due to encrustation of the lumen of the catheter , necessitating surgical removal (endoscopic or dif \201 cultly , either around the suprapubic site or per urethra. (SCC of the bladder): there is con \202 icting evidence CHAPTER 4 Bladder outlet obstruction 114 whether managed with indwelling catheters, ISC, or sheath drainage and so the presence of t he catheter per se is not enough to induce development of a cancer. Screening cystoscopy st udies have either failed to result in a downstaging of bladder cancer when compared with no n-screened patients or have simply not detected any cases of bladder cancer. Screening cyst oscopy remains a subject of debate.5 Catheter care \200 When should the \201 rst change be done and who should do it? BAUS suprapubic catheter pr actice guidelines state \200\230It is not necessary for the \201 rst catheter change to be carried out by the team who inserted the catheter; the \201 rst change is generally de ferred for at least 2 weeks (and typically 6 \200\22312 weeks) after catheter insertion to allow the track to \200\230mature \200\231. How often should the catheter be changed? Usua lly 6 weekly to 3 monthly, but there is no hard and fast rule that a catheter must be chang ed at a given interval. To maintain bladder capacity over the long term, should the cathete r be clamped and should long-term anticholinergic medication be given? Nice idea in theory, but no evidence of ef \201 cacy of either method. Can a \202 ip- \202 ow valve be used to allow intermittent bladder emptying? Yes, as long as the patient does not get autonomic dysre \202 exia with bladder distension and does not leak urethrally with a full bladder. Can the patient or carer change the SPC? Yes, if adequately trained. What should I do for bypassing of urine (leakage of urine either per urethra or around the SPC)? Try anticholine rgics and if this fails bladder botox injections. If all else fails, a bladder neck or uret hral closure may be necessary. The catheter keeps blocking. What can I do? BAUS suprapubic catheter practice guidelines state that \200\230Repeated catheter blockages are frequently related to the development of bladder calculi \200\231. The author agrees that blockages a re \200\230related to \200\231 the same process that causes bladder stones, but catheter b lockages are not caused by bladder stones for in the authors \200\231 experience of managin g many, many hundreds of patients with bladder stones, such stones are often far too large to block the catheter eye-holes. Catheter blockages and bladder stones are caused by the sa me process \200\224chronic bacterial colonization of the bladder and any arti \201 cial de vice left within the bladder such as a catheter, followed by the development of a bio \201 lm around the colonies of bacteria, followed by in \201 ltration of this bio \201 lm wit h calcium and phosphate. This is the process of catheter encrustation (which blocks cathete rs) and it is also the process of bladder stone formation. Where blockages become problemat ic, increase the SPC size, increase \202 uid intake, and consider bladder washouts (daily or every few days) \200\224the evidence base for the ef \201 cacy of all of this is weak. The evidence base for in vivo use of a \202 ip- \202 ow valve to stop blockages is non- existent. In the authors \200\231 experience, full-dose courses of antibiotics or low-dose prophylactic antibiotics only very occasionally resolve this problem and more often than no t, lead to the emergence of multiresistant bacteria in the urine. \200 TECHNIQUE OF SUPRAPUBIC CATHETERIZATION 115 1 Ahluwalia RS, Johal N, Kouriefs C, et al. (2006) The surgical risk of suprapubic catheter insertion and long-term sequelae. Ann R Coll Surg Engl 88: 171 \200\2236. 2 Sheriff MK, Foley S, McFarlene J, et al. (1998) Long-term suprapubic catheterization: cli nical outcome and satisfaction survey. Spinal Cord 36:171 \200\2236. 3 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. 4 Subramonian K, Cartwright RA, Harnden P, Harrison SCW (2004) Bladder cancer in patients w ith spinal cord injuries. Br J Urol Int 93:739 \200\22343. 5 Hamid R, Bycroft J, Arya M, Shah PJ (2003) Screening cystoscopy and biopsy in patients wi th neuropathic bladder and chronic suprapubic indwelling catheters: is it valid? J Urol 170 (2 Pt 1):425 \200\2237. Further reading Harrison SCW, Lawrence WT, Morley R, Pearce I, Taylor J (2011) British Association of Urolo gical Surgeons \200\231 (BAUS suprapubic catheter practice guidelines (BAUS) suprapubic cat heter practice guidelines. Br J Urol Int 107:77 \200\22385. Hamid R, Bycroft J, Arya M, Shah PJ (2003) Screening cystoscopy and biopsy in patients with neuropathic bladder and chronic suprapubic indwelling catheters: is it valid? J Urol 170(2 Pt 1):425 \200\2237. Ord J, Lunn D, Reynard J (2003) Bladder management and risk of bladder stone formation in s pinal cord injured patients. J Urol 170:1734 \200\2237. Sabbuba NA, Stickler DJ, Long M, et al. (2005) Does the valve-regulated release of urine fr om the bladder reduce the encrustation and blockage of indwelling catheters by crystalline Proteus mirabilis bio \201 lms? J Urol 173:262 \200\2236. Stickler DJ, Zimakoff J (1994) Complications of urinary tract infections associated with de vices for long-term bladder management. J Hosp Infect 28:177 \200\22394. Warren JW, Muncie HL, Hebel JR, Hall-Craggs M (1994) Long-term urethral catheterisation inc reases risk of chronic pyelonephritis and renal in \202 ammation. J Am Geriatr Soc 42:1286 \200\22390. CHAPTER 4 Bladder outlet obstruction 116 Management of nocturia and nocturnal polyuria Nocturia is often particularly resistant to t reatment. First, establish whether the patient is polyuric (>3L of urine/24h) by getting them to comp lete a frequency volume chart. If they are polyu- ric, this may account for their daytime a nd night-time voiding frequency. Establish whether they have a solute or water diuresis and the causes thereof (Box 4.1). If non-polyuric (<3L urine output/24h), determine the distribution of urine output over the 24h period. If >1/3 of urine output is between the hours of midnight and 8 a.m., then the patient has nocturnal polyuria (NP). If there is nocturnal polyuria, exclude other medical causes \200\224diabetes mellitus and inspidus, adrenal insuf \201 ciency; hypercalcaemia; liver failure; polyuric renal failure ; chronic heart failure; obstructive sleep apnoea, dependent oedema; chronic venous stasis; calcium channel blockers; diuretics; selective serotonin reuptake inhibitor antidepressant s. Non-polyuric nocturia BPH medical therapy The impact of alpha blockers, 5 -reductase inhib itors, and anticholinergics on nocturia is modest. TURP Nocturia persists in 20 \200\22340% of men after TURP. Medtronic Interstim therapy for nocturia Patients preselected on the basis of a favorable s ymptomatic response to a test stimulation can experience a reduction in nocturia,1 but not all patients respond to the test stimulation and the treatment is expensive and not yet wid ely available in all countries. Treatment for NP The evidence base for NP treatments is limited (very few randomized, place bo-controlled trials). Fluid restriction Many patients have reduced their afternoon and evening \202 uid intake in an attempt to reduce their night-time diuresis. Diuretics Diuretics, taken several hours before bedtime, reduce nocturnal voiding frequency in some patients.2,3 DDAVP A synthetic analog of arginine vasopressin (endogenous ADH) which, if taken at night, can reduce urine \202 ow by its antidiuretic action. It has been suggested that NP may b e caused by a lack of endogenous produc- tion of ADH in elderly people. However, adults bot h with and without NP have no rise in ADH at night (i.e. ADH secretion remains remarkably c onstant throughout the day in adults with and without NP). Furthermore, MANAGEMENT OF NOCTURIA AND NOCTURNAL POLYURIA 117 the diuresis in adults with NP is a solute diuresis due to a nocturnal natriu- resis.4 Thus , lack of ADH secretion at night is not the cause of the diuresis in nocturnal polyuric adu lts and, therefore, from a theoretical perspec- tive, there is no logical basis for using d esmopressin in NP.5 There is limited evidence that it reduces night-time voiding frequency (at least in responder enrichment studies) and increases sleep duration in a propor- tion o f patients with NP.6 in 5% of patients. Side effects Hyponatraemia (Na <130mmol/L) Measure serum Na 3 days after starting DDAVP and stop if hyponatraemia develops.3 Box 4.1 Investigation of the polyuric patient (urine output >3L per 24h) \200 Urine osmol ality? \200 \200 Solute diuresis (e.g. post-operative diuresis), diuresis following rel ief of HPCR. Water diuresis (nephrogenic \200\224e.g. lithium therapy, central \200\224ADH de \201 ciency). >250mOsm/kg = solute diuresis. <250mOsm/kg = water diuresis. : poorly controlled diabetes mellitus, saline loading : primary polydipsia, diabetes insipidus Nocturia and sleep apnoea Obstructive sleep apnoea (OSA) is highly prevalent in those over 65y of age. It is often manifested by snoring. There is a strong association between OSA sy mptoms and nocturia.7 Large negative intrathoracic pressure swings may trigger a cardiac-me diated natriuresis and hence, cause NP. 1 Spinelli M (2003) New sacral neuromodulation lead for percutaneous implantation using loc al anesthesia: description and \201 rst experience. J Urol 170:1905 \200\2237. 2 Reynard JM, Cannon A, Yang Q, Abrams P (1998) A novel therapy for nocturnal polyuria: a d ouble-blind randomized trial of frusemide against placebo. Br J Urol 81:215 \200\2238. 3 National Institute for Health and Clinical Excellence (2010) The management of lower urin ary tract symptoms in men [online]. Available from: M www.nice.org.uk/CG97. 4 Matthiesen TB, Rittig S, Norgaard JP, Pedersen EB, Djurhuus JC (1996) Nocturnal polyuria and natriuresis in male patients with nocturia and lower urinary tract symptoms. J Urol 156 :1292 \200\2239. 5 McKeigue P, Reynard J (2000) Relation of nocturnal polyuria of the elderly to essential h ypertension. Lancet 355:486 \200\2238. 6 Mattiasson A (2002) Ef \201 cacy of desmopressin in the treatment of nocturia: a double- blind placebo-controlled study in men. Br J Urol 89:855 \200\22362. 7 Umlauf M (1999) Nocturia and sleep apnea symptoms in older patients: clinical interview. Sleep 22:S127. CHAPTER 4 Bladder outlet obstruction 118 Chronic retention Anyone who retains a certain volume of urine in their bladder after void- ing or attempted voiding can be said to be in chronic retention. For those who retain the ability to pass urine, such a situation can be termed \200\230chronic retention \200\231 a nd this may be low pressure (normal creatinine and absence of hydronephrosis on ultrasound) or high pressure (raised creatinine which falls post-catheterization, usually with hydrone phrosis on ultrasound). Those with chronic retention who suddenly become unable to pass uri ne (and this is usually painful) can be said to have developed acute-on-chronic retention. Again, this can be low pressure or high pressure. A workable de \201 nition (one that is r elated to the outcome of TURP) for the acute setting of painful inability to void is that a cute retention (non-chronic) is painful inability to void with a catheterization volume of <800mL and acute-on-chronic retention is painful inability to void with a catheterization v olume of >800mL.1 In the context of chronic retention, precisely what \200\230a certain volume \200\231 mean s is variably de \201 ned. Some say a patient has chronic retention when they consistently leave 300mL behind post-void, others 800mL2,3, and NICE4 describes it as a residual volume >1000mL or the presence of a palpable/percussable bladder (though the bladder can certainl y be pal- pated or percussed when containing <1000mL so this de \201 nition is not strictl y consistent). The 2010 NICE guidelines on management of LUTS in men provide a useful algorithm for manage ment of chronic retention (Fig. 4.3). A creati- nine and renal ultrasound are done. Raised creatinine or hydronephrosis Yes No Bothersome LUTS Active surveillance monitor residual urine volume creatinine, renal ultraso und No bothersome LUTS Catheterize Active surveillance monitor residual urine volume creatinine, renal ultrasound Consider TUR P Consider ISC or long term indwelling catheter before offering TURP Consider TURP Fig. 4.3 NICE guidelines for management of LUTS in men \200\224modi \201 ed version. CHRONIC RETENTION 119 1 Reynard JM (1999) Failure to void after transuretural resection of the prostate and mode of presentation. Urology 53:336 \200\2239. 2 Mitchell JP (1984) Management of chronic urinary retention. BMJ 289:515 \200\2236. 3 Abrams P, Dunn M, George N (1978) Urodynamic \201 ndings in chronic retention of urine and their relevance to results of surgery. BMJ 2:1258 \200\22360. 4 National Institute for Health and Clinical Excellence (2010) The management of lower urin ary tract symptoms in men [online]. Available from: M www.nice.org.uk/CG97. CHAPTER 4 Bladder outlet obstruction 120 High-pressure chronic retention (HPCR) In the 2nd edition of this book, this was de \201 n ed as maintenance of void- ing, with a bladder volume of >800mL and an intravesical pressur e above 30cmH2O, accompanied by hydronephrosis1,2 and since this de \201 nition has been s hown to be helpful in predicting the outcome of the commonest surgical treatment for urinar y retention,1 it is one that I have decided to keep for this 3rd edition. Over time, this l eads to renal failure. When the patient is suddenly unable to pass urine, acute-on-chronic high-pressure retention of urine has occurred. A man with high-pressure retention who continues to void spontane- ously may be unaware tha t there is anything wrong. He will often have no sensation of incomplete emptying and his b ladder seems to be insensitive to the gross distension. Often, the \201 rst presenting sy mptom is that of bedwetting. This is such an unpleasant and disruptive symptom that it will cause most people to visit their doctor. Visual inspection of the patient \200\231s abdome n may show marked distension due to a grossly enlarged bladder. The diagnosis of chronic re tention can be con \201 rmed by palpation of the enlarged, tense bladder which is dull to percussion. Acute treatment Catheterization relieves the pressure on the kidneys and allows normaliza- tion of renal function. A large volume of urine is drained from the bladder (often in the o rder of 1 \200\2232L and sometimes much greater). The serum creatinine is elevated and an u ltrasound will show hydronephrosis with a grossly distended bladder if the scan is done bef ore relief of retention. Anticipate a profound diuresis following drainage of the bladder due to: \200 Excretion of salt and water that has accumulated during the period of renal failure. Loss o f the corticomedullary concentration gradient, due to continued perfusion of the kidneys wi th diminished \202 ow of urine through the nephron (this washes out the concentration gra dient between the cortex and medulla). An osmotic diuresis caused by elevated serum urea co ncentration. A small percentage of patients have a postural drop in blood pressure. It is wise to admit patients with HPCR for a short period of observation until the diuresis has settled. A few will require intravenous \202 uid replacement if they experience a symptomatic fall in bl ood pressure when standing. De \201 nitive treatment TURP or a long-term catheter. In those unable to void who have be en catheterized, a TWOC is clearly not appropriate in cases where there is back pressure on the kidneys. Rarely, a patient who wants to avoid a TURP and does not want an indwelling c atheter will be able to empty their bladder by ISC. HIGH-PRESSURE CHRONIC RETENTION (HPCR) 121 1 Reynard JM (1999) Failure to void after transuretural resection of the prostate and mode of presentation. Urology 53:336 \200\2239. 2 Mitchell JP (1984) Management of chronic urinary retention. BMJ 289:515 \200\2236. CHAPTER 4 Bladder outlet obstruction 122 Bladder outlet obstruction and retention in women Relatively rare (75% of women undergoing pressure \202 ow studies have BOO, compared with 60% of unselected men with LUTS).1,2 It may be symptom-free, and present with LUTS or as acute urinary retention. In broad terms , the causes are related to obstruction of the ure- thra (e.g. urethral stricture, compress ion by a prolapsing pelvic organ such as the uterus, post-surgery for stress incontinence) or have a neurological basis (e.g. injury to sacral cord or parasympathetic plexus, degener ative neurological disease, e.g. MS, diabetic cystopathy). Voiding studies in women Women have a higher Qmax, for a given voided volume than do men. W omen with BOO have lower Qmax than those without BOO. There are no universally accepted uro dynamic criteria for diagnosing BOO in women. Treatment of BOO in women Treat the cause (e.g. dilatation of a urethral stricture; repair of a pelvic prolapse). Where this it is not possible (because of a neurological cause such as MS or SCI), the options are: \200 \200 \200 ISC or intermittent catheterization by a carer. Indwelling catheter (preferably suprapubic rather than urethral). Mitrofanoff catheterizable stoma. Where urethral intermittent self-catheterization is technically dif \201 cult, a catheteri zable stoma can be constructed between the anterior abdominal wall and the bladder, using t he appendix, Fallopian tube, or a narrowed section of small intestine. This is the Mitrofan off procedure. It is simply a new urethra which has an abdominal location rather than a per ineal one and is, therefore, easier to access for ISC. For women with a suprasacral SCI with preserved detrusor contrac- tion and urinary retentio n due to DSD, sacral deafferentation combined with a Brindley stimulator can be used to man age the resulting urinary retention. Fowler \200\231s syndrome A primary disorder of sphincter relaxation (as opposed to seconda ry to, for example, SCI). Increased electromyographic activity (repetitive dis- charges on external sphincter EMG) can be recorded in the external ure- thral sphincters of these wome n (which, on ultrasound, are of increased volume) and is hypothesized to cause impaired rel axation of external sphincter. Occurs in premenopausal women, typically aged 15 \200\22330, often in association with polycystic ovaries (50% of patients), acne, hirsutism, and menst rual irregularities. May also be precipitated by childbirth or gynaeco- logical or other su rgical procedures. They report no urgency with bladder volumes >1000mL, but when attempts a re made to manage their reten- tion by ISC, they experience pain, especially on withdrawing the catheter. BLADDER OUTLET OBSTRUCTION AND RETENTION IN WOMEN 123 Pathophysiology: may be due to a channelopathy of the striated urethral sphincter muscle, l eading to involuntary external sphincter contraction. Treatment: ISC, sacral neuromodulation with Medtronic Interstim (90% void post-implantation and 75% are still voiding at 3y follow-up). The mechanism of action of sacral neuromodulat ion in urinary retention is unknown. 1 Madersbascher S, Pycha A, Klingler CH, et al. (1998) The aging lower urinary tract: a com para- tive urodynamic study of men and women. Urology 51:206 \200\22312. 2 Swinn MJ, Wiseman OJ, Lowe E, Fowler CJ (2002) The cause and treatment of urinary retenti on in young women. J Urol 167:151 \200\2236. CHAPTER 4 Bladder outlet obstruction 124 Urethral strictures and stenoses A urethral stricture is a scar in the subepithelial tissue s of the corpus spongiosum which constricts the lumen of the urethra. Since it is only the anterior urethra that is surrounded by the corpus spongiosum, by consen- sus, urethral stri ctures are said only to affect the anterior urethra (Mundy).1 A narrowing of the caliber of the posterior urethra is termed a stenosis. Anterior urethral strictures The process of scar formation occurs in the spongy erectile ti ssue (corpus spongiosum) of the penis that surrounds the urethra \200\224spongio \201 bros is. \200 In \202 ammation (e.g. balanitis xerotica obliterans \200\224BXO), gonococcal i nfection leading to gonococcal urethritis (less common nowadays because of prompt treatment of gonorrhea). Trauma. \200 \200 Straddle injuries \200\224blow to bulbar urethra (e.g. cross-bar injury). Iatrogenic \200 \224instrumentation (e.g. traumatic catheterization, traumatic cystoscopy, TURP, bladder ne ck incision). The role of non-speci \201 c urethritis (e.g. Chlamydia) in the development of anterior ur ethral strictures has not been established. Posterior urethral stenoses Fibrosis of the tissues around the urethra results from trauma \200\224pelvic fracture or surgical (radical prostatectomy, TURP, urethral instrumenta- tio n). By consensus, they are now described as stenosis and are no longer described as strictu res. These are essentially distraction injuries (leading to a stenosis of the urethra), whe re the posterior urethra has been pulled apart and the subsequent healing process results i n the formation of a scar which contracts and thereby narrows the urethral lumen. Symptoms and signs of urethral stricture \200 \200 \200 Voiding symptoms \200\224hesitancy, poor \202 ow, post-micturition dribbling. Urinary ret ention \200\224acute, or high pressure acute-on-chronic. Urinary tract infection \200\224pr ostatitis, epididymitis. Management of urethral strictures Where the patient presents with urinary retention, the di agnosis is usually made following a failed attempt at urethral catheterization. In such cas es, avoid the temptation to \200\230blindly \200\231 dilate the urethra. Dilatation may be the wrong treatment option for this type of stricture \200\224it may convert a short stric ture, which could have been cured by urethrotomy or urethroplasty, into a longer and more d ense stricture, thus committing the patient to more complex surgery and a higher risk of re current stricturing. Place a suprapubic catheter instead and image the urethra with retrogr ade and antegrade urethrography to establish the precise position and the length of the str icture. Similarly, avoid the temptation to inappropriately dilate a urethral stric- ture diagnosed at \202 exible cystocopy (urethroscopy). Arrange retrograde urethrography so appropriate treatment can be planned. URETHRAL STRICTURES AND STENOSES 125 Treatment options Urethral dilatation: designed to stretch the stricture without causing mo re scarring; bleeding post-dilatation indicates tearing of the stricture (i.e. fur- ther in jury has been caused) and re-stricturing is likely. Internal (optical) urethrotomy: stricture incision with an endoscopic knife or laser. Divid es the stricture, followed by epithelialization of the incision. If deep spongio \201 bros is is present, the stricture will recur. Best suited for short (<1.5cm) bulbar urethral str ictures with minimal spongio \201 brosis.2 Leave a catheter for 3 \200\2235 days (what evi dence there is suggests keeping a catheter for 3 days reduces the risk of extravasation of urine and infective complications that may result;1 longer catheterization does not reduce long-term re-stricturing). Consider ISC for 3 \200\2236 months, starting several times dail y, reducing to once or twice a week towards the end of this period. For strictures in other parts of the anterior urethra or where there has been a previous optical urethrotomy or di latation, an optical urethro- tomy will almost certainly fail to cure the stricture. Avoid optical urethro- tomy for sphincter strictures (e.g. post-TURP) because the sphincter may b e rendered incompetent \200\224dilatation is a safer option. Excision and reanastomosis or tissue transfer: best chance of cure; excises the area of spo ngio \201 brosis with primary re-anastomosis or closure of defect with buccal mucosa or pe dicled skin \202 ap. Stricturotomy and buccal mucosal grafting, rather than transecting t he entire urethra and then re- anastomosing it, is becoming increasingly popular (but not f or strictures that obliterate the entire urethral lumen). A stepwise progression up this \200\230reconstructive ladder \200\231 (the process of star ting with a simple procedure and moving onto the next level of complexity when this fails) is not appropriate for every patient. For the patient who wants the best chance of long-ter m cure, offer excision and re-anastomosis or tissue transfer up front. For the patient who is happy with lifelong \200\230management \200\231 of his stricture (with repeat dilatatio n or opti- cal urethrotomy), offer dilatation or optical urethrotomy. Balanitis xerotica obliterans (BXO) Genital lichen sclerosis and atrophicus in the male. Hy perkeratosis is seen histologically. Appears as a white plaque on the foreskin, glans of th e penis, or within the urethral meatus. Most common cause of stenosis of the meatus. Foresk in becomes thickened and adheres to the glans, leading to phimosis (a thickened, non-retrac tile foreskin). Patients with longstanding BXO and meatal stenosis often have more proximal urethral strictures. 1 Mundy AR, Andrich DE (2010) Urethral strictures. BJU Int 107:6-26. 2 Pansadoro V, Emiliozzi P (1996) Internal urethrotomy in the management of anterior urethr al strictures: long term follow-up. J Urol 156:73 \200\2235. This page intentionally left blank 127 Chapter 5 Incontinence and female urology Incontinence: classi \201 cation 128 Incontinence: causes and pathophysiology 130 Incontin ence: evaluation 132 Stress and mixed urinary incontinence 136 Surgery for stress incontine nce: injection therapy 138 Surgery for stress incontinence: retropubic suspension 140 Surge ry for stress incontinence: suburethral tapes and slings 142 Surgery for stress incontinence: arti \201 cial urinary sphincter 146 Overactive bladder: conservative and medical treatments 148 Overactive bladder: options for failed conventional therapy 150 Overactive bladder: intravesical botulinum toxin-A therapy 152 Post-prostatect omy incontinence 154 Vesicovaginal \201 stula (VVF) 156 Incontinence in elderly patients 158 Management pathways for urinary incontinence Initial management of urinary incontinence in women 160 Specialized management of urinary i ncontinence in women 161 Initial management of urinary incontinence in men 162 Specialized management of urinary incontinence in men 163 Management of urinary incontinence in frail o lder persons 164 Female urethral diverticulum (UD) 166 Pelvic organ prolapse (POP) 170 CHAPTER 5 Incontinence and female urology 128 Incontinence: classi \201 cation De \201 nition Urinary incontinence (UI) is the complain t of any involuntary leakage of urine.1 It results from a failure to store urine during the \201 lling phase of the bladder due to dysfunction of the bladder smooth muscle (detruso r), urethral sphincter, or anatomical abnormalities (congenital or acquired). Urine loss is either urethral or extraurethral (i.e. due to ectopic ureter or vesicovaginal \201 stula ). Prevalence There is wide variation in the reported prevalence of UI worldwide. It affects a bout 3.5 million people in the UK. The prevalence is approxi- mately twice as common in fem ales compared to males and increases with age (Table 5.1).2 International studies show a gr adual increase in the prevalence of female UI during adulthood to 30%, stabilizing between the ages of 50 and 70y old, before rising again.3 Approximately 50% of women suffer stress UI, 11% urgency UI, and 36% mixed UI.3 Classi \201 cation Stress urinary incontinence (SUI): involuntary urinary leakage on effor t, exertion, sneezing, or coughing.1 It is due to hypermobility of the bladder base, pelvic \202 oor and/or intrinsic urethral sphincter de \201 ciency. When con- \201 rmed on u rodynamic testing, it is termed urodynamic stress incontinence. It was further categorized by Blaivas4 (using videourodynamics) into: - - Type 0: Type I: bladder base below the upper border of the symphysis pubis. Type II: descen t (>2cm) that occurs only during stress (IIa) or is permanently present (IIb). bladder neck and proximal urethra are already open at rest Type III: (with or without descent), which i s also known as intrinsic sphincter de \201 ciency (ISD). report of UI, but without clinical signs. leakage that occurs during stress with <2cm desce nt of the leakage on stress accompanied by marked bladder base Urgency urinary incontinence (UUI): involuntary urine leakage accompa- nied by or immediate ly preceded by urgency (a sudden, strong desire to void).1 Previously called \200\230urge \200\231 urinary incontinence, it is due to an over- active detrusor muscle. The urodynamic diagnosis is termed \200\230detrusor overactivity incontinence \200\231. It is a componen t of the overactive bladder syndrome (see OAB b p. 148). Mixed urinary incontinence (MUI): involuntary leakage associated with urgency and also with exertion, effort, sneezing, or co ughing.1 It contains symptoms of both SUI and UUI. Over \202 ow incontinence: is leakage o f urine when the bladder is abnormally distended with large residual volumes. Typically, me n present with chronic urinary retention (with a degree of detrusor failure) and dribbling incon- tinence. This can lead to back pressure on the kidneys and renal failure in 30% of p atients. BOO must be corrected; detrusor failure can be managed with clean intermittent sel f-catheterization (CISC) or indwelling catheter. INCONTINENCE: CLASSIFICATION 129 Nocturnal enuresis: the complaint of loss of urine occurring during sleep.1 The prevalence in adults is about 0.5%5 and 7 \200\22310% in children aged 7y old.6 Nocturnal enuresis can be further classi \201 ed into primary types (never been dry for longer than a 6-month pe riod) or secondary (the re-emergence of bedwetting after a period of being dry for at least 6 \200\22312 months; see b p. 694). In an adult male, nocturnal incontinence may be an ind icator of high-pressure chronic retention (see b p. 120). Post-micturition dribble: involun tary loss of urine immediately after the individual has \201 nished passing urine, usuall y after leaving the toilet in men or after rising from the toilet in women.1 In men, it is due to pooling of urine in the bulbous urethra after voiding. A recent standardization report by the International Urogynaecology Association and the Int ernational Continence Society on female pelvic \202 oor dysfunction7 recommend new de \201 nitions, including: - Continuous incontinence: loss of urine. Insensible incontinence: been unaware of how it occ urred. Coital incontinence: coitus. the complaint of continuous involuntary the complaint of UI where the women has the complaint of involuntary loss of urine with Table 5.1 Prevalence of urinary incontinence in the UK Age (y) Females Males 15 \200\22344 5 \200\2237% 3% 45 \200\22364 8 \200\22315% 3% 65+ 10 \200\22320% 7 \200\22310% 1 Abrams P, Cardozo L, Fall M, et al. (2002) The standardization of terminology of lower ur inary tract function: report from the standardization sub-committee of the International Co ntinence Society. Neurourol Urodyn 21:167 \200\22378. 2 Royal College of Physicians. Incontinence: causes, management and provision of services. Report of a working party. London: RCP 1995. Available from: M www.rcplondon.ac.uk. 3 Hannestad YS, Rortveit G, Sandvik H, et al. (2000) A community-based epidemiological surv ey of female urinary incontinence: The Norwegian EPINCONT Study. J Clin Epidemiol 53:1150 \200\2237. 4 Blaivas JG, Olsson CA (1988) Stress incontinence: classi \201 cation and surgical approa ch. J Urol 139:727 \200\22331 5 Hirasing RA, van Leerdam FJM, Bolk-Bennink L, et al. (1997) Enuresis nocturna in adults. Scan J Urol Nephrol 31:533 \200\2236. 6 Abrams P, Cardozo L, Khoury S, Wein A (2009) Epidemiology of Urinary and Fecal Incontinen ce and Pelvic Organ Prolapse. 4th International Consultation on Incontinence, pp 39 \200 \22341. London: Health Publications Ltd. 7 BT Haylen, D de Ridder, RM Freeman, et al. (2010) An International Urogynecological Assoc iation (IUGA)/International Continence Society (ICS) joint report on the terminology for fe male pelvic \202 oor dysfunction. Int Urogynecol J 21:5 \200\22326. CHAPTER 5 Incontinence and female urology 130 Incontinence: causes and pathophysiology General risk factors for UI Predisposing factors - - - - Gender (female > males). Race (Caucasian > Afro-Caribbean). Genetic predisposition. Neurolo gical disorders (spinal cord injury ( sclerosis, Parkinson \200\231s disease). Anatomical d isorders (vesicovaginal \201 stula, ectopic ureter in girls, urethral diverticulum, ureth ral \201 stula, bladder exstrophy, epispadias) Childbirth (vaginal delivery, increasing p arity) and pregnancy. Anomalies in collagen subtype. Pelvic, perineal, and prostate surgery (radical hysterectomy, prostatectomy, TURP), leading to pelvic muscle and nerve injury. Ra dical pelvic radiotherapy. Diabetes. SCI), stroke, multiple - Promoting factors - - - - - - - - - - Smoking (causing chronic cough and raised intra-abdominal pressure). Obesity. Infection ( I ncreased \202 uid intake. Medications (i.e. alpha blockers in women). Poor nutrition. Age ing. Cognitive de \201 cits. Poor mobility. Estrogen de \201 ciency. UTI). Pathophysiology Urodynamic studies can help determine the underlying etiology for UI. Bladder abnormalities Detrusor overactivity: a urodynamic observation characterized by invo l- untary bladder muscle (detrusor) contractions during the \201 lling phase of the bladd er, which may be spontaneous or provoked and can consequent- ly cause UI. The underlying ca use may be neuropathic where there is a relevant neurological condition or idiopathic where there is no de \201 ned cause. It leads to the symptoms of urgency incontinence and overa ctive bladder (OAB). The pathogenesis of detrusor overactivity is most likely to be multifac- torial. Theories include: - Myogenic hypothesis: increased excitability and activity betwee n muscle cells.1 Neurogenic hypothesis: muscle cells.2 partial detrusor denervation, leading to disruption of primary neural control in INCONTINENCE: CAUSES AND PATHOPHYSIOLOGY 131 detrusor muscle is arranged in modules Integrative hypothesis: which are thought to be controlled by a peripheral myovesical plexu s composed of intramural ganglia and interstitial cells. Detrusor overactivity results from abnormal or exaggerated peripheral autonomic activity (within this plexus).3 Low bladder compliance: characterized by a decreased volume-to-pres- sure relationship wher e there is a high increase in bladder pressure during \201 lling due to alterations in el astic properties of the bladder wall or changes in muscle tone (secondary to myelodysplasia , SCI, radical hysterectomy, interstitial or radiation cystitis). Urethral and sphincter abnormalities In females, there may be functional abnormalities of u rethral hypermobility and/or ISD. These are the main causes of SUI. Urethral hypermobility: due to a weakness of pelvic \202 oor support, caus- ing a rotatio nal descent of the bladder neck and proximal urethra during increases in intra-abdominal pr essure. If the urethra opens concomitantly, there will be urinary leaking. Intrinsic sphincter de \201 ciency: describes an intrinsic malfunction of the sphincter, r egardless of its anatomical position, which is responsible for type III SUI (described by M cGuire). Causes include inadequate urethral compression (previous urethral surgery, ageing, menopause, radical pelvic surgery, anterior spinal artery syndrome) or de \201 cient uret hral support (pelvic \202 oor weakness, childbirth, pelvic surgery, menopause). In males, the urethral sphincter may be damaged after prostatic or pelvic surgery (TURP, radical pro statectomy) or radiotherapy. Theories for the pathogenesis of SUI include: Integral theory: ligaments, causing bladder neck hypermobility.4 Hammock hypothesis: fascia and vaginal wal l.5 laxity of anterior vaginal wall and pubourethral failure of support of urethra by the endopelvic 1 Brading AF (1997) A myogenic basis for the overactive bladder. Urology 50:57 \200\22367 2 De Groat WC (1997) A neurological basis for the overactive bladder. Urology 50:36 \200 \22352. 3 Drake MJ, Mills IW, Gillespie JI (2001) Model of peripheral autonomous modules and a myo- vesical plexus in normal and overactive bladder function. Lancet 358:401 \200\2233. 4 Petros PE, Ulmsten UI (1990) An integral theory of female urinary incontinence. Experimen tal and clinical considerations. Acta Obstet Gynecol Scand Suppl. 153:7 \200\22331. 5 DeLancey JO (1994) Structural support of the urethra as it relates to stress urinary inco nti- nence: the hammock hypothesis. Am J Obstet Gynecol 170:1713 \200\22320. CHAPTER 5 Incontinence and female urology 132 Incontinence: evaluation History Aim: to establish the type of incontinence (stress, urgenc y or mixed). Enquire about LUTS (storage or voiding symptoms); triggers for inconti- nence (cough, sneezing, exercise, position, urgency); frequency, severity, and degree of bother o f symptoms. Establish risk factors (abdominal/pelvic surgery or radiotherapy, neurological disorders, obstetric and gynaecol- ogy history, medications). Enquire about bowel function and symptoms of sexual dysfunction and pelvic organ prolapse in women (see b p. 170) A vali dated patient-completed questionnaire is helpful to assess initial symp- toms and patient-r eported outcome following intervention (ICIQ-UI short form,1,5 ICIQ-FLUTS,2 ICIQ-MLUTS,3 SF 36 QoL4) (Fig. 5.1). \200\230Red \202 ag \200\231 symptoms which require further speci \201 c investigation are incontinence associated with pain, haematuria, recurrent UTI, signi \201 cant voiding or obstructive symptoms, and a previous history of pelvic surgery/ radiotherapy. Physical examination Women Perform a chaperoned pelvic examination in the supine, standing, and left lateral position with a Sim \200\231s speculum. Ask the patient to cough or strai n and inspect for anterior and posterior vaginal wall prolapse, uterine or vaginal vault de scent, and urinary leakage (stress test). Internal pelvic ex- amination can be performed to assess the strength of voluntary pelvic \202 oor muscle strength and for bladder neck mo bility. Inspect the vulva for estrogen de \201 ciency (causing vaginal atrophy), which may require topical estrogen treatment. Calculate of body mass index (BMI) as a tool to counse l patients as higher BMIs are associated with incontinence. Both sexes Examine the abdomen for a palpable bladder (indicating urinary reten- tion if th e patient has recently passed urine). A neurological examination should include assessment of gait, anal re \202 ex, perineal sensation, and lower limb function. DRE should be perfo rmed to exclude constipation, a rectal mass, and to test anal tone. \200\230Red \202 ag \200\231 signs requiring further investigation include (new) neurolo gi- cal de \201 cit, haematuria, urethral, bladder or pelvic masses, and suspected \201 stula. INCONTINENCE: EVALUATION 133