some data to suggest that if your detrusor leak point pressure is greater than 40, you may affect that hydrodynamic coming from the upper urinary tract and potentially elicit damage over time. This is largely a neurogenic measurement. The valsalva leak point pressure, however, is a urethral measurement, okay? We see this, we use this often, even in women with stress incontinence and in men with post-prosthetic incontinence. This is basically a measurement of urethral resistance. So it's basically the intravesical pressure at which urine leakage occurs due to the increased abdominal pressure in the absence of a detrusor contraction. So what am I saying? So my patient is sitting or however you have the patient's position, they're filling the bladder, you ask them to bear down. The bladder is normal. It's storing urine normally. You ask them to bear down, push, push, push, push, push, and the intravesical pressure at which they leak, okay, is the valsalva or abdominal leak point pressure. And so really what that is is in some ways an indirect measure of urethral resistance. So in other words, if I bear down just a little bit and I leak, I don't have much urethral resistance. If I have to bear down more and more and more, and then I leak, I've got more urethral resistance. So a lower number means more urethral incompetence, okay? And so back in the old days, these were the grading scales that we used to use a number of years ago. And the only reason why I still keep it on this slide is to let you know that the lower the number of the valsalva leak point goes, the more impaired that outlet is, okay? And still some people use the number 60 to signify something called intrinsic sphincter deficiency. For me, in the neurogenic population, and even with women with stress incompetence, it's more of a continuum. But just remember the rule here, the lower the valsalva leak point pressure, the more impaired your urethra is. So the detrusional leak point pressure, as I mentioned again, is basically essentially a measurement of the resistance of the sphincter to basically a poorly compliant bladder, okay? That's basically what it is. And so if you're having to have significantly elevated bladder pressures to overcome the sphincter resistance, then you can start getting a loss of bladder compliance. And this is back to that index patient that I was showing you about that did develop that poor compliance. And if you notice his leak point pressure, 65 centimeters of water, okay? So this gentleman is at risk for significant upper tract damage, significant deterioration of his upper tracts. So the abdominal leak point pressure, again, is that measurement of the competence of the urethra as a result of resisting someone bearing down to push urine out, if you would. So it's a measurement of urethral function, and it's commonly used to quantify the degree of sphincter deficiency. So just remember, for all of you, when you're doing this measurement, whether you call it balsalva leak point pressure, abdominal leak point pressure, I'll have to have a beer with you and discuss that one one day. But what you do wanna make sure is that your detrusor pressure is normal. If you're having a bladder contraction or an involuntary bladder contraction, while you're trying to measure this, you can't. The bladder has to be at rest to really get this measurement. And again, I put this down here again, just to show you the concept, the lower the number, the worse your urethra. So here's another patient of mine, same lab. As you can see, once again, zero to atmosphere. Bladder looks pretty good here. Normal compliance, no erectivity. But notice that she starts to bear down at 50, 51, 53, 64. She's leaking, okay? Leak, leak, leak, leak. So I'm observing it visually, she's leaking. So she has a fairly impaired urethral resistance. This is a woman that I actually did an autologous sling on who had failed a previous outlet procedure and had significant impairment of urethral resistance. And there you see it there. So the other part of the sphincter complex is the skeletal muscle of the pelvic floor. So basically the external urinary sphincter. So we can measure this somewhat indirectly by basically measuring the activity of the pelvic floor through EMG. It's usually more commonly done with surface patch electrodes. Needles can be done, but you have to be very proficient at it. Obviously there's some degree of patient discomfort. And basically what this does is it helps us determine whether the voiding is synergistic, meaning the pelvic floor relaxes appropriately, or it's dyssynergic, meaning the pelvic floor doesn't relax appropriately, okay? And so it may increase in activity during voiding, okay? And that's a very, very important concept. And in these patients, often I need to know that. I usually don't do EMG on my neurologically intact patients who are coming in for stress and confidence or OEB evaluation, but I do do it on all patients that I suspect as having any degree of neurogenic bladder or to some degree dysfunctional voiding. So what is detrusor sphincter dyssynergia? That's a very important term here, which I find is one of the most common misdiagnoses on urodynamic studies that I get. First and foremost, this is seen in exclusively in neurologic disease. If you're gonna make this diagnosis, you're basically telling this patient's got a neurogenic bladder, okay? And so you need to begin to start to investigate that or figure that out. What it is is involuntary contractions of the striated sphincter musculature during an involuntary detrusor contraction, okay? Remember, super sacral. It's all uncoordinated. One's exciting the other, and it's like a dog chasing his tail. It just keeps happening over and over and over again, okay? Now I borrowed this urodynamic study from a friend of mine named Steve Krause, and I think that this shows it very, very well. Notice as the bladder compliance gets poor, and that's because this patient has probably gone for years with this condition, and it just gets worse and worse and worse over time. This is the bladder compliance getting poor, and notice as this pressure goes up instead of relaxing, the sphincter goes up. It's uncoordinated. This person is trying to expel urine at high pressures against a brick wall, essentially, okay? This is a totally neurogenic condition. Most commonly you'll notice and see a top appearance of the urethra. Here it is here, okay? And as you go higher up along the spinal cord, you may see some internal sphincter dyssynergia, which you see there. And notice this almost beginning of a pyramidal type of Christmas tree configuration of the bladder. That's also mainly consistent with DSD because of the outlet obstruction, okay? So this is a neurogenic condition, and it's detrusor external sphincter dyssynergia. So this is a massive contraction of the pelvic floor. For some of the patients that I see with high cervical injuries or high thoracic injuries, many times they'll have internal sphincter dyssynergia. This will stay shut. So I can't see the spinning top urethra because nothing's filling, because the internal sphincter is closed, but I do see the EMG activity. That's how I know, okay, on those patients. So last part of this complex study is fluoroscopy. So let's think about this. This tells you a lot, doesn't it? So if you look at this patient, a lot of times you don't even need to know and see the urogynamic center. This patient's in trouble, okay? This patient has, at the level of pelvic floor, a contraction causing the dilation. This is a beautiful spinning top urethra, beautiful, okay? In addition to that, you can see here, concentric beginning to contract the bladder neck. So he's got mainly external sphincter dyssynergia, some degree of internal sphincter dyssynergia, of course, vesicle ureflux, and a poor capacity bladder. This is all from pressure. This is all from poor compliance. This bladder can't store anything, and he's already blowing out his upper tracts. He's had multiple episodes of pylo, et cetera, et cetera, et cetera. So this has given you some significant anatomic detail, okay? So remember our index patient with the high leak point pressure and the poorly compliant bladder? This is him, okay? So this gives you all the detail that you really, really need to know and be able to tell this patient what's going on. This is a guy I ultimately wound up doing a sigmoid augment on because I couldn't control him even with Botox, and so I had to do an augment on this patient, okay? And so I did a sigmoid because he had another bowel work at the same time. Usually I do helium. But anyway, so this patient has multiple factors of having potentially developing, it has developed upper tract deterioration. So when do we do these? Understand when somebody has a neurologic injury, even a stroke, it's called shock. They have a neurologic shock, and for a spinal cord injury, it's a spinal shock. It occurs immediately after the neurogenic injury, okay? And then the bladder remains fairly aeroflexic, okay? For those patients, we'll give them intermittent catheterization, try to keep the pothoids around 500. It lasts up to six weeks to three months, and then it generally returns by about three months. So I'll do the urodynamics at three months, post-injury, or if something develops sooner, like in confidence or return of refluxes, okay? That's how that works. So let's start to put it all together. We already talked about the suprapontine lesion, which is neurogenic detrusor of activity with synergistic sphincter activity, and I've already showed you an example of that. This is a stroke patient, or a brain tumor, or something like that. This is considered a more lower risk neurologic injury. Suprasacral spinal cord, loss of coordination, still excitable, sphincter and bladder not working together. So notice this involuntary bladder contraction, contraction of the pelvic floor, interruption of urinary flow. This is autonomic, I'm sorry, this is detrusor sphincter dyssynergia with neurogenic detrusor of activity. This is a patient with a spinal cord injury, spinal tumor, MS plaque in the spine, anything really involving the spine like transverse myelitis. What about multiple sclerosis? The most common thing that we see in our patients with multiple sclerosis is detrusor overactivity, remember a new term, overactivity in about two-thirds of the patients or 75% of the patients. Overactivity of the bladder and DSD occur in that population about 50% of the time, but remember up to a third of the patients almost 40% can get impaired contractivity because the plaque is in the sacral core. So these patients have a varying degree of urodynamic findings and varying degree of presentation given the fact that the plaques can occur at different areas. This is one of my patients that had MS that looks just like a spinal cord injury patient because her plaques were in the spine, okay, and so as you can see the again the overactivity with the with the pelvic floor contracting. So I'm going to throw a sidebar. Why am I telling y'all so much DSD? Because when you get a lot of urodynamics questions that's what you're going to get on the exam because this is probably the most significant thing that you're going to see. Lastly, we talked about the sacral cord things being a reflexic, right? So bladder is out, okay, it's not doing anything. Bladder is denervated, you can't really feel anything. This is actually somebody with a fixed external sphincter, okay, so it's not that it's uncoordinated, it's just fixed though, it's just fixed. So this patient has no sensation, no rise in bladder pressure, so largely a low pressure bladder which is less risk. So we talked about our goals of management. Preserve the upper tracts, confidence, try to maintain an infection, and do this in a matter that has the best impact on a patient's quality of life, right? So how do we achieve that? We've got to do something that's going to allow adequate urine storage at low pressure. We've got to adequately empty in the absence of obstruction. Whether we can do that for the patient to do it on their own or that we have to do catheterizations for the patient, okay? We've got to make sure that we have adequate competence of the urethra to make sure that these patients hold and store their urine appropriately, and it's best to do it with the less invasive treatment option or individually tailored to the patient. So the reason why I do this because it's pretty simple. Here's how it works. You can either fill it empty or fill you to store, okay? That's the functional classification of this. So you either don't empty well because your bladder doesn't work or because your sphincter won't let it, okay? Or you don't store urine because the bladder can't hold it or the sphincter can't hold it. So it's pretty simple. So either of a truser or a sphincter cause of a failure to empty or a failure to store, okay? And so when you're evaluating these patients, you need to think about emptying status, you think about storage status, you think about the bladder, and you think about the sphincter. And if you do that every time and you answer those questions, when you do your investigation, you'll be able to classify this bladder, I'm sorry, this patient more appropriate, and then you'll be able to start talking about treatment options. So Peter, do we have enough time to talk about treatment options? Are we good on time? We are right now. We have two minutes till we hit the 45 minutes, so we can do a quick overview for treatment before. All right, so give me about five minutes. So I'm going to go through these slides real quick, but I'm trying to give you an overview of this. So we look at failure to store, okay? There's a detrusor cause of it, meaning we've got to control bladder overactivity or loss of compliance, and there's a sphincter cause of it, okay? So the sphincter is open, it's not holding the urine. So that's an incompetent outlet. So we're going to try to fix the incompetent outlet. How can we do that? In a woman, most commonly in a neurogenic patient with a really bad urethra, they're going to get a pubovaginal sling. Rarely, very rarely, they're going to get an artificial sphincter. They're either going to largely get, in my practice, usually a pubovaginal sling or possibly even a urethral closure. In some women, you can do a mid-urethral sling, but you have to be very, very selective in that urethra can't really be that bad to do that. So what about the bladder? How can we treat the bladder? So there are a number of different ways to do it, and as you can see here, we can give drugs. We know about the drugs. I'm not going to get into that. We can give Botox, which is very efficient in this population, or we can augment the bladder or even do urinary diversions, okay? So just to go through that a little bit, the mainstay of therapy of drugs, antimuscarinic and beta agonists, and we all know about botulinum toxin, which basically blocks the ACH fusion. Therefore, it's released to stimulate the muscle, okay? It blocks it, and this is highly effective in the neurogenic population. Here's one of the landmark studies. Not going to repeat it, but we've actually seen compliance almost normalized in patients after Botox. It's pretty fascinating, but sometimes with Botox drugs, we can't get it to work. So what's next? We can do surgical procedures to augment the bladder. This just shows basically placing intestine on the bladder, a number of different ways to do it, but it basically becomes a big storage reservoir, okay, that stores urine under low pressure that the patient can catheterize, okay? So we can get into the goals of it, but the bottom line is store adequately under low pressure and maintain confidence. So what about other surgeries? Well, we can also, in some bad instances, patients can't catheterize themselves. They have a combined problem with bladder and outlet. We can divert them. We can do either an ileal vesicostomy, a bladder chimney, which I tend to do largely in more of my quadriplegic males who can't catheterize because generally they have a good outlet, and then it just basically allows them to have an appliance and just drain directly into that. Or we can do an ileal conduit. Many of you have seen that, an ileal conduit. I tend to do more of that in women because they have less, they have more problems with the outlet, and so for some women who can't catheterize, very reasonable operation for them improving their quality of life. You can also do a continent diversion, but of course, they have to be able to catheterize themselves. So what about patients who can't empty? Well, the problem is there's very little that I can do to actually make the bladder function normally again, okay? So I'm basically going to have to look at these options here. Butcher tube drainage, which we tend to try to avoid, although I will tell you I use a lot of tubes in properly select patients and just kind of follow them closely. Intermittent catheterization is clearly the hallmark here, clearly the hallmark here, and very rarely do I proceed to sphincterotomies. Again, diversions not unreasonable in some of these patients. Last closing comments on intermittent catheterization. You need to make sure these patients are storing urine under low pressure, and if you've got somebody with a bad bladder, like I told you before, sometimes you need to repeat the urinamics to make sure that you've improved the pressure. But there are a lot of studies to suggest that if you do intermittent catheterization, you lower the pressure, that you can actually resolve upper tract problems. In addition to that, remember the urinary tract becomes colonized, so you're really only treating clinical UTIs, fever, hematuria, epididymitis, pain, things that you can attribute directly to a urinary tract infection. Not odorous urine, not cloudy urine, which is what the vast majority of your patients are going to call you for, okay? So I'm going to stop there by concluding that, you know, this is really, this condition knows a lot about trying to understand the pathophysiology, making the most accurate diagnosis that you can, trying to identify both bladder and urethral function during both the storage and emptying phase, and then essentially tailoring the treatment individually to each one of your patients. And to be honest with you, that's the art of the science. So I'm going to stop there. Thank you all very much for your time and your attention, and I appreciate it. It's been good being with you guys. Thank you. Thank you very much, Dr. Winners, for this. Right now, we would like to get questions. If anyone has any questions, please use the Q&A feature on the Zoom webinar. It's on the bottom, and once you type down the question, we will be able to see it. We have a couple of questions coming in, Dr. Winners. First question is, why are synthetic slings not an option for management of sphincter causes of failure to store? Okay, so I'm not going to say that they're not an option, okay? Well, what I will tell you is, the message that I like to take home is, is that many times these urethras have open, patchless bladder necks. Urethral resistance is very, very impaired, and quite frankly, you need many times to get some compression, which you don't want to do with a synthetic sling. So for these types of slings, they're going to be a little bit more occlusive, because you need to actually try not only to the mid-urethral sling basically restores competence by preventing urethral descensus and allowing it to close off during that voluntary, if you will, that reflex dynamic contraction of the pelvic floor during increasing abdominal pressure. That's not necessarily the way a pupal vaginal sling works in this case. We need to basically compress the urethral bit, a bit more compressive effect, and you also need more bladder neck closure. So basically, when we do the pupal vaginal slings, we're going all the way to the bladder neck, across the proximal urethra, up into basically the mid-urethra. So it's a very, very different operation, and many of these patients require that degree of urethral occlusion. Regarding the pupal vaginal slings that are winner, how do you counsel patients on the treatment outcomes for this in terms of percentage of improvements when placing patchless slings and quality of life improvement? Repeat it again for me one time. How do you counsel the patients on the outcomes and the percentage of improvement when placing pupal vaginal slings on those patients? Yeah, so there are a lot of different factors there that may affect how I counsel them. So I will tell, in other words, if the bladder is poor, then their outcomes will be worse. Even the same is honest for a mid-urethra sling too. I mean, you've got to store it right. So I will tell you that a pupal vaginal sling, I would tell this patient has an 80% chance of significantly improving their symptoms, not necessarily potentially completely curing it, but improving their symptoms to make it a lot easier for them to manage. I also tell them that there is a higher probability that it's going to potentially impair emptying than compared to the traditional mid-urethra sling for sure. And many of these patients may require, if they weren't doing it before, they may require catheterization after because their bladder may not be able to empty if they need an occlusive sling. So it really does depend on the bladder dynamic as well, and also if they're urinating or not. And so there are a lot of different little nuances in that. But globally, if you look at the at the results of a pupal vaginal sling in the neurogenic population in someone with ISD, I would say anywhere between probably in the worst case scenario, 50 to 65%, but the best case scenario, probably around 80 to 85% that they would expect to see and be pleased, if you will, that they have the operation and be able to manage their bladder more effectively. Okay, thank you. Another question, how do you differentiate DESD from dysfunctional voiding from inappropriate pelvic floor contractions? Very, very good question. And I regret taking the slide out of the talk because I have an illustration of that. And if somebody wants to email Peter or me, I'll be happy to send you the comparison slide. But basically, remember the DE, there's two things. Number one, DESD occurs in a neurologically impaired individual. Okay. Dysfunctional voiding technically should not, because it's either a learned behavior, etc. So it should not be somebody with a known specific discreet neurologic impairment. Secondly, the bladder storage characteristics of those patients are certainly not going to be an abnormality of compliance. Okay, it's going to potentially, there's going to be potentially some coexistent overactivity, or if you will, the little phasic to choose overactivity, maybe some urgent confidence, but largely for the most part, the storage characteristics of these blood patients are going to be much, much more normal. And it's going to be mainly when they're attempting to urinate, that they will then start to have either a delayed relaxation of the sphincter or intermittent dysfunction of the sphincter that actually interrupts urine flow. So I look at the storage characteristics of the bladder, I look at the history of the patient to determine that, and I've never seen that I'm aware of a dysfunctional voiding case where they have pretty significant abnormal compliance, which most of my DESD patients have. Another question, what is a good alternative if video urodynamics is not available, and you have concern about emptying function or C-compliance issues on non-video urodynamics? Yeah, so in one of my areas, it's not. And in some instances, what I will do is I will do a VCUG, which allows you to see the patient urinate under fluoro. Sometimes your radiologist can do that for you, or you could do it in your systole suite if you want it. Sometimes if there is a urodynamics machine in the systole suite, I'll hook up the urodynamics catheter to it at least to see them urinate and get some pressure measurements. But for the most part, you can do a urodynamic study and then do a VCUG as an alternative if you really feel like, for me, I do like to see that anatomy, particularly in some patients who are having emptying disorders and they're a bit elusive. So I guess I would say do a VCUG as well as a urodynamic study, a pressure flow study with EMG. Alrighty, we have a question. Who are you offering SNS for non-obstructive urinary retention? Fully functional spine and biveta? So let's start off the question by, let's start off the answer by saying there is no, the FDA, no neurogenic bladder condition technically is approved by the FDA. So that's a disclaimer that if you're going to do it, you should be telling your patients that. I would say the most area in patients with neurogenic disorders that we are using neuromodulation in is in patients who have MS and in patients a little bit less so with Parkinson's patients. I have not yet really done a significant amount of SNS in patients with actual core disruption or spina bifida, et cetera, at least in my practice. I know there are a few places that are experimenting with that but I think it's important to tell you, but most of the work has been done and I do know that there's going to be a trial starting in MS relatively soon for SNS and I have seen in some of those patients that it's worked very well. Yes, it's indicated in non-obstructive retention but it's a non-neurogenic obstructive retention, non-obstructive retention as its indication is. And one last question, Dr. Reyners, can you review the risks of long-term catheters on suprapubic catheter patients and when do you use them? Yeah, give me two seconds. Sure. There you go. So the review, the indwelling catheterizations, whether it's a SP tube, if you will, or it's a actual Foley catheter, the stone formation rate is probably a bit higher. Of course, it's debatable as to whether the infection rate, that data, is it really true infections? What was it? How was it measured? So every tube is going to colonize, right? So they're going to be chronically, theoretically, bacteoric. But with some of the catheters, particularly in women, having a urethral catheter can lead to bladder, neck, and urethral destruction, relative tissue erosion. We've seen traumatic hypospadias things in men. So therefore, if I am going to put a catheter in, I do try to put an SP tube in to avoid some of these things. In women, obviously, it's a little bit less successful because the outlet tends to be a little bit more of a concern in women where they're going to leak more through the bottom, but still, I have a very significant number of women that I've been able to manage successfully with SP tubes. Bladder wall fibrosis. So in other words, if the tube is in there, it does create, probably relative to an SP tube, whether it's the same, but bladder wall fibrosis is a concern. There is some associated risk, particularly squamous cell neoplasia. So patients start to develop gross hematuria, etc. You probably should be at least looking to work that up and possibly biopsying. And then there is some evidence to suggest that vesicle reflux and hydronephrosis can occur. But remember, some of this data was before Botox. So I have some patients that I manage with indwelling tubes, and I'll periodically will give them Botox to try to decrease the bladder pressure to see if I can avoid some of these sequelae. And then, of course, stones as well. So those are the risks that are associated with chronic indwelling tubes. But I will tell you, there are some studies, if you go back and look, that say these patients can be managed successfully with indwelling tubes. I have a lot of women with MS. I have a lot of patients who can't catheterize wearing catheters, but they need to be followed still. And I think part of the reason why these risks existed is because many patients would get their tubes and they'd just go away, and they wouldn't be followed. You still need to follow them to make sure that they're not getting pyelitis, they're not getting problems, they're not getting stones, they're not getting symptomatic infections. Because if you are, most of that's usually due to bladder pressure. And if you lower that pressure, many of these things can slow down. So we really don't know the real difference between intermittent catheterization and an indwelling catheter, although I still think probably the indwelling catheter is a bit more risky probably in the long run. Thank you very much, Dr. Reyners. I think we're running out of time. On behalf of OX, I'd like to thank Dr. Reyners and everyone for joining us today. Please, everyone, be sure to register for the upcoming OX webinar on November 16th. There is a webinar on starting a pedipartum pelvic floor disorders clinic, why and how. And December 21st is the season for good laxation, how to more effectively treat individuals with chronic constipation. Thank you very much for attending this and have a good night. Y'all have a great night. Thank y'all. Thanks for your time. Good luck to you guys. Bye-bye.

Functional Anatomy

Lower Urinary System

Neuroanatomy

Bladder Storage

Bladder Emptying

Neurogenic Bladder Disorders

Urinalysis

Bladder Management

Treatment Options