Welcome to the Oggs Urogynecology webinar series. I am Dr. Taji Yazdani, Oggs Education Committee Chair and the moderator for today's webinar. Today's webinar is titled Diagnosis and Management of LUTs in MS, Parkinson's, and Spinal Cord Injury Patients. Our speaker today is Dr. Jahar Santiago-Lastra. Dr. Lastra is director of UC San Diego Health Women's Pelvic Medicine Center, which provides comprehensive and multidisciplinary care for a wide range of urogynecologic and pelvic floor dysfunctions. She specializes in diagnosing and treating a wide range of urogenital conditions in both men and women, including those caused by neurologic disorders. These include pelvic organ prolapse, urinary incontinence, voiding dysfunction, overactive bladder, neurogenic bladder, ureteral strictures, and post-prostatectomy incontinence, among other pelvic floor disorders. Her other areas of expertise includes procedures such as neuromodulation for overactive bladder, bladder augmentation, and urinary diversion. She also works with patients with congenital urologic malformations who are transitioning from pediatric to adult care. Outside of work, she enjoys traveling with her family and writing nonfiction. Dr. Santiago-Lastra is from San Juan, Puerto Rico, and speaks Spanish and French fluently. Just a couple of reminders. So before we begin, I'd like to review our housekeeping items. This presentation will be at 60 minutes. The first 45 minutes will consist of lecture, and the last 15 minutes of webinar will be dedicated to Q&A. Oggs designates this live activity for a maximum of one American Medical Association, AMA credits, so you get one credit. To claim your CME credit, you must log into the Oggs e-learning portal and complete the evaluation following the completion of the webinar. The webinar is being recorded and livestreamed, and the recording of the webinar will be made available in the Oggs e-learning portal. Please use the Q&A feature of the Zoom webinar to ask any of the speaker any questions you have. We will answer them at the end of the presentation, and use the chat feature if you have any technical issues, and Oggs staff member will be monitoring the chat and can assist. Dr. Santiago-Lastra, you may begin. Thank you. Thank you very much, Tarvi, for that wonderful introduction. I am really excited to talk to you guys today about this topic. A lot of times in urology, especially for those of us who so specialize in urogynecology and pelvic reconstructive surgery, neurogenic bladder becomes one of the areas of focus where we can be very useful to our colleagues. But first of all, I have no disclosures, but I do disclose that NLUTD, or neurogenic lower urinary tract dysfunction, can have profound effects on quality of life and long-term health for our patients, and it goes way beyond continence. There can be serious complications like infections, kidney damage, autonomic dysreflexia. Recognizing and addressing these issues early is very critical. So let's go over those. The objectives are listed here. And we'll go over them a little by little. So why is it important to worry about neurogenic lower urinary tract dysfunction? Initially, we called this neurogenic bladder, but because it goes way beyond the bladder to the bladder outlet, the pelvic floor, the upper tracts, lower urinary tract dysfunction is the broader term that's more appropriate. As a quick bullet point, you can see three of the main reasons why this is such an important issue to tackle. Firstly, because anything related to deterioration of the bladder or affecting the storage or emptying function of the bladder may result in upper tract deterioration, and we'll go over why. And I'll add a fun fact here, back before the advent of clean intermittent catheterization routinely for patients with high risk neurogenic bladder or patients, for example, with spinal cord injury, many of those patients would not survive past 10 years and renal failure was the largest cause of death. Now, the main cause of death tends to be either old age or pulmonary complications for the higher level spinal cord injury, and it is because the implementation of bladder management and specifically intermittent catheterization that we have seen survivorship increase so well. Symptoms, when not life-threatening, can also be really detrimental to quality of life, and there can also be other genitourinary complications, including recurrent infections, specifically cystitis, that can be quite bothersome. So we're going to go over now a little bit of a crash course into physiology. The bladder spends most of its time in storage where that urine needs to be stored at low pressure with a normal sensation and a closed outlet in order for the patients to have normal storage. And this is also how I like to teach urodynamics to my learners is to think about what should be normal in the storage phase so that you can then detect what is abnormal. And for a storage phase to be normal, those three things are very important. For the emptying phase, you want to have volitional control. You want to have a sphincter that relaxes first and completely, and then have a detrusor contraction of adequate duration and strength. And all of this requires the neural access to be intact. You need the both sympathetic and parasympathetic nervous system. You need the somatic nervous system to be intact. And then the structures involved, the CNS, the brain or cerebral cortex, the pons, and that will provide that voluntary control that we need and the synergy that we need to switch from storage to emptying. This here is a schematic of those parts involved and let's go over them little by little. So as the bladder begins to store, the bladder will fill with urine and there is a tonic contraction of the outlet or the sphincter. And then there is passive relaxation of the bladder. And it's really incredible how the bladder is able to fill with urine under relatively low pressure or sometimes even zero pressure in women. And that is mediated by sensory afferents that come up those spinal cord tracks and send information about the bladder stretching. You then have the pontine micturition center, which in the background, not under voluntary control, will send inhibitory signals down the spinal tracts and through the hypogastric nerve, send signals that mediate the relaxation or inhibition of bladder contraction. And that is mostly a sympathetically mediated phenomenon. At some point, the bladder is going to reach a critical volume in which those afferent signals send some excitatory signals to the periaqueductal gray, which then starts to create that cortical control and awareness of the bladder being full. And once the cortex is informed that the bladder is full at some point, we will decide volitionally that it is time to empty our bladder. That will send an excitatory signal down to the pons, which then shuts off its inhibition of the bladder and the outlet. At that point, the sphincter will relax and the bladder will contract and we will empty. And then the whole process starts again. It's a very sophisticated process and we can see how any injury in any of these levels is potentially going to produce a different type of symptom. And we will go over that a little later in the schematic. So initially when we see patients, even when we know bladder physiology and neural physiology down thick and can recite it from memory, patients will present to us with a whole variety of symptoms. I always tell patients, well, you know, patients don't read the textbook, so they will present in many different ways. There is a guideline-based way to evaluate the patients in order to assess what type of risk they have of having those devastating complications that we described in the first slide. And as usual with any evaluation, a good history, an exam, some labs, and then an evaluation of the upper and the lower tracks is going to be very useful. So here are some highlights, and I included here in green, you'll see those interspersed around the talk, some pearls that come through from the guidelines. And so we want to know what the duration of the neurologic injury has been or what the diagnosis is and any associated urinary symptoms. There are many times where I am unable to tell the patient whether their urinary symptoms are arising from the neurologic injury itself or simply present because they're post-menopausal or because they're postpartum or they've had babies, and that's sort of the natural history of their birth injury, et cetera. So it's important to get a sense of the timeline of those urinary symptoms, and then also get a sense of how they're managing their bladder in the current moment and whether they're satisfied with that method of management because sometimes that method is not totally acceptable to us or not ideal, but if the patients are not symptomatic from it, it can sometimes be a little bit difficult to get them to change it. And there are some other things, especially bowel function that we really want to assess as well. I always tell patients that the bowels and the bladder are like two wings on the same bird, and then there's some higher risk things like autonomic dysreflexia that can affect certain patients with NLUTD that we want to be aware of as well. One guideline pearl is that at the initial evaluation, we need to identify whether patients are low risk, unknown risk, or high risk for stratification. And we'll go into a little bit more what that means because stratifying into those risk categories is gonna determine how we manage the patients in surveillance. Let's get into autonomic dysreflexia a little bit because it is a very important part of the initial evaluation of a patient with neurogenic lower urinary tract dysfunction that we really need to know because if we plan on ordering any studies for the patient or on evaluating the patient thoroughly, this can be something that we'll encounter. You want to think about autonomic dysreflexia when you have a patient with a spinal lesion that is at the level of the T6 level or above. And what happens with autonomic dysreflexia? It's a trigger of sympathetic reflex, reflex vasoconstriction that comes from having received a noxious injury. So something painful or irritating happens before the spinal cord injury, like a full bladder or constipation, tight clothing, sexual intercourse. And then that signal, that noxious signal travels up the spinal cord injury, but because there is, up the spinal cord, but because there is an injury, that signal is blocked from reaching the brain. So what happens is that the nerves below the injury overreact and send signals that cause vasoconstriction, which causes a sudden spike in blood pressure. The brain detects that there's been this sudden rise in blood pressure and it tries to fix it. It tries to slow the heart rate and cause vasodilation so that patients look really flushed in the face. They get reflexive bradycardia, but the blood pressure is not controlled because there's actually no communication past the level of the injury. And that bradycardia with elevated blood pressure can actually be quite life threatening. And it's important to recognize not just that it's happening, but that it can happen because it can be deadly. And what is the guideline pearl for this? If you have a patient that's T6 injury or higher, consider autonomic dysreflexia as being a risk factor for any evaluation or procedure that you might do. You want to make sure you have bladder drainage if you're performing a study. And if the cycling of the blood pressure during that evaluation shows that there's persistently elevated blood pressure, you want to institute pharmacologic management, which typically in our clinic involves the addition of nitro paste. You can also use morphine. Some others use other treatment options like nifedipine, but I really do recommend nitro paste. And you want to escalate this care quickly because the unopposed rise in blood pressure can lead to stroke or seizure, even death if not treated quickly enough. So that's really important about autonomic dysreflexia. For urologists seeking board certification, that is always a common question that will be asked. Then we go to the examination phase. And this is where it can get a bit overwhelming for people who are evaluating patients with neurogenic lower urinary tract dysfunction because there can always be some additional factors to consider. The skin breakdown, the body habitus may be different. These can often be patients that are wheelchair bound, have difficulty transferring. And so it can even be difficult for them to engage in an exam sometimes. So what I try to impart often when we're evaluating these patients is to really think about it in the basics that you know. Your abilities as a pelvic floor specialist, as a urogynecologist and reconstructive surgeon are all the tools that you need to recognize what is happening with your patients and how to assist them. So with regards to ASIA score, typically if it's a spinal cord injury patients, they'll come with that injury categorization and it has to do with the motor and sensory function. You do not need to get an ASIA score when you evaluate the patient. It's just important to recognize that there are sensory and motor deficits associated with that injury that you should know. Mobility is gonna be a huge factor for patient's urinary function. Obviously a lack of mobility can lead to a functional incontinence if patients have an urgency to urinate. And for example, just can't make it to the toilet in time and end up voiding in a diaper because they just can't make it to a commode or can't sit in a commode. The skin breakdown associated, all of these things can be easily evaluated just from having the patient present and they're at the pelvic examination table, sometimes even just putting them in throgleg or just examining them in the stretcher where they are. And those are valuable clues that you can use to inform your categorization of the patient. And so as you're evaluating a patient, you have to start thinking, why are some NLUTD conditions higher risk than others? And what the basic issue is, is whenever you have a lesion that disrupts transmission between the pontine mcturition center and the sacral spinal cord, you're going to have a higher risk injury. So that's going to include your spinal cord injury patients, your MS patients with a high volume of spinal lesions, your spina bifida patients, for example, your patients who have had a spinal stroke. Those are automatically because of the type of injury that they have going to be a high risk NLUTD patient. But that is not the only type of patient that will be an NLUTD patient. This I highlight here. So the patients that lose the disrupted control from their pontine mcturition center by definition are going to have a high risk spinal cord injury. And why is that? The pontine mcturition center, as we discussed quickly previously, are going to be patients that as their bladder fills, you do not have that inhibitory signal from the pons trying to maximize the viscoelastic properties of the bladder so that the bladder relaxes and continues to store urine at a low pressure while it fills. And so over time, the lack of that inhibitory signal and the associated issues with the outlet as well are going to lead to some changes within the lining of the bladder and within the tracer itself that will cause trabeculation. Diverticula, increased storage pressures and overall impaired bladder compliance. So that's where the high risk category for those lesions is coming from. But establishing that level of risk is going to be incredibly important for most patients with neurogenic lower urinary tract dysfunction. And that's why one of the important guideline mediated recommendations for patients when you first assess them, particularly if they have neurogenic lower urinary tract dysfunction is to get a post-void residual urine volume. So if a patient comes in to see you and they have normal stable renal function, they have a low residual urine volume and they have stable urinary tract imaging and synergistic voiding, meaning that PONS synergy mediation is intact, that is going to constitute a low-risk patient. Any patient that does not have those categories is going to be categorized as a moderate risk. And then higher risk patients are going to have renal function abnormalities already. They may have scarring, hydronephrosis, poorly compliant bladder on neurodynamics, et cetera. And we're going to go over how to strategize with this and how to evaluate those lower and upper tracts little by little on these slides. So let's first go into our lower genitourinary tract evaluation. So remember in that first visit, when you see the patient, you're getting a history of their symptoms, of their bowel bladder management, their mobility, what's troubling them, how are they managing, what was the injury? And then you're going to get an examination and you're going to get that post-void residual urine volume. And that constitutes a part of that initial evaluation. You'll notice here in bold that really the only thing that you have to do in that initial visit is something that you're probably already doing for your pelvic floor patients to begin with. And it's to get a post-void residual urine volume and get a urinalysis. That's going to give you the first inkling of risk on these patients. So you'll get a PVR and you'll get a urinalysis. There are a bunch of other things that you may want to do when the patients first present, particularly if you know that they're already high risk. Like I mentioned, if they have a spinal lesion, that's going to be a patient that's high risk that you're going to want to evaluate further. Like those recommendations stratified them. But if it's a patient, for example, has Parkinson's disease or multiple sclerosis where you're just not sure what risk category they are, post-void residual urinalysis is really what you need to think about. Here, I'm showing you an example of a patient who obtained one of those additional studies. This patient got avoiding cystourethrogram. And I wanted to make a comment about the VCUG because we think of VCUGs a lot in pediatric urology, but all of us who do video or fluoroscopic urodynamics are doing VCUGs during those studies. And so you can see here, this patient, a female patient has several abnormalities of their VCUG that are worth noting that constitute this high risk category. Firstly, look at their bladder shape, multiple diverticula and sort of a cone shaped bladder instead of it being a smooth walled bladder. They have a catheter here, you can see the balloon, but you can also see that as the bladder fills, you have this massive vesicle ureteral reflux on the left and massive vesicle ureteral reflux on the right. And that's why video urodynamics is so important for the patients you suspect could have a high risk neurologic injury, because if you just get conventional urodynamics without the fluoroscopy or without the video component, you may be actually imaging and seeing that the storage pressures perhaps look normal, but it's because the patient has developed what we call a pop-off valve, which has allowed the reflux and dissemination of that storage pressure up to the upper tract. That's one of the long-term sequelae and complications of that poor compliance that we discussed earlier. And the video component of that study allows you to see that reflux and make adjustments to your assessment, knowing that, hey, we got a pretty normal compliance measurement on this urodynamics, but she has massive reflux on either side. So that probably is a pop-off valve. So that bladder is probably poorly compliant. And you can deduce that from your finding. These are some additional imaging studies that we might order for patients that help us further re-stratify them. Typically, urologists are the ones that are ordering these by far, but it's really important to have a good knowledge of these because they can be really useful tools, especially if you are in a lower resource setting. So a renal ultrasound and a KUB are my go-tos. A renal ultrasound will tell me if there's hydronephrosis, and it'll also show me the cortex of that kidney. And that helps you to determine whether this is an acute injury or whether it's a longer term dilation that's resulted in scarring or loss of cortical renal function. A KUB is excellent because it also gives you a measure of stool burden. And I even will sometimes get it for able-bodied women who have severe constipation, just to see if their regimen is actually working for them. Cross-sectional imaging like a CT will be indicated if patients have microscopic or gross hematuria. And then there are a lot of different ways to assess renal function, including the most accurate, which is the 24-hour creatinine clearance. A nuclear renal scan, it helps assess kidneys for obstruction. The serum creatinine tends to be unreliable, particularly with patients who have muscle wasting. And then one expensive, but very useful test is a cystatin C. So just to summarize that piece of the evaluation, you complete all of those assessments. Let's say you get your exam, you get your post-void residual urine, you get your urinalysis, and you're like, okay, there's elevated PBR. There is an abnormal urinalysis. I will get an ultrasound. The ultrasound looks abnormal. I will assess the bladder storage with a urodynamics. What is the surveillance schedule for this patient? How do you need to follow these patients up? So the patients with moderate risk neurogenic bladder should be assessed with an annual history and symptom assessment, an annual test of renal function, and upper tract imaging every one to two years. Notice how the guidelines do not include urodynamics. However, if they have high risk neurogenic bladder, then the assessment changes to yearly imaging, and then the urodynamic study, which may be repeated if clinically indicated. So let's go into a little bit of the urodynamic because it does have a rationale for its implementation, and it's a great baseline functional assessment for lower urinary tract function. I will say that the guidelines, both the AUASUFU guideline and the European Association of Urology Guidelines have gone away from recommending routine urodynamic evaluation for any patient with neurogenic lower urinary tract dysfunction because of the risk categories that have now been implemented. And why is that? To utilize our resources wisely. A patient who has post-stroke urinary incontinence, for example, and we'll go over later how those patients will classically have normal bladder emptying and storage, but will have a lot of detrusor overactivity. Those patients don't need to have a urodynamic study necessarily if their PVR is normal and their urinalysis is normal, and they have no hydronephrosis on their urinary tract evaluation if it's obtained. So not every patient who comes in through the door with neurogenic bladder necessarily needs to have urodynamics. But it does provide a really great objective assessment of the lower urinary tract, and it might help you identify patients who need an earlier intervention, like patients who have high storage pressure or poor bladder compliance or patients with dyssynergia. And notice, again, those two urodynamic findings that I noticed, again, have to do with that disruption of the connection between the pontine mcturition center and the sacral nerves and the control of storage versus emptying function. So how do we actually define what's happening with their bladder when we get the urodynamic study, and how do we translate that into what we know about each disease state, and how do we treat it? So I really love the schematic that was popularized back in like the 90s, 2000s about dividing the bladder symptoms into like failure to store and failure to empty and dividing that between the bladder and its outlet. So you can see here failure to store. We see it for the bladder, known as neurogenic detrusor overactivity as an example, or impaired compliance as another example. And you can have outlet failure to store as in intrinsic sphincter deficiency, and I gave you some examples there. We're gonna go over this in a little more depth shortly. But then you have failure to empty. You can have an areflexic detrusor, now called detrusor underactivity, or detrusor hypocontractility, and that can happen in multiple sclerosis, rarely in stroke, happens a lot in peripheral nerve injuries, and in spinal cord injury, especially in the early period of spinal shock. You can also have a failure to empty of the outlet, and one very common and high-risk one is detrusor sphincter dyssynergia, or sphincter bradykinesia, which happens in Parkinson's. And we're gonna go over those common urodynamic patterns found in patients with neurogenic lower urinary tract dysfunction. So typically, we may see any of these abnormalities, and I highlighted the hostile storage again, because I wanna hammer home what some typical findings could be, and what some really concerning high-risk findings might be, which is the loss of bladder compliance and a high detrusor leak point pressure, and we'll go over that in depth. Let's start with detrusor areflexia. So I brought you some colored-in urodynamic tracings, because it's hard to see the lines on a webinar format. So let's first go with detrusor areflexia, or a contractile detrusor, as in the parlance of modern times. So this can include detrusor underactivity, or hypocontractility, as it was called previously, and then impaired contractility as well. This is diminished detrusor contraction. And so you can see here, our vesicle pressure in this tracing is pretty flat, as is the abdominal pressure and the detrusor pressure. So you can see, as the bladder starts to fill, look at the fill volume on this patient. It's 738. So many times, patients with these flaccid bladders or a contractile detrusors have some storage issues as well. They have diminished sensation, which allows their bladder to fill to these supraphysiologic volumes and don't have a sensation of needing to empty at all. So one very helpful thing is to follow these patients with a detrusor leak point pressure. What that means is filling the patient to what would be considered a normal storage, like 480 mLs, and to see whether there is incontinence associated with that filling in the absence of a detrusor contraction. That's a detrusor leak point pressure, and it is a secondary finding of impaired compliance if that detrusor pressure is greater than 40 centimeters of water. That's a really commonly tested question, perhaps not in URPS boards, but it is very commonly asked of urologists. And so these patients who have chronic detrusor areoflexia may not need consistent urodynamic studies if their bladder symptoms don't change, but an upper tract evaluation is going to be necessary every one to two years based on those risk categories we discussed previously just to make sure that the upper tracts are safe. And it's not just about hydronephrosis, but urinary stasis, which is very common in a contractile detrusor because it doesn't empty, can lead to bladder and or kidney stones. So that tends to be what does them in, gets them back to the urologist offices and stones. So now let's talk about bladder compliance. So a little different than the tracing we saw previously, right? Because before we just saw pretty flat lines, and here we see a rising vesicle pressure. Always try to look at your vesicle pressure first, but here we can see the vesicle pressure is very different from the abdominal pressure. We can see that rising detrusor pressure here. And look at the video component of this bladder. You can see a lot of diverticula, really abnormal bladder shape, and almost like a cone shape to the outlet. So this is a classic finding of impaired bladder compliance, and this is incredibly common in patients who have any sort of neurogenic injury. And it can also be common in patients with devastated bladders. So again, we talked about the detrusor leak point pressure and how it is a secondary marker for impaired compliance. And now we can see here in this bladder, it's hard to see on this screen, but you can see the bladder here, you can see reflux here, and then the impaired compliance. This patient still had an abnormal compliance tracing, but often if the patients have severe reflux, you could even see this as being pretty flat and you see massive reflux off top. I've even seen a patient that had such massive upper tracts that they were able to insert a Foley all the way up into the ureter and drain the upper tract, which is insane to me. So here is another example of pathology that you might find when you evaluate your neurogenic bladder patients, and it's detrusor overactivity. If you think patients with OAB have bad DO, wait till you see it in a neurogenic bladder patient. There are all different types of detrusor overactivity. There's phasic DO, which is very commonly seen as involuntary. It has a characteristic waveform and it may or may not lead to incontinence, but you see it very clearly on the urodynamic tracing. Terminal DO is when patients cannot volitionally empty their bladder completely, but they reach a certain critical bladder capacity and it can be different for each patient. And then the bladder has a very high amplitude contraction resulting in them almost completely emptying their bladder at capacity. So that's why it's called terminal DO. When you have a patient with terminal DO on your urodynamic study, it can be really hard to give them permission to void because they just kind of empty when they have that big DO contraction. So that compels you to perhaps fill them very slowly, just let them empty whenever they're going to empty. And the goal there is to make sure that they can actually empty their bladder completely. And it can be very difficult to restore continence for patients who have this. There's a detrusor overactivity incontinence, and then neurogenic detrusor overactivity, which could be a classification for any one of these if it's associated with a relevant neurological condition. And then another one, which is detrusor overactivity with impaired contractility is going to be very difficult to treat in patients with neurogenic bladder because it could mean that they have both storage and emptying symptoms. And a lot of those patients do have to be canceled about intermittent catheterization. This is a classic one. It's usually the one that first comes to mind when you ask clinicians what the most common urodynamic finding is for patients with neurogenic lower urinary tract dysfunction. But that's actually not the case. Detrusor sphincter dyssynergia is only encountered in neurologic injuries above the level of the sacrum. So it's defined as an involuntary contraction of the sphincter during an involuntary detrusor contraction. And again, it typically occurs with super sacral lesions, very testable item, and it's uncommon with lower cord lesions. And this can result in elevated intravesical pressures and neurological complications because of the high storage and voiding pressures encountered with this phenomenon. And you can see here that when the bladder contracts, there's a characteristic increase in the EMG. You can also see this patient not only has detrusor sphincter dyssynergia, but they also have impaired bladder compliance. And this is a very classic shape of a bladder with DSD. You can see the spinning top appearance of the bladder outlet and bladder neck. And then you can see the cone-shaped detrusor itself. So again, we talked about what types of pathology patients have and how does it correlate with the lower urinary tract. And this is a great guide to sort of make that determination, but it doesn't necessarily mean that patients are gonna manifest this every single time you evaluate them. But you can see that for the cortical lesions, where really what you've lost is that excitatory control over the pons that gets it to initiate the switch from storage to emptying. When you don't have that, the pons is just on autopilot, and that results in detrusor overactivity of varying levels. When the lesion is at the level of the spinal cord, then you can see you can have detrusor overactivity because you lose that input from above, but you also lose the synergy that the pons brings to the table. And these are the lesions where you have the detrusor-sphincter dyssynergia. And then as you get lower into the cauda equina and the pelvic plexus, the peripheral nerves, you start to have the acontractile detrusor, the impaired contractility, and you may even see some sphincteric dysfunction as well. So now let's focus. Now we showed the urodynamic findings and what they can show. Now let's focus on each of the individual diseases and what we see in each of those so we learn it back and forth, right? So we can have Parkinson's disease, these patients, one important pearl for these patients is the pseudodyssynergia that they can experience, which is often misdiagnosed as detrusor sphincter dyssynergia. But the reason that Parkinson's disease patients have a urodynamic tracing like the one I'm showing here where you can see the detrusors contracting and then you have increase in the EMG and not the relaxation is due to bradykinesia. And that's a movement disorder problem, which is impairing the relaxation of the urinary sphincter and causing hesitancy. This is really important because as you can see here, many women with Parkinson's disease will experience detrusor overactivity, but you wanna make sure that you remember that they may also experience some of this bradykinesia and you want to counsel them on timed voiding, double voiding so that you can ensure that even with treatments for bladder storage, that they still get a good opportunity to empty their bladder fully or to participate in intermittent catheterization if necessary. Traumatic spinal cord injury very similarly has some pearls to remember. The big one for spinal cord injury is to remember that when they have initially suffered their injury, they may be in a period of spinal shock. And at that point, they may have a completely a contractile detrusor and then they will, after about six months, start to recover some of their, what will be their baseline or stable phase of the injury. And the level of the injury may correlate with their expected function, but you can see here, there's all across the board, different symptoms. As you go up the level of the spinal cord, you can see more sphincter dyssynergia. And then as you go more towards the lumbar and the sacral level, you start to see more a contractile detrusor. Multiple sclerosis is a really common one. And I feel like we are in an era of improved treatments for multiple sclerosis. So we are now seeing, for example, there's a clinical trial that's currently underway through the SUFU collaborative network where patients are being recruited to receive sacral nerve stimulation early on with their MS because MS treatments of this demyelinating condition have improved so much that it is possible that they may stand to benefit more from these typically overactive bladder treatments than they did in the past. But this is, again, really affects women at the peak of their urogynecological years or childbearing years. It's more common in females, and a lot of them will have overactive bladder-like symptoms with urgency, frequency, urge incontinence, et cetera. Diabetic cystopathy I include here because it is a very commonly overlooked type of neurogenic lower urinary tract dysfunction. Many of these patients will start to present classically after about 10 years. They can experience sensory impairments, reduced contractility. If you see here in women with diabetes, 44% are going to have some type of diabetic cystopathy. And add to this an observation is that a lot of these women get started on medications that give them glucocerea, and that actually elevates their urinary symptoms and can also elevate their UTI symptoms. So it is something we see very commonly in clinic and have to do a lot of education and teaching to make them understand that not just the patients, but also providers of medicine understand that this is a very common cause of neurogenic lower urinary tract dysfunction and can result in both storage and emptying issues. And then finally, the last one I wanted to focus on, and again, there are many, many to discuss is the pelvic plexus injury, which can occur with any major pelvic surgery. Pelvic surgery, you see here, APRs, radical hysterectomy is super relevant to the gynecologist, pelvic fractures, tumors, et cetera. What this may be is a neuropraxia, which means that there is the possibility that there may be recovery from these symptoms, but often several branches of these three nerves are affected. And even though improvement may be expected in many cases, in many ways, patients may experience in very commonly an acontractile or underactive ladder that has to be managed with treatment ranging from times voiding to even intermittent catheterization and sometimes a sacral nerve stimulation in the right patient. So developing a treatment plan with all of these types of patients requires shared decision-making. These are the goals that I think of when I'm trying to develop a plan on how to manage their lower urinary tract. We want to improve compliance of the bladder. We want to improve emptying because we want to reduce the mortality risk that comes with the upper tract deterioration in those higher risk patients. We also want to control or alleviate their symptoms. You want to meet them halfway because they have an agenda. Your agenda is to protect their kidneys. That may not be on their agenda. And then the other part is that the treatment may often be dictated by the UDS findings rather than symptoms. And this is really common, particularly in patients with spinal cord injury. So let's end here. We have a few more patient scenarios, slides about different treatment options and going over them, but we're at 447-ish. So let's look at the five important principles that I want you to take away when you see these patients and it's preserving their renal function, making sure that if they either have good renal function or you're managing their bladder in a way that protects their renal function, that their bladder is safe, meaning that those bolded items I mentioned before, the sphincter dyssynergia, elevated residual urine volume, impaired compliance are assessed for in your evaluation that you're thinking about the potential for that when you stratify them. Thinking about how to manage their contents because socially it is so important. Optimizing their quality of life and then meeting them halfway on their perspective and what their goals are. Let's pause there and see sort of what questions we have and then we can do some scenarios if we have time. Wonderful, thank you so much for that. And we do have one question. So if a patient has coordinated EMG activity during filling but is not coordinating during a pressure flow or voiding, is that DSD? It could be. So we may need to qualify that question. So I'm assuming if you are thinking whether they have coordination when storing, when you do maneuvers. So you're asking them to cough and they're doing cough stress testing or Valsalva and you're seeing an uptick in the abdominal and vesicle pressures along with coordinated EMG activity. That is actually a measure of what's called ONIF's nucleus and the guarding reflex. That is different from the coordination that comes between storage and emptying. So they may have an intact guarding reflex but actually be discoordinated in their storage and voiding because they don't have the input, higher up input from the ponds to mediate that switch from storage to emptying. So they're not able to generate a coordinated voiding response, but when you do maneuvers, they have an intact guarding reflex. Hopefully that answered your question. And when deciding between video urodynamics and regular urodynamics, what do you use? How do you decide which one to use for which? Yeah. So I think that for a patient where you are performing the urodynamic evaluation because you've determined that it is possible because either they have a level of injury that makes it very likely that they're high risk or they have several findings already that suggest to you that there is a high risk neurogenic bladder. Let's say you see a patient in clinic, they've had bladder exstrophy or Parkinson's disease or MS, for example, and they have an ultrasound already with them that shows that they have hydronephrosis. Then that's somebody that you're like, okay, what is this hydronephrosis coming from? You have to rule out that it's from a bladder issue. And if you add the video component to that study, it will allow you to assess for potential reflux and it will also allow you to assess bladder shape. You will still get a compliance tracing from a conventional multichannel urodynamics, but you could miss reflux and you could also miss normal tracing for compliance that actually has severe vesicle ureteral reflux. But in a patient that you've already determined is unlikely to be in that high, high risk category, getting conventional urodynamics, if it will help you just determine detrusor function so the patient can undergo a Botox injection, for example, you don't need to get a video for that if it's not available. And I practice in clinics where we don't necessarily have the video component and you can just get a VCUG and radiology and correlate it that way as well. It doesn't have to be a video at the time of the urodynamics to make those conjectures. Okay, thank you. So we might have time for one of your cases. We have like maybe about five minutes. So I don't see any- Okay, let's do an easy one. Let's do an easy one so we can talk about. So we were talking about MS. So we have this 45 year old woman. She has a 10 year history of MS and she presents to her clinic with urgency, incontinence, difficulty emptying her bladder per her report. You were very diligent. You followed the guidelines and you obtained a post-void residual measurement in the office and it's 250. Otherwise she doesn't have hematuria. She doesn't have flank pain or fever. Because she had that elevated residual urine volume and she's had this longstanding history of MS and she's tried previous treatments and failed. And based on that initial figure that I showed you, some of those criteria put her in that unclear or moderate risk category. You decide to get urodynamic studies. And so those urodynamic studies demonstrated detrusor overactivity with impaired contractility, a detrusor pressure of 15 centimeters of water during voiding, which is like moderate for obstruction and an MCC of 280, which is slightly diminished. So what is the most appropriate next step in managing this patient's urinary dysfunction? Should we offer sacral nerve stimulation because it's not gonna affect her emptying? Should we recommend antibiotics for UTIs? Should we talk about initiating clean intermittent catheterization or should we continue anticholinergics and monitor? As sad as it makes me, this is the time to make this converse, to give this conversation. And I'll tell you some little clues that I put in the scenario that may not have come initially to mind. And this only comes with seeing a lot of neurogenic bladder patients. So this isn't beyond the scope of this talk. But this patient is 10 years with MS. Most of the time patients who have MS towards as they get to the 10 year mark, many will progress with their symptoms and progress with their bladder despite all of those wonderful treatments I told you are available these days. And because of that and her borderline residual urine volume of 250 and the impaired contractility that we saw on the urodynamics, we want to help her initiate clean intermittent catheterization. It is very difficult for some women, especially if they're in a wheelchair to empty their bladder and catheterize. So starting that education early, even if you plan on enrolling her in the trial of sacral nerve stimulation, which is not FDA approved for MS just yet, but enrolling her in a trial for her symptoms or recommending Botox and still allowing self-alloyed with a residual urine volume, she is a candidate to learn intermittent catheterization based on the guidelines. And I think we will, should we wrap it up there? Do we have time for another question? I think we have a couple minutes. Yeah, I think we have a couple minutes. All right, let's see. So which of the following statements aligns with the AUA recommendations regarding management of urinary dysfunction in neurogenic bladder? Is it A, that urodynamic studies are required in all patients with neurogenic lower urinary tract dysfunction? Or B, that anti-muscarinic or beta agonist therapy is first line for patients with storage dysfunction due to neurogenic detrusor overactivity? Is it C, intravesical Botox is contraindicated in patients with neurogenic bladder? Or D, patients with neurogenic lower urinary tract dysfunction should undergo annual upper tract imaging. So we talked about the guidelines have steered away from recommending urodynamic studies to all comers so we can eliminate that. Despite everything we talked about the different types of conditions or the fact that your whole armamentarium of pelvic floor treatments should be considered for these patients and case by case, you can determine the safety and feasibility of those treatments. Are we still relying on medications as first line just like we do for our IRPS patients? C, intravesical Botox is contraindicated. That's clearly untrue. And then patients with neurogenic lower urinary tract dysfunction should undergo annual tract imaging. We talked about risk stratifying them. If they risk stratify to a higher risk, then absolutely yes. If they don't, then they don't need to undergo annual imaging. And the answer is anti-muscarinic or beta-agonist therapy is first line for patients with storage dysfunction due to neurogenic detrusor overactivity, highlighting that for a lot of these patients, a lot of the treatments that are included within our OAB guidelines, for example, are considered feasible treatments for these patients as well. The only difference is that we want to consider clean and unwritten catheterization much more thoughtfully and early for these patients, especially when their residual urine volumes are elevated because they will have a higher risk of incomplete emptying. All right. I think that is probably my last one. Well, we have like a minute left and there's one last question. So we'll end on this. Oh, awesome. Do you- Yay. Thank you for everything. Do you counsel your MS patients on Botox versus sacro-neural modulation in the same way as your non-MS patients? I tell them about the data supporting Botox versus sacro-nerve stimulation, the same as I do for my idiopathic overactive bladder patients, except that I will mention that when it comes to patients with a neurologic injury, there is clear FDA approval for Botox, whereas there have been trials that show that sacro-nerve stimulation is not as effective in patients with neurogenic lower urinary tract dysfunction as it is for patients with idiopathic OAB. And then I'll introduce the conversation on the trial that we're having for sacro-nerve stimulation in MS. And prior to that trial being available, I would tell patients that anecdotally in my practice, I have tried sacro-nerve stimulation in MS patients who do not have progressive MS, who actually have relapsing remitting MS and have flares, but then go back to a pretty normal baseline and who have a normal residual urine volume, not because sacro-nerve stimulation would change that, but because I think they usually stand to benefit the most from the treatment. And obviously they need to have the functionality to be able to manage the device and the operative risk stratification, all of those things. But I do implement it in my practice more frequently. Now, if the patient is having to intermittently catheterize and they do have progressive MS, that's higher risk. I'll typically counsel them that it is unlikely to be successful and usually steer towards Botox, especially if on the urodynamics, they have changes in their bladder shape, diverticula, and that distressor sphincter dyssynergia. I think those patients do much better with Botox for their DO. Well, on behalf of AUGS, I'd like to thank our faculty, Dr. Santiago-Lastra, for her webinar. Be sure to register for upcoming AUGS education webinar on April 9th with Dr. Leyshan Kuros. And she is presenting, her talk is titled, Anal Sphincter Injury, Diagnosis and Implications for Future Pregnancy. Follow AUGS on Twitter and Instagram and check our website for information on all upcoming webinars. Thank you and have a great evening, everyone. Bye. Thank you.

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