Thank you for the opportunity to present our research, titled Imaging Bladder Fluid Dynamics Using MRI. We have no disclosures. Our study objectives were to develop a method for imaging bladder fluid dynamics within a healthy human bladder using conventional MRI and to understand normal bladder flow patterns. The first question that comes up is what do we know about urine flow within the bladder? We actually know quite a lot about the anatomical course of urine as it flows through the urinary system from the kidneys into the ureters, filling the bladder for storage and then out through the urethra. What we know less about or have less significant understanding about is the fluid dynamics within the bladder or the motion of fluid. As urogynecologists, every day we understand that bladder pathologies influence flow. For example, when urine is blocked in bladder outlet obstruction, when it is trapped in systoceles or diverticulae, when it's reversed in vesicourital reflux, or when it is stalled in detrusor underactivity. So when these bladder pathologies alter urine flow, it follows that there's more to be learned about the relation between structure and the role of flow in urinary function. Additionally, we know in nature that changes in flow patterns have been shown to alter microbiological systems. The urine has its own microbiome, so understanding flow may help us understand more about the role of the flow in microbiome and UTI recurrence. This study in particular is looking at what normal and abnormal flow is in the bladder and finding a way to actually look at it using conventional imaging. We have plenty of imaging modalities to take a look at the urogenital system, but this tends to look more at bulk urine flow and tells us little about detailed fluid dynamics. So what we like to do is look a little bit deeper and more complex. Conventional fluid dynamics is an established engineering tool for the study of complex physiologic flows in order to analyze fluid systems and to design interventions. More specifically and simply, conventional medical imaging can be translated into complex flow analysis. This has already been done to a significant degree in cardiology, where analysis of the flow patterns within blood vessels, aneurysms, and across heart valves has led to increased understanding of the forces at play, leading to better temporal and spatial resolution within possible and clinical methodology, and optimizing medical device design. This is still in its infant stages in urology. A recent study used computational fluid dynamics as a non-invasive urodynamic model. However, this is a small study. Only male subjects were examined. Computational models were based on structural assumptions without considering the actual bladder deformation during micturition, and there's no visualization of real-time in vivo global flow patterns. Our study wants to use conventional MRI to see if we can visualize these flow patterns, which we think we can, and that there are consistent bladder fluid flow patterns in healthy bladders. This is a pilot study of five healthy women and three healthy men without urinary symptoms or contraindications to MRI. Subjects were instructed not to void for three hours prior to the study. Real-time MRI images were acquired during spontaneous voiding attempt in a supine position, and urine spillage was controlled with a diaper and an enema ring collection device that you can see on the right. Radiologically, we used a 3-Tesla Prisma MRI scanner and a balanced steady-state free-procession sequence. For the non-radiologists in the room, this sequence is very susceptible to the effects from flow, which causes off-resonance effects, which reduces the signal. So usually this would be considered an artifact. We used that artifact to our advantage to study these flow patterns. Images were acquired in a mid-sagittal plane, crossing the symphysis pubics and the coccyx, and reconstructed in a spatial resolution of 1.6 millimeters squared. Let's look at a full bladder first. You can see clear images within the static bladder of urine, and three times throughout this video, you'll see ureterial jets pictured. You also slowly notice that there's a laminar vortex developing and stretching in the bulk fluid of the bladder. And just one last time, we'll have another strong ureterial jet that you can easily visualize near the blue arrow. Let's take another look at a full bladder at rest. In this, you can see a recirculating flow pattern at a smaller time-length scale, generated around the urethrovespinal junction, or UVJ, and this migrates toward the inner bladder. You can also see, once again, a small ureterial jet. Next, we take a full bladder and apply valsalva pressures. So you can very clearly see here the flow, and that the complex vortical flow patterns are best seen on valsalva, which makes sense, since you're applying abdominal force to the bladder and changing the position of the fluid. Again, you can also see this vortex recirculation pattern initiating around the urethrovespinal junction. Now we're looking at micturition. The flow pattern here is different, in that you see a laminar parallel flow, which is noted at the urethrovespinal junction during early micturition. This stays this way, and it becomes more complex as terminal emptying, when valsalva to empty the bladder completely shows, once again, complex vortical flow patterns. We did all this with male patients, so this is a little bit different than what we're used to. But this is also showing laminar parallel flow at the UVJ. This movie takes a second for him to really start the urination process, which is right about here, when you start to see the increase in signal. You can also see more complex flow noted in the prostatic and bulbous urethra. This last image wasn't one of our ideal subjects, but it does show the best contrast of the flow within the bladder of all of our subjects. It will recycle in just a moment, but you can again see that laminar parallel flow noted at the urethrovespinal junction during early micturition, right about now. So this is a novel demonstration that urinary flow can be visualized on MRI within the normal bladder, and that flow patterns appear qualitatively similar in different subjects. There are consistent flow patterns. Laminar vortex circulation of fluid is seen at rest, while laminar parallel flow is seen during micturition. And there's a consistent recirculation pattern suggesting that the position and orientation of the UVJ has an impact on the global flow patterns. The limitations of this study is that it is quite difficult for subjects to avoid an unnatural supine position of an MRI scanner. It's difficult to standardize the starting bladder volume with our protocol, because we did not use invasive catheterization for this study to fill the bladder. Most importantly, imaging of flow can only be done in two dimensions. It is possible to simultaneously image multiple planes during these voids, however, the resolution dramatically decreases and you can no longer see flow. Our next and very important steps are working with our Georgia Tech mechanical engineering partners, who are currently in the process of analyzing this data. They'll take our MRI images, make 3D reconstructions of the surface, triangulate the surface, and then make a temporal mesh, and finally perform the computational fluid dynamics. We actually just this week got our first 3D reconstructed bladder image from one of our first subjects, and from this they'll do temporal flow evaluation, develop an interpolation algorithm, and then predict the flow structures, taking into account the temporal bladder deformation. And finally, phase two of the study will repeat this optimized MRI protocol and analysis in subjects with known bladder abnormalities. Here are my references, and I welcome any questions. Thank you. Excellent study. Very interesting. Do you have thoughts on maybe how to account for the supine position, or how to image? Yes. We don't have a model to really account for that change in position now. We are very limited by MRI technology of how we can perform these studies. There are sitting, standing MRI machines that exist, but those are only to a maximum of 1.5 tesla, and don't have anywhere close to the resolution we need for this. So, although it's not really, I mean, no one's usually voiding on their back with a diaper on, this is something that we can at least start to view these flow patterns. Come back again and show us some more. I'd be happy to. Thank you for your time. Thank you for the Scientific Society for the opportunity to give the presentation. So, this is my disclosure. So, as we all know, anal incontinence is not uncommon, and the prevalence of fecal incontinence reported varies from 2% to 24% in women in the United States. And many studies have investigated risk factors of anal incontinence. Some studies show that anal incontinence has less prevalence among black women compared to white women, but some don't. So, here we have the question, what is the relationship between race and AI, and how the symptoms change over time? To answer these questions, we generate two hypotheses. First, black and white women are equally likely to have AI symptoms. Second, asymptomatic black and white women are equally likely to develop AI over one year. We analyzed the data collected from mothers' outcome after delivery study, mode study. It is a longitudinal cohort study of Paris women. Participants recruit 5 to 10 years from the first delivery and followed annually up to 9 years. And at each visit, epidemiology of prolapse and incontinence questionnaire was completed by each woman. And our outcome here, AI score, is obtained from this questionnaire. AI score measure border from incontinence of solid stool, liquid stool, or gas with a range from 0 to 100. Zero means no symptoms at all, and AI score greater than 22.8 indicates clinically significant AI. So, for this study, our outcome is AI score, and exposure is race, which only pertains to white versus black here. And other co-variants include mode of delivery, OASIS, BMI, age, and parity. Univariable and multivariable logistic regression models using generalized estimation equation methods were applied. And for our first hypothesis, the analysis is at the visit level. But for the second hypothesis, our analysis is at the visit pair level, which is two sequential visits from any participants, and it is one year apart of average. So, this figure shows our study population. 1528 women were enrolled in the mode study, and we excluded women who only attended one visit, as well as the women who didn't report race or reported other race. So, finally, we got 1256 women with 6902 visits, and 5872 visit pairs. And among the 1256 women, there are 189 black women and 1067 white women. So, here, in the following, I'm going to only show the difference in terms of the characteristics between these two groups. First, the black women tend to be younger at the first delivery, and about 59% of black women had cis-hearing, which is lower than among white women. But white women are more likely to have OASIS, 10% versus 4% of black women. So, in addition, black women are also more likely to have obesity and more likely to have less parity. Then, let's come to our results. So, recall that our first hypothesis is black and white women are equally likely to have AI symptoms. So, for this hypothesis, we compared the odds ratio of having AI score above zero at visit level for white women versus black women. And after adjusting for modem delivery, BMI, age, and parity, the odds ratio is 1.8. So then, move to the second part. So, recall that our second hypothesis is symptomatic black and white women are equally likely to develop AI over one year. So, for this hypothesis, our analysis is at visit pair level, and we only focused on the visit pair which has AI score equal to zero at time t. So, this part shows the distribution of AI score at visit t plus one above those pairs. So, for the black women who have AI score equal to zero at time t, about over 94% of the AI score remains zero at time t plus one, which is higher than among white women, 90%. So, if we draw a line at 22.8, which is catapult for the clinically significant AI. So, among black women who are symptomatic at time t, about 1.3% of the visit pairs have AI score above 22.8 at visit t plus one, which is lower than it among white women. And adjust the odds ratio is 2.6. Similarly, if we draw a line at 11.4, which is half of the 22.8. So, among the black women who are asymptomatic at time t, about 2.5% of visit pair have AI score above 11.4 at time t plus one, which is also lower than it among white women. And adjust the odds ratio is 2.3, which is consistent with the odds ratio we got when we used the 22.8 as our catapult. So, in conclusion, white race were significantly associated with AI symptoms at any time point in time, as well as to the development of AI over one year of observation in analysis controlled for mode of delivery, OASIS-B, obesity, age, and parity. So, our study have some limitations. First, our findings are limited to only two race groups and rely only on AI score to assess the severity of symptoms may be too simple. But our study also have some significant strengths. First, the pair study is in longitudinal design. Second, it is unlikely to have misclassification for our exposure. We also are able to control for several confounders and account for time-varying matters. In the end, thank you to our team and all the moms. Thank you. We've got time for some questions. I was surprised at the high C-section rate in your groups and also the high rate of OAC injuries. And I wondered how typical this population would be, how you could generalize it. Yeah, so that's a very good question. So, in terms of generalization, we have to understand the study population. So, I didn't give a very thorough introduction for this cohort study. Actually, this cohort study where you recruit all the people, all the women, they are kind of matched by the delivery, the mode of delivery. So, that is why this mode study has a higher C-section proportion than the general study. Yeah, that is by design. Thank you very much. Thank you. Thank you so much for giving us an opportunity to present our research. I'd like to acknowledge my co-authors. The following are our disclosures. Robotic sacral copalpexy can be a challenging procedure to teach due to complex anatomy and multiple surgical steps. Simulation, however, provides a safe learning environment. We created the following model that includes both pre-sacral dissection and mesh attachment for learners to practice in a simulation setting. In these pictures, you see the construction of our model with mostly reusable parts. In the first photo, you see the bony pelvis with silk surgical tape over the sacral promontory simulating the anterior longitudinal ligament. Next, you see the pelvic model with the addition of vasculature, the right ureter, and the vaginal cuff. In the next photo, you see the addition of quilt batting to simulate areolar tissue. And finally, you see a simulated peritoneum attached to the pelvic model with binder clips. The objectives of our study were to validate a simulation model that includes the multiple steps of sacral copalpexy, including pre-sacral dissection, vaginal mesh attachment, sacral mesh attachment, and peritoneal closure. The study was IRB-exempt with participants from seven U.S. institutions who were recruited with an emailed invitation. Our expert participants included FPMRS surgeons who regularly perform robotic sacral copalpexy. Our trainees were current fellows. After each participant completed a pre-procedural demographic questionnaire, they watched a video orienting them to the model and its use in sacral copalpexy. They then completed a post-procedural questionnaire. Three surgeon reviewers scored and timed de-identified videos. Construct validity was measured both with the Global Evaluative Assessment of Robotic Skills, or GEERS, tool and procedural time. Inter-rater reliability was assessed with intra-class correlation coefficients for the total GEERS score. Face validity was assessed with a five-point post-procedural questionnaire. To establish construct validity, the three surgeon reviewers underwent calibration training using the GEERS assessment tool. GEERS is a validated robotic surgery assessment tool composed of six domains, with higher scores indicating greater degree of proficiency. The highest total score one can achieve is 30. Each of our participants was graded with this tool on the sacral copalpexy procedure as a whole. Timing data was collected in a standardized manner from each of the following steps. For example, sacral dissection started with identification of the sacrum and then concluded with the exposure of the anterior longitudinal ligament. Each of these steps had been shown in the pre-procedural video that each of the participants watched immediately before starting their procedure. This is the post-procedural questionnaire that was used to establish face validity. The first question assesses the model's ability to mimic live surgery. The second question assesses the use in teaching and learning. And the third question assesses its use as a tool to ascertain a learner's readiness to perform robotic sacral copalpexy in a live surgery environment. Here are the details of our validation methods. GEERS scores and procedural times were assessed for normality of distribution and non-parametric tests were used. Interrater reliability was assessed with an interclass correlation coefficient with a score of greater than or equal to .8, indicating an acceptable level of interrater reliability. And then face validity was assessed with percentage of agreement or strong agreement on the post-procedural questionnaire. Our trainees included 17 fellows from 7 U.S. institutions with an even distribution amongst years of training. And our experts were 9 board-certified FPMRAS surgeons and 5 out of 7 taught fellows. The median number of yearly robotic sacral copalpexy performed by each group is listed in the bottom line. So using our simulation model, experts' total GEERS scores were significantly higher than trainees. Additionally, experts' GEERS subscale scores were also higher than trainees. Cumulative distributions of both groups' GEERS scores were then plotted and the contrasting groups' method of standard setting was applied to determine a minimum path in GEERS scores of 20, as indicated by the vertical arrow. As expected, experts performed the procedure faster than trainees with a median time of 42 minutes and trainees performed the procedure with a median time of about 64 minutes. Experts were also faster with each of the individual sub-steps of the procedure. Inter-rater reliability was high for the three video reviewers, as demonstrated by the high inter-class correlation coefficients between each pair of reviewers. I'm going to show you this short video to illustrate the difference between expert and novice mesh manipulation and knot tying skills used in our model. To orient you, the expert is demonstrated on the left. As you will see, the expert finishes tying the knot prior to the trainee actually starting their knot. So current robotic virtual reality simulation technology offers the practice of many skills, but at this time we believe the knot tying skill is suboptimal in the virtual reality environment platform, and we believe our model might be able to help bridge this gap. So this second video demonstrates suturing of the mesh at the sacral promontory. You can see the difference in efficiency and dexterity between the two participants here. Again, the expert is on the left. Finally, feasibility was established with our model, as all subjects agreed or strongly agreed that the model closely approximated live robotic sacral copalpexy and the model would be useful for teaching and learning the procedure. 92% agreed or strongly agreed that the model would be useful in assessing the learner's ability to perform robotic sacral copalpexy before a live surgery. In conclusion, our robotic sacral copalpexy simulation model demonstrated construct validity with experts consistently scoring higher than trainees in the total GEERS score in each GEERS domain. Timing data supported this differentiation of surgical skill. There was high inter-rater reliability between all viewers of the procedural videos, and face validity was also established. Finally, we would like to make the following acknowledgments and welcome any questions you may have. Thank you. We'll take any questions. One question I had, Megan, fabulous model and study. Two questions, actually. One, is the model reusable? And two, completely unrelated, did you actually use it? We did. Those are both excellent questions and included in the manuscript. So most of the fellows, we had an even distribution between all years of training. Most of them had independently done about 5 to 20. And so there was quite a range about how much consult time they had. The model is reusable. I think it's important to note that the model is reusable. We have this published in our draft for the manuscript. The abdominal wall model that this has to fit in is a semi-cylindrical model that's different than the FLS box trainer. It costs about $600, but I think the price could be negotiated down with the company that makes that. And the pelvis is about $170. So with all the reusable parts, the total cost for the model is $170. So with all the reusable parts, the total cost for the model would be about $900 to $1,100. I was using a lot of reusable parts for our validation work, so we actually ran many, many people through, and we had things that tore. So the flexible things can be rotated and reused, and the quilt batting is a minimal cost. If you compare that to the cost of time in the operation room, it's nothing. Nothing at all. Your words impact me. Hi, Amanda from Hartford. Did you compare the fellows based on what year they were? Did you compare the fellows among each other? That's a good question. We did not do that. But that would be an interesting thing to look at. I mean, we have small numbers, but it is one of the larger validation studies, so maybe we could take a look at that. Thank you. I think that was great. Thank you very much. Thank you. Thank you. Thanks for the introduction. This is my disclosure. As we all know, synthetic permanent meshes are associated with lots of clinical complications in the long term, and it's mainly based on unmatched biomechanical properties between the mesh and also the native tissue, and inappropriate tissue integration, which results in fibrosis at the end. Based on these complications, actually, the European Committee suggested to focus on the mostly absorbable implants and regenerative approaches to treat pelvic organ prolapse. That's why, actually, we were working on fully resorbable implants in the last couple of years, and mainly P4HP, let's say. It already has an FDA clearance, and already in use for ligament repair and reconstructive surgery, as well. It's a quite good material because it doesn't cause any acidic environment when it degrades, and the in vivo degradation is more than 12 months. We were conducting cell experiments, and we showed that the mechanical properties is quite comparable with the native tissue, the stiffness, and also it supports the vaginal fibroblast attachment, proliferation, and collagen deposition. Based on these results, actually, we are currently conducting a couple of projects based on P4HP material, focusing the cellular interactions as well as immune response in both in vivo and in vitro conditions. And, actually, we already have a human study for stress urinary incontinence, which was presented on Wednesday. Today, I'm going to present some data on the short-term follow-up in large animal model. So, for this study, we implanted 14 sheep, both abdominally and vaginally, with P4HP material, and on the right side, you can see the type of the constructs that we used. It's in diamond shape, and we observed the biomechanics and host response after 60 days and 180 days. During the explantations, we didn't observe any adverse effects, and when we compared this data with the retrospective polypropylene data, actually, three of the sheep had some complications. In P4HP, with SEM images, we saw good tissue implant integration as well as good fibroblast interaction, and with the HNA stainings, we saw mild foreign body response, which was evidenced with the foreign body giant cells, as well as new vessel formation. And smooth muscle activity was there, and the collagen deposition as well as new vascularization was increased between 60 days and 180 days, and when we compared it with polypropylene data, the connective tissue vascularization and neuronal growth was higher in P4HP group. And when we checked the M2M1 ratio to assess the wound healing and tissue remodeling, we saw that between implantation—explantation times, M2M1 ratio was increased, and again, when we compared with restorative data, in P4HP group, this ratio was higher compared to native tissue and also restorative. And when we assessed the vaginal functionality with the contractility assay, between, again, the explantation points, we saw increasing vaginal functionality compared to polypropylene as well, but compared to polypropylene, actually, the difference was not that big. And also, we are using an incident dark field imaging to assess the microcirculation with a non-invasive technique, actually, and we still have to evaluate the data for vessel density and geoarchitecture. But we saw a high vessel density, which is an evidence for more oxygenation, and eventually it results in better functionality and wound healing. Here you can see the flow, and flow is also an indication of the functionality as well. And we checked the degradation of the material and also how this affects the biomechanics of the tissue, and we saw gradual degradation of the material, and after six months almost half of the material was degraded. And it's a combination of hydrolysis and surface aeration, and you can see it on the SEM images. And when we checked the biomechanical properties of the vaginal tissue, we can see that between explantation days, the stiffness of the tissue was increased, and in 180 days it was comparable with native tissue. And since we know the material is degraded, we can say that based on the tissue reorganization and remodeling, tissue was taking over the mechanical load from the implant, and it can support itself, let's say. So in conclusion, this short-term follow-up shows us the P4-HB implant supports vaginal reinforcement without adverse effects, and when it's compared to P4-HB restoral and native tissue, P4-HB favors more collagen deposition, vaginal functionality, and better wound healing. And based on these results, we can say maybe P4-HB can be a good candidate or an alternative to permanent meshes. Of course, we know that long-term follow-up is needed, that's why currently we are conducting a long-term follow-up to investigate the effects of P4-HB in the long-term, and to see how the tissue biomechanics will change after polydegradation of the implant. These are the collaborators. Thanks for listening. Thank you. Some questions from the floor? Thank you for the presentation. So I saw a part about the vagina functionality and contractility. Could you give a brief introduction about how you measure this? It was based on KCL application, actually. You are gradually adding KCL to the environment and to see how it affects the contractility of the vagina. Okay, thanks. I think that's a really interesting study, and I was very encouraged to see the neovascularization Can you comment on how you think that might help in an era when everyone is using lasers? Would you think that might also potentially help women with symptomatic atrophy as well? Yeah, actually, we have another study also focusing on atrophy in the sheep model, and we are using microcirculation as one of the main outcomes, because, yeah, actually, after also implantation or in an atrophy model, you can see eventually the vessel network is changing more like a network to the loop shape for better functionality. And we believe that it's a good model to study neovascularization. It's also non-laser, so it's quite practical as well. It's really interesting. I had one quick question as well. In terms of the neovascularization, what do you think the effect of age is on that, like the applicability to younger women versus postmenopausal women in the future? Yeah, actually, maybe my colleague who is more expert on microcirculation can answer that better, but I know that premenopausal or postmenopausal women have a different structure in the neovascular network. So, yeah. Thank you very much. Yeah. Our next speaker, please. Well, thank you so much for the opportunity to present our work this morning. We have no significant disclosures. Fecal incontinence or accidental bowel leakage, as most of us know, is uncontrollable leakage of liquid or solid stool that is a debilitating condition that disproportionately affects older women. So the numbers are something like 17 percent incidence rate in women 65 and over over four years. Typically, a conservative treatment approach is recommended for the initial management of FI, and this often includes diet modification. However, both providers and patients report that they have inadequate access to dietary advice regarding fecal incontinence. Thus, the goal of our project was to develop a diet modification intervention for older women with fecal incontinence, one that was culturally competent, age appropriate, and socially relevant, and we wanted to make sure it was something that would be accessible to providers who see older women with FI. The objective of my talk today is to describe the iterative process of creating this intervention. So this is sort of a schema. I'll go into each one of these, but we, in order to create the intervention, we did a lit review. We did focus groups. We got some expert input. And after creating the intervention, we got some patient input about the intervention. So first, we started with a pretty in-depth, systematic review of the published literature looking at the impact of diet on FI and what dietary modifications or interventions were out there. And basically what we found, and this is published in the Blue Journal, was that there's not a lot of information out there. There were a few things on what women do, what women think were associated with the FI symptoms, and a couple of studies looking at private supplementation, but basically there wasn't a lot of information. We also did a review of subject-specific websites. So these are academic and clinical centers that treat women with FI to see what kind of information to provide. Again, fewer than five websites, but mostly based on expertise, experience, and again, you know, it's like change your diet and modify your fiber, but not a lot of information. We also reviewed general nutrition guidelines for older women, so looking at national guidelines on nutrition, including something like My Place for Older Adults, which we actually got permission to include in our intervention. After the literature review, we conducted a focus group study, this is published in the Gold Journal, where we looked at women 65 and older with FI and we asked them about their diet and FI symptoms, what kind of strategies they used, and how they thought we could disseminate this information. So, you know, you can read the study in the Gold, but, you know, three focus groups, six to eight women in each group, and we got some good information. The big takeaway was that really the process of diet modification and changing your diet is a trial and error system. Women figured out different triggers and made changes. They gave us some strategies they used, which we then incorporated into the intervention we created. Along that, we created, set up an advisory group where we got representation from geriatricians, nutritionists, urogynes, gastroenterologists. We really wanted to make sure that whatever things we, the intervention we created would be compatible with, you know, national guidelines, that would conform to best practices, and we thought that, you know, we needed input from this group of people to make sure that the intervention was pragmatic. And then after creating the intervention, like I said previously, we got patient input. We did this in the form of a qualitative study where we conducted two rounds of cognitive interviews in women with FI and we, you know, making sure that the materials we developed were, they were able to comprehend the materials we developed, that they thought that this was feasible, and again, get their input on how we could disseminate this information. So, our results. The main message of our intervention and what we wanted to make sure women got out of this was three things. One, that it's really important to try to identify triggers and, you know, making sure women understand the association between FI and diet and the common trends. But really, again, making sure that women understand that this is an iterative and personal process. We talked about trigger elimination or even conscious indulgence where some women said, I know this is going to cause problems, but I want to be able to plan for it. And then mindful fiber intake. So those were sort of the messages we wanted to make sure they got out of the intervention. The intervention itself was, we created two booklets and then a diary where in the first booklet we talked about, you know, an overview of FI, ideology, information about demographic specific nutrition and strategies for managing FI. So, it's like a 20-page booklet, lots of information for women and different sort of like strategies they could try. The second booklet really talked about ways to increase dietary fiber. So, as we went through this process of creating the intervention, we got a lot of feedback on, oh, people tell me, eat more fiber. One, I don't know what that is. How do I do that? Give me practical ways to do this. And so, you know, this has an overview of dietary fiber, good versus bad sources. We have a sample meal plan in there. We really, you know, provided a sample grocery shopping list for these women, but really a lot of information that they can then make the advice we give them practical. And then the intervention includes the seven-day food and bowel diary. Again, it's a way for women to, you know, write down what they're eating and what symptoms they have and really be able to start to make this connection between diet and FI. So then, again, like I said, we created an intervention and the material and then we did the cognitive interviews to get women's feedback. These are our participants, a racially diverse group. Everyone above 65. I think our oldest lady was 87. And basically what we found was all the women found the material to be understandable. And again, the salient themes we got from the cognitive interviews that we then put into the revisions of the material were terminology preference. So things like, you know, use older rather than senior women or like, you know, making sure that the print and the material were more senior friendly, which we then incorporated recommendations from the NIA on how to do that. We asked women about feasibility. Mostly, you know, most women thought it was going to be feasible. Some participants shared reservations. Things like optimal journal length, how long do you want to keep a diary for, you know, what kind of hidden barriers. And so we made lists and we gave recommendations. And women said, you know, this is too costly. This is, the packing is bad. Listen, I'm by myself. I don't need to buy this amount of food. Things around us. So we got feedback like that. The sample grocery list came out of some of this feedback. And then we also included a guide on reading nutrition labels. I am almost done. We got some feedback on dissemination. Two seconds. Making sure we minimize visit burden. They really talked about widely disseminating this information, avoiding specialized testing. And then really importantly, we confirmed that in this demographic, printed material was the way they wanted the information provided. Strength of our study really, creation of all this stuff was rooted in behavioral theory. We used a qualitative approach with iterative analysis. We had a racially diverse population, which is really important when you think about diet because people eat different things. It's limited because this is all non-institutionalized women who have control of their diet. And so that's who this is made for. In conclusion, we created an intervention for older women with FI. Really using an ongoing involvement of stakeholders and trying to rigorously evaluate intervention as we went along, we are conducting studies currently on the feasibility and effectiveness of the diet intervention. I am grateful for funding from the NIA and my collaborators, and I can take questions. There will be shortly. Can you repeat your question? Oh, she just asked, are the booklets available? And I said yes. So one way is that I've conducted a pre-postpilot, and once we publish that, we'll make the booklets available. But yeah, that's the whole point. One of the, this is amazing. Like, so great. Thank you. So glad that you did this. And really, really a lot, so much intelligence in it. One of the big barriers for helping women with their nutrition that I see is that Medicare doesn't cover for nutritional counseling unless you're diabetic after, you know, so that cuts out that option for a lot of women. And the other thing is, in my geographic area, the nutritionists are really into this thing that came out of, I think it's New Zealand, the FODMAP elimination diet. And I'm just wondering if that was something you encountered, and if you find any utility to that. Love it. Great. So two questions and two things I'll comment on. So I think the first point was, you know, access to nutritionists, which is a really good point and came up early in this process when we talked to women. So, you know, one of the quotes from the focus group study was, listen, I see six, seven different doctors. I'm not adding a nutritionist to that list. And so it's really hard for women to then add this extra person with the co-pay, a lot of our older patients on fixed incomes. And so really part of this intervention is to make sure that it's something that's accessible to, you know, generalists. You know, primary care doctors, NPs, you know, your guys that can give this information out. So I do think that that's a barrier, sending patients to an actual nutritionist. The second point about FODMAP, I think that's just a paper that came out. I read the abstract a few days ago where they looked at FODMAP in women with FI and saw some improvement in symptoms. I don't know the full details, but I know that people are looking at that. I've heard that sort of from women qualitatively where women say, oh, when I change my diet and I adhere to a FODMAP diet, that does help my symptoms. So I think you're on to something there, absolutely. Thank you very much. Thank you. I'd like to introduce Roger Dzemierski, who's an invited speaker for the many state-of-the-art sections, and he's going to be talking about lower urinary tract symptoms, the under and over bladder storage. Thank you very much. It's a great pleasure to be here. I want to thank the Congress organizers for asking me. I hope you've enjoyed Nashville. It's a wonderful city and certainly has been growing up over the last two decades since I've been here. So my remit today is to speak about lower urinary tract symptoms and the under and over bladder storage, which is a relatively unique title, so I hope you don't mind the directions I've gone with this particular mini state-of-the-art. It's not working. These are my conflicts of interest. So I always like to start off lectures by a thought-provoking sort of concept, and I was searching a few weeks ago when I created this lecture for a pictograph of what pristine is. So we use the word pristine with something that's clean and clear and obviously lucid, and it's interesting how many of the images on Google about pristine involve some aspect of beautiful clear water and mountainscapes and whatnot. Certainly unfortunate that we use this term now with all the corruption of our oceans, which is very sad. But nonetheless, I'm using the term pristine, though, for some of the linguistics and the terminology that we use around lower urinary tract symptoms. And the problem with our terminology is that it is muddled, to say the least. And we use some terms that have relative specificity but without real integrity of the specificity, and I'll drive that home, I hope, in the next few minutes when we look at some of the terms. This is obviously a conflation of the entire over- and underactive realm, and we obviously are very symptom-bound when we create these sort of definitional terms, and obviously there are a set of symptoms that are uniquely attributed to one or the other side of the divide. As I hope you will see, though, in the next few minutes, perhaps the divide should not be as arbitrary as we've made it. Clearly with OAB, we have some concerns about the ravages of the symptom complex, including urinary tract infection, perineal breakdown, possible sepsis, when there's a very significant infection associated with it. With underactive bladder, our concerns obviously are related to storage failure and the potentiation of issues up to and inclusive of renal decompensation, which obviously is the one thing that we as public-court specialists want to do everything we can to prevent. There's a variety, though, of suppositions that have been made from a pathophysiologic basis related to the underpinnings, if you will, of what we discuss in these relative terminologic discussions, and that is, is this dichotomization of over- and underactive bladder fair? Obviously this is a bit of a dated article, but obviously my chancellor has done a lot of thinking about this, and obviously he sort of melds the over- and the underactive into the whole issue about, does aging have something to do with this? Is aging a major component of this? And I would put it to you that perhaps aging has a subtle variability to the presentation of this whole conflated complex of symptoms, but perhaps it's something a bit more that is often associated with aging, but as many will agree, vascular phenomena is not all about aging. This is some work that was published several years ago looking at the histopathology of the lamina propria and epithelium associated with ischemia. On the left is normal bladder, on the right is ischemic bladder, and as you can see, there's vascularization, loss of mucosal integrity, and significant fibrosis being laid down in the interstitium. This is sort of an acute one-hit model, if you will, of vascular inflow phenomena change. Carl Eric Anderson, who in my opinion remains one of the world's leaders in thinking about the underpinnings of the pathophysiology of over- and underactive bladder, has done a great job with Professor Yamaguchi and Nomiya looking at sort of the interrelationship of vascular dysfunction and atherosclerosis, which again often is associated with aging, but again in Western society can be independent of aging, dependent upon diet and obviously genetics. And this issue about acute versus chronic ischemia and the potential oxidative stress that basically underpin both conditions have this downflow, if you will, this cascade of injuries, re-hit injuries with vascular inflow, again acute obstruction, and then final chronic ischemic changes that actually can produce either complex under- or overactivity, depending upon the model, or the actual time frame with which we've captured the pathophysiologic cascade, if you will. And this is from a different paper, same author, Carl Eric again is one of the leads, looking at the effects of chronic bladder ischemia, oxidative stress, and the production of really either side of this dichotomized, pseudo-dichotomized hermenologic schema that we have been using for lower urinary tract symptoms in both genders. So let's focus for a minute, there have been several very good presentations during the past few days of overactive bladder, and I wanted to spend a few moments looking at whatever underactive bladder is. So we use two terms, again, relatively non-homogenous terms, but they're meant to be almost synonymous and they truly aren't. Underactive bladder, UAB, and detrusor underactivity, DU. And the various Venn diagrams here show the various possibilities of these conditions, that they are absolutely separate, that they overlap, also unlikely, and that there is some partial overlap, much as you see with underactivity and overactivity. So what is, and how do we define, how do we make better sense of these concepts of underactivity and underactive bladder? Well, do we want symptoms only? Do we want specific measures, inclusive of urodynamic measures? Or do we want to be able to characterize in a way that is pertinent to the patient? And obviously, as we come forward and try to struggle through the cascading, terminologic, divisive discussions regarding these conditions, we have to have the patient voice represented. So I do think quality of life is a significant component for these conditions. The one problem with detrusor underactivity, underactive bladder, is what do you do with the form FRUSP, where you have a patient who presents with silent urinary retention and has no prodrome for symptoms? It makes it very difficult to interpret these conditions based upon symptoms only. So this is the first sort of ICS consensus committee, and we've had now several of these sort of grappling with some of the words, the English linguistics of the terms. And obviously, these linguistics are pertinent to English, but may not be pertinent to some of the other romance languages and other languages. But obviously, the first sort of essay into this was a symptom complex characterized by prolonged urination time with or without a sensation of incomplete bladder emptying, usually with hesitancy, reduced sensation, unfilling, and a slow stream. So what should underactive bladder be? Well, it should ideally be a clinical condition where we look at both symptoms and objective measures in some balance. And again, when we have symptomatic silence, obviously we are then left with objective measures, postvoid residual ultrasound, detrusor contractility index, etc., etc. How do we measure and quantify these? Well, obviously, symptoms and measures should be rated in such a way that a score can indicate severity, and that should be generally accepted. And this really applies to all of our conditions. We are much further along with overactive bladder in some of these scores and metrics that we use, but I don't believe we've also scaled, we've reached the summit of Everest either with overactive bladder also. As we progress through these symptomatic definitions, a more advanced definition was lower urinary tract symptoms, and they're not disease-specific. The symptoms of hesitancy, strained void, and a slow stream can be characteristics of both outflow obstruction and detrusor underactivity. And the underactive bladder, again, is characterized by hesitancy, a feeling of incomplete emptying, bladder emptying, a reduced sensation of filling with or without leakage or nighttime frequency. So again, a focus on the patient's voice, the patient's symptoms where appropriate, but also remembering that detrusor underactivity as a germinal term actually has a very specific need for some other criteria to define it. So this was, again, the progression of the definition that I showed you initially, and notice now there are some post-void and voiding symptoms associated with the addition of post-micturition dribbling, et cetera, often with storage symptoms. Again, implying that although we would like these to be clean and clear-cut as a definitional difference, they're truly not. There is tremendous overlap, as you saw in one of the prior Venn diagrams. So the final decision, and the final current decision of the underactive bladder working group is that, again, you see symptoms that are suggestive of both voiding and storage symptomatology, which, again, is implicating that we really need to understand detrusor underactivity, detrusor overactivity as the true paradigm of a, if you will, of a progression and where two conditions can clearly coexist. So there are some corollary considerations when we look at these definitions. Again, there are a diverse set of pathophysiologies that can produce underactive bladder. I've really referenced and framed the reference on vasculogenic pathologies, but we know there's a variety of other pathologies that can instigate and cause lower urinary tract symptoms for underactive bladder. Additionally, patients perceive their storage symptoms in a variety of manners. Perhaps it's predominantly nocturia, perhaps it's predominantly daytime frequency, perhaps it's a bit of everything as in a Chinese food menu. So, again, the underlying mechanisms of storage disease are diverse and not only vasculogenic, obviously, but obviously we should keep in mind the metabolism of the individual that supports the lower urinary tract symptoms. Specifically in women, detrusors are obviously less caused by anatomical obstruction. It can occur, but it's relatively unusual as compared to the male gender. And so detrusor underactivity and functional causes of outlet obstruction are much more likely, such as dysfunctional voiding, and clearly our English colleagues have done a great job with this from some of the considerations of conditions such as Fowler syndrome and whatnot. The estimates of the prevalence of detrusor underactivity and, again, you see a bias potentially towards an older population, specifically the older frail population or let's just leave it at the frail population. And I think as we move forward, aging and age, the chronologic age of an individual is less important than the comorbidities and the other baggage, if you will, that that individual brings forward for the discussion and evaluation of their symptomatology. This is work that Chris Chappell did in his papers to underactivity, myogenic, afferent, and cerebral control. You can also have a very similar, if you will, algorithmic diagram for overactive bladder. Again, the importance of not being so, if you will, philosophic about making a speciation between the two. There is tremendous overlap even in the unique individual patient that we see. I would like to focus on some work that's been done by in my mind, one of the great minds that is looking at basic science models and clinical evolution, translational medicine, that being Phil Smith in Connecticut who's done a lot of work looking at underactive bladder and again, he has really focused on the afferent aspect of the, if you will, of the bladder functionality. And the afferent aspect is again something that we historically have not paid much attention to because we didn't understand it until really two decades ago the importance of afferent behavior. And again, afferent behavior, loss of volume sensitivity can be a primary urothelial dysfunction and I'm sure that exists but obviously look at the conditions that are commonly associated with that afferent dysfunction. Aging, diabetes, ischemia, again there's that vascogenic component. And then something that is one of my great areas of interest which is what happens with our autonomic nervous system and how does this part of the nervous system impact the bladder? Obviously very significantly. We, in my institution, have a large referral basis for POTS syndrome, postural orthostasis tachycardia syndrome, which has a high predominance in women especially middle-aged women. And in our experience virtually 100% of those patients have afferent behavioral aspects to their bladder function such that they either have detrusor over, under or usually a combination of both activity of their bladder. What can we do for this? Again, this is a summary again from Carl Eric looking at how we might modify the underactive bladder and modify the mechanisms that create this condition. Many of these mechanisms though obviously appertain to the overactive bladder as well and as we progress one of my great pleas is we are still at the point of, if you will, a post hoc management of these conditions. And I think much like cardiovascular disease, we should treat the bladder as a unique vascular environment and begin to think about condition prevention. And part of that is understanding the individual and their comorbidities such that we can best prevent these conditions from developing. Because it's fairly clear with what we have in hand right now and our understanding of the pathophysiology of the bladder, we don't have very good techniques for really reverting the patient back to their normal symptom prior to the onset of the condition of either under, over, or mixed activity. So some parting thoughts. We do have a common condition that we think we can recognize but we really can't define it well or quantitate it. There's often a contributory factor in emptying and it's very common in LUTs that there's really no condition or no, if you will, intervention that routinely allows us to help these patients except for urinary retention when obviously we are left with catheter management. What's the way forward? Do we need urodynamic criteria for all patients? Well, that's simply not doable in the current status and current assumptions of the healthcare delivery. We should have agreed upon indications for treatment. Part of that should again include the patient voice. We should also have agreed upon outcome parameters for success. Again, involving the patient's considerations. And again, a benefit-risk categorization of treatments is critical although, albeit that our universe of treatments is relatively limited. We have pharmacologic possibilities possibly with the chance for sensory activation in the future. Possible roles for reinnervation. Possible roles for stem cells. None of this yet. These are hoped for attributions but not definitive by any means. OAB is not underactive. However, the pathophysiologic pathways are common, at least in my reading of the evidence. Neither has particularly effective treatment paradigms associated with them. Patient dissatisfaction is high with both conditions but it's not continuous and certainly we are able to make positive impacts, at least on some individuals. And for both conditions, interestingly enough, the natural history is variable. So however, we should consider LUTs as not a single symptomatic entity. It really is a need to understand the contributing components of it. So differential segregation is ideal but not often easily possible, especially when we use only symptomatic criteria for that segregation. So therefore, I would stress that we need new algorithms driven by patient factors inclusive of their expectations. So a couple of last words. We use the word dichotomy and I've used it several times. So dichotomy implies essentially a separation of outcomes. Really, we are much closer to this, which is the yin and yang of the bladder. There is a building here that we must recognize especially as we move forward and hopefully complete that treatment for these individuals who are very bothered. I'll leave you with one last consideration. There's a wonderful word that we have adopted from Greek called chimera. It's obviously a Greek mythologic term. I would focus you on the second aspect of the definition, which is a thing that is avocationally hoped or wished for but in fact is illusory or impossible to achieve. So this is the an Athenian shield from circa 3rd century B.C. showing what a chimera is. It's usually a two-headed animal representing something that is illusory or impossible to achieve. I hope in my plea and I hope that the young people in the audience will help us with this because obviously my generation is not going to be able to do this but with the new techniques and new capabilities and the new frame of reference in terms of being able to incorporate patients in their treatment paradigms that this the ability to manage LUTs will not be a chimera, not being an illusory goal but actually a matter of fact. Obviously this may take a decade or two, more but we are well on our way. Thank you very much. Thank you. Applause Applause Applause

Lower urinary tract symptoms

LUTS

overactive bladder

OAB

underactive bladder

UAB

urgency

frequency

urge incontinence

hesitancy