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    • Adult Neurogenic Bladders: From Basics to Advanced Management Wednesday, May 21, 2008 10:00 a.m. - 1:15 p.m. COURSE 109 PG FACULTY Jacques Corcos, M.D. Course Director Anthony Stone, M.D. Angelo E. Gousse, M.D. American Urological Association Education and Research Inc. 2008 Annual Meeting, Orlando, FL May 17-22, 2008 Sponsored by: The American Urological Association Education and Research, Inc.
    • Adult Neurogenic Bladders: From Basics to Advanced Management Wednesday, May 21, 2008 10:00 a.m. - 1:15 p.m. COURSE 109 PG FACULTY Jacques Corcos, M.D. Course Director Anthony Stone, M.D. Angelo E. Gousse, M.D. American Urological Association Education and Research Inc. 2008 Annual Meeting, Orlando, FL May 17-22, 2008 Sponsored by: The American Urological Association Education and Research, Inc.
    • Meeting Disclaimer Regarding materials and information received, written or otherwise, during the 2008 American Urological Association Education and Research, Inc. Annual Meeting Instructional/Postgraduate MC/EC and Dry Lab Courses sponsored by the Office of Education: The scientific views, statements, and recommendations expressed in the written materials and during the meeting represent those of the authors and speakers and do not necessarily represent the views of the American Urological Association Education and Research, Inc.® Reproduction Permission Reproduction of all Instructional/Postgraduate, MC/EC and Dry Lab Courses is prohibited without written permission from individual authors and the American Urological Association Education and Research, Inc. These materials have been written and produced as a supplement to continuing medical education activities pursued during the Instructional/Postgraduate, MC/EC and Dry Lab Courses and are intended for use in that context only. Use of this material as an educational tool or singular resource/authority on the subject/s outside the context of the meeting is not intended. Accreditation The American Urological Association Education and Research, Inc. is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education (CME) for physicians. The American Urological Association Education and Research, Inc. takes responsibility for the content, quality, and scientific integrity of the CME activity. CME Credit The American Urological Association Education and Research, Inc. designates each Instructional Course educational activity for a maximum of 1.5 AMA PRA Category 1 credits™; each Postgraduate Course for a maximum of 3.25 AMA PRA Category 1 credits™; each MC Course for a maximum of 1.0 AMA PRA Category 1 credits™; each EC Course for a maximum of 2.0 AMA PRA Category 1 credits™; each MC Plus Course for a maximum of 2.0 AMA PRA Category 1 credits™; and each Dry Lab Course for a maximum of 2.5 AMA PRA Category 1 credits™. Physicians should only claim credits commensurate with the extent of their participation in the activity. Disclosure Policy Statement As a provider accredited by the Accreditation Council for Continuing Medical Education (ACCME), the American Urological Association Education and Research, Inc., must insure balance, independence, objectivity and scientific rigor in all its sponsored activities. All faculty participating in an educational activity provided by the American Urological Association Education and Research, Inc. are required to disclose to the audience any relevant financial relationships with any commercial interest to the provider. The intent of this disclosure is not to prevent a faculty with relevant financial relationships from serving as faculty, but rather to provide members of the audience with information on which they can make their own judgments. The American Urological Association Education and Research, Inc. must resolve any conflicts of interest prior to the commencement of the educational activity. It remains for the audience to determine if the faculty’s relationships may influence the educational content with regard to exposition or conclusion. When unlabeled or unapproved uses are discussed, these are also indicated. Evidence-based Content As a provider of continuing medical education accredited by the Accreditation Council for Continuing Medical Education (ACCME), it is the policy of the American Urological Association Education and Research, Inc. to review and certify that the content contained in this CME activity is evidence-based, valid, fair and balanced, scientifically rigorous, and free of commercial bias.
    • 2008 AUA Annual Meeting 109PG Adult Neurogenic Bladders: From Basics to Advanced Management 5/21/2008 10:00 - 1:15 p.m. Disclosures According to the American Urological Association’s Disclosure Policy, speakers involved in continuing medical education activities are required to report all relevant financial relationships with any commercial interest to the provider by completing an AUA Disclosure Form. All information from this form is provided to meeting participants so that they may make their own judgments about a speaker’s presentation. Well in advance of the CME activity, all disclosure information is reviewed by a peer group for identification of conflicts of interest, which are resolved in a variety of ways. The American Urological Association does not view the existence of relevant financial relationships as necessarily implying bias, conflict of interest, or decreasing the value of the presentation. Each faculty member presenting lectures in the Annual Meeting Instructional or Postgraduate, MC or EC and Dry Lab Courses has submitted a copy of his or her Disclosure online to the AUA. These copies are on file in the AUA Office of Education. This course has been planned to be well balanced, objective, and scientifically rigorous. Information and opinions offered by the speakers represent their viewpoints. Conclusions drawn by the audience members should be derived from careful consideration of all available scientific information. The following faculty members(s) declare a relationship with the commercial interests as listed below, related directly or indirectly to this CME activity. Participants may form their own judgments about the presentations in light of full disclosure of the facts. Faculty Disclosure Jacques Corcos, M.D. Course Director Coloplast: Board Member, Officer, Trustee Triton pharma: Board Member, Officer, Trustee Watson/Paladin: Consultant or Advisor Q MED: Consultant or Advisor GyneCare: Consultant or Advisor; Mentor: Consultant or Advisor; Novartis: Consultant or Advisor; Pfizer: Consultant or Advisor; Investigator Anthony Stone, M.D. AMS: Meeting Participant or Lecturer, Other GSK/Astellas: Meeting Participant or Lecturer; GyneCare: Other Angelo E. Gousse, M.D. Miller School of Medicine University of Miami: Board Member, Officer, Trustee; Roche: Investigator; Lilly: Consultant or Advisor
    • Disclosure of Off-Label Uses The audience is advised that this continuing medical education activity may contain reference(s) to unlabeled or unapproved uses of drugs or devices. Please consult the prescribing information for full disclosure of approved uses. Faculty and speakers are required to disclose unlabeled or unapproved use of drugs or devices before their presentation or discussion during this activity. A special AUA value for your patients: www.UrologyHealth.org is a joint AUA/AFUD patient education web site that provides accurate and unbiased information on urologic disease and conditions. It also provides information for patients and others wishing to locate urologists in their local areas. This site does not provide medical advice. The content and illustrations are for informational purposes only. This information is not intended to substitute for a consultation with a urologist. It is offered to educate the patient, and their families, in order for them to get the most out of office visits and consultations.
    • AUA 2008 Neuro Urology Workshop Wednesday, May 21, 2008 10.00 a.m. – 1:15 p.m. Program 10.00 – 10.10 Introduction J. Corcos 10.10- 10.25 Initial management T. Stone 10.25 – 10.35 Discussion 10.35 – 10. 50 Urodynamic aspects of Neurogenic bladders Technique and results J. Corcos 10.50- 11.00 Discussion 11.00 – 11.15 Catheterizations and stents T. Stone 11.15 – 11.25 Discussion 11.25 – 11.40 Break 11.40 – 11.55 Oral and intravesical pharmacotherapy A. Gousse 11.55 – 12.05 Discussion 12.05 – 12.45 Surgery (8’ presentation) • Indications and preparation J. Corcos • Artificial Sphincters T. stone • Catheterizable channels J. Corcos • Bladder augmentations A. Gousse 12.45 – 13.15 General discussion and case presentations
    • AUA Workshop: Neurourology Initial Management • SCI o Initial bladder management usually carried out in rehab unit. Unless specifically associated with this, urologists are not usually involved at this point. Standard rehab bladder management will be described, with emphasis on urologic problems that may be encountered. o Spinal shock (suprasacral injuries) Acontractile/areflexic detrusor Closed outlet Lasts 2-3 months (occasionally longer) Mechanism: lack of suprasacral facilitation, depression of interneuronal activity. o Patients usually transferred to rehab unit with indwelling foley o Principles of management Preserve upper tracts Prevent infection Provide efficient bladder emptying Provide appropriate urine collection o Management philosophies Resist instrumentation/catheterization at ‘all costs’ • Crede, suprapubic tapping, ‘balanced bladder’ Intermittent catheterization • Clean (most common) v sterile (hospital setting?) Most units now favor intermittent catheterization. o Potential urologic complications/consults, in initial rehab phase Infection (urine) • Residual bactiuria following foley removal • Initial response to starting CIC o Appropriate course of antibiotics Infection (other) • Epididymo-orchitis Urolithiasis • Usually small bladder calculi from indwelling foley management. • Renal calculi (rare)
    • • Urolithiasis may be exacerbated by hypercalcemia, hypercaliuria occasionally seen in the initial phase of SCI Incontinence • Cause: a. Sphincteric incompetence(LMN), b.Overflow, c.Detrusor overactivity (resolution of spinal shock phase) Autonomic dysreflexia • May also occur as spinal shock phase resolving Priapism • Resolution of spinal shock, mostly high suprasacral injuries • Differentiate from reflexogenic erection • Always high flow • Manage conservatively • o Initial workup KUB, renal ultrasound Urine culture Urodynamics • Wait until resolution of spinal shock • Synchronous fluoro • Sphincter emg? • Ice water test? Bibliography 1. Ditunno JF, Little JW, Tessler A, Burns AS. Spinal shock revisited: a four-phase model. Spinal Cord. 2004 Jul;42(7):383-95. 2. Wyndaele JJ, Madersbacher H, Kovindha A. Conservative treatment of the neuropathic bladder in spinal cord injured patients. Spinal Cord. 2001 Jun;39(6):294-300. 3. Bycroft J, Hamid R, Bywater H, Patki P, Craggs M, Shah J. Variation in urological practice amongst spinal injuries units in the UK and Eire. Neurourol Urodyn. 2004;23(3):252-6; discussion 257. 4. Maynard F, Diokno A, Urinary Tract infection and complications during clean intermittent catheterization following spinal cord injury. J. Urol 1984; 132:943- 946
    • • Spina bifida o Initial management philosophy Urodynamics as soon after back closure as possible • Synchronous fluoroscopy very useful o Bladder shape, vu reflux, bladder neck function, evidence of DSD Start intermittent catheterization as early as possible • Prevents subsequent bladder ‘deterioration’ • Child/parent compliance • Prevents upper tract deterioration, infection Start antimuscarinic meds (usually ditropan) if indicated by urodynamics Follow with urodynamics/renal ultrasound Bibliography 1. Woodhouse CR. Progress in the management of children born with spina bifida. Eur Urol. 2006 May; 49(5):777-8. 2. Stone AR. Neurourologic evaluation and urologic management of spinal dysraphism. Neurosurg Clin N Am. 1995 Apr;6(2):269-77. 3. Dik P, Klijn AJ, van Gool JD, de Jong-de Vos van Steenwijk CC, de Jong TP.Early start to therapy preserves kidney function in spina bifida patients. Eur Urol. 2006 May;49(5):908-13. Epub 2006 Jan 19.
    • Catheterizations and Stents o Intermittent catheterization o Standard management o Issues: Clean v. sterile technique Hydrophilic v. standard Reusable v. individual use Prophylactic antibiotics Incidence, significance, prevention of bactiuria Does technique reduce infection When to treat infection • Evidence for or against these are mixed and will be discussed o Complications Bleeding from urethral trauma UTI False passages Most complications related to the neurogenic bladder dysfunction are reduced significantly o Indwelling catheter management o Urethral v suprapubic Urethral catheters should be avoided, occasionally indicated o Severe disability o Temporary drainage • Complications: prostatitis, epididymo-orchitis, urethral trauma, urethral diverticulae, fistulae, stones, squamous cancer Suprapubic catheters • Indications: Poor hand function, poor mobility, severe disability, unable to perform catheterization • Similar complications to urethral catheters (less urethral complications)
    • o Stents o Better, more durable alternative to external sphincterotomy? o Sphincterotomy largely abandoned as drainage technique Need to be repeated, diminished detrusor contractility, condom appliance issues o Endoscopically deployed Urolume: cobalt chrome alloy, expand when deployed Memokath: Nickel titanium alloy, temperature sensitive expansion and contraction. Allows easier removal Problems: urethral blockage from epithelial reaction to stent, urolume is difficult to remove, similar long term problems to conventional sphincterotomy o Not presently standard management, Memokath potential for temporary use? Bibliography 1. Sugimura T, Arnold E, English S, Moore J. Chronic suprapubic catheterization in the management of patients with spinal cord injuries: analysis of upper and lower urinary tract complications. BJU Int. 2008 2. Seoane-Rodríguez S, Sánchez R-Losada J, Montoto-Marqués A, Salvador-de la Barrera S, Ferreiro-Velasco ME, Alvarez-Castelo L, Balsa-Mosquera B, Rodríguez-Sotillo A.Long-term follow-up study of intraurethral stents in spinal cord injured patients with detrusor-sphincter dyssynergia. Spinal Cord. 2007 Sep;45(9):621-6. 3. Kovindha A, Mai WN, Madersbacher H.Reused silicone catheter for clean intermittent catheterization (CIC): is it safe for spinal cord-injured (SCI) men? Spinal Cord. 2004 Nov;42(11):638-42. 4. Hamid R, Arya M, Wood S, Patel HR, Shah PJ. The use of the Memokath stent in the treatment of detrusor sphincter dyssynergia in spinal cord injury patients: a single-centre seven-year experience. Eur Urol. 2003 May;43(5):539-43. 5. Wilson TS, Lemack GE, Dmochowski RR. UroLume stents: lessons learned. J Urol. 2002 Jun;167(6):2477-80. 6. Nambirajan T, Woolsey S, Mahendra V, Stone AR, Walsh IK. Urethral stents for detrusor sphincter dyssynergia. BJU Int. 2005 Feb;95(3):350-3.
    • Artificial sphincter o Indications o Male spina bifida, incompetent outlet o Male spinal cord injured patient following sphincterotomy or lower motor neurone lesion with sphincteric involvement o Rarely indicated in female neurogenic patients o Facilitates urethral intermittent catheterization (compare with bladder neck reconstruction) o May require augmentation cystoplasty to improve bladder storage characteristics (spina bifida) o Age: usually >7, must be compliant with catherization. o Technique: bladder neck cuff placement (better efficacy, higher complication rate in perineum?) o Suprapubic incision, incise endopelvic fascia, blunt disection behind bladder neck, facilitated by opening bladder anteriorly. o Cuff size 6-10cm, bladder neck and inferior trigone. o Reservoir placed intra-peritonealy or in perivesical retroperitoneal space o Pump in scrotum o Connections above fascia o Suprapubic bladder drainage for 2 weeks, restart IC then o Activate at 6 weeks o Routine follow up mandatory due to high infection rate o Upper tract monitoring especially when done without cystoplasty o Complications o Infection, system leaks, bladder perforation (cystoplasty), erosion rare o Results: published results poor in long term Bibliography 1. Patki P, Hamid R, Shah PJ, Craggs M. Long-term efficacy of AMS 800 artificial urinary sphincter in male patients with urodynamic stress incontinence due to spinal cord lesion. Spinal Cord. 2006 May;44(5):297-300. 2. Toh KL, Tan JK. Artificial urinary sphincter in adult male with neurogenic stress urinary incontinence: a rare indication. Ann Acad Med Singapore. 2005 Jun;34(5):389-90. 3. Hussain M, Greenwell TJ, Venn SN, Mundy AR. The current role of the artificial urinary sphincter for the treatment of urinary incontinence. J Urol. 2005 Aug;174(2):418-24.
    • Chapter 38 from CORCOS & SCHICK TEXTBOOK of the NEUROGENIC BLADDER Second edition, Martin Dunitz London May 2008 Evaluation of neurogenic bladder dysfunction: basic urodynamics Christopher E Kelly and Victor W Nitti Classification of neurogenic voiding dysfunction The main objective in assessing patients with suspected neurogenic lower urinary tract (LUT) dysfunction is to determine what effect the neurologic disease has on the entire urinary tract so that treatment can be implemented to relieve symptoms and prevent upper and lower urinary tract damage. The functional classification system described by Wein (Figure 38.1) is a useful framework with which to conceptualize neurogenic voiding dysfunction and provides a basis for the discussion of various diagnostic and treatment modalities.1 This simple and practical system can be easily applied to our diagnostic criteria (e.g. urodynamics). Of equal importance is the fact that treatment options can be chosen based on this system. The functional classification system is based on the simple concept that the LUT has two basic functions: storage of adequate volumes of urine at low pressures, and voluntary and complete evacuation of urine from the bladder. For normal storage and emptying to occur there must be proper and coordinated functioning of the bladder and bladder outlet (bladder neck, urethra, external sphincter). Hence, neurogenic LUT dysfunction can be classified under the following rubrics: ‘failure to store’, ‘failure to empty’, or a combination thereof. Abnormalities in LUT function may be the result of bladder dysfunction, bladder outlet dysfunction, or a combined dysfunction. Figure 38.2 summarizes how neurologic disease can adversely affect the bladder and/or the bladder outlet, causing storage and emptying dysfunction. Figure 38.1 Functional classification of voiding disorders. Figure 38.2 Effects of neurologic disease on storage and emptying function. Prior to our discussion, it is important to emphasize that symptoms do not always indicate the magnitude to which the disease is affecting the urinary tract, especially in neurologic disorders. Serious urinary tract damage can result in the absence of symptoms. It is also vital to realize that patients with neurologic disease are at risk for developing the same urologic and gynecologic problems as persons of the same age without neurologic disease.2 For example, just because a woman has had a cerebro vascular accident does not exclude her from having stress urinary incontinence. And, lastly, the clinician should remember that neurologic lesions may be ‘complete’ or ‘incomplete’. Hence, urologic manifestations of neurologic disease may not always be predictable. A complete neuro-urologic evaluation of patients with neurogenic voiding dysfunction is therefore important. In this chapter we will discuss the evaluation of patients with neurogenic LUT dysfunction with urodynamics. Prior to this discussion, a working knowledge of the neurophysiology of micturition is essential. This topic is covered in Chapter 6. Additionally, the effect of particular neurologic diseases on lower urinary tract function is covered elsewhere in the book. Assessment of patients with neurogenic lower urinary tract dysfunction History and physical examination Any patient with obvious or suspected neurogenic voiding LUT dysfunction deserves a neurologic work-up. Controversy exists as to how often patients should be reassessed urologically. We recommend that patients be reviewed at least annually, and the complete work-up be repeated if significant changes occur in the neurologic status or LUT signs or symptoms. Prior to urodynamic testing a complete history and physical examination are imperative. A thorough understanding of the patient’s condition and symptoms are essential so that urodynamic investigations can be ‘customized’ to answer questions relevant to that particular patient. Initial evaluation of patients with suspected neurogenic LUT dysfunction should include a thorough history of the patient’s general health and neurologic disease. It is important to understand how the neurologic disease affects daily activities, whether it affects other systems, and whether its course is stable or changing. In patients who do not have a history of neurologic disease (i.e. occult neurologic disease), it is important to carefully and directly question them even about their more subtle neurologic complaints.2
    • A standard and complete urologic examination should be performed on all patients with suspected neurogenic LUT dysfunction. A good general neurologic examination to assess sensation, strength, dexterity, and mobility is essential, as all of these can affect treatment of neurogenic LUT dysfunction. A specific and comprehensive evaluation of the sacral nerve (S2-S4) reflex arc is critical. A digital rectal examination will establish rectal tone and control. The bulbocavernosus reflex and perianal sensation should also be assessed. Finally, lower extremity spasticity along with patellar and ankle reflexes should be evaluated. Laboratory studies Basic serum and urine tests, including renal function tests and serum electrolytes, should be performed. Urinalysis and urine culture are essential, particularly in patients with an increased risk for developing urinary tract infections: those with chronic indwelling catheters, on intermittent self- catheterization, or those carrying high post-void residual volumes. Noninvasive urodynamic assessment Noninvasive studies such as uroflowmetry and measurement of post-void residual urine can be readily performed to give an initial assessment of the patient’s ability to empty the bladder. While nonspecific for underlying dysfunction, uroflowmetry is often used as a screening test for voiding dysfunction and as a means for selecting patients for more sophisticated urodynamic studies. It also provides an objective way to monitor the emptying in patients who have specific diagnoses and are followed with observation or specific therapy. Since the upper urinary tract in neurogenic voiding dysfunction can be adversely affected by secondary reflux, ascending infection, hydronephrosis, chronically elevated bladder storage pressures or stones, we recommend some baseline imaging studies. The choice of study depends on the clinical question being answered. A renal ultrasound or intravenous pyelogram can be used to assess for anatomic abnormalities, hydronephrosis or stones. Bladder ultrasound provides a non-invasive method of measuring residual bladder urine and may assist in ruling out bladder calculi, which are associated with chronic indwelling catheterization.3 Voiding cystourethrogram whether alone or part of videourodynamics, can help diagnose vesico-ureteral reflux.4 Radionucleotide renography may be helpful when more detailed information on renal function is required, such as obstruction or cortical scarring. Although it is an invasive technique, a few words on cystourethroscopy are important. It is indicated in those with indwelling catheters on a yearly basis. Besides evaluating for bladder calculi, epithelial changes can be detected. These patients carry a 5% lifetime risk of developing squamous cell carcinoma of the bladder.5-7 Urodyamics Multichannel urodynamic evaluation is the mainstay of evaluation in patients with neurogenic LUT dysfunction. The goals of urodynamic testing in patients with neurologic disease are: 1. To provide documentation of the effect of neurologic disease on the LUT. 2. To correlate the patient’s symptoms with urodynamic events. 3. To assess for the presence of urologic risk factors associated with urologic complications: detrusor striated sphincter dyssynergia (DESD), impaired bladder compliance, sustained high-pressure detrusor contractions, and vesicoureteral reflux. The urodynamic evaluation consists of several components, including the uroflowmetry, cystometrogram (CMG), abdominal pressure monitoring, electromyography (EMG), and voiding pressure-flow studies. Simultaneous fluoroscopic imaging of the entire urinary tract during urodynamics (i.e. videourodynamics) can be helpful in cases of known or suspected neurogenic voiding dysfunction. It is not unusual to repeat a study several times in order to fulfill the above goals. Cystometrogram The filling CMG is used to mimic the bladder’s filling and storage of urine while the pressure- volume relationship within the bladder is recorded. It is best to fill the bladder at a rate of 30 ml/min or less. In our experience, faster filling rates can exaggerate urodynamic observations. Important bladder parameters with respect to neurologic disease are bladder sensation, the presence of involuntary detrusor contractions (IDC), compliance (storage pressures), and cystometric capacity. IDCs associated with neurologic disease are referred to as neurogenic detrusor overactivity according to the International Continence Society (Figure 38.3).8 The magnitude, or
    • pressure, of IDCs is often determined by the amount of resistance provided by the bladder outlet. For example, in cases of high outlet resistance such as DESD or anatomical obstruction, detrusor pressure with IDC can be quite high, whereas in cases of low outlet resistance, the IDC pressure is often low with subsequent incontinence. Neurogenic detrusor overactivity is caused by lesions above the sacral micturition center, including the spinal cord and brain. Simply stated, the inhibition of the spinal micturition reflex from suprapontine centers is blocked. Figure 38.3 Filling phase of a urodynamic study in a 68-year-old woman with urge incontinence after cerebrovascular accident. Note the involuntary detrusor contractions (arrows). There is a rise in total bladder pressure (Pves) and detrusor pressure (Pdet), but no change in abdominal pressure (Pabd). There are several very important points regarding involuntary contractions: 1. The clinician must be absolutely sure that the contraction is indeed involuntary. Sometimes a patient may become confused during the study and actually void as soon as he feels the desire. 2. It is extremely important to determine whether or not a patient’s symptoms are reproduced during the involuntary contraction. However, in cases of neurologic disease, IDCs can occur with symptoms and should not be discounted. 3. The volume at which contractions occur and the pressure of the contractions should be recorded. 4. It is often worthwhile to repeat the CMG at a slower filling rate if the patient experiences uncharacteristic symptoms (e.g. incontinence or spasms) or detrusor activity. 5. If the patient experiences incontinence during an involuntary contraction (urge incontinence), this should be noted. Sometimes the involuntary contraction will bring on involuntary voiding to completion (precipitant micturition).9 Compliance is defined as the change of volume for a change in detrusor pressure and is calculated by dividing the volume change (ΔV) by the change in detrusor pressure (ΔPdet) during that change in bladder volume. It is expressed in milliliters per centimeter H2O (ml/cmH2O). The spherical shape of the bladder as well as the viscoelastic properties of its components contribute to its excellent compliance, allowing storage of progressive volumes of urine at low pressure. When the pressure begins to rise with increasing volumes, compliance is decreased or ‘impaired’. Impaired compliance is not uncommon in neurogenic voiding dysfunction and is potentially hazardous. The degree of impaired compliance in neurogenic voiding dysfunction is often dependent on outlet resistance. However, poor compliance can also occur with chronically catheterized bladders. Impaired compliance leads to high bladder storage pressures. The calculated value of compliance is probably less important than the actual bladder pressure during filling. This is because the compliance value can change, depending on the volume over which it is calculated. This is probably why compliance, despite being a well-known and accepted parameter, is rarely reported in terms of a discrete or well-defined value in the urologic literature. Normal compliance has been difficult to establish. Toppercer and Tetreault evaluated a group of normal asymptomatic women and women with stress incontinence and found mean compliance to be 55.71 ± 27.37.10 If two standard deviations are used, normal would be between 1 and 110 ml/cmH2O. When compliance is calculated as a single point on the pressure-volume curve it becomes a ‘static’ property. Gilmour et al point out that this oversimplifies the concept of compliance and may lead to potentially erroneous conclusions.11 For example, an abrupt and potentially dangerous rise in pressure may occur as compliance rapidly decreases. However, the value for compliance will be very different, depending on whether it is calculated over the entire filling volume or over the volume in which the change in pressure actually occurred. McGuire and associates have shown that sustained pressures of 40 cmH2O or greater during storage can lead to upper tract damage.12 Storage pressures in this range are dangerous, regardless of the volume in the bladder or calculated compliance value ( Figure 38.4). In poorly compliant bladders in children, Churchill and associates have suggested determining compliance between initial filling and the point at which detrusor pressure exceeds 35 cmH2O.11 More recently, these investigators have applied the concept of dynamic compliance and argue that the amount of time spent with bladder compliance less than 10 ml/cmH2O (an empirically derived value) will strongly influence upper tract deterioration.13 Figure 38.4 Impaired compliance in a 35-yearold male with a T8 spinal cord injury. Note that there is an initial rise in both total vesical pressure (Pves) and abdominal pressure (Pabd), but the Pves and, thus, the detrusor pressure (Pdet) continue to rise to pressures exceeding 40 cmH2O.
    • We would certainly agree that prolonged high-pressure storage is an ominous urodynamic finding, independent of any discrete value of compliance. One must remember that compliance may be dependent on filling rate during a urodynamic study; overly rapid filling rates may produce erroneously lower compliance values. Lastly, neurogenic detrusor overactivity can mimic impaired compliance. Two methods of differentiating these two entities are (1) stopping the infusion rate and, if necessary, (2) having the patient perform a sustained Kegel maneuver to suppress possible involuntary contractions. Involuntary detrusor contractions can also occur in the face of impaired compliance ( Figure 38.5). Figure 38.5 Involuntary detrusor contractions occurring in the face of impaired compliance in a teenage girl with myelomeningocele. The left arrow indicates where detrusor pressure equals and then exceeds 40 cmH2O. The right arrow indicates where leakage occurs-at a bladder leak point pressure of 53 cmH2O. Pves, total vesical pressure; Pdet, detrusor pressure; Pabd, abdominal pressure. Storage parameters – leak point pressures During the filling portion of the cystometrogram, urinary storage can also be assessed. Assessment of storage is important because patients with neurogenic bladders often have issues pertaining to urinary incontinence and/or storage pressures. Urinary leakage can be secondary to a bladder dysfunction (neurogenic detrusor overactivity or impaired compliance) and/or a sphincteric dysfunction (e.g. intrinsic sphincter deficiency). The bladder, or detrusor, leak point pressure (DLPP) test measures the detrusor pressure required to cause urinary incontinence in the absence of increased abdominal pressure.8 The DLPP is a direct reflection of the amount of resistance provided by the external sphincter. The higher the bladder outlet resistance (e.g. as in detrusor-sphincter dyssynergia), the higher the DLPP. High storage pressures and high DLPP are potentially dangerous to upper urinary tracts (Figure 38.5). Knowledge of the DLPP is useful because it allows the clinician to determine the volume at which detrusor pressure reaches dangerous levels. Urinary leakage secondary to sphincteric dysfunction can be measured by the Valsalva or abdominal leak point pressure (ALPP).8,14 The ALPP is an indirect measure of the ability of the urethra to resist changes in abdominal pressure as an expulsive force.15 Clinically, it is used to determine the presence of stress urinary incontinence and the degree of sphincter incompetence ( Figure 38.6). Normally, there is no physiologic abdominal pressure that should cause incontinence, and therefore there is no ‘normal ALPP’. Unlike the DLPP, an elevated ALPP does not indicate potential danger to the kidneys. Figure 38.6 Urodynamic tracing of a female patient with stress incontinence. Tracing shows progressive Valsalva maneuvers until leakage occurs (arrow) at an abdominal pressure of 109 cmH2O, which is the abdominal leak point pressure (ALPP). Note that there is no rise in detrusor pressure. Pves, total vesical pressure; Pdet, detrusor pressure; Pabd, abdominal pressure. Voiding phase As important as filling and storage is the voiding or emptying phase, known as micturition. Prior to urodynamic assessment, one must determine how the patient voids. If voiding is voluntary, the strength and duration of the detrusor contraction is assessed. Detrusor contractility may be impaired in particular types of neurologic disease, particularly with lower motor neuron or denervating lesions. This can cause impaired contractility or areflexia. Aside from detrusor contraction, outlet resistance can be measured while voiding. Although the most common cause of outlet resistance in neurogenic voiding dysfunction is DESD, bladder outlet obstruction can occur anywhere distal to the bladder. Several nomograms and formulas exist to categorize pressure–flow relationships in terms of nonobstructed, obstructed, or equivocal.16–20 It is important to note that interpretation of bladder outlet obstruction during urodynamics should be performed at the point at which the patient was actually given permission to void. If the patient has an involuntary bladder contraction and empties the bladder prematurely, this pressure-flow relationship should not be misinterpreted as being equivalent to normal physiologic voiding. Electromyography during urodynamics permits the urologist to evaluate the striated sphincter function during micturition. Often, surface patch electrodes are used, but needle electrodes permit more accurate placement and more accurate recording. Normally, voluntary voiding is preceded by a complete relaxation of the striated sphincter. Detrusor-external sphincter dyssynergia refers to obstruction to the outflow of urine during bladder contraction caused by involuntary contraction of the striated sphincter during an IDC.21,22 It is secondary to a neurologic lesion and is not associated with a learned voiding dysfunction such as dysfunctional voiding. DESD results in a functional
    • obstruction that usually affects emptying, and ultimately leads to high storage pressures secondary to impaired compliance and incomplete emptying. True DESD is seen in patients with suprasacral spinal lesions (Figure 38.7). Depending on the level of the lesion, patients also may develop detrusor-internal sphincter dyssynergia. In such cases the bladder fails to open appropriately with a bladder contraction due to autonomic dysfunction. It typically occurs in lesions above T10. Detrusor-internal sphincter dyssynergia is best diagnosed by videourodynamics (Figure 38.8). Figure 38.7 Urodynamic tracing of an 18-year-old woman with frequency, urgency, and urge incontinence who was diagnosed with a tethered cord. Note the involuntary detrusor contraction (IDC, arrow) associated with highvolume urine loss as registered in the flow meter. There is increased sphincter activity, as demonstrated by increased electromyograph (EMG) activity consistent with detrusor-external sphincter dyssynergia (DESD). On the second fill there is again an IDC, but this time the patient is instructed to void (double void). Note that there is increased EMG activity throughout the IC and ‘voluntary void’. Detrusor pressures with IDCs are quite high because of the resistance of the contracting striated sphincter. Pves, total vesical pressure; Pdet, detrusor pressure; Pabd, abdominal pressure. Figure 38.8 Detrusor-external sphincter dyssynergia (DESD) and detrusor-internal sphincter dyssynergia in a 35-year-old male with a high cervical spinal cord injury. There are two IDCs with associated increased electromyograph (EMG) activity consistent with DESD. However, the fluoroscopic picture taken at the time of the second IDC shows an incompletely opened bladder neck consistent with detrusor-internal sphincter dyssynergia. This patient underwent a striated sphincterotomy as well as a bladder neck incision to facilitate emptying and lower pressures. Pves, total vesical pressure; Pdet, detrusor pressure; Pabd, abdominal pressure. Videourodynamics Videourodynamics, or simultaneous fluoroscopic monitoring of the urinary tract during urodynamics, is the most comprehensive and accurate way of assessing neurogenic lower urinary tract dysfunction (Figures 38.8 and 38.9).23 During the evaluation of filling and storage, videourodynamics allows for the determination of vesicoureteral reflux and the pressure at which this occurs. Moreover, assessment of the DLPP or ALPP is facilitated as fluoroscopy is often more sensitive than direct observation in determining urinary leakage. Videourodynamics also permits the radiographic evaluation of the bladder neck during filling and anatomic abnormalities such as bladder and urethral diverticula and fistula. During the voiding phase, fluoroscopy permits an accurate determination of the site of obstruction when highpressure/low-flow states exist. Videourodynamics also provides an excellent way of evaluating sphincter behavior during voiding, especially in cases where EMG tracing is imperfect or equivocal. Videourodynamics is the definitive test to determine the presence of detrusor-internal sphincter dyssynergia by the lack of opening of the bladder neck on fluoroscopy during a detrusor contraction. Using fluoroscopy with EMG can help make the diagnosis of detrusor-internal and detrusor-external sphincter dyssynergia.24 Figure 38.9 Videourodynamic study in a 3-year-old boy with myelomeningocele who is on anticholinergic medication but remains wet between catheterizations. There is mild left hydronephrosis on renal ultrasound. Pves, total vesical pressure; Pdet, detrusor pressure; Pabd, abdominal pressure. EMG, electromyography.This study shows that leakage occurs as a result of impaired compliance: bladder leak point pressure (DLPP) = 20 cmH2O.Video portion shows left vesicoureteral reflux occurring at a relative low detrusor pressure of 10cmH2O (upper left arrow), and confirms the DLPP of 20 cmH2O (lower right arrow). Conclusion In patients with known neurologic disease, careful urodynamic evaluation may be necessary to gauge any deleterious effect on the urinary tract, to determine the etiology of LUT symptoms, and to screen for any urologic risk factors. Often times, urodynamics are necessary for the asymptomatic patient because the effects of the disease on the urinary tract can be ‘silent’. Patients without a history of neurologic disease whose urologic evaluation is suspicious for neurogenic LUT dysfunction should be evaluated for occult neurologic disease. References 1. Wein AJ. Classification of neurogenic voiding dysfunction. J Urol 1981; 125:605. 2. Gades NM, Jacobson DJ, Girman CJ et al. Prevalence of conditions potentially associated with lower urinary tract symptoms in men. BJU Int 2005; 95: 549-553. 3. Ku JA, Jung TYL, Park JK et al. Risk factors for urinary stone formation in men with spinal cord injury: a 17- year follow-up study. BJU Int 2006; 97 (4): 790-793. 4. Bunts RC. Management of urological complications in 100 paraplegics. J Urol 1958; 79:733–736.
    • 5. Bejany BE, Lockhart JL, Rhamy RK. Malignant vesical tumors following spinal cord injury. J Urol 1987; 138:1390–1392. 6. Bickel A, Culkin J, Wheeler J. Bladder cancer in spinal cord injury patients. J Urol 1991; 146:1240–1241. 7. Broecker BH, Klein FA, Hackler RH. Cancer of the bladder in spinal cord injury patients. J Urol 1981; 125:196–197. 8. Abrams P, Cardozo L, Fall M, et al. The standardization of terminology of lower urinary tract function. Neurourol Urodynam 2002; 21:167–178. 9. Nitti VW. Cystometry and abdominal pressure monitoring. In: Nitti VW, ed. Practical urodynamics. Philadelphia: WB Saunders, 1998:38–51. 10. Toppercer A, Tetreault JP. Compliance of the bladder: an attempt to establish normal values. Urology 1979; 14:204. 11. Gilmour RF, Churchill BM, Steckler RE, et al. A new technique for dynamic analysis of bladder compliance. J Urol 1993; 150:1200. 12. McGuire EM, Woodside JR, Borden TA. Prognostic value of urodynamic testing in meylodysplastic children. J Urol 1981; 126: 205. 13. Churchill BM, Gilmour PE, Williot P. Urodynamics. Ped Clin NA 1987; 34:1133. 14. McGuire EJ, Fitzpatrick CC, Wan J, et al. Clinical assessment of urethral sphincter function. J Urol 1993; 150:1452–1454. 15. McGuire EJ, Cespedes RD, O’Connell HE. Leak point pressures. Urol Clin N Am 1996; 23:253–262. 16. Abrams PH, Griffiths DJ. Assessment of prostate obstruction from urodynamic measurements and from residual urine. Br J Urol 1979; 51:129–134. 17. Schafer W. Principles and clinical application of advanced urodynamic analysis of voiding function. Urol Clin N Am 1990; 17:553-566. 18. Abrams P. Bladder outlet obstruction index, bladder contractility index and bladder voiding efficiency; three simple indices to define bladder voiding function. BJU Int 1999; 84:14–15. 19. Blaivas JG, Groutz A. Bladder outlet obstruction nomogram for women with lower urinary tract symptomatology. Neurourol Urodyn 2000; 19:553–564. 20. Lemack GE, Zimmern PE. Pressure flow analysis may aid in identifying women with outflow obstruction. J Urol 2000; 163(6):1823–1828. 21. Blaivas JG, Singa HP, Zayed AAH, Labib KB. Detrusor-external sphincter dyssynergia. J Urol 1981; 125:541–544. 22. Blaivas JG, Singa HP, Zayed AAH, Labib KB. Detrusor-external sphincter dyssynergia: a detailed EMG study. J Urol 1981; 125:545–548. 23. Blavais JG. Videourodynamic studies. In: Nitti VW, ed. Practical urodynamics. Philadelphia: WB Saunders, 1998:78–93. 24. Watanabe T, Chancellor MB, Rivas DA. Neurogenic voiding dysfunction. In: Nitti VW, ed. Practical urodynamics. Philadelphia: WB Saunders, 1998:142–155.
    • Neuro-urology Workshop AUA 2008 Oral & Intravesical pharmacotherapy Muscarinic receptors: lower urinary tract Muscarinic receptor selectivity • 5 subtypes (M1-M5) • M1: salivary glands (dry mouth) & brain • Non-selective: • M2: heart; detrusor contraction in NGB – Tolterodine (acts more on bladder than on salivary • M3: normal micturition contraction glands) • M5: eye (ciliary musle) – Solifenacin (long acting) • Urethra: – Trospium – Alpha & beta adrenoceptors – Estrogen receptors • M3 selective (M3 vs. M1): darifenacin (11-fold) • Bladder: • Mixed activity (antimuscarinic + direct + calcium – Adrenergic: beta 1, beta2 & beta 3 channel blockade) : oxybutynin (on M1 & M3) – M2 and M3 – Estrogen receptors Wein AJ, et al. J Urol, suppl., 2006; 175: S5-S10 Wein AJ, et al. J Urol, suppl., 2006; 175: S5-S10 Abrams P. Avery K. Gardener N, et al. J Urol 2006; 175 (3 Pt 1): 1063-6 Abrams P, et al. J Urol 2006; 175 (3 Pt 1): 1063-6 Neurogenic OAB Points to remember • Placebo effect • OAB – WET: urgency, frequency, • Side effect profile incontinence • Maximal response may take 6 weeks • OAB – DRY: no urinary incontinence • Patient preference Abrams P, et al. Urology. 2003; 61: 37-49
    • Targets and Effects of pharmacotherapy Molecular action Site of Effects on target action bladder function Muscarinic Antagonist Cholinergic ↓ contractility Levels of (M2M3) evidence: K channels Activation DSM CM ↓ contractility Andersson (K+ATP) nerve cells(?) KE. 2006 Ca channels Inhibition DAM CM ↓ contractility (L-type) Adrenocoptor Adrenergic ↓ contractility Antagonist CNS, DSM (α1A subtype) Antimuscarinic agents Targets and effects of OAB therapeutic agents For FAILURE TO STORE (bladder) Molecular Drug Site of Effects on Contraindicated in narrow-angle glaucoma target action action Bladder function Mechanism: inhibit acetylcholine binding to M-receptors in bladder wall & reduce DO Adrenoceptor Agonist Adrenergic ↓ Bladder cap (β2β3 subtypes) postjunc DSM contractility Adverse effects •Blurred vision Vanilloid Activation Bladder sensory ↓ Activation of •Dry mouth (Capsaicin, RTX) nerve pathways mict. reflex •Palpitations Neurokinin Antagonist Bladder & urethra sen ↓ Activation of •Drowsiness Nitti VW, et al. J Urol 2007;1 (NK-1, NK2) nerve pathways mict. reflex 78(6):2488-94 •Constipation, facial flushing P 2X, recp Antagonist Bladder sensory ↓ Activation of •Impaired mental alertness and physical coordination nerve pathways mict. reflex OXYBUTYNIN, TOLTERODINE, TROSPIUM, DARIFENACIN, SOLEFENACIN, FESOTERODINE Current antimuscarinic agents Oxybutynin • M1, M2, and M3 muscarinic receptor antagonist • Oxybutynin IR: 5 mg TID • 80% discontinuation rate • Oxybutynin ER: 15 mg QD • First pass metabolism: – N-desethyloxybutynin (metabolite) responsible for • Tolterodine IR: 2 mg BID systemic side effects • Tolterodine ER: 4 mg QD • OROS delivery system: • Trospium: 20 mg BID – Stable plasma levels • Solifenacin: 5 mg/10 mg QD – Diminished first pass metabolism: low side effects • Darifenacin: 7.5 mg/15 mg QD • S-oxybutynin: increased receptor affinity & improved tolerability Franco I, et al. J Urol. 2005;173(1):221-5 Abrams P. Avery K. Gardener N, et al. J Urol 2006; 175 (3 Pt 1): 1063-6 Kelleher C, Cardozo L, et al. Br J Obstet Gynaecol 1997; 104:988–993
    • Tolterodine Oxybutynin vs. tolterodine 1. Competitive muscarinic receptor antagonist • OPERA trial: – Tolterodine ER 4 mg QD vs. oxybutynin ER 10 mg QD 2. Comparable efficacy to oxybutynin: – Equivalent efficacy on incontinence episodes – Oxybutynin more effective on wkly frequency & total dryness – 20% reduction in frequency of micturition (no incontinence) – 45% reduction in incontinence episodes – Dry mouth more with oxybutynin – Reduction in weekly UUI episodes, daily urgency/frequency Diokno AC, Appell RA, Sand PK, et al. Mayo Clin Proc 2003; 78 (6): 687-95 – Increase in bladder capacity – Improved QOL • OBJECT trial: 3. Safety: – Oxybutynin ER – 10 mg QD vs. 2 mg BID of tolterodine IR – Oxybutynin more effective than tolterodine in reducing – No safety concerns incontinence episodes & micturition frequency episodes – Better tolerability then Oxybutynin Abrams P. Avery K. Gardener N, et al. J Urol 2006; 175 (3 Pt 1): 1063-6 Appell RA, Sand P, Dmochowski R, et al. Mayo Clin Proc 2000; 76(4): 358-63 Kredcr KJ. Brubakcr L, Mainprize T. BJU Int 2003 Sep: 92 (4): 418-21 Trospium chloride : Sanctura • Quaternary ammonium compound • Does not cross bladder-brain barrier (BBB) Dmochowski R. Drug Safety 2005; 28(7): 583-600 Dmochowski R. Drug Safety 2005; 28(7): 583-600 Study completion & withdrawal rates Solifenacin Haab F, et al. Eur Urol 2005; 47: 376–84 Haab F, et al. Eur Urol 2005; 47: 376–84
    • Darifenacin Propiverine – M3 selective • Anticholinergic + Ca antagonist – low lipophilicity—does not penetrate CNS—low • 15 mg PO TID cognitive side effects (M1) • Useful for incontinence – Low incidence of dry mouth (5-fold lower affinity • Efficacy similar to oxybutynin for M1) • Adverse effect: dry mouth – Little effect on heart rate (M2) – Minimal effect on visual accommodation (M5) • No long term outcome data Abrams P. Avery K. Gardener N, et al. J Urol 2006; 175 (3 Pt 1): 1063-6 Abrams P. Avery K. Gardener N, et al. J Urol 2006; 175 (3 Pt 1): 1063-6 Kredcr KJ. Brubakcr L, Mainprize T. BJU Int 2003 Sep: 92 (4): 418-21 Kredcr KJ. Brubakcr L, Mainprize T. BJU Int 2003 Sep: 92 (4): 418-21 Combined anticholinergics & Tricyclic antidepressants musculotropic relaxants For FAILURE TO STORE (bladder) • Oxybutynin Mechanism: Increase norepinephrine & serotonin • Propiverine HCl Anticholinergic & direct muscle relaxant effects on the urinary bladder and bladder neck • Flavoxate Example: imipramine Appell RA. J Urol 1994 Dec;152(6 Pt 1):2086 Dmochowski R. Drug Safety 2005; 28(7): 583-600 Castleden CM, et al. J Urol 1981; 125: 318 Duloxetine Calcium Antagonists For mixed stress and urge incontinence • Terodiline, Nifedifine, Diltiazem, 20mg BD for 2 weeks; increase to 40mg BID Verapamil Caution: nausea at the start of treatment Slow withdrawal over 2 weeks by halving the dose every few days if need to stop • torsades de pointes medication Dmochowski R. Drug Safety 2005; 28(7): 583-600 Dmochowski R. Drug Safety 2005; 28(7): 583-600
    • Other agents Newer agents • K channel openers (hyperpolarization): cromakalim, pinacidil • Beta adrenergic agonists: terbutaline (tachycardia, tremor) • Alpha adrenergic antagonists: phenoxybenzamine, prazosin, terazosin, doxazosin, tamsulosin Dmochowski R. Drug Safety 2005; 28(7): 583-600 Yoshimura N, Chancellor MB. J Urol 2002; 168: 1897-1913 Intravesical therapy Botulinum toxin A (BOTOX) • FAILURE TO STORE (bladder) • Hyperexcitability of C-fiber bladder afferents & FAILURE TO EMPTY (outlet – • Lidocaine DSD) • Oxybutynin: 55-90% symptomatic improvement • Mechanism: • Inhibition of Ach release at • Capsaicin (effectivein C-fiber mediated OAB) neuromuscular junction • Relaxes sphincter when DSD • Resiniferatoxin (potent sensory antagonist): present – Vanilloid receptor subtype 1 • Effect not permanent (Q 6 months) – Desensitizes unmyelinated afferent c-fibers – Off-label intradetrusor injections – 30 ml @ 10 micromoles/L x 30 min (200-300 units) Mochless I, et al. J Urol. 2006; 176(4 Pt 2):1767-70 Seki N, et al. J Urol 2001 Dec;166(6):2368-9 – Intrasphincteric Injections for DSD (transurethrally or transperineally) Dmochowski R. Drug Safety 2005; Kaplinsky R, et al. J Urol 1996 Aug;156(2 Pt 2):753-6 28(7): 583-600 Brendler CB, et al. J Urol 1989; 141: 1350 Adapted from Allergan Technique For Botox Injection
    • Where To Inject ? Neurogenic OAB and Botulinum Toxin A Adapted from Allergan Neurogenic OAB Results: Urinary Incontinence Episodes • Double blind, randomized, placebo controlled, Reduction in Number of UI Episodes Compared to Baseline (%) parallel group study 300 U BTX-A 200 U BTX-A Placebo 80 • 59 patients - urinary incontinence, failed *† anticholinergics, performed cic 60 † *† *† † † † • 53 - spinal cord injury, 6 - multiple sclerosis 40 † • 1:1:1 ratio to 300 U Botox, 200 U Botox or 20 placebo groups 0 Week 2 Week 6 Week 12 Week 18 Week 24 *P<0.05 for differences between BTX group and placebo †P<0.05 for difference within-group changes from baseline Schurch B et al. J Urol Vol. 174,196-200, July 2005 Schurch, et al: J Urol. 2005;74:196-200. Results: Urodynamics - MCC Results: Urodynamics - MDP Mean Increase in MCC from Baseline (mL) Mean Reduction in MDP (cm H2O) 300U BTX-A 200U BTX-A Placebo 300 U BTX-A 200U BTX-A Placebo 250 *† 80 *† *† *† 200 *† *† *† 60 *† 150 *† *† 40 *† 100 * 20 50 0 0 Week 2 Week 6 Week 24 Week 2 Week 6 Week 24 *P<0.05 for within-group changes from baseline *P<0.05 for within-group changes from baseline †P<0.05 for pair-wise contrasts between BTX groups versus placebo †P<0.05 for pair-wise contrasts between BTX groups versus placebo Schurch, et al: J Urol. 2005;74:196-200. Schurch, et al: J Urol. 2005;74:196-200.
    • Results: Quality of Life Findings Increase in Total I-QoL Score From Baseline (%) 300 U BTX-A 200U BTX-A Placebo • Decreased urinary incontinence 100 *† • Improvement in urodynamic parameters 80 *† *† 60 *† *† *† *† *† • Improved quality of life scores *† 40 *† • Urinary tract infections in 13/59 pts (22%) 20 • No drug-related side effects 0 Week 2 Week 6 Week 12 Week 18 Week 24 • No difference between the 200 U and 300 U groups *P<0.05 for pair-wise contrasts between BTX groups and placebo †P≤0.002 for within-group differences from baseline Schurch, et al: J Urol. 2005;74:196-200. Results Gousse et al: ICS 2007 Conclusion Urinary Leakage Urinary Frequency Kruskal-Wallis test p<0.01 Kruskal-Wallis test p=0.001 Inj-1 Inj-2 80% * Significant Lower than Baseline 90% * Significant Lower than Baseline (pairwise comparison) • Cornerstone of treatment for # Subjects Leakage / N # Subjects with with UF / N 70% Inj-1 Inj-2 (pairwise comparison) 80% 60% 70% *p=0.005 Inj-3 neurogenic OAB: anticholinergics 60% 50% *p=0.0004 p=0.20 * p=0.04 50% *p=0.0003 * p=0.02 40% 40% *p=0.0001 * p=0.08 *p=0.0002 * p=0.01 • Refractory cases: 30% *p<0.0001* p=0.0002 30% 20% * p=0.006 – Botulinum toxin type A 20% * p<0.0001 10% 10% *p=0.006 p=0.23 – Bladder augmentation 0% 0% Baseline; 2wk; Baseline; 2wk; 6wk; 6wk; 3mon; 3mon; 6mon; 9mon; 12mo; 15mo; 18mo; 6mon; 9mon; 12mo; 15mo; 18mo; n=19 n=16 n=19 n=16 n=16 n=16 n=15 n=15 n=12 n=12 n=10 n=10 n=9 n=9 n=4 n=4 n=2 n=2
    • Indications Bladder Augmentation in Decreased bladder capacity Neurogenic Bladder Decreased compliance Neuro-urology Workshop Intractable involuntary bladder contractions AUA 2008 causing wet neurogenic OAB, recurrent UTI’s/pyelonephritis and/or progressive renal insufficiency Scope Etiology Goals Decrease intravesical pressure Restore urinary continence Spinal cord injury Preserve upper urinary tracts by alleviating reflux and hydronephrosis Multiple sclerosis Myelodysplasia Can combine with a continent abdominal stoma (catheterizable channel using appendix, tapered ileum) Tethered spinal cord Consider in patients: who are able and motivated to perform CIC Reflex voiders wishing to convert to CIC Females with paraplegia Selection of tissue Effect of bowel segment used Augmentation Advantages Disadvantages Ileum Ureter Mucus(-), Rarely available Large intestine electrolyte(-) Stomach Stomach Renal insufficiency, Hematuria-dysuria acidosis, short gut, syndrome Ureter stones: few Autoaugmentation Ileum Electrolyte absorption, Easy to work, mucus(+), peristalsis Large available intestine infection↑ Rawashdeh IF, et al. J Urol 2004 Jun;171(6 Pt 2):2654-6
    • Selection of tissue Selection of tissue Renal insufficiency or significant metabolic Ileum and large intestine: acidosis gastric segment (O) handle well surgically Massively dilated ureter excellent intestinal segments for ureterocystoplasty and nephrectomy augmentation Neuropathic causes (spina bifida) good mobility, no tension no peristalsis (detubularized) distal ileum and cecum (X) ileocecal valve to fecal continence mucus Ileocystoplasty Continent catheterizable Augmentation sigmoidocystoplasty conduits Mitrofanoff principle 15 cm sigmoid colon Appendix Cup pouch Ureter Fallopian tube Tapered ileum
    • Appendiceal conduit Appendix continent conduit In situ (Issa, J Urol 1989; 141: 1385) Snodgrass WT, Elmore J, Adams R. Cecal disconnection with or without cecal lengthening (Snyder & Duckett, 1991; English & McGuire, 1998) Submucosal tunnel Mitrofanoff neourethra Appendix only (preferable) Snodgrass WT, Elmore J, Adams R. J Urol 2007 Apr;177(4):1510-4 Appendicovesicostomy Reconfigured ileum Continence: 97.3% Monti (standard & spiral) Stomal revision: 6.4% Channel revision: 6.4% Monti. J Urol 1999 Difficult catheterization: 5% Caine. J Urol 1999 Monti. Urol 1997; 49:112 Dussinger, Cain et al. 2004 Continent ileal (tapered Monti ileovesicostomy ileum) stoma Continence: 95% 95% dry on CIC Early complications: 7% No stomal complications Stomal revision: 8% 1/19 reservoir perforation Channel revision: 9.5% 3/7 small bowel obstruction 1/19 wound infection 1/7 enterocutaneous fistula 1/7 pelvic abscess 1/7 empyema Rink et al. 1991 Dussinger, Cain et al. 2004
    • Sphincter enhancing procedures Complications Perforation: 6% Not needed always Causes: ischemia, infection, inflammation, overdistention, CIC Pubourethral sling Neurourol Urodyn 1995; 14(4): 297-309 AUS Rivas et al (1996) in animal model: stressed with infused volume: rupture dome (7/11), suture line (4/11) Urology 1996 Jul; 48(1): 40-6 Pediatric surgery VI volume 2 1698-1705 Complications Complications Mucus and urolithiasis Metabolic derangements Mucus: outlet obstruction absorbs chloride and ammonia: ↑infection ↑serum chloride,↓serum bicarbonate nidus for urolithiasis acidosis Large > small intestine growth retardation and bone density Daily irrigation regimen loss Metabolic abnormalities Complications Stomach: Hematuria/dysuria syndrome hypochloremia Hypokalemia 33% with a gastric segment: Metabolic alkalosis dysuria, hematuria, and perineal Hematuria-dysuria syndrome Jejunum: irritation (low urine pH) Hyponatremia @ Low urine volume, incontinence, Hyperkalemia sensate abdomen and pelvis Metabolica acidosis Ileum: B-12, bile salt & fat malabsorption Treatment: H2 blocker, PPI Ileum & Colon: Hypercholoremia; Metabolic acidosis
    • Complications Malignancy 14 cases of malignancy in literature Mean time to malignancy: 18 years Mostly adenocarcinomas Filmer and Spencer (1990) -Yearly cytology & cystoscopy - Biopsy: 10 years after surgery J Urol 1990 Apr; 143(4): 671-8
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