Hello, everybody, welcome to the AUG's urogynecology webinar series. I'm Joel Weiner, the moderator for today's session. Today's webinar is titled the urethra, what we know and how much we don't. Our speaker today is Roger Demikowski. He is a professor in the department of urology, the professor of surgery and a professor of obstetrics and gynecology at Vanderbilt University in Nashville. He was the director of the section of female pelvic medicine and the program director for the fellowship in pelvic medicine at Vanderbilt for the past 18 years. He's also a clinical assistant professor in surgery at the Uniformed Services University of Health Sciences in Bethesda, Maryland. He is associate surgeon in chief, vice chair, section of surgical sciences at Vanderbilt University Medical Center, executive medical director for perioperative services and surgery, and the associate chief of staff and medical director of risk management at Vanderbilt University Health System. He also recently completed a one-year tenure as the interim vice president of surgical services. Dr. Demikowski received his medical degree from the University of Texas Medical Branch at Galveston, completed his internship and residency in surgery and urology at the University of Texas Medical School at Houston and at MD Anderson Hospital and Tumor Institute in Texas. In addition, he is subspecialty fellowship trained in female urology, neuro urology, urodynamics and reconstructive urology. He is board certified in urology and female pelvic medicine and reconstructive surgery. He received a master's in medical management from the Owen School of Business at Vanderbilt in 2012. He has published in numerous articles, probably nearly 400 or more now, over 112 book chapters, 500 abstracts, and soon to be, if not in his CV yet, 300 presentations, national and international meetings, if not more. Dr. Demikowski is on the editorial board for the World Journal of Urology, and he's a reviewer for the Journal of Urology and Urology, separate journals. He is the editor-in-chief of neuro urology and urodynamics. He is a fellow of the American College of Surgeons and a member of the American Urological Association and International Continent Society. He is a trustee of the American Board of Urology. Dr. Demikowski has been granted the Zimskin Distinguished Service Award and Lifetime Achievement Awards from the Urodynamic Society for his accomplishment in clinical treatment for incontinence. He has received a Presidential Citation, Distinguished Service Award, and Pelotono Award for services to the American Urologic Association and was the past chair of the Practice Parameters, Standards, and Guidelines Committee for that organization. His current research interests are outcomes of incontinence therapies with a particular emphasis on quality of life issues, patient literacy, and informed consent related to pelvic floor interventions. He is also active in biomaterials evaluation. He is a trustee of the American Board of Urology and has just completed his term as president of the board. He is also the vice chair of the Urology Residency Review Committee for the ACGME. A few last minute reminders. The presentation will run around 45 minutes and then the last 10-15 minutes will be devoted to Q&A. Before we begin, just a few housekeeping items. This webinar is recorded and live streamed. A recording will be made available through the AUG's e-learning portal later. Please use the Q&A feature within Zoom to ask any questions and we'll address them at the end of the presentation. The chat feature is there if you have any technical issues and the AUG staff will be monitoring it and can hopefully help you. With that, I will turn it over to Dr. Demikowski. Thank you, Joel. Very kind of you. Good evening, everyone. I'm Roger Demikowski. I'm at Vanderbilt. Just a couple of clarifications I did start the fellowship at Vanderbilt. I am no longer the fellowship director as of about a year and a half, two years ago. Stuart Reynolds is that. I'm also no longer the division director. Melissa Kaufman is that. As I was asked to step down to do a variety of institutional responsibilities that took time. And also just for complete clarity, I have completed my tenure on the Board of Urology, so I'm no longer on that. But I do remain on the RRC. And one thing that would be of interest to you, I serve on the sub-RRC that merges the GYN and Urology RRC in the oversight of the FPRMS program. So I've had a lot of experience with that. And as many of you know, we've just completed the milestone development for the fellowships, milestone 2.0, that is. And so obviously we can talk about those at some point if you'd like to as well. So my remit tonight is to talk about the urethra, what we know and how much we don't. And I think you'll find that at the end of this, we have some simplistic assumptions about urethral function and treatment. But in reality, as with all things simple, the answer is not as simple as perhaps we historically have thought about it. And I'm going to give you a couple of references, one specifically that I really would like you to read because I think it'd be very helpful. That has just been penned by one of the leaders in our field who has thought a lot about pelvic floor structure function and integrity. And I think you'll find the results of that paper very interesting. So as I think about this topic, I think about the Holy Grail. And of course, the Holy Grail is an analogy to finding a variety of things. And there's all sorts of attributes given to the Grail, but obviously it is considered one of the ultimate aspects of existence. And if we can find it, we've gotten a lot of answers to many of the questions of existence. And I think the analogy to urethral function and reparation of same in the individual who's incontinent or needs urethral reconstruction is very true because we do a lot of things surgically and a few things medically for the urethra, but in reality, we are way under treating the urethra. And unfortunately, until we have much better biologic interventions, such as reconstructive materials made of self and a better understanding of the really fine infrastructure that supports urethral function, we are really, but treating a over essentially wallpapering a hole in a wall, because we really don't completely understand the reasons for urethral dysfunction. More on that in a second. So let's start easily. Obviously the anatomy of the urethra is such that obviously it courses through the central pelvis. And we'll talk a little bit about the sphincteric mechanism. There's a lot of weight put into the pubo urethral ligaments, which allegedly stabilize the mid urethra. And obviously we try to recapitulate those ligaments with mid urethral slings at the time of repair for women with urinary incontinence. But in addition to the fibromuscular investments of the urethra and the internal external sphincteric components, which I'll talk about more in a moment, there's this concept of the seal mechanism. And the seal mechanism is a marvelous concept. It's essentially a, if you will, a viscous plug-like mechanism in a continent patient or continent person that completely prevents the loss of urine. And one of the debates is what is ISD? And ISD intrinsic sphincteric deficiency has always been associated with quote unquote, the loss of the seal effect. And I would argue with you to you that although we do a lot of things to treat all women with a variety of very simple interventions, unfortunately the seal effect is one that we still are struggling to replicate. And in reality, many of us now feel that the intrinsic seal effect and loss of the appropriate function of the intrinsic seal effect actually is one of the real major and perhaps the major underpinning of stress urinary incontinence in women. So we know the bladder control is a complicated factor. I think all of you are aware of not only the pelvic, but also the sacral, super sacral, and obviously super tentorial functionality that subtend normal bladder function. And one of the important aspects of, especially when we consider the pelvic innervation of the bladder, are the short neuronal circuits that actually link bladder to urethral function. And you don't see them on many of the drawings and the suppositions made about urethral function, but local reflexes are really critical for normal urethral function. And unfortunately we see a lot of patients who obviously have open bladder necks. And why would their, all of a sudden their smooth sphincteric mechanism be awry? Some of them are neurologic and they are attributable to definable neurologic lesions in the central neuro axis, but some are peripheral. And we see that not only in patients who have perhaps subtle neurologic diseases that we as yet can't put a name on, but we also see that as sometimes associated with peripheral neuropathies, such as that is associated, for instance, with diabetes. So, uh, and again, the, the local effects, again, the pelvic ganglia, not only takes care of bladder and, and, and, uh, and, and bladder body function, but also sort of bladder neck function. And that bladder neck function is really critical to maintenance, if you will, the intrinsic sphincteric functionality of the urethra, a little bit different than the seal mechanism. The seal mechanism is again, a little bit more of a complicated structure, which we'll talk about in a second. But again, you have this interplay of both, um, uh, higher levels as well as local levels that, uh, uh, comport not only normal bladder, but also normal urethral function and interruption of those normal bladder and urethral functions is also mediated by many of these local reflex arcs that are so critical to normal functionality of both storage and voiding phase in the continent woman. Now, if we really, uh, if you will, uh, hone in on the urethra again, uh, it's very important to remember there really are two components to continents and women. We focus a lot on the rhabdo sphincteric, the pelvic floor, again, where the pubo urethral ligaments, if you will provide a suspension effect for the mid urethra, but there is this proximal mechanism that is a smooth sphincteric mechanism. Again, that's under the control, not only of neurologic, but also passive factors, which is also very important. And when we see patients with open bladder necks, this part of the sphincteric mechanism is not functional. And that's a problem for the management of these individuals, because sometimes a simple sphincter won't address a completely patchless bladder neck. And that's something critically that we have to be aware of as we evaluate patients, especially neurologic patients with complex presentations for their incontinence. Now, one last bit about the seal effect. So the seal effect again is, is basically this viscous spongy effect that really is comported by the rich vascular venous plexus that exists in the lamina propria of the healthy urethra. Uh, and also is imparted by the muscularity internally urethral muscularis, and also an intact external urethral fascial envelope, the periurethral fascia. And if any of these mechanisms are problematic, that seal effect is likely to be not as, uh, um, co-active if you will, as we would like. And of course we cannot forget the importance of the urethra and the integrity of the urethra and the urethra's ability to basically collapse on itself and create, if you will, a plug-like effect in, in, in the, uh, in the, um, non, in the, in the storage phase that keeps a woman dry until such point as she wants volitional, uh, wishes volitional emptying of her bladder. And this seal mechanism is clearly a vascular and neural phenomenon, which we are just now beginning to understand, but the seal effect is very much affected by the local neuronal architecture of the proximal urethra and bladder neck, which of course are subtended by the central neuraxis and also the pelvic ganglia. So you have this multi-component, if you will, construct that gives women continence, which is this marvelous construct, uh, that when it works well, works really well. And unfortunately when it doesn't work well, we have a limited number of assessments that we can utilize to evaluate the seal and the sphincteric mechanisms. And we even have a fewer number of really apropos interventions to help these women with a very disabling condition known as urinary stress incontinence. This obviously is a histopathologic exam, uh, rather micro, um, uh, microgram of a urethra demonstrating the importance of the urethral mucosa in the seal effect and notice the redundancy of the mucosa and the thickness of the mucosa in an otherwise, um, uh, premenopausal woman with, with essentially risk, rich vascular supply. And remember one of the things we see in, in Mary perimenopausal and post-menopausal patients is loss of this mucosal height. And obviously when you lose that mucosal height, you lose the ability, the stickiness, if you will, the urethra to itself. And then you get these interstices, which make it harder for the seal mechanism to be functional. When you couple that then with the loss of vasculature and thinning of the vascular plexus that really provides that seal coaptation, you can see how you can get a seal defect, a urethral seal defect, which again, in the old days, we used to call ISD. People still use that term, but ISD really is a loss of functionality of the plug-like mechanism that keeps a continent patient continent. Um, and when that, when she loses that mechanism, she obviously then can experience urinary continents, uh, which can then be exacerbated by hypermobility and, or fixed urethra. So intrinsic sphincteric deficiency historically has meant a mobile, no urethral hypermobility associated with low leak point pressures. And this, this definition has sort of stayed around for quite a while and has been sort of what I grew up with certainly as, as a physician taking care of patients with pelvic floor. But in reality, is this meaningful nowadays? And I would have to tell you this definition has clearly evolved, uh, in one that we need to really take a step back, especially in light of some of the information I'm going to present to you. This is a way that I would say we thought about the pathophysiology of stress urinary incontinence. Even a decade ago, we had this, this significant component of hypermobility, sort of a crescendo increase of intrinsic sphincteric deficiency until you have patients who only have ISD. And these, again, the, the, if you will, the, the, um, representation of ISD in this far right with those patients was fixed, sometimes radiated, sometimes neurologic urethras that have no mobility and are patchless and just leak at all times. And these are very problematic, uh, patients because again, they, uh, are, uh, provide sort of the worst case if you will. But I think even a decade ago, what we became, what we became aware of was that ISD really exists in any patient who leaks. Urethral hypermobility contributes to that, but ISD really is a substantial component and contributor to stress urinary incontinence and to urethral dysfunction. So again, I think it's important to understand that we've had this sort of progression of knowledge as we move forward in our understanding of the urethra. So what is ISD and does it affect the treatment of choice? Well, again, the, the, the, the concept of hypermobility and, and, and lack thereof came from McGuire. Uh, they identified it initially in patients, uh, about 40 years ago who underwent retropubic procedures and had fixed patchless urethras. Some of them are also radiated patients. They often had open bladder necks and their proximal urethra did not move at rest. Uh, and basically the concept was ISD was an intrinsic malfunction of the urethral, the sphincter, regardless of anatomic position. And that aspect of the definition of ISD, I think has persisted. ISD really is a failure of the seal mechanism and it can exist whether or not the urethra is mobile. Mobility of the urethra is, if you will, a follow on the ISD is the real core and key component to urethral function. And that, which we really, unfortunately still don't have the ideal intervention for management and, and, uh, remediation thereof. Uh, just historically, I think it's important that, uh, from that you'd be aware that as you can see way back in 1988, there were the classes of, or types of urethral incontinence were classified and notice what we historically called type, uh, or ISD was this type three component was essentially an open bladder neck at rest. But a lot of these other types were related to the presence or absence of hypermobility and the degree of hypermobility. And of course, type zero was a patient who had a history for stress incontinence, but you couldn't demonstrate it. So now what we would call again, if you will, cryptic incontinence, incontinence that only the patient could complain. And we go through all sorts of testing to try to prove that needed stress. And we really worry that we're making a misdiagnosis. So they weren't far off, but this was representative of technology that was really trying to very much simplify what really is a very complicated mechanism. I know many of you are familiar with, um, um, MUF, MUCP, maximum urethral closure pressures. Uh, I tend to use leak point pressures. That's what I grew up with. But of course, leak point pressures are a reflection of abdominal pressure and the reflection on the urethra causing leakage and that magnitude of pressure, which results in leakage is that pressure, which we call the leak point pressure. And that's also true for MUCP, obviously. Um, but the problem with these pressures are, is that one, they are somewhat difficult to reproduce even in the same individual and the reproducibility across individuals doesn't necessarily correlate with the magnitude of the symptomatic volumetric loss of incontinence or the bother that the patient has. So it's a number, it's a part of a measure, but in reality it's only a perhaps even a partial directional measure. It's not really very beneficial for anything else, though. Historically, we used it as part of our assessment and our assessment. Still, this date includes objective evaluation, including the stress test, hypermobility and physical examination of the urethra. Of course, that has to be coupled with the stress subjective components of the condition, including the patient's bother, um, patient's willingness to treat and really the patient's expectations and for outcomes. Because again, from the standpoint of outcomes of treatment, we have to have reasonable outcomes. And I will just say this now, and I'll say it again, when we talk about some of the interventions, a patient should not leave your office with the expectation that any treatment that you give them is going to be 100% successful, because that's just not true. Because again, as you see, we really don't fully understand all the issues associated with the causation of urethral dysfunction across the general population. So the Q-tip test is sort of the test we've used historically to evaluate hypermobility. It involves placing a Q-tip in the urethra and assessing the descensus of the urethra to, if you will, the baseline of the urethra. And again, usually 30 degrees of descensus is considered significant hypermobility. This is what you'll see in a lot of the tests in historical FDA reports on various things, such as bulking agents, and even some of the Sling FDA trials have used Q-tip testing to measure the degree of hypermobility. And of course, this is a relatively, there is some subjectivity on the examiner's part to this test, but it is a historical test that is still used to this date. That is often now, and historically has also been utilized and compared to descensus of the proximal urethra and bladder neck with Valsalva or cough vent. And as you can see, this is sort of the normal plane, and you can see the descensus and rotational descent of the proximal urethra and bladder neck in this case with the Valsalva effort. So again, you can add a video fluoroscopic underscoring of the findings on the Q-tip test, but the Q-tip test is a fairly reasonable test if you want really a first order approximation of urethral hypermobility as a part of your examination of the individual. Many of us now, after having done this for many, many years, you'll get a visual concept of hypermobility, and so many people don't have to use a Q-tip, but a Q-tip is a nice starting way to get comfortable with the degrees of descensus and hypermobility associated with urinary incontinence. Now I measured leak point pressure, and again, historically there's been a gradation of pressures utilized that have stressed the magnitude and have tried to correlate the severity of leakage with the severity of depression of leak point pressures, and the same is true for MUCP as well, and urethral pressure profiles, and unfortunately none of these really have been consistently representative of urethral dysfunction. Over the last two decades, 100 centimeters of water was sort of popularized as being that which is the cutoff between normal and abnormal urethral function or high and low leak point pressure, but again, as you'll, if I can give you one thing to take away from the lecture is leak point pressure in and of itself indicates a diseased urethra. No matter what the pressure is, even if it's 150 or 200 centimeters of water, if the patient leaks with that, that's still significant for the individual and still indicative of a seal mechanism failure or at least a seal mechanism inaccuracy that allows the patient to leak, and so because if you think about it, a continent woman should have a leak point pressure that's essentially infinite. She should not leak under any circumstances, and so this is where we get into this discussion. What is the value of these pressures, and do they really give us any guidance? I mean, yes, if you've got a patient with pressures in the single digits are very, very low. Often that's associated with severe incontinence, but there's been some very reasonable objective data that has shown that unfortunately even patients with very low leak point pressure sometimes don't have as magnitude of volumetric leakage as you might anticipate. So again, all of these are relative, if you will, contributions to the impressionistic picture which you have to come away in terms of telling the patient about the magnitude of her incontinence and what her options are. This simply shows the ability to use fluoroscopy associated with leak point pressures, mainly to look at the bladder neck at the time of leakage to determine if there is some form of urethral hyperactivity that basically is causing the bladder neck to open because of urine presenting itself to the posterior urethra, but it also allows you to determine visually the point of leakage as well as around the catheter. So fluoroscopy does add a bit to this, but again, if you're doing a good study, you should be able to determine visually just the loss of urine around the catheter and the pressure which that occurs at. So perhaps the take-home message is an excellent paper which appeared in Neuro-Urology, and you can tell who the senior author is. He needs no explanation as far as I'm concerned. He is still one of the great anatomists and neurophysiologists in our understanding of the female pelvis, both from the standpoint of prolapse and urinary function, and this was a paper that appeared in February this year as part of a debate feature in the journal, and you can see the title of the paper. It's urethral failure is a critical factor in female urinary incontinence, and as you have guessed from what I'm saying, I agree with that. So now what? And John makes some very good points in this paper, and I highly recommend you read it. So he talks about this concept of a three-factor paradigm, and if you'll harken back to that figure that showed sort of the splitting and mixing of hypermobility and ISD until you get to the point of ISD, well, you can see that his three-factor paradigm essentially looks at not only support loss, which is pure stress, but also urethral failure, and notice where he has in this three-factor paradigm urethral failure actually contributes to pure stress as well. So it's no longer just a supportive issue. There is urethral failure that perhaps is not the major part in some women with significant hypermobility, but it's something to consider, especially if you have a patient who doesn't have substantial improvement after a standard well-done mid-urethral sling or retropubic fascial sling. John then in his paper looks at the various interactions of the, if you will, of the environment of the pelvis, and as you can see, he looks at not only, in this case, he's looking at the development of cancer, but this could be also the development and or abnormal development of urethral mucosa, because urethral mucosa, as you know, is plenipotentiary and can develop into many things, but one of the receptor mechanisms for urethral mucosal cells are not only the peripheral, but also the central nervous system, and the various feedbacks, notice as you do this trickle down through the macroscopic, if you will, neurologic system, and then you get into the microscopic cellular system and the importance of cellular interactions, not only in oncogenesis, but also in maintenance of normal tissues and potentially the loss of things such as TGF-beta and normal macrophage function and normal endothelial function, and the impact that that has on the normal environment and the normal function of both the mucosa, the transitional lining of the bladder, and the transitional lining of the proximal and mid urethra, really critical, and these things really complicate, because that, when you start thinking about all these factors, how do you make sense of this? In reality, we don't have the ability for the unique individual at this time to make sense of this, but I'm calling this to you because some really smart people are thinking about this, and this is not as simplistic as it's been made out to. This is from John's work, and this again looks at the importance of the sacral spinal connections, in this case in a rodent model, and the importance of peripheral nerve stimulation for normal continence based upon unique sacral and sub-sacral reflex arcs, and so at some intraspinal in terms of the importance of maintenance, if you will, of the functionality of the urethra. So, again, from the standpoint of the complexity of this, what John has very nicely done is he sort of said, well, let's think of this as a dichotomous or bicameral system. One is involved on sensory function and one is on motor function, and most people would agree that the bladder and lower urinary tract have a predominant sensory now function and also a predominant motor function, and those functions cross, and what you see is, as you look at the ascending normal and normality of urethral function, normality of urethral sensory and motor function, you see most patients are continent as you go up the scale for both of those. As you go down the scale, most patients are incontinent, but notice you have individuals, unique individuals, who appear outside the realm of what you would consider normality. In other words, they should, by all criteria that we have currently, normal sensation, normal motor function, they should be continent. Guess what? They're not. So, this just tells us that, you know, by a first order of magnitude, we're okay in assessing the urethra, but we've got a long way to go to really individualize, to personalize the therapy for urinary incontinence in women, and this is a real challenge for all of you in the next generation because you're going to be confronted with a lot of biologic parameters that will need to be perhaps modified, evaluated, tested, assessed as part of your evaluation of these patients, even for some such simplistic things, seemingly simplistic things, as urinary incontinence. So, John's conclusion in this paper is a very interesting thing, and basically I've just taken on, this is from his conclusion, he said, basically there's a little bit of a preamble. There exists the need to utilize the tools of modern science, and he lists them there. Notice computational models and predictive models are part of this, as well as the involvement of systems diagrams, and remember we've got neural, vascular, anatomic, structural systems that are all interacting for normal urethral function to move this field forward, to yet uncover undiscovered diseases and disease mechanisms, and to provide new approaches for going beyond current success rates, and what John is implicitly saying, and we all explicitly acknowledge, is we're okay in the treatment of urinary incontinence, but we're not perfect by any means, and we've got a long way to go, and please, as unique surgeons, remember to comport that information to your patients, because if a patient leaves your office and thinks that some intervention is going to make her perfect, and she's guaranteed of that, and her results are less than perfect, you obviously have a very dissatisfied patient. So, part of our job is taking this very complex conclusion and distilling it down for the individual, such that the individual understands we're going to do our best with the information that we have, but we cannot make promises or guarantees of perfection in the management of urinary incontinence, or for that matter, prolapse. So, let's spend the last bit of this lecture talking about therapy, and I'll keep it very simplistic. There's a lot of wonderful things going on with the understanding of therapy for the urethra, but as we know, one of the treatments for seal mechanism deficit is bulking, and there's a variety of bulking agents. Bulking agents take a urethra that allegedly is patchless, like the one showing here, and then with basically the creation of some bulk effect by any of the materials available, you create this, if you will, recapitulation, re-ontologic derivation of the mechanism that's the seal bulking mechanism, if you will, of the urethra. We can see that ultrasonographically, and when we look at these various materials that we look at, some obviously are much more hyperechoic than others, and again, this is a treatment that's often reserved for individuals who fail or have less than optimal stress incontinence interventions related to slings, and one of the things we all have to be aware of is that bulking is a very reasonable option for patients, minimally invasive, and one that provides individuals with perhaps a stopgap mechanism, and as the bulking agents get better, perhaps this becomes much more of an intervention that we consider as more of a frontline therapy for patients who are primary individuals who haven't undergone sling interventions. What have we attempted to do with slings? Well, we've attempted to recapitulate support, and again, as I mentioned, you know, if you can imagine these being the pubourethral ligaments, these are actually sutures for a patched sling, and again, the goal for slings is to essentially recreate support around the urethra such that when the urethra moves, individuals who have hypermobility as an aspect of their incontinence to try to prevent that hypermobility from resulting in opening of the urethra with urinary descensus, and slings have gone from partial slings to full slings as demonstrated here. Often the full slings nowadays are mesh materials, but certainly I'm of a generation that used full slings for autologous slings as well, so we've seen a real derivation of these procedures, but one of the key learning points is that where we know that the slings must have contact is with the endopelvic fascia. These slings must go through the endopelvic fascia to allow ingrowth of fibrous tissue to provide adequate support for hypermobility, and however you anchor them, suture or mesh or whatnot to the rectus fascia or to the obturator areas, that's where the support sort of gets anchored, but the main components really are at the level of the entry of the material through the endopelvic fascia, and again what we're trying to do is recreate or recapitulate the effects of the pubocervical and periurethral fascia on urethral function, and that's what these various sling materials have attempted to do for us over the years of intervention. So stress incontinence equals intrinsic sphincteric deficiency, and I would say yes, any patient who has stress incontinence has some component of intrinsic sphincteric deficiency. Some have more than others, and again because of our relatively blunt assessment tools, I'll have to say that we still as yet aren't really as precise as we would like to be, and many of us have argued for the use of dynamic ultrasound such as IVUS ultrasound that is now being used for a lot of the cardiac tools in the urethra to assess not only the seal, if you will, the urethra, but also, if you will, the ability of the contractile ability and also the tensile ability of the external fascia in terms of its ability to support urethral function, because again remember it's a syncytium, and one part of the syncytium, if it's non-functional and poorly functional, will affect all aspects of the syncytium. So just a brief roll down memory strain, memory lane rather, we all appreciate the autologous pubovaginal sling as being the gold standard for those patients who failed. Historically it was used for patients with low leak point pressures. It was then extended to patients with hypermobility. Many people have demonstrated the value of repeat slings, but these are these are procedures that are much more invasive than the than the standard midurethral sling and still really aren't perhaps ideal for the individual patient who's had no interventions and who wants to return to her degree of activities relatively rapidly. I mean our autologous slings, really I tell patients to take it easy for about six weeks, and that's not really compatible with some expectations for patients. So again the post-operative management of these individuals is really critical in terms of optimizing their expectations and also optimizing their benefit from whatever intervention we utilize. We know the tension-free slings have been used both in ISD and hypermobility, but the ISD described in most of the sling papers has been in patients with some degree of hypermobility, and what's clear there is some data to suggest not only the TBTs are less favorable in patients with very low leak point pressures, but also the absence of hypermobility may adversely impact outcomes, especially with obturator tapes, perhaps less so with transvaginal tapes, but again the concern is as we place more and more tension on transvaginal tapes, the risk of erosion into urethra and or bladder when these slings are placed under tension. So can we do a TVT after a standard sling, or can we repeat a TVT after another sling, after a prior TVT? The answer is absolutely yes, and there is some data to support that. However again it's a careful, careful consideration of workup of the individual is really critical to make sure you're you're opting for the best option for that individual, rather than just sort of pigeonholing her into what maybe fits best in the algorithms that that exist at the current time frame. This is simply some intraoperative photographs. I do use a needle pronteria. This is sort of the standard length of sling that we use. I do use two suspension slings. I use PDS as my material. Some people still use permanent material, but again once the sling is affixed to the endopelvic fascia, you really don't need permanent material because the sling gets its support actually from the periurethral fascia, not so much from the rectus fascia. The sling dimensions usually are eight to ten centimeters in length, and two to three centimeters in width. Two is the ideal width, and this can be obtained through a small patch obtained through a relatively small incision on the interabdominal wall with relatively little morbidity, but again it is a second incision, and the individual patient has to be aware of that second incision, especially from a cosmesis standpoint. The slings are can be placed and actually can cover quite a bit of the urethra as demonstrated here. You see the coverage really from almost mid to distal urethra all the way to bladder neck, so you did get a very good, very reasonable coverage of the overall geography of the urethra with these materials, and it does supply you with much more support than, for instance, a standard TBT, but obviously these sort of tapes or these sort of mesh self rather autologous slings are again more reserved for either failures or for patients who have neurogenic disease, who require some tension to be placed on the sling to actually compress the sling for continence basis. We know there's lots of data. This is just a few of the data points. This again, some of McGuire's end of career data looking at the four-year outcome data. Notice there was a high degree of satisfaction, but the continence rates were less than 90%. And there was some de novo urgency that developed in 4% harvest site rate issues, such as seromas, which is the most common in our experience, as well as wound infection. Long-term results were also encountered by this group. And they noted that although there was high degrees of satisfaction, what we've seen in all the studies is the longer you follow these patients, the less likely they are to be completely dry under all circumstances. Again, getting to the point that we still don't understand all the reasons why urethras become dysfunctional. And certainly one of those is temporal change over time. And that temporal change over time obviously impacts patients negatively. And the Ward and Hilton studies done in the early 2000s very nicely show the differences between the various interventions followed over time. And the reality is nothing is perfect over time. And patients need to be aware of that. There is sort of a timestamp that is problematic for long-term effectiveness of their procedures. Patient satisfaction, despite the fact that there is this sort of limitation on long-term results is still very good. And actually with slings, it's better than birches. And that's been shown sort of repetitively now because a sling probably is a better anatomic operation or at least a better restorative operation than the birch from a standpoint of a patient's viewpoint. So the autologous sling is, I still think, represents a reasonable, if you will, salvage mechanism for the non-functional, poorly functional urethra. Certainly remember all the guidelines now recommend self-tissue when you're doing a diverticulectomy and concomitant stress incontinence procedure, or you're doing some form of urethral reconstruction. Don't put mesh over a fresh urethral incision because you'll be guaranteed an erosion almost definitively. And again, autologous slings probably have the only role when you're trying to place a patient in retention for a patient with a really patchless urethra who's had injury from long-term Foley catheter management or who's a neurogenic patient who has desirous of intermittent catheter-based surgical retention for purposes of urinary incontinence. So let me conclude by saying that severe incontinence is intrinsic sphincteric deficiency, but stress incontinence of all types is intrinsic sphincteric deficiency. It's probably a form factor of how much, and I think we all have to, again, assess our patients carefully. Hypermobility is key, especially if you're going to consider a transvaginal tape because, again, hypermobility, if it's not present, is less likely to respond to a tape than the person who has hypermobility present. And again, if I can leave you with anything else, we need to have a better understanding of that seal mechanism and how it's formed and how we can restore it and also maintain it. And my real hope is that, with much of the biologic research being done, that we'll have biologic agents, perhaps based upon some of the new technologies that we're seeing, mRNA technologies, et cetera, that will help provide restorative medicine to the proximal urethra and seal mechanism such that we can restore continence to individuals without subjecting them to such invasive surgical procedures. That's easily probably another decade away, but I do think we're now closer to much better interventions than we've ever been, and we're also a good deal closer to understanding the true root causes of stress incontinence and the problems that can be imparted by a variety of conditions that heretofore we didn't worry about as much or we perhaps placed secondary to the patients presenting symptomatology. And again, I use diabetes as one of my key components here because diabetes with a small neuronal impacts can really impact urethral sensory function, also bladder sensory function, and obviously much lighter motor function. So I think these things are all key and critical to consider. And one thing that I've learned over the years, if a patient has peripheral neuropathy, they often have pelvic neuropathy as well. And so be thinking about that, especially in the individual has sort of a mixed presentation with a spontaneous component because they actually, maybe individual has relatively advanced peripheral sensory neuropathy and are missing some urge events because of the impacts of their diabetes. So it's a very interesting field and one that continues to evolve and one that I hope that you all will continue to remain engaged in as long as you are in the field of female pelvic medicine. It's a wonderful field. I certainly have myself. I'm grateful for many of my mentors and also grateful for the people like John Valanci in the world who are really pushing the envelope forward in terms of our knowledge. And those individuals who are also helping us with patient education, patient health disparity resolution, and also helping patients with their health literacy. Because again, one of the key and critical components I've learned in all these years is that health literacy is really a very, very important aspect of a happy patient. And we as a specialty really need to sort of relook at that in terms of not only helping our patients understand their conditions, but also helping create reasonable expectations for our patients in terms of the interventions that we're currently doing and perhaps for the future of any interventions that we may offer. So Joel, thank you. I will shut up and let's see if anybody has any questions. I muted myself. So one question from the Q and A is asking if you could please update us on the latest state of urethral sphincter for female urethra. Okay. So the urethral sphincter has historically and remains approved for use in women. It has been recently revitalized by the use of robotics to implant the bladder neck sphincter, which is obviously how it's implanted in women. So obviously you'll have to have some ability to expose the proximal urethra and bladder neck and places sphincter such that you don't disrupt the vaginal wall at the time of placement. So you have to develop the urethral vaginal plane for purposes of placement of the sphincter. But the sphincter actually is a very nice option. The problem with the sphincter is chronically, we've noticed this in management of men with post prostatectomy incontinences, continuous pressure creates urethral atrophy. And in a woman, once you've gotten urethral atrophy, there's really no options, because in men you can move the sphincter to a different area of the urethra. In women, obviously the sphincter's width is essentially 50% or so of the length of the urethra, and you don't really have any other place to put it. So I think most of us would reserve the sphincter in women for those women who have really no other options and it's sort of a last gasp maneuver, if you will. The philosophy, frankly, is a little bit different in France. The French have the greatest experience with this and are actually quite happy with their experience with the urethral sphincter in women. But again, the problem is the sphincter has about a 10-year life expectancy. And so as you think about replacing the sphincter, you'll get urethral atrophy and it becomes problematic in terms of getting reasonable coaptation with replaced sphincters and replaced cuffs because the cuffs really have less tissue to compress and then you get into issues with erosion. So it's definitely out there and robotics have certainly re-added some interest in it, but it really has, once you get to the point where, as you do with all our procedures, it starts failing, you don't really have a good option for replacement. Okay. Next, we're asked if stress incontinence is intrinsic sphincter deficiency, is the reverse also true? Yes. I mean, I think if you are following what Delancey has put forward and what I clearly believe is that ISD is a component of all stress incontinence. So stress incontinence is ISD. Now, the stress equals ISD does not give any shrift, if you will, to hypermobility and hypermobility is present in some women. The opposite, which is ISD equals stress incontinence is true because ISD, if it's present, does cause stress incontinence. And if you don't have ISD, you're not gonna leak. There you go. A couple more. So if a previous TOT mesh failed and you plan to repeat with a TVT mesh sling, what is your practice in that situation? Or would you use an autologous fascial sling for any TOT mesh? Yeah, if a TOT has failed, I'm less likely to put another TOT in. I think you need a little bit more support so I'm more than likely going to do a TVT or an autologous, excuse me, a retropubic majorethral or a retropubic autologous sling in that individual. And then would you remove, there's like a sub question, would you remove the previous sling at the time or just place the new one sort of around or under it or near it? Yeah, it's a bit of a judgment call. The answer is if it's a TOT, it's a bit of a judgment call. The answer is if it's not eroded and not associated with pain, I'll usually leave it in because I've not had any issues with that. But if there's an erosion, a fornoceal erosion, or there is any degree of pain of the sling, then I'll remove them. And then one request, if you had any comments about urethral pain. Yeah, urethral pain is very interesting. I mean, you have real causes of urethral pain. I seem to have had a run of women with intraurethral condylomita that have been referred to me with urethral pain that do well with laser fulguration of, or laser ablation, excuse me, of those lesions, especially at the distal urethra. But there are also women who have urethral pain that can be either very localized or global in the urethra. And that is problematic. Obviously, you need to consider infectious etiologies. Certainly, I've had some patients with multiple sclerosis who have urethral pain. They have a complex regional pain syndrome associated with a multiple sclerosis. They also may have other anatomic defects that result in pain, such as diverticulum, ectopic urethrus, ectopic ureters. So all those things need to be excluded. The management of urethral pain is really hard. I mean, if a patient has fixed urethral pain, it's a component of her painful pelvis disorder, they really have some real issues. Some patients clearly have an epithelial component, and they do well with coating agents, such as finazopyridine and other agents such as that. But some patients have deeper-seated pain, and I've actually done periurethral blocks on those individuals, intraurethral lidocaine, xylocaine gel for those individuals, self-administered on a timed basis. There's a variety of treatments for those individuals. Occasionally, they also required pelvic ganglia blocks to help them because their pain is so severe. Clearly, many of them have had an etiology of instigated by some infective event and whatnot, as much as we see with painful bladder syndrome. And unfortunately, you're left without any further infection, but you're left with this severe urethral hypersensitivity, which is very problematic and very difficult to treat. And I do use gabapentanoids and whatnot in those individuals because they probably do have polysynaptic-based pain. And so any management from a gobergic standpoint that you can use is probably helpful for them. Okay, and then another question, if you have any thoughts on the role of neuromodulation for stress incontinence. Yeah, as many of you know, there has been some dorsal genital stimulation for stress incontinence that has been put forward. Obviously, there's no as yet approved neuromodulation per se for stress incontinence. There's clearly intravaginal devices that could be considered neuromodulatory that are beneficial for treating the pelvis for women with stress incontinence. But there's no real good implantable technology at this time that's approved. There's certainly stuff that's been evaluated, but nothing that really has borne the test of time and obviously nothing approved. And again, if you have an individual who has mixed incontinence and she has some stress and a lot of urge, you're going to benefit the urge with neuromodulation. You can always come back and manage the stress a bit later should she still be bothered by that. Okay, and one last question, which was going back to the role of the urethral submucosal tissue and mucosal tissue. So thanks for the good talk. And then that is very encouraging that people are investigating the urethral function and incontinence mechanisms more and more. And that you had mentioned that there's a decrease in urethral submucosal tissue with aging. And is that based on a human urethra study? And do you think that plays a role in the decreased leak point pressure or maximum urethral closure pressure? Yeah, there's actually quite a few pathologic studies that have demonstrated the loss of not only the abundance of the lamina propria of the urethra, but also thinning of the mucosa and also atrophy of the muscular layers of the urethra associated with the especially advanced menopausal change. So the answer is yes, I definitely think that impact is there and definitely think that that contribution is definable and obviously something that I use a lot of topical vaginal estrogen, not so much for treatment of the stress, but to try to rebuild the, to resuscitate the tissues to some degree for any of the subsequent interventions that we discussed earlier. And then, yeah, is there any follow-up on that specific question? Was if you think there's a way we can uniquely evaluate patient-specific reasons for incontinence in terms of what component that mucosal change has on their dysfunction? I would say not at this time. I think we can get some hints from your dynamics and physical examination, but we really don't have the divining rod that can give us a direct interaction. I mean, certainly you can get a view of the lay of the land based upon other vaginal changes about the degree of atrophy and whatnot. And it's a fair assessment that if you have significant vaginal atrophy, you're going to have some impact on the internal urethral seal mechanism. And we can keep coming in. And then if you have any thoughts on the effect of sensory urgency on the urethral sphincter function and tone. Well, sensory urgency obviously is a real component. Sometimes sensory urgency comes from the presence of urine in the posterior urethra associated with stress events. Sometimes it's a learned phenomena. It does have an impact on tone because women, basically, if you have urgency, you're going to tense your muscularis, your external sphincter. So there is external sphincteric tone increase associated with sensory urgency, especially as the urgency, if you will, reaches its crescendo. So it's sort of a positive feedback mechanism between the two. And one last question was just whether or not you use single incision slings, we had mentioned. I used a lot of single incision slings in my life. I'm, for transparency purposes, a medical monitor on a single incision sling study. Now, I think they have a role, but I think it's a very selective role in women who have reasonably good vaginal tissues, demonstrable hypermobility, and reasonable anchoring tissues for the slings. Because again, you really depend on a relatively short bit of material to give you that anchoring to the endopelvic fascia on either side. Clearly works for some individuals, but it's not a generalizable thing, and certainly not in individuals who lack hypermobility. And as I will, I'll just wrap up now to answer the last questions. Yes, this recorded webinar will be available through the AUGS portal. And so just on behalf of AUGS, I just wanna thank you, Dr. Demikoski, and everyone for joining us today. And just remind everyone to please register for the upcoming webinars, which are on September 21st, Male and Female Genital Microbiome on October 19th. It is Congenital Anomalies on October 25th, Incorporating Pelvic Floor Ultrasound into Your Practice. Thank you very much, everyone. Have a good evening. Take care. Thank you.

webinar

The Urethra

stress urinary incontinence

intrinsic sphincteric deficiency

urethral sphincter

female urinary incontinence

treatment options

research

personalized approaches