BLADDER MANAGEMENT TECHNIQUES 619 blurring of vision (due to intraocular muscle effects \200\224very rare, but very disabling ); and dif \201 culty taking a deep breath and/or swallowing (two cases in 10y in the auth or \200\231s experience, both resolving spontaneously within 2 \200\2233 weeks and neither required in-hospital observation). All of these side effects are uncommon, will last weeks or a few months, require no speci \201 c treatment, and usually do not recur with subseque nt repeat injections. Deafferentation Division of dorsal spinal nerve roots of S2 \200\2234 to convert the hyperr e \202 exic, high-pressure bladder into an are \202 exic, low-pressure one. Can be used w here the hyperre \202 exic bladder is the cause of incontinence or hydrone- phrosis. Bladd er emptying can subsequently be achieved by ISC or implanta- tion of a nerve stimulator pla ced on ventral roots (efferent nerves) of S2 \200\2234 to \200\230drive \200\231 micturiti on when the patient wants to void (a pager-sized exter- nally applied radiotransmitter acti vates micturition (Figs. 14.3 and 14.4). Also useful for DSD/incomplete bladder emptying ca using recurrent UTIs and retention. 1 Reynard JM (2003) Sphincterotomy and the treatment of detrusor \200\223sphincter dyssyner gia: cur- rent status, future prospects. Spinal Cord 41:1 \200\22311. 2 Reitz A, Knapp PA, M ntener M, Schurch B (2004) Oral nitric oxide donors: a new phar- ma cological approach to detrusor-sphincter dyssynergia in spinal cord injured patients. Eur U rol 45:516 \200\22320. 3 Mamas MA, Reynard JM, Brading AF (2001) Augmentation of external uretheral sphincter nitr ic oxide: a potential pharmacological treatment for detrusor-external sphincter dyssynergia in spinal cord injury. Lancet 357:1964 \200\2237. 4 Cain MP, Rink RC (2010) Augmentation for neuropathic bladder dysfunction \200\223 A thin g of the past? J Urol 183:2124 \200\2235. 5 Cui M, Khanijou S, Rubino J, Aoki KR (2004) Subcutaneous administration botulinum toxin t ype A reduces formalin-induced pain. Pain 107:125 \200\22333. 6 Chuang YC, Yoshimura N, Huang CC, Chiang PH, Chancellor MB (2004) Intravesical botulinum toxin A administration produces analgesia against acetic acid induced bladder pain response s in rats. J Urol 172:1529 \200\22332. 7 Schurch B, de S ze M, Denys P,et al. (2005) Botox detrusor hyper-re \202 exia study tea m. Botulinum toxin type A is safe and effective treatment for neurogenic urinary incontinen ce: results of a single treatment, randomized, placebo controlled 6 month study. J Urol 174 :196 \200\223200. 8 Khan S, Game X, Kalsi V, et al. (2011) Long term effect on quality of life of repeat detr usor injections of botulinum neurotoxin-A for detrusor overactivity in patients with multip le sclerosis. J Urol 185:1344 \200\2239. 9 Anger JT, Weinberg A, Suttorp MJ, Litwin MS, Shekelle PG (2010) Outcome of intravesical b otulinum toxin for idiopathic overactive bladder symptoms: a systematic review of the liter ature. J Urol 183:2258 \200\22364. 10 Grise P, Ruf \201 on A, Denys P, Egon G, Chartier Kastler E (2010) Ef \201 cacy and to lerability of botulinum toxin type A in patients with neurogenic detrusor overactivity and without concomitant anticholinergic therapy: comparison of two doses. Eur Urol 58:759 \200 \22366. 11 Game X, Khan S, Panicker JN, et al. (2010) Comparison of the impact on health related qu ality of life of repeated detrusor injections of botulinum toxin in patients with idiopathi c or neurogenic detrusor overactivity. BJU Int 107:1786 \200\22392. 12 Kuo HC (2006) Will suburothelial injection of a small dose of botulinum A toxin have sim ilar therapeutic effects and less adverse events for refractory detrusor overactivity. Urol ogy 68:993 \200\2237. CHAPTER 14 Neuropathic bladder 620 Fig. 14.3 A sacral anterior root stimulator used to \200\230drive \200\231 micturition fol lowing a deafferentation (external components). Fig. 14.4 KUB X-ray showing the sacral electrodes positioned on the ventral roots of S2, 3, and 4. This page intentionally left blank CHAPTER 14 Neuropathic bladder 622 Catheters and sheaths and the neuropathic patient Many patients manage their bladders by in termittent catheterization (IC) done by themselves (ISC) or by a carer if their hand functi on is inad- equate, as is the case with most (though remarkably not all) tetraplegics. Many others manage their bladders with an indwelling catheter (urethral or suprapubic). Both me thods can be effective for managing incontinence, recurrent UTIs, and BOO causing hydroneph rosis. Intermittent catheterization Requires adequate hand function. The technique is a \200\230c lean \200\231 one (simple handwashing prior to catheterization) rather than \200\230steril e \200\231. Gel-coated catheters become slippery when in contact with water so providing lu bri- cation. Usually done 3 \200\2234 hourly. Problems - - Recurrent Recurrent incontinence: check technique (adequate drainage of last few drops of u rine). Suggest increasing frequency of ISC to minimize volume of urine in the bladder (redu ces bacterial colonization and minimizes bladder pressure). If incontinence persists, consi der intravesical botulinum toxin. UTIs. Long-term catheterization Some patients prefer the convenience of a long-term catheter. Oth ers regard it as a last resort when other methods of bladder drainage have failed. The supr apubic route (SPC) is preferred over the urethral because of pressure necrosis of the ventr al surface of the distal penile urethra in men (acquired hypospadias \200\224 \200\230kippe ring \200\231 of the penis) and pressure necro- sis of the bladder neck in women which beco mes wider and wider until urine leaks around the catheter ( \200\230patulous \200\231 ureth ra) or frequent expulsion of the catheter occurs with the balloon in \202 ated. Problems and complications of long-term catheters - Recurrent source of recurrent infection. Catheter blockages are common: of the catheter wit h bacterial bio \201 lms. Proteus mirabilis, Morganella, and Providencia species secrete a polysaccharide matrix. Within this, urease-producing bacteria generate ammonia from nitrog en in urine, raising urine pH and precipitating magnesium and calcium phosphate crystals. T he matrix \200\223crystal complex blocks the catheter. Catheter blockage causes bypassing w hich soils the patient \200\231s clothes. Bladder distension can cause autonomic dysre \202 exia, leading to extreme rises in BP which can cause stroke and death! Regular bladder washouts and increased catheter size sometimes help. Impregnation of catheters with antiba cterials (e.g. triclosan) are under investigation.1 Intermittent \201 lling and emptying of the bladder using a \200\230 \202 ip- \202 ow \200\231 valve may reduce the frequency of catheter blockages. UTIs: colonization with bacteria provides a potential due to encrustation of the lumen CATHETERS AND SHEATHS AND THE NEUROPATHIC PATIENT 623 develop in 1 in 4 patients over 5y.2 chronic in \202 ammation (from bladder stones, recurr ent Bladder stones: Bladder cancer: UTIs, long-term catheterization) may increase the risk of s quamous cell carcinoma in SCI patients. Some studies report a higher incidence of bladder c ancer (whether chronically catheterized or not); others do not.3 Condom sheaths These are an externally worn urine collection device, consisting of a tubu- lar sheath applied over the glans and shaft of the penis (just like a contra- ceptive condo m, only without the lubrication to prevent it slipping off). Usually made of silicone rubbe r with a tube attached to the distal end to allow urine drainage into a leg bag. They are u sed as a convenient way of preventing leakage of urine, but are obviously only suitable for men. Detachment of the sheath from the penis is prevented by using adhesive gels and tapes . They are used for patients with re \202 ex voiding (where the hyperre \202 exic bladder spontaneously empties and where bladder pressure between voids never reaches a high enough level to compromise kid- ney function). They are also used as a urine collection device fo r patients after external sphincterotomy (for combined detrusor hyperre \202 exia and sphi ncter dysynergia where incomplete bladder emptying leads to recur- rent UTIs and/or hydrone phrosis). Problems The principal problem experienced by some patients is sheath detach- ment. Despite the fact that a man walked on the moon 30y ago, we have been unable to design a condom she ath that will consistently prevent urine leakage in all men. This can be a major problem an d in some cases, requires a complete change of bladder management. Skin reactions some- tim es occur. 1 Stickler D, Jones GL, Russell AD (2003) Control of encrustation and blocked Foley cathete rs. Lancet 361:1435 \200\2237. 2 Ord J, Lunn D, Reynard J (2003) Bladder management and risk of bladder stone formation in spinal cord injured patients. J Urol 170:1734 \200\2237. 3 Subramonian K, Cartwright RA, Harnden P, Harrison SC (2004) Bladder cancer in patients wi th spinal cord injuries. BJU Int 93:739 \200\22343. CHAPTER 14 Neuropathic bladder 624 Management of incontinence in the neuropathic patient Causes High-pressure bladder (detruso r hyperre \202 exia, reduced bladder compli- ance); sphincter weakness; UTI; bladder stone s; rarely, bladder cancer (enquire for UTI symptoms and haematuria). Hyperre \202 exic per ipheral re \202 exes suggest bladder may be hyperre \202 exic (increased ankle jerk re \202 exes, S1 \200\2232, and a positive bulbocavernosus re \202 ex indicating an intact sa cral re \202 ex arc, i.e. S2 \200\2234 intact). Absent peripheral re \202 exes suggest th e bladder and sphincter may be are \202 exic (i.e. sphincter unable to generate pressures adequate for maintaining continence). Initial investigations Urine culture (for infection); KUB X-ray for bladder stones; bladder and renal USS for residual urine volume and to detect hydronephrosis; cytol- ogy and cysto scopy if bladder cancer suspected. Empirical treatment Start with simple treatments. If the bladder residual volume is large, regular ISC may lower bladder pressure and achieve continence. Try an anticholinergic drug (e.g. oxybutynin, tolterodine). Many SCI patients are already doing ISC and simply increasi ng ISC frequency to 3 \200\2234 hourly may achieve continence. ISC more frequently than 3-h ourly is usually impracti- cal, particularly for paraplegic women who usually have to trans fer from their wheelchair onto a toilet and then back onto their wheelchair (Table 14.1). Management of failed empirical treatment Determined by videocystourethrography (VCUG) to as sess bladder and sphincter behavior. Detrusor hyperre \202 exia or poor compliance High-pressure sphincter (i.e. DSD): treating the high-pressure bladder is usu- ally enough to achieve continence. - Bladder treatments: (auto-augmentation), bladder augmentation (ileocystoplasty). All will u sually require ISC for bladder emptying. Long-term SPC. Sacral deafferentation + intravesical botulinum toxin, detrusor myectomy ISC or Brindley implant (SARS). Low-pressure sphincter. Treat the bladder \201 rst. If bladder treatment alone fails, con sider a urethral bulking agent, a transvaginal tape (TVT) or blad- der neck closure in wome n, or an arti \201 cial urinary sphincter in either sex (Fig. 14.5). Detrusor are \202 exia + low-pressure sphincter - - - - Urethral bulking agents. TVT. Bladder neck closure in women. Arti \201 cial urinary sphinc ter. MANAGEMENT OF INCONTINENCE IN THE NEUROPATHIC PATIENT 625 The arti \201 cial urinary sphincter (AUS) The AUS essentially consists of two balloons co nnected by tubing to a control pump. One of the balloons is con \201 gured as a cuff aroun d the bul- bar urethra or bladder neck. The other balloon (placed deep to the rectus muscle ) applies a constant pressure (usually 61 \200\22370cmH2O pressure) to the cuff via a contr ol pump located in the scrotum or labia (Fig. 14.5; The AMS (American Medical Systems) 800 AUS). Pressure in the cuff is main- tained until the control pump is squeezed by the patien t. This forces \202 uid from the cuff (so it temporarily no longer occludes the urethra) into the balloon. Pressure from the balloon then re \201 lls the cuff via delay resistors in the control pump over a minute or so. Indications Incontinence - - Following prostatectomy (post- In the neuropathic patients ( de \201 ciency. Following tra uma to the pelvis or perineum. TURP or radical prostatectomy). SCI, spina bi \201 da) due to intrinsic sphincter Relative contraindications - Poor bladder compliance (risk of dangerous and silent elevation of bladder pressure, with t he development of hydronephrosis). Untreated involuntary bladder contractions (persistent i ncontinence common). Urethral stricture. Incision can expose the underlying cuff, leading t o AUS infection. Poor cognitive function such that the patient is unable to appreciate the need to de \202 ate the cuff several times a day. Preparation prior to insertion - Videourodynamics (to assess bladder pressure and con \201 rm the presence of sphincter wea kness incontinence). Usually not necessary in \200\230simple \200\231 post-radical prostat ectomy patients (cause of incontinence usually obvious). Flexible cystoscopy to exclude ure thral stricture. Urine culture. Treat infection with an appropriate antibiotic for a week o r so before insertion. Bulbar cuff placement: for post-radical prostatectomy incontinence, pre- vious surgery or t rauma (pelvic fracture) in the region of bladder neck (increased risk of rectal perforation ). Bladder neck cuff placement: women (obviously), children (bulbar urethra too small for the available cuff sizes), men who wish to maintain fertility by preserving antegrade ejaculati on, neuropathic patients where ISC is or may be required. A deactivation button prevents return of \202 uid from the balloon to the cuff so allowin g catheterization or instrumentation. CHAPTER 14 Neuropathic bladder 626 Outcomes Improved continence in 60 \200\22390%. Complications in 5 \200\22330% \200\224infe ction, urethral erosion, urethral loosening under the cuff (atrophy), device ( \200\230mech anical \200\231) failure.1 Alternatives - - Injectable urethral bulking agents. Male urethral sling: suburethral); bone anchored perine al (InVanceTM); transobturator (AdVanceTM). Said to improve continence by bulbar urethral r epositioning (rather than compression). Good (short-term) outcomes for less severe incontin ence \200\224 \201 ve or fewer pads per day; poor outcome if six or more pads per day.2 Lo ng-term outcomes and those for transobturator slings remain undetermined. Extraurethral ret ropubic adjustable compression devices: local or regional anesthesia, two small silicone ba lloons are introduced percutaneously via a perineal approach and positioned on each side of the urethra close to the bladder neck. Subcutaneous ports allow volume adjustment post-ope ratively to increase (for persistent leakage) or decrease urethral resistance (for voiding dif \201 culty). Questions remain over its safety (e.g. 10% urethral or bladder perforatio n, balloon migration, \202 uid leakage) and continence outcomes. three types \200\224bulbourethral (suprapubic to under 1 Hussain M, Greenwell TJ, Venn SN, Mundy AR (2005) The current role of the arti \201 cial urinary sphincter for the treatment of urinary incontinence. J Urol 174:418 \200\22324. 2 Castle EP, Andrews PE, Itano N (2005) The male sling for post-prostatectomy incontinence: mean follow-up of 18 months. J Urol 173:1657. MANAGEMENT OF INCONTINENCE IN THE NEUROPATHIC PATIENT 627 Table 14.1 Summary of treatment for incontinence High bladder pressure Low bladder pressure ISC* Lower bladder pressure by ISC + anticholinergics or botulinum toxin type A or augmentation High sphincter pressure Low sphincter pressure Lower bladder pressure by (ISC + anticholinergics or botox or augmentation) + urethral bulk ing agent TVT or bladder neck closure or arti \201 cial urinary sphincter Urethral bulking agent, TVT, bladder neck closure, arti \201 cial urinary sphincter High sphincter pressure is usually enough to keep patient dry. Fig. 14.5 Arti \201 cial urinary sphincter implanted around the bulbar urethra. CHAPTER 14 Neuropathic bladder 628 Management of recurrent urinary tract infections (UTIs) in the neuropathic patient Causes o f recurrent UTIs - Incomplete bladder emptying. - Kidney stones. - Bladder stones. - Presen ce of an indwelling catheter (urethral or suprapubic). History What the patient interprets as a UTI may be different from your de \201 nition of UTI. The neuropathic bladder is frequently colonized with bacteria and often contains pus c ells (pyuria). From time to time, it becomes cloudy due to the precipitation of calcium, ma gnesium, and phosphate salts in the absence of active infection. The presence of bacteria, pus cells, or cloudy urine in the presence of non-speci \201 c symptoms (abdominal pain, t iredness, headaches, feeling \200\230under the weather \200\231) is frequently interpreted as a UTI. Indications for treatment of UTI in the neuropathic patient It is impossible to eradicate b acteria or pus cells from the urine in the presence of a foreign body (e.g. a catheter). In the absence of fever and cloudy smelly urine, we do not prescribe antibiotics, the indiscr iminate use of which encourages growth of antibiotic-resistant organisms. We prescribe anti biotics to the chronically catheterized patient where there is a combination of fever, clou dy, smelly urine and where the patient feels unwell. Culture urine and immediately start em pirical antibiotic therapy with nitrofurantoin, ciprofoxacin, or trimethoprim (the antibiot ics sensi- tivities of our local \200\230bacterial \202 ora \200\231), changing to a mor e speci \201 c antibiotic if the organism is resistant to the prescribed one. Investigations For recurrent UTIs (= frequent episodes of fever, cloudy, smelly urine and f eeling unwell), organize the following: - - KUB Renal and bladder hydronephrosis and to measure pre-void bladder volume and post- void residual urine volume. X-ray \200\224looking for kidney and bladder stones. USS to determine the presence/absence of Treatment In the presence of fever and cloudy, smelly urine, culture the urine and start an tibiotics empirically (e.g. trimethoprim, nitrofurantoin, amoxicillin, cipro \202 oxacin), changing the antibiotic if the culture result suggests resist- ance to your empirical choi ce. \200\230Response \200\231 to treatment is suggested by the patient feeling better and their urine clearing and becoming non-offensive to smell. Persistent fever with constitutio nal symptoms (malaise, rigors) UTIs IN THE NEUROPATHIC PATIENT 629 despite treatment with a speci \201 c oral antibiotic in an adequate dose is an indication for admission for treatment with intravenous antibiotics. Management of recurrent UTIs (Table 14.2) If there is residual urine present, optimize blad der emptying by IC (males, females) or external sphincterotomy for DSD (males). IC can be d one by the patient (ISC) if hand function is good (paraplegic) or by a carer if tetraplegic . An indwelling catheter is an option, but the presence of a for- eign body in the bladder may itself cause recurrent UTIs (though in some, it seems to reduce UTI frequency). Table 14.2 Summary of treatment for recurrent UTIs Low bladder pressure High bladder pressure + DSD* ISC ISC IDC IDC External sphincterotomy \200\224surgical, botox, stent Deafferentation/SARS Remove stones, if present \200\224cystolitholapxy for bladder stones, PCNL for staghorn sto nes. * A new potential option for DSD is augmentation of external sphincter nitric oxide (N O), a neuro-transmitter which relaxes the external sphincter, thereby encouraging antegrade \202 ow of urine and potentially, therefore, lowering residual urine volume. NO donors s uch as nifedipine or GTN can be used. There is theoretical and some experimental evidence t o support this.1,2 1 Mamas MA, Reynard JM, Brading AF (2001) Augmentation of external urethral sphincter nitri c oxide: a potential pharmacological treatment for detrusor-external sphincter dyssynergia in spinal cord injury. Lancet 357:1964 \200\2237. 2 Reitz A, Knapp PA, M ntener M, Schurch B (2004) Oral nitric oxide donors: a new phar- ma cological approach to detrusorspincter dyssynergia in spinal cord injured patients. Eur Uro l 45:516 \200\22320. CHAPTER 14 Neuropathic bladder 630 Management of hydronephrosis in the neuropathic patient An overactive bladder (detrusor hyp erre \202 exia) or poorly compliant blad- der is frequently combined with a high-pressure sphincter (DSD). Bladder pressures during both \201 lling and voiding are high. At times, the bladder pressure may overcome the sphincter pressure and the patient leaks small quant ities of urine. For much of the time, however, the sphincter pres- sures are higher than th e bladder pressures and the kidneys are chronically exposed to these high pressures. They a re hydronephrotic on USS and renal function slowly, but inexorably, deteriorate. Treatment options for hydronephrosis Bypass the external sphincter - IDC ISC- Treat the ext ernal sphincter - (indwelling catheter). + anticholinergics. Sphincterotomy: surgical incision via a cystoscope inserted down the urethra (electrically heated knife or laser), botulinum toxin type A injections into sphincter, urethral stent. D eafferentation + ISC or SARS. Treat the bladder - - - Intravesical botulinum toxin type A + ISC. Augmentation + 1 + ISC or SARS. Deafferentation ISC. Deafferentation converts the high-pressure sphincter into a low-pressure sphincter and the high-pressure bladder into low-pressure bladder. This page intentionally left blank CHAPTER 14 Neuropathic bladder 632 Bladder dysfunction in multiple sclerosis, Parkinson \200\231s disease, spina bi \201 da, after stroke, and in other neurological disease Multiple sclerosis (MS) Seventy- \201 ve p ercent of patients with MS have spinal cord involvement and in these patients, bladder dysf unction is common. The most common symptoms in patients with MS are urgency, frequency, noc turia, and urge incontinence (due to DH) occurring in 32 \200\22397% of individuals, depend ing on the duration and severity of their MS.1 Bladder pressures are rarely high enough to cause upper tract problems (hydronephrosis). The mainstays of treatment are anticholinergic s, ISC, and bladder botox injections. Parkinson \200\231s disease (PD) PD is a cause of parkinsonism (tremor, rigidity, bradykine sis \200\224slow movements) and is due to the degeneration of dopaminergic neurons in the s ubstantia nigra in the basal ganglia. The principal urological manifesta- tion of PD is the development of LUTS, affecting 30 \200\22340% of patients with PD.2 In the 30 \200\22340% of patients with PD and LUTS, nocturia is reported by 90%, urinary frequency and urgency by 70%, and urge incontinence by >40% (the symptoms that classically respond least well to TU RP). The most common urodynamic abnormality is DH (the basal ganglia may have an inhibitory effe ct on the micturition re \202 ex). L-dopa seems to have a variable effect on these symptom s and DH, improving symptoms in some and making them worse in others. Impaired detrusor con tractility can also occur, albeit uncommonly. Sphincter function during spontaneous (desire d) voiding is synergic, i.e. there is no sphincter dyssynergia. Thus, the patient with PD h as unobstructed voiding, unless they have coexist- ent benign prostatic obstruction. Poor s triated sphincter function can also occur. Both DH and poor striated sphincter function can predispose to post-TURP incontinence.3 Urological lore is that patients with PD have had a poor outcome after TURP3 (de novo urina ry incontinence rate of 20%). However, this is prob- ably because of inclusion of patients with multisystem atrophy in previous studies,3 which is associated with a particularly poor outcome after TURP.4 If a patient with PD has urodynamically proven BOO, symptomatic out- comes after TURP can be good4, at least in patients with mild PD of less than 5y duration. Multiple system atrophy (MSA; formerly Shy \200\223Drager syndrome) A cause of parkinsonism characterized clinically by postural hypotension and detrusor are \202 exia. Loss of cell s in the pons leads to DH (symptoms of bladder overactivity), loss of parasympathetic neuro ns due to cell loss in the intermediolateral cell column of the sacral cord causes poor bla d- der emptying, and loss of neurons in Onuf \200\231s nucleus in the sacral anterior BLADDER DYSFUNCTION IN NON-SCI NEUROLOGICAL DISEASE 633 horns leads to denervation of the striated sphincter causing incontinence. The presentation is usually with DH (i.e. symptoms of bladder overac- tivity), followed over the course of several years by worsening bladder emptying. Spina bi \201 da The term \200\230spina bi \201 da \200\231 (more correctly, spinal dysr aphism) describes the clinical manifestations arising from the failure of fusion of the neu ral and bony elements of the spine. The entity of spina bi \201 da includes spina bi \201 da cystica (myelomeningocele and meningocele) and spina bi \201 da occulta (lipomeningoce le, intradural lipoma, and tethered cord). Urinary incontinence, recurrent UTI, bladder and renal stone formation, and re \202 ux nephropathy are common problems. McGuire introduced the concept of detrusor leak point pressure as an indicator of risk of u pper tract deterioration in spina bi \201 da patients.5 In 42 patients with myelodysplasia followed over 15y, urethral urine leakage occurred in 20 patients at intravesical pressure s <40cmH2O (the detru- sor leak point pressure) and in 22 at pressures >40cmH2O. While no p atient with a leak point pressure <40cmH2O had VUR and only two had ureteral dilatation on intravenous urography, in contrast, VUR was present in 15 patients (68%) and ureteral dilat ation in 18 (81%) in those patients with a leak point pressure >40cmH2O. As a result of thi s study (later supported by others), an end \201 ll pressure <40cmH2O is taken as an indi cation that upper tract deterioration will not occur and an end \201 ll pressure >40cmH2O is taken as an indication of the potential for upper tract deterioration. The hallmark urodynamic \201 nding in spina bi \201 da is loss of bladder com- pliance c ombined with increased outlet resistance secondary to abnor- mal bladder neck function or D SD6 (62% of patients; 38% had what was described as detrusor are \202 exia which, in reali ty, described a group of 34 patients, 30 of who had poor bladder compliance with high end \201 ll pressures). Most patients have a \201 xed (static) external sphincter and 10 \200\22315% of patients have DESD. The mainstay of management is directed towards maintaining a low- pressure, continent bladd er with anticholinergics combined with ISC.7 In those with increased detrusor leak point pr essures, this decreases the probability of upper tract deterioration.8 Where anticholinergi cs fail to achieve continence or fail to eliminate hydronephrosis, the next step is to try bladder botox injections combined with ISC, though the poorly com- pliant bladder that is s o characteristic of spina bi \201 da seems to be more resistant to botox than the purely h yperre \202 exic bladder. If anticholinergics or botox combined with ISC are not be able to achieve safe storage pres sures in the small capacity, poorly compliant bladder augmentation cystoplasty with or with out a Mitrofanoff stoma to make ISC easier (especially in the wheelchair-bound patient) may be required to achieve safe lowering of bladder pressure. Where continence cannot be achie ved by reducing bladder pressure alone, bladder neck clo- sure, urethral support (e.g. a TV T in women), or an arti \201 cial sphincter may be required. Leak point pressure can predi ct (with reasonable accuracy) those patients who have adequate bladder outlet resistance (t hose with a CHAPTER 14 Neuropathic bladder 634 leak point pressure >40cmH2O generally) to obviate the need for bladder outlet surgery. Those patients with spina bi \201 da and impaired cognitive ability (who rep- resent a sig ni \201 cant proportion of the spina bi \201 da population) may not be able to cope with the requirement for regular and frequent bladder emp- tying with ISC or with the use of the AUS. For such patients, an SPC may be a safer method of achieving continence and protectin g renal function. Furthermore, while it is possible to improve continence with LUT recon- s tructive surgery, there is evidence that this may not be paralleled with substantial improv ements in overall quality of life.9 Quality of life scores seem to be no different between patients with spina bi \201 da who undergo successful surgery for incontinence and matched controls who do not (it is dif \201 cult to improve quality of life by correcting just on e system in a complex, multisystem disability such as spina bi \201 da). Cerebrovascular accidents DH occurs in 70%, DSD in 15%. Detrusor are \202 exia can occur.1 0 Frequency, nocturia, urgency, and urge incontinence are common. Retention occurs in 5% in the acute phase. Incontinence within the \201 rst 7 days after a CVA predicts poor survi val.11 Other neurological disease Frontal lobe lesions (e.g. tumors, arteriovenous malformations ( AVMs)) May cause severe frequency and urgency (frontal lobe has inhibitory input to the pon s). Brainstem lesions (e.g. posterior fossa tumors) Can cause urinary retention or bladder over activity. Transverse myelitis Severe tetraparesis and bladder dysfunction which often recovers to a s ubstantial degree. Peripheral neuropathies The autonomic innervation of the bladder makes it \200\230vulnerab le \200\231 to the effects of peripheral neuropathies such as those occurring in diabetes m el- litus and amyloidosis. The picture is usually one of reduced bladder con- tractility (p oor bladder emptying, i.e. chronic low-pressure retention). BLADDER DYSFUNCTION IN NON-SCI NEUROLOGICAL DISEASE 635 1 de Seze M, Ruf \201 on A, Denys P (2007) The neurogenic bladder in multiple sclerosis: r eview of the literature and proposal of management guidelines. Mult Scler 13:915 \200\22328 . 2 Winge K, Skau AM, Stimpel H, Nielsen KK, Werdelin L (2006) Prevalence of bladder dysfunc- tion in Parkinsons disease. Neurourol Urodyn 25:116 \200\22322. 3 Staskin DS, Vardi Y, Siroky MB (1988) Post-prostatectomy continence in the parkinsonian p a- tient: the signi \201 cance of poor voluntary sphincter control. J Urol 140:117 \200 \2238. 4 Roth B, Studer UE, Fowler CJ, Kessler TM (2009) Benign prostatic obstruction and parkinso n \200\231s disease should transurethral resection of the prostate be avoided? J Urol 181: 2209 \200\22313. 5 McGuire EJ, Woodside JR, Borden TA, Weiss RM (1981) Prognostic value of urodynamic test- ing in myelodysplastic patients. J Urol 126:205 \200\2239. 6 Webster GD, el-Mahrouky A, Stone AR, Zakrzewski C (1986) The urological evaluation and ma nagement of patients with myelodysplasia. Br J Urol 58:261 \200\2235. 7 Edelstein RA, Bauer SB, Kelly MD, et al. (1995) The long-term urological response of neo- nates with myelodysplasia treated proactively with intermittent catheterization and antich olinergic therapy. J Urol 154:1500. 8 Wang SC, McGuire EJ, Bloom DA (1988) A bladder pressure management system for myelo- dysp lasia \200\224clinical outcome. J Urol 140: 1499 \200\223502. 9 MacNeily AE, Jafari S, Scott H, Dalgetty A, Afshar K (2009) Health Related Quality of Lif e in Patients With Spina Bi \201 da: A prospective assessment before and after lower urina ry tract recon- struction. J Urol 182:1984 \200\22392. 10 Sakakibara R, Hattori T, Yasuda K, Yamanishi T (1996) Micturitional disturbance after ac ute hemispheric stroke: analysis of the lesion site by CT and MRI. J Neurol Sci 137:47 \200 \22356. 11 Wade D, Hewer RL (1985) Outlook after an acute stroke: urinary incontinence and loss of consciousness compared in 532 patients. Q J Med 56:601 \200\2238. CHAPTER 14 Neuropathic bladder 636 Neuromodulation in neuropathic and non-neuropathic lower urinary tract dysfunction This is the electrical activation of afferent nerve \201 bres to modulate their function. Electrical stimulation applied anywhere in the body preferentially depo- larizes nerves (hi gher current amplitudes are required to directly depolar- ize muscle). In patients with LUT dysfunction, the relevant spinal segments are S2 \200\2234. Indications: urgency, frequenc y, urge incontinence, chronic uri- nary retention where behavioral and drug therapy has fai led. Several sites of stimulation are available, the electrical stimulus being applied directly to nerves or as close as possible: - - SNS Pudendal nerve: vagina, anus, pelvic \202 oor muscles) or via stimulation of dorsal p enile or clitoral nerve (DPN, DCN). Posterior tibial nerve stimulation ( . direct pelvic \202 oor electrical stimulation (of bladder, PTNS).1 PTNS PTN (L4,5; S1 \200\2233) shares common nerve roots with those innervating the bladder. PTNS can be applied transcutaneously (stick-on surface elec- trodes) or percutaneously (ne edle electrodes). Percutaneous needle sys- tems include the SANS (Stoller) and the UrgentPC system. Stimulation is applied via an acupuncture needle inserted just above the medial ma lleolus with a reference (or returns) electrode \200\22430min of stimulation per week, over 12 weeks. Thereafter, 30min of treatment every 2 \200\2233 weeks can be used to maintain t he treatment effect in those who respond. PTNS has not been compared with placebo ( \200 \230sham \200\231 stimulation) and, therefore, reported ef \201 cacy may represent a place bo response. In a single-blinded, placebo- controlled study (gastrocnemius muscle stimulati on without PTNS), 71% of patients receiving PTNS (12 treatments; 3 per week over 4 weeks) r eported >50% reduction in urge incontinence episodes.2 SNS (sacral nerve modulation \200\224SNM) A sacral nerve stimulator (Medtronic Interstim) d elivers continuous electrical pulses to S3 via an electrode inserted through the sacral for amina and connected to an electrical pulse generator which is implanted subcu- taneously. S upported by NICE3 for patients with urge incontinence who have failed lifestyle modi \201 cation and behavior and drug therapy. A test stimulation (the peripheral nerve evaluation, PNE) is performed, under local anesthe tic, by a percutaneous test electrode placed in S3 foramina to con \201 rm an appropriate clinical response (a reduction in urgency, frequency, or incontinence episodes). A permanen t implant is offered if there is a 50% reduction in frequency and urgency. This is placed i n a subcutaneous pocket and is connected to the sacral elec- trode. It can be switched on a nd off and the amplitude varied within set limits. About 50 \200\22360% of patients have a successful PNE. A multicentre study, randomizing non-neuropathic patients with a successful PNE test NEUROMODULATION IN LOWER URINARY TRACT DYSFUNCTION 637 to immediate vs delayed (for 6 months) implantation (the control group), showed signi \201 cantly better symptomatic outcomes in the implant group, 50 \200\22370% reporting resoluti on of their urge incontinence and 80% report- ing >50% reduction in incontinence episodes, persisting for at least 3 \200\2235y.4 Longer term follow-up studies report a durable respo nse.5,6 Numbers of neuropathic patients treated with SNS are too small to draw meaningful c onclusions.5 For non-obstructive urinary retention of those responding to PNE (68 of 177, 38%) and who w ere subsequently implanted, 58% no longer required ISC at 18 months of follow-up,7 results mirrored by others (50 \200\22355% stopping ISC) at a mean of 41 \200\22343 months (70% wit h Fowler \200\231s syndrome stopped ISC).8,9 The exact mechanism of action of SNM in patients with bladder dys- function is not known. 1 Andrews B, Reynard J (2003) Transcutaneous posterior tibial nerve stimulation for the tre at- ment of detrusor hyper-re \202 exia in spinal cord injury. J Urol 170:926. 2 Finazzi-Agro E, Petta F, Sciobica F, Pasqualetti P, Musco S, Bove P (2010) Percutaneous t ibial nerve stimulation effects on detrusor overactivity incontinence are not due to a plac ebo effect: a randomized, double-blind, placebo controlled trial. J Urol 184:2001 \200\2236 . 3 National Institute for Health and Clinical Excellence (2004) Sacral nerve stimulation for urge incontinence and urgency-frequency [online]. Available from: M http://publications.ni ce.org.uk/ sacral-nerve-stimulation-for-urge-incontinence-and-urgency-frequency-ipg64. 4 Schmidt RA, Jonas U, Oleson KA, et al. (1999) Sacral nerve stimulation for treatment of r efractory urinary incontinence. Sacral Nerve Stimulation Study Group. J Urol 162:325 \200 \2237. 5 Bosch JLHR (2010) An update on sacral neuromodulation: where do we stand with this in the management of lower urinary tract dysfunction in 2010. BJU Int 106:1432 \200\22342. 6 Groen J, et al. (2009) Five-year follow-up of sacral nerve neuromodulation in 60 woen wit h idiopathic refractory urge incontinence. Neurourol Urodyn 28:795 \200\2236. 7 retention: results 18 months after implantation. J Urol 165:15 \200\2239. Jonas U, Fowler CJ, Chancellor MB, et al. (2001) Ef \201 cacy of sacral nerve stimulation for urinary 8 Datta SN, Chaliha C, Singh A, et al. (2008) Sacral neuromodulation for urinary retention: 10 year experience from one UK center. BJU Int 101:192 \200\2236. 9 De Ridder D, Ost D, Bruyninckx F (2007) The presence of Fowler \200\231s syndrome predict s suc- cessful long-term outcome of sacral nerve stimulation in women with urinary retentio n. Eur Urol 51:229 \200\22333. This page intentionally left blank 639 Chapter 15 Urological problems in pregnancy Physiological and anatomical changes in the urinary tract 640 Urinary tract infection (UTI) 642 Hydronephrosis of pregnancy 644 CHAPTER 15 Urological problems in pregnancy 640