1. 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.

2. 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.

3. 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.

4. 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

5. 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.

6. 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

8. 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)

9. • 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

10. • 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.

11. 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)

12. 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.

13. 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.

14. 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

15. 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

16. 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.

17. 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

18. 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.

19. 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.

26. 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

27. 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

28. 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

29. 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

30. 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

31. 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.

32. 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

34. 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

35. 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

36. 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

37. 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

38. 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

39. OFFICE OF EDUCATION
Improving Practice and Patient Care Through Affordable Quality Urological Education
AUA EDUCATIONAL PRODUCTS
2008 AUA Courses
Subject-Oriented Seminars Surgical Learning Center Courses
∗ AUA Annual Review Course ∗ Hand-assisted Laparoscopy: Nephrectomy,
June 5-8—Dallas, TX Nephroutererectomy & Partial Nephrectomy
Course Directors: Daniel A. Shoskes, MD & Allen F. Morey, MD June 7-8—Houston, TX
∗ Basic Sciences for Urology Residents Course Director: R. Ernest Sosa, MD
June 13-18—Charlottesville, VA ∗ Introductory Urodynamics
Course Director: William Steers, MD August 1-3—Reno, NV
∗ 2008 Summer Research Conference Course Director: Timothy Boone, MD
August 7-9— Baltimore, MD ∗ Hands-on Ultrasound
Course Director: Arthur L. Burnett, MD October 25-26—Dallas, TX
∗ Cutting Edge Topics in Urology Course Director: Pat F. Fulgham, MD
October 3-5—Scottsdale, AZ ∗ Mentored Laparoscopy
Course Director: Gopal Badlani, MD November 8-9—Houston, TX
∗ Female Urology & Advanced Urodynamics Course Director: Stephen Y. Nakada, MD
October 16-18—New Orleans, LA ∗ Hand-assisted Laparoscopy: Nephrectomy,
Course Director: Victor Nitti, MD Nephroutererectomy & Partial Nephrectomy
∗ 4th International Congress on the History of Urology December 6-7—Houston, TX
November 7-9—Baltimore, MD Course Director: R. Ernest Sosa, MD
Rainer Engel, MD
∗ AUA Coding Seminars
∗ Female Sexual Dysfunction – Move to the Forefront
December 12-13—Washington, DC July 12— Las Vegas, NV
Course Director: Irwin Goldstein, MD August 9— Washington, DC
September 20—Tampa, FL
Other AUA Educational Products
New Products! Monographs/DVDs/Webinars
∗Prostate Cancer Webinar Series ∗Annual Meeting Webcasts
∗Basic Ultrasound DVD ∗Update Series
∗Urolithiasis DVD (not for CME) ∗Self Assessment Study Program—Print, CD, and Internet
For more information: ∗Practice Management Webinar Series (not for CME)
Email CME@AUAnet.org or call 1-866-Ring-AUA ∗Advanced Laparoscopy Surgical DVD
Visit the AUA Product Store in the Registration Area