23.2.1.1.1 Urodynamics

The term ‘urodynamics’ encompasses all tests of function, assessment of pressure or flow in the LUT, including uroflowmetry, measurement of postvoid residual (PVR) urine, pad tests, filling cystometry, pressure or flow cystometry, video cystometrography, and ambulatory urodynamics.

Urodynamic studies provide a snapshot in time. The observations are specific to the individual patient and relevant to the duration of the test. This is borne out in studies that have shown results of urodynamic tests to be variable even in the same individual at different time points [2]. The results of urodynamics do not appear to influence the outcome of treatment for stress UI [2].

Urodynamics, as the name suggests, is a dynamic test, and therefore, interpretation of results is dependent on the interpreter being present for the duration of the test. Review of traces ‘after the fact’ can be misleading, unless the events and occurrences during the test are described in detail in the report. Figure 23.1 depicts the various traces for the corresponding complaints.

The use of urodynamics is largely a matter of preference, expertise, and availability. It is a urologist’s tool, and when used appropriately, can help inform management decisions. Equally, when used inappropriately or without the required expertise, it may at best put the patient at unnecessary risk and embarrassment, and at worst, cause significant harm.

23.2.1.1.2 Urine Flow Rate

The rate of urine flow depends upon the expulsive force developed by the detrusor and the outflow resistance during micturition. Both factors can be affected by psychological factors and flow rate measurements on a voided volume of less than about 150 ml may not be reliable. A uroflow measurement will usually give a graphic read out which presents the pattern of flow, its maximum (Qmax) and average (Qave) rate, as well as the total volume of urine passed (Vcomp) (Figure 23.2). A single flow measurement should be treated with caution, but most normal men should be able to produce a maximum peak flow of 15 ml s⁻¹ or more. A maximum flow of less than 10 ml s⁻¹ is usually taken as abnormal. A normal flow rises to a peak which is sustained for most of the void. Infravesical obstruction produces a flattened curve (Figure 23.3), which classically has a box shape when the obstruction is caused by urethral stricture. Obstructed voiding due to failure of sphincter relaxation typically gives a pattern of intermittent flow (Figure 23.4). This picture is seen in the detrusor–sphincter dyssynergia of neurological disease as well as the rather less well‐explained failure of voluntary relaxation of the external sphincter which afflicts some men, especially when they attempt to void in public places.

The urine flow rate is normally greater in women who may be able to generate maximum rates in excess of 25 ml s⁻¹ if 50 years of age or younger and > 18 ml s⁻¹ if 50 years of age or older.

23.2.1.1.3 Filling Cystometry

Compliance is the change in intravesical pressure which occurs with a given change in volume (ml/cm H₂O). There is very little increase in the pressure within the normal bladder as it fills (i.e. compliance is very high). There is a cessation of detrusor activity possibly mediated in part by the sympathetic nervous system. At some point, which partly depends upon the filling rate, the subject becomes aware of a sensation from the bladder. This first sensation is succeeded by an urge to void which can be suppressed even though it is associated with a transient rise in intravesical pressure. Further bladder filling is usually uncomfortable.

The technique of filling cystometry varies, but the principle is simple. Starting with an empty bladder, a catheter is used to fill the bladder while intravesical pressure is measured by means of a second catheter. A pressure line in the rectum measures variations in intra‐abdominal pressure which are electronically subtracted from the intravesical pressure to give a graphic read out of the calculated detrusor pressure (Figure 23.5).

During the filling study, the patient is asked to report sensations from the bladder. The volumes at which first sensation is felt and when there is an urge to void are taken as important measures of bladder sensation. The pressure trace is scanned to detect rises in pressure which reflect abnormal detrusor contractions. The onset of these contractions may be affected by the rate of filling and the temperature of the filling fluid, and patients may be asked to perform other manoeuvres (e.g. to cough or to change position) to provoke them. If they occur, the patient is asked to attempt to suppress them, and a note is made as to whether this is possible.

Abnormalities of the Filling Cystometrogram

Sensory Frequency or Urgency

Even if patients are carefully selected for filling cystometrography because they have unexplained urgency and frequency with or without incontinence, the detrusor pressure trace is often normal, with an end filling pressure of less than 15 cm H₂O and no abnormal detrusor contractions. A proportion of these patients report their first sensation and urge to void at a smaller filling volume than would be expected; they are labelled as suffering from ‘sensory urgency’. Because this may be the result of intravesical pathology, a cystoscopy is always indicated. If there is no bladder lesion, the term might be taken to imply a hypersensitivity of the bladder, but no adequate explanation of the pathophysiology of this condition has ever been offered.

Detrusor Overactivity

Uninhibited detrusor contractions during filling that cannot be suppressed and give rise to detrusor pressures of more than 15 cm H₂O (Figure 23.6) are characteristic of ‘idiopathic detrusor overactivity’ in patients without neurological disease. In the presence of neurological disease, this is termed ‘neurogenic detrusor overactivity’. The urethral sphincter can withstand high intravesical pressures up to a point, but beyond that threshold (which will vary from individual to individual and is usually higher in men than in women) leakage will occur. If detrusor overactivity leads to intravesical pressures that overcome sphincteric resistance that leads to leakage, this is termed ‘urge urinary incontinence’ (UUI).

Poor Detrusor Compliance

Sometimes the detrusor pressure shows a steady rise during filling to reach an end filling pressure greater than 15 cm H₂O (Figure 23.7). This may be due to ‘small bladder syndrome’ from fibrosis after radiotherapy or extensive bladder surgery. Alternately, it is seen against a background of neurological disease, especially of the lower segments of the spinal cord. It may also be seen sporadically in neurologically intact individuals and is then difficult to explain, but is thought to be due to failure of the neurally mediated normal bladder compliance mechanism.

23.2.1.1.4 Voiding Pressure Studies

In some patients, it is impossible to tell whether they have BOO just from a measurement of flow rate and postmicturition residual volume, and in these patients, it may be useful to measure the detrusor pressure as the patient voids. In men, the upper limit of normal voiding pressure is about 60 cm H₂O and in women 40 cm H₂O. In those with outflow obstruction, the voiding pressure may be significantly higher and may or may not be associated with a low flow. There is a tendency for the urethral pressure line to be expelled during voiding, and to get a true measurement, it may be necessary to insert a line through a suprapubic needle. As the bladder outlet obstructs, the pressure‐flow dynamics are generally thought to follow a pattern of going from ‘normal pressure, normal flow’ to ‘high pressure, normal flow’ to ‘high pressure, low flow’ and finally ‘low pressure, low flow’ as the obstruction gets steadily worse. The perceived wisdom is that once the stage of ‘low pressure, low flow’ is reached then the success rate of interventions such as a transurethral resection of prostate (TURP) is generally poorer.

23.2.1.1.5 Videocystometry

If X‐ray fluoroscopic equipment is available, important anatomical information can be obtained by using water‐soluble X‐ray contrast medium to fill the bladder. This will demonstrate the saccules, the thickened bladder wall, and the ‘fir tree’ appearance of the high‐pressure neuropathic bladder. In stress incontinence, weakness of the supportive tissues around the bladder neck may become evident with descent of the pelvic floor during coughing and at the same time contrast may enter the urethra to give the appearance of ‘beaking’ (Figure 23.8) or be seen to leak all the way through in frank incontinence. Urethral hypermobility during coughing or valsalva is an important screening observation and should be noted during video cystometry for stress incontinence. Another advantage of video screening is the ability to assess for vesicoureteric reflux, although the value of this observation in adults with normal renal function is limited.

Uroflow, filling and voiding cystometry, with or without video, along with measurement of the postmicturition residual urine volume are the elements of a standard urodynamic study. Other investigations including urethral pressure profilometry and the fluid bridge test for stress incontinence are research tools which are insufficiently standardised for general use.

23.3.1.1.1 Definition and Incidence

OAB is defined as urgency, with or without urgency incontinence, usually associated with frequency and nocturia. OAB has been described as a ‘syndrome’ due to the multitude of commonly associated symptoms, but the hallmark symptom classically described is urgency (Table 23.1).

Two types of OAB are distinguished in the literature: OAB dry and OAB wet (i.e. associated without or with UI).

The prevalence of OAB ranges between 8 and 30%, depending on the definitions used and age of patients [3, 4]. Risk factors associated with OAB are increasing age (nearly 20% of >40 s will suffer OAB symptoms), high body mass index (BMI), cognitive impairment, depression, and diabetes [3, 5, 6].

23.3.1.1.2 Aetiology

Urgency and OAB symptoms are manifestations of bladder smooth muscle contraction during the filling phase of the bladder. What causes these contraction is yet to be determined. The probable cause of dysfunction is in the afferent sensory nervous pathways from the bladder. This is an area of ongoing study, as is the role of different sensory receptors. The classical muscarinic receptors have been targets for therapy for a number of years, but more recently, the beta‐receptors (specifically beta‐3) have been a source of great interest.

23.3.1.1.3 History, Physical Examination, and Important Differential Diagnoses

Important points in the history (applicable to OAB and UI) are:

• Duration and severity, such as number of pads or change of clothes per day.
  
• Circumstances around the incontinence – whether associated with any particular activity, change of position or exercise; ‘key‐in‐the‐door syndrome’; associated urgency.
  
• Bowel function, such as faecal incontinence, constipation/diarrhoea, digitation.
  
• Red flag symptoms (pain, haematuria, recurrent UTI, incomplete emptying, lack of sensation and neurological symptoms) – presence of any of these symptoms requires urgent specialist referral.
  
• Past medical history, including diabetes, cardiac failure, or glaucoma.
  
• History of previous pelvic radiotherapy or surgery.
  
• Drug history, particularly use of anticholinergics, antidepressants, diuretics, oestrogens, laxatives, over‐the‐counter, and illicit drugs.
  
• Obstetric history, including episiotomy and any other assisted delivery.
  
• Mobility.
  
• Dexterity.

It is important to examine all patients to rule out other significant associated features such as neurological disease, stigmata of chronic kidney dysfunction, vaginal dryness and atrophy in women, vaginal prolapse, chronic retention (more commonly in men), rectal examination of the prostate in men, etc.

Other pathologic conditions, like bladder stones and UTIs, must have been excluded to diagnose OAB. The combination of urgency, frequency, and nocturia is suggestive of detrusor overactivity (DO). However, DO is a urodynamic finding and not a clinical one [7], and not all patients with symptoms of OAB will have demonstrable DO on urodynamic investigation.

Frequency can be both an initial symptom and a coping strategy in patients with urgency. In fact, urgency is often more troublesome than established UUI. A patient who is OAB dry may live in fear of leakage all day every day, whereas a patient who is OAB wet patient might just wear some containment device, and their life will no longer be ruled by the distance from the nearest toilet.

The following alternative diagnoses need to be considered and excluded to diagnose idiopathic OAB:

• Intravesical pathology (e.g. stones, bladder cancer, carcinoma in situ, or UTI).
  
• Neurogenic bladder dysfunction.
  
• BOO (e.g. benign prostatic enlargement [BPE] or urethral strictures).

DO can be triggered by certain events, such as key‐in‐the‐door syndrome, or exertion. The latter is likely to complicate the diagnostic process because it is different from true stress UI.

23.3.1.1.4 Investigations

Initial investigations are as previously mentioned, and if satisfactory, urodynamic tests may be indicated. However, the absence of DO during a urodynamic study does not exclude DO in the patient, rather one can only conclude that DO could not be demonstrated at the time of the study. It is crucial to note whether the patient’s symptoms were reproduced during the study and what was seen at that time. Any urodynamic study that failed to reproduce the patient’s symptoms is of little value. Equally, the absence of DO on urodynamics should not preclude pharmacological therapy for OAB if clinically indicated.

23.3.1.1.5 Treatment

1. Conservative treatment or lifestyle modification

General advice includes regular exercise and to stop smoking.

In patients who are overweight or obese, it is useful to start with weight loss to improve the symptoms of UI and OAB. It has been shown that losing weight can also be preventative in developing UI, especially in patients suffering from diabetes [8, 9]. Several studies have shown a correlation between constipation and UI and OAB, although no causal relationship has been established. If constipation is apparent, it should be addressed [1, 10, 11].

A number of patients report very high (>3 l) or very low (<1 l) fluid intake in their bladder diaries. Adaptation of fluid intake may result in an improvement of symptoms. Patients who are constipated might resolve their constipation by increasing their fluid intake [12].

Some patients have a high caffeine intake associated with OAB. A reduction in caffeine intake may improve OAB symptoms in some patients, especially symptoms of urgency and frequency [13].

In patients with UUI, MUI and OAB, bladder training can be an effective initial therapeutic strategy. However, there is a general lack of understanding as to what constitutes ‘bladder training’. It is sometimes used interchangeably with timed voiding, behavioural changes, scheduled voiding, bladder drill, etc. A fairly comprehensive definition is: ‘A program of patient education along with a scheduled voiding regimen with gradually adjusted voiding intervals. Specific goals are to correct faulty habit patterns of frequent urination, improve control over bladder urgency, prolong voiding intervals, increase bladder capacity, reduce incontinent episodes and restore patient confidence in controlling bladder function’. The optimal duration remains unclear, but it is suggested to be a minimum of six weeks [14].

2. Medical treatment

Before considering the different classes of drugs available to treat OAB symptoms, it is important to distinguish the real‐world difference in treating urgency and treating incontinence. Too often these objectives are confused, and the evidence from drug trials is heavily weighted towards the treatment of urgency and frequency. When evaluating the literature for studies on anticholinergics or beta‐3 agonists, it is therefore important to note the primary outcome measure used because this will guide the reader to determine whether the study was aimed at evaluating treatment of urgency or frequency or urge incontinence.

The use of anti‐muscarinic drugs has been proven to be an effective treatment for OAB and UUI in 50–75% of patients. The muscarinic receptor blockade leads to a decreased ability of the detrusor muscle to contract and a decreased sensation of urgency. It also leads to increased bladder capacity and increased mean volume voided, all of which lead to reduction in symptoms. A wide range of anti‐muscarinic drugs are available, such as oxybutynin, tolterodine, solifenacin, darifenacin, trospium chloride, and fesoterodine [3], but none of these specific drugs has been proven to be more effective than others in the treatment of OAB [15].

Optimal efficacy of anti‐muscarinic drugs may take up to four weeks. When no satisfactory improvement can be established after four weeks, an increase in dose or change in drug may be indicated [14].

Anti‐muscarinic drugs are commonly known to have a high incidence of adverse events due the wide presence of muscarinic receptors throughout the body (Table 23.6). Side effects include dry mouth, blurred vision and constipation. Cognitive impairment, particularly in the elderly, has become a recent focus of attention [16]. Side effects can cause discontinuation rates of up to 86% after 12 months of treatment [17].

Oxybutynin, trospium chloride, and tolterodine are nonselective muscarinic blockers. Solifenacin is selective M2and M3, and darifenacin is selective for M3.

Myasthenia Gravis, narrow angle glaucoma, significant BOO, active ulcerative colitis, toxic megacolon, and gastrointestinal obstruction are contraindications of anticholinergics.

Oxybutynin and tolterodine are currently off‐patent and therefore standard formularies would recommend them as first‐line treatment, with other anticholinergics available as second‐line in treatment failures or in case of intolerable side effects. There is evidence that Oxybutynin may worsen cognitive function in the elderly, and in these patients, fesoterodine, solifenacin, or darifenacin may be better alternatives [2].

The use of adrenergic drugs, such as the beta‐3 adrenoceptor agonist mirabegron, for OAB and UUI has been introduced in recent years. It promotes receptive relaxation during the storage phase by binding to and activating the beta‐3 adrenergic receptor (Chapter 17) [18]. Mirabegron has been shown to be better than placebo for the treatment of urgency or frequency symptoms, but the evidence for cure of incontinence is weak. Head‐to‐head studies comparing it to standard anti‐muscarinics are currently lacking. However, it is interesting to note with mirabegron that most of the randomised studies were conducted on participants who had failed on anti‐muscarinic therapy; hence, it may be underrepresenting its real‐world effectiveness in treatment‐naïve patients. National Institute for Health and Clinical Excellence (NICE) currently states, ‘Mirabegron is recommended as an option for treating the symptoms of overactive bladder only for people in whom anti‐muscarinic drugs are contraindicated or clinically ineffective, or have unacceptable side effects’ (NICE TA290).

Comparison of adverse events seems to favour mirabegron [19], but a recent safety update has been issued, warning against its use in patients with uncontrolled hypertension.

3. Botulinum toxin A (BoNT‐A)

Botulinum toxin A (BoNT‐A) is a neurotoxin produced by the gram‐positive Clostridium botulinum bacteria. There are eight distinct serotypes, but only types A and B are licenced for therapeutic purposes. Botulinum toxin A has five subtypes, the most commonly used being onabotulinum toxin A (e.g. BOTOX™) and Abobotulinum toxin A (e.g. DYSPORT™). Botulinum toxin acts by binding to the synaptic vesicle protein (SV2) on the presynaptic nerve terminal. Once in the cells, it causes proteolysis of the synaptosomal associated protein, SNAP‐25, one of the SNARE proteins (an acronym derived from ‘SNAP [Soluble NSF Attachment Protein] REceptor’) which are responsible for vesicle fusion with the cell membrane (i.e. endocytosis). It thus inhibits the release of Ach at the neuromuscular junction of cholinergic neurons, and hence, induces a flaccid paralysis of the detrusor muscle. In addition it reduces the expression of neuronal receptors such as the transient receptor potential cation channel subfamily V member 1 (TrpV1) (vanilloid receptor 1) and the purinoreceptor P2X3 on sensory nerves, leading to reduced sensation [20].

Injections with BoNT‐A in the bladder can be performed in an outpatient setting under local anaesthesia or in the operating theatre under sedation or general anaesthesia. The starting dose of 100 U for idiopathic OAB with or without UUI is optimal, but doses up to 200 U or, in rare cases, 300 U may be used. For neurogenic DO, a dose of 300 U is commonly required. The recommendation from the manufacturer of BOTOX™ is to dilute the required dose in 10 ml of saline and inject the solution in 0.5 ml aliquots to 20 sites in the submucosa of the bladder wall avoiding the dome (risk of extravesical injection) and trigone (theoretical risk of ureteric paralysis and reflux, although this has not been demonstrable in clinical trials).

The effects are noticeable by the first week and last between three and nine months. BoNT‐A appears to have a much higher rate of cure of UUI compared to anti‐muscarinics, with patients reporting on average 50% reduction in UUI episodes a day and 23% of patients reporting being completely dry [21].

Repeat injections are necessary because of the mean effectiveness of three to nine months, and there is no evidence so far that repeat injections have reduced efficacy. About 5–10% of the patients with OAB develop significant PVR (>150 ml) and sometimes urinary retention after intravesical BoNT‐A injections, and this is more common in the elderly. Therefore, as a precaution, all patients should be instructed how to perform clean intermittent catheterization (CIC) before the first BoNT‐A injections, or at least should be made aware that this may become necessary, and they must be willing to learn the technique if required. Haematuria is a common procedural complication. Also, UTIs are common [22, 23] with rates of up to 25%. Rarely systemic side effects occur such as generalised muscular weakness, difficulty in taking a deep breath or swallowing, or blurred vision due to intraocular muscle weakness. These are usually self‐limiting, resolving within a few weeks.

Patients with Myasthenia gravis or Eaton‐Lambert syndrome are contraindicated for Botulinum toxin injections due to the risk of increasing muscular weakness or paralysis. Aminoglycosides enhance the effects of the toxin and should be avoided.

4. Posterior tibial nerve stimulation (PTNS)

The posterior tibial nerve is stimulated using an electrode inserted above the ankle near the medial malleolus. This can be done percutaneously (P‐PTNS) or transcutaneously (T‐PTNS). Thirty‐minute treatment is delivered on a weekly basis for 12 weeks. It is indicated in patients suffering from OAB who have not benefitted from anti‐muscarinic therapy and is minimally invasive. P‐PTNS gives rise to an improvement of >50% in symptoms [2, 24]. In addition, compared to anticholinergic treatment, it showed similar satisfactory results [25]. Note that results with anti‐muscarinics, in real‐world practice, are extremely variable, and so with PTNS also.

5. Neuromodulation with sacral nerve stimulation (SNS)

An invasive treatment that can be considered to treat refractory OAB symptoms. The third sacral nerve is electrically stimulated and during a test phase with a temporary percutaneous lead electrode the effectiveness of the stimulation is evaluated. The percutaneous nerve evaluation (PNE) lasts one week and patients who show an improvement of more than 50% in their symptoms and mean voided volume are eligible for placement of a permanent electrode and a pulse generator in the buttock of the patient. This requires major surgery under an anaesthetic; therefore, careful patient selection and optimisation is essential. It is also worth noting that this surgery requires prone positioning, and therefore, is not suitable for patients with a high BMI due to the risk of respiratory compromise.

The pulse generator is programmed with stimulation activated just above the threshold of a sensation in the urogenital area. Patients can choose between different programmes [26]. The average life span of the Interstim II battery is 4.5 years. This treatment modality has shown satisfactory results in up to 60% of the patients during long‐term follow‐up [27]. Complications involve occasional wound infections and surgical revision of the generator or tined lead [23].

6. Augmentation cystoplasty

Much less commonly performed for OAB these days, augmentation of the bladder may be performed in patients who are non‐responsive to or who are not eligible for sacral neuromodulation and BoNT‐A. An ileal intestinal segment is most commonly used, but any segment of the bowel may be adapted. The isolated segment is detubularised before placement in the bladder wall. The bladder wall is incised, either sagitally or transversely, after which the bowel segment is sutured in the gap to ‘augment’ the capacity of the bladder. The aim is to create a low‐pressure bladder with increased capacity and improved continence. Long‐term results indicate a success rate of 50%. Augmentation has been associated with high complication rates, ranging from stones to metabolic complications, fistulae, and changing bowel habits [28]. CIC is often needed after augmentation due to impaired bladder emptying, mucus production, and high PVR [3].

7. Urinary diversion may also be performed in the most severe of cases.

23.3.1.2.1 Definition and Incidence

Urinary incontinence is defined as any involuntary leakage of urine. This definition is problematic in its simplicity; there is no mention of how often or how much involuntary leakage needs to occur before a patient is deemed ‘incontinent’ of urine.

Prevalence rates range between 30 and 60% [3, 29], while treatment is sought by approximately 35% of patients [29–31], and this is significant because it shows that the majority of patients either do not seek treatment because they are not bothered or do not know that treatment is available.

23.3.1.2.2 Aetiology

There are a number of theories proposed for the mechanisms behind stress UI, the most widely stated being the integral theory, urethral hypermobility, and intrinsic sphincter deficiency.

The integral theory states that vaginal laxity, either due to altered collagen or elastin in the vaginal connective tissue or in its ligamentous supports, causes not just loss of urethral support and therefore, stress UI, but also activation of bladder base and proximal urethral stretch receptors, therefore, precipitating urgency or frequency and UUI. The urethra is sometimes described as resting in its vaginal ‘hammock’, and the laxer the hammock, the higher the likelihood of incontinence. Urethral hypermobility due to factors aside from vaginal laxity may also play a role, and intrinsic sphincter deficiency can cause a loss of outlet resistance, resulting in leakage from smaller rises in bladder pressure. Mechanically, continence is dependent on bladder pressure and outlet resistance; anything that causes the former to exceed the latter may result in leakage (i.e. abnormal rises in bladder pressure or loss of outlet resistance). Therefore, the evaluation of the patient should be aimed at identifying what is causing the imbalance and understanding how best to correct it with the tools and techniques available.

The biggest risk factor to develop UI seems to be increasing age. Other associated risk factors include pregnancy, vaginal deliveries, high BMI, constipation, UTIs, and previous pelvic surgery, or radiotherapy. Other risk factors are for patients with neurological disorders such as multiple sclerosis, spina bifida, or spinal cord injury.

23.3.1.2.3 History, Examination, and Differential Diagnoses

UI is classically subdivided into stress UI (SUI), urgency UI (UUI), and mixed UI (MUI) [7].

• SUI (50%) is defined as the complaint of involuntary leakage of urine on effort or exertion or on sneezing or coughing.
  
• UUI (10–20%) is defined as the complaint of involuntary leakage of urine accompanied by or immediately preceded by urgency.
  
• MUI (30–40%) is defined as the complaint of involuntary leakage of urine associated with urgency and also with exertion, effort, sneezing, or coughing.

Women younger than 50 years of age more often suffer from SUI, whereas UUI and MUI show an increase in prevalence in women older than 50 years of age [32].

A thorough history is important in the evaluation of the incontinent patient. A provisional classification of SUI, UUI, or MUI can often be made based on history alone. Important points in the history are as stated for OAB. Often the history will be the only clue suggesting UUI. SUI, on the other hand, is usually demonstrable on physical examination.

Physical examination should include assessment of BMI, abdominal palpation (masses, enlarged bladder), and inspection and digital exam of the external genitalia [33]. During inspection in women, assess the extent of vulvovaginal atrophy, visibility of any pelvic organ prolapse (POP), and perform a cough stress test to assess SUI. The digital exam is used to determine the contraction strength of the pelvic floor and severity of any POP using the POP‐Q scale.

Primary SUI is much less common in men due to the more substantial external sphincter. However, men who have had bladder outlet surgery (such as TURP, bladder neck incision [BNI], or radical prostatectomy) and who are therefore more likely to have sphincter dysfunction, are at increased risk of SUI. This is now usually classified as a separate subtype of SUI.

UUI by definition is part of the OAB symptom complex, and therefore patients with pure UUI should be assessed and managed as per the algorithm set out in the OAB section.

Aside from the three classically described forms of UI, other types are also recognised: nocturnal enuresis, continuous UI, inappropriate urethral relaxation incontinence, post‐TURP incontinence, and postprostatectomy incontinence, as well as incontinence in special situations, such as incontinence during sexual intercourse or giggle incontinence.

Nocturnal enuresis. Nocturnal enuresis is the complaint of loss of urine occurring during sleep. This is most commonly encountered in the paediatric setting and is discussed in Chapter 10. The main reason for new nocturnal enuresis during adulthood is chronic retention, usually due to BOO, but it can be due to poor detrusor contractility or both. If new nocturnal enuresis is present, it should always prompt a full LUTS history, PVR measurement, and (in men) a flow test.

Continuous urinary incontinence. The presence of continuous urinary incontinence should always prompt careful examination and investigation for possible fistulae and urethral diverticula. However, in the absence of any fistulae, continuous incontinence can result from particularly poor sphincter function, as can occur in occasional female patients after long‐term urethral catheters use for many years or from particularly frequent SUI or UUI, such that individual episodes are not distinguished.

The treatment of urethral fistulae should be conducted by specialists experienced in such surgery. The most commonly performed procedure for fistula repair is the Martius fat pad interposition [34].

Inappropriate urethral relaxation incontinence. Inappropriate urethral relaxation incontinence is a term given to incontinence occurring due to sphincter relaxation with no measurable detrusor contraction. It is extremely rare and only occurs in women. However, detrusor pressure often shows no measurable rise in healthy women during normal micturition. As such, inappropriate urethral relaxation incontinence may represent an unconsciously activated micturition reflex. Treatment is usually the same as for SUI.

Post‐TURP incontinence. Post‐TURP incontinence is perhaps more common than previously thought and can be caused by: (i) un‐masked UUI (not previously apparent due to the prostatic obstruction) or (ii) sphincter injury during the operation causing SUI. A careful history may help distinguish one or the other, but video urodynamics may be necessary to confirm. Patients should always be carefully counselled regarding the risk of incontinence post TURP, particularly those who complain of significant storage LUTS and urgency preoperatively. Treatment is as for primary UUI or SUI. It is important to note that in a man with mixed LUTS, often it is more pragmatic to treat the obstruction first before considering invasive treatment (such as botulinum toxin injections) for OAB and UUI because of the risk of urinary retention with these treatments. Also there is significant reduction in storage symptoms post‐TURP without any other therapy.

Postradical prostatectomy incontinence. Postradical prostatectomy incontinence is common irrespective of the surgical modality (i.e. open, laparoscopic, or robot‐assisted), and men should be counselled accordingly. Pelvic floor exercises and physiotherapy help in restoring continence postoperatively, and many men will achieve acceptable levels of continence in 12–18 months postoperatively. However, nearly 5% of men will require treatment, and this is usually in the form of a male sling or an artificial urinary sphincter. Evaluation of persistent postradical prostatectomy incontinence before considering surgical treatment should consist of a flexible cystoscopy to exclude bladder neck stenosis and video urodynamics to assess the nature and degree of incontinence. The general consensus is that mild to moderate degrees of incontinence could be treated with a male sling, and more severe incontinence will require insertion of an artificial urinary sphincter [2].

Incontinence during sexual intercourse. This can be a symptom of both SUI and UUI. It is important to rule out other causes, such as UTI, and to take a gynaecological history for other associated symptoms.

Giggle incontinence. Isolated giggle incontinence sometimes occurs in young girls, but it is rarely a problem persisting into adulthood. If it persists, investigation, and management would be as for an adult presenting with UI.

23.3.1.2.4 Investigations

Outpatient investigations: three‐day bladder diary, urine dipstick, PVR, and uroflowmetry.

Uroflowmetry can suggest dysfunctional voiding but should be interpreted with caution. A reasonable voided volume is required (at least 100–150 ml) and although arbitrary Qmax figures of 10 ml s⁻¹ have been suggested as a cut‐off for clinically significant obstruction, a single reading is probably of minimal diagnostic value.

Questionnaires can be used to evaluate the impact of the urinary dysfunction. Several scales are available, measuring general urinary dysfunction and also specific UUI, pelvic floor dysfunction (PFD), and sexual dysfunction. These questionnaires can also be used to report on the effectiveness of certain treatments [33]. The International Consultation on Incontinence has recommended to use, amongst others, the following symptom specific short questionnaires: UID‐6 and IIQ‐7 for UI, PFDI‐20 and PFIQ‐7 for PFD, and FIQL and FISI for faecal incontinence [35].

Patients who prove to be refractory to conservative or pharmacological treatment, or those with complicated UI, may benefit from further investigations, such as cystometrography (CMG or video CMG). CMG can objectively demonstrate SUI and DO, although the absence of demonstrable SUI or DO during a test does not preclude the diagnosis. Some studies have suggested that surgical treatment of SUI also relieves DO and symptoms of OAB in up to 30% of cases, although this figures varies widely.

The Valsalva leak point pressure (VLPP) can be helpful to determine the severity of SUI. Stress leakage at a pressure of <60 cm H₂O suggests intrinsic sphincter deficiency, while pressures >90 cm H₂O indicate urethral hypermobility [36]. The implication of this in terms of choice of treatment remains unclear in women. However, in men with postprostatectomy incontinence, there is a general trend to treat men with moderate decrease in VLPP with a male sling and those with severe decrease in VLPP with an artificial urinary sphincter (AUS).

Detrusor hypocontractility or detrusor underactivity can be defined as a bladder contraction of reduced strength, which prolongs urination and may lead to significant PVR or urinary retention. The significance of detrusor underactivity may be particularly important in men with voiding symptoms, as surgical treatment of presumed BOO may not improve their symptoms. Urodynamic demonstration of detrusor underactivity may therefore be an important factor when counselling men for consideration of bladder outlet surgery.

23.3.1.2.5 Treatment of UI

The treatment algorithm for UUI is as stated for OAB. However, it must be noted that patients with significant UUI are less likely to be cured of their incontinence by medical therapy and are more likely to require invasive treatments.

1. Conservative treatment or lifestyle modification

A wide variety of treatment options is available for UI and OAB. Choice of treatment is dependent on the severity and duration of symptoms, comorbidities, and local expertise. It is recommended to start with conservative treatment before proceeding to more invasive treatment [23]. For patients with MUI, the most bothersome symptom should be treated first.

Overall, conservative treatment modalities are similar to those stated for OAB: regular exercise, smoking and caffeine cessation, weight loss, adequate hydration, and treating constipation.

Pelvic floor muscle training (PFMT). PFMT is aimed to improve control over the pelvic floor muscles. PFMT has not been standardised and can include pelvic floor muscle exercises, biofeedback and electrical or magnetic stimulation [33, 37]. Supervised PFMT should be carried out for at least three months with at least eight contractions three times a day [33]. It has been shown to be beneficial in improving symptoms and quality of life (QoL) in SUI, and to a lesser degree for MUI and anterior POP [14, 38, 39].

2. Medical treatment of SUI

Antidepressants. Duloxetine can be used as a second‐line treatment for SUI in patients who are not eligible for surgical interventions or do not wish to have surgical intervention. It is a serotonin and noradrenaline reuptake inhibitor and increases sphincteric muscle activity by increasing the pudendal nerve and Onuf’s nucleus stimulation. A significant reduction of symptoms by >50% is seen during the use of duloxetine, but adverse events may lead to discontinuation in some cases. It is important to counsel patients that they must not discontinue duloxetine abruptly and should wean off it gradually. It should be used only in select patients and rarely effects cure. The effects are also limited to while the patient stays on the drug.

3. Surgical treatment of SUI
   
   
   
   1. Midurethral slings or tapes

Currently the gold‐standard surgical treatment for SUI. It is a minimally invasive procedure in which a synthetic sling is placed under the middle urethra to provide support and reduce urethral mobility during stress. The synthetic tapes are type I (pores are >75 μm) monofilament polypropylene meshes. Others include type II (pores are <10 μm), type III (macro‐multifilament), and type IV (sub‐micron pores). Continence rates higher than 80% have been described with the standard retropubic and transobturator approach, equivalent to Burch colposuspension but with considerably less associated morbidity. The advantages of this procedure include short operation times, minimal blood loss, and short hospital stay [40].

In the transobturator procedure, the tape is inserted with two trocars through a vaginal incision beneath the mid‐urethra, anchored to the obturator foramina on either side. Both outside‐in and inside‐out approaches have been described [41].

The originally described retropubic tension‐free vaginal tape (TVT) procedure involves two needles, which are blindly passed through the retropubic space. No fixation sutures are necessary in the TVT approaches. The transobturator approach has been shown to result in less complications like bladder perforation and urinary retention, but postoperative pain (groin or thigh pain) is more common compared to the retropubic route. Other complications include de novo bladder overactivity, urethral infection or erosion, and rarely, bowel or blood vessel injury.

The inside‐out insertion has less postoperative complications compared to the outside‐in insertion and might be the preferred route [23]. Satisfaction declines over time, but the urinary continence rates remain high [42]. The use of single‐incision slings does not appear to have satisfactory long‐term results compared to standard midurethral slings but can be performed under local anaesthesia and may be effective in experienced hands [43].

2. Colposuspension

This procedure can be performed open (Burch) or laparoscopic with or without robotic assistance. The general principles do not differ between the different approaches. The anterior vaginal wall is attached by paravaginal sutures on both sides to the ileopectineal ligaments. The anchor site, types of sutures, and extraperitoneal and abdominal approach may vary.

Studies have shown that although the colposuspension is more invasive, continence outcomes are similar to midurethral sling procedures. The open approach has proven to be effective in the long‐term with continence rates of about 80% after five years. An increased risk of POP is reported following colposuspension compared to other surgical techniques [44].

3. Autologous fascial sling

The autologous fascial sling is a traditional suburethral sling, which uses the patient’s own tissue obtained from the rectus fascia or the tensor fascia lata. A combined vaginal and abdominal approach is used to place the suburethral sling. After mobilising fascial tissue, it is tunnelled under the urethra, and then fixed with sutures to the periurethral fascia or anchored to the rectus fascia using the sling‐on‐a‐string technique, similar to insertion of a synthetic retropubic sling. This results in a mechanical compression of the urethra [45].

Long‐term results are similar to colposuspension and midurethral slings for incontinence improvement rates, and a recent study has suggested improvement rates may in fact be more durable with autologous slings. However, postoperative voiding dysfunction is found more frequently compared to colposuspension and CIC might be needed. The autologous rectus fascia seems to be favourable over other biological materials [46].

4. Urethral bulking agents

Urethral bulking agents can be used as second‐line treatment. The results are inferior to midurethral slings and colposuspension and have usually only short‐term beneficial effects. However, bulking agents might be considered in patients who are not fit for more invasive surgery, or those who do not want to undertake the risks of other surgery. Hyaluronic acid, polyacrylamide hydrogel, polytetrafluoroethylene (PTFE), collagen, adipose tissue (autologous fat), and silicon agents have been injected submucosally into the proximal urethra until coaptation has been reached. Repeat injections are often needed to maintain a significant improvement of symptoms [47, 48].

5. Artificial urinary sphincter and adjustable continence therapy

Patients needing third‐line treatment for SUI or complicated SUI have often already undergone conservative or second‐line treatment. The management of complicated SUI should be provided in specialised centres, where enough expertise and experience are available. The AUS and adjustable continence therapy (ACT) have shown good results for this group of patients. AUS are indicated for patients with sphincter deficiency, usually seen in men after prostatectomy or transurethral surgery, or in patients who had pelvic radiotherapy or a pelvic fracture or failed other UI treatments. Nonetheless, if associated with OAB symptoms, the bladder needs to be treated first because this might alleviate the UI. Patients need to have good manual dexterity and cognitive function to understand the principle and be able to work the pump mechanism.

AUS is comprised of a pressure‐regulating balloon, a pump, and a cuff. To void, the patient squeezes the pump, which deflates the fluid‐filled cuff, transferring the fluid to the balloon. Over a three‐minute period, the fluid slowly fills the cuff again. Depending on the site of cuff placement, the pressure can be 61–70 mm Hg for vulvar urethral placement or 71–80 mm Hg for bladder neck placement.

The AUS is inserted through an abdominal approach followed by cuff placement around the bladder neck between periurethral fascia and vagina [49]. A high number of patients reported improvement during long‐term follow‐up (85–86%). Complication rates range between 17 and 26% [50, 51]. The ACT is placed as follows: the bladder neck is identified with fluoroscopy. A trocar is introduced through incisions in the labia majora laterally of the urethra and balloons are placed paraurethrally just under the bladder neck. The ACT shows 66–78% improvement rates and significant improvement in QoL. Explantation or revision rates range between 19 and 31% [52].

Complications requiring revision include urethral atrophy or erosion, mechanical failure, and infections. Other complications include de novo bladder overactivity and urinary retention due to urethral strictures or bladder neck contracture.

23.3.1.3.1 Definition and Incidence

Painful bladder syndrome (PBS) is the complaint of suprapubic pain related to bladder filling, accompanied by other symptoms such as increased daytime or nighttime frequency, in the absence of proven UTI or other obvious bladder pathology. It is chronic in its nature (>6 months) with pain being the major complaint. The diagnosis is one of exclusion. Other names for this condition are interstitial cystitis (largely historical) and bladder pain syndrome.

23.3.1.3.2 Aetiology

Prevalence within a population can be variable ranging from 0.06 to 30%, with a 10 : 1 female: male ratio, [53]. It has no easily identifiable aetiology; multiple triggers may manifest as a final common bladder response to different types of stimuli or insult. It can be considered a major part of the painful bladder disease complex that includes other painful bladder conditions with established aetiology such as radiation cystitis. Other disorders such as depression, irritable bowel syndrome, and fibromyalgia are more prevalent in patients with PBS.

Although the pathology is poorly understood, PBS usually affects the patient during the storage phase and appears to originate within the bladder. Possible or postulated causes include deficiencies in the glycosaminoglycan (GAG) layer, infiltration with mast cells, neurogenic inflammation, excessive sympathetic activity, stress, recurrent UTIs, autoimmunity, and allergy. Females are 10 times more likely to be affected than males. The natural history is one of remissions and exacerbations. Some patients ultimately develop a small fibrotic bladder.

23.3.1.4.1 Definitions and Incidence

Nocturia is the complaint that the individual has to wake at night one or more times to void (symptom). Nocturia is also the number of voids recorded during a night’s sleep: each void is preceded and followed by sleep. Polyuria is urinating >3 l over a 24 hours period. Nocturnal polyuria (NP) is present when an increased proportion of the 24‐hour output occurs at night (normally during the eight hours whilst the patient is in bed). The nighttime urine output excludes the last void before sleep but includes the first void of the morning. An ‘increased proportion’ is defined as >20% in patients younger than 65 and > 33% in those 65 years of age or older.

A single episode of nocturia does not usually affect quality fo life, but two or more voids per night may. Patients will vary in their assessment of this and should be counselled accordingly. Incidence of nocturia (two episodes or more) increases with age from the sixth decade of life onwards, with around 50% of the population affected by age 80. Comparative prevalence is greater in young females than young males, but greater in elderly males than elderly females.

23.3.1.4.2 Aetiology: LUT Related

Nocturia in elderly males is often believed to be secondary to BPE, but rates of improvement after treatment of BPE are variable. Nocturia is part of the OAB symptom complex and is also common in reduced bladder capacity due to any cause (e.g. BPS, neurogenic bladder dysfunction, LUT obstruction of any cause, LUT cancer, bladder calculi, detrusor failure, urogenital atrophy, and UTI).

23.3.1.4.3 Aetiology: Non LUT Related

Nocturia is more common in patients who are obese and very common in pregnancy. Exercise appears to protect against nocturia in some studies. Polydipsia causes polyuria, and depending on timing, may cause nocturia and nocturnal polyuria.

Medical conditions which may cause nocturia and should be excluded are diabetes, coronary heart disease, congestive cardiac failure, obstructive sleep apnoea (i.e. large negative intrathoracic pressure fluctuations can cause the heart muscle cells to secret atrial natriuretic peptide causing NP), and neurological diseases (e.g. multiple sclerosis, stroke, and Parkinson disease). Diuretic use should also be considered, and if possible, the timing of intake should be altered.

One must remember that nocturia could also occur if the person wakes for any other reason and decides to void before returning to sleep. As such, the potential list of causes could include any sleep disturbance such as insomnia, dementia, depression, anxiety, chronic pain, a baby crying in the house, or noisy neighbours!

Polyuria can be either solute or water diuresis. In patients who have undergone surgery, the more common causes are poorly controlled diabetes, diuresis seen in patients with high‐pressure retention once obstruction is relieved, postoperative loading with saline, and primary polydipsia. A long list of medical causes is beyond the scope of this chapter.

23.3.1.4.4 History and Examination

Patients with nocturia need a detailed medical and surgical history, as well as examination of the abdomen, pelvic and rectal examination, and assessment of any ankle swelling. Further examination is guided by symptoms, such as possible neurological disease. It is important to ask whether the patient is bothered by their nocturia. It is often helpful to ask partners regarding snoring or interrupted breathing during sleep because the patient themselves may not know.

23.3.1.4.5 Investigations

Baseline investigations include BMI, forced vital capacity (FVC, including a marker for going to bed and for getting up), urine dipstick, flow rate, pelvic examination, and urea and electrolytes. Further urological investigations are only indicated if LUT pathology is suspected. In patients who are polyuric, urine osmolality to determine if solute (>250 mOsml kg⁻¹) or water (<250 mOsml kg⁻¹) diuresis.

23.3.1.4.6 Treatment

1. Conservative treatment or lifestyle modification and referrals

Simple measures to avoid nocturia are fluid advice, in particular avoiding fluid intake in the evening, encourage exercise, elevate legs to above heart level in the afternoon, changing diuretic doses to the morning or afternoon, and improving the sleep environment.

Depending on the results of history, examination and baseline investigations, it may be appropriate to refer the patient to other specialists for further assessment, such as the cardiologist, sleep specialist, neurologist, psychologist, or endocrinologist.

2. Medical and surgical treatment

Medical and surgical treatment of nocturia should be aimed at the underlying cause.

An afternoon dose of loop diuretic can be used for nocturnal polyuria.

In patients with nocturnal polyuria not responsive to other measures, desmopressin (a synthetic analogue of vasopressin antidiuretic hormone) therapy can be used, provided serum sodium is >135 mmol l⁻¹. Sodium levels should be monitored at three and seven days for hyponatraemia, detection of which is an indication to discontinue treatment.

23.3.1.4.7 Other Considerations

Nocturia raises the potential dangers of walking to the toilet in the dark, most notably causing falls, and in some cases, fractures in the elderly. Its impact should therefore not be underestimated.

23.3.1.5.1 Definition and Incidence

With increased bladder sensation, the individual feels an early and persistent desire to void, with actual voided volumes usually being small.

23.3.1.5.2 Aetiology

Increased bladder sensation can be caused by any inflammation of the bladder or urethra or could be idiopathic. This includes radiation cystitis, chemical cystitis, PBS, and urethral pain syndrome. The most common cause, however, is a UTI.

23.3.1.5.3 History, Examination, and Common or Important Differential Diagnoses

A careful history often reveals storage symptoms and may reveal dyspareunia or any relationship with the menstrual cycle or previous hysterectomy. Examination may be negative but may reveal a urethral caruncle (which is a mucosal prolapse) or bladder tenderness.

23.3.1.6.1 Definition and Incidence

With reduced bladder sensation, the individual is aware of bladder filling but does not feel a definite desire to void. With absent bladder sensation, the individual reports no sensation of bladder filling or desire to void.

23.3.1.6.2 Aetiology

Reduced bladder sensation is either idiopathic, neurogenic (will be discussed in Section 23.4), or secondary to chronic retention. It often coexists with atonic bladder (Section 23.4).

23.3.1.6.3 History, Examination, and Common or Important Differential Diagnoses

There is usually isolated infrequent voiding. Other symptoms can include straining to void, feeling of incomplete emptying, UI, recurrent UTIs, chronic retention of urine, known neurological injury, or disease. Examination should assess sacral dermatomes.

23.3.1.6.4 Investigations

All patients need a voiding diary, PVR, and pressure or flow cystometry; any further investigations are guided by the history. In idiopathic cases, there will simply be reduced sensation, but otherwise normal filling and voiding with a low PVR.

23.3.1.6.5 Treatment

Treatment of reduced bladder sensation consists of bladder retraining (voiding by the clock and double voiding), and if necessary CIC or a trial of α‐blockers.

23.3.2.1.1 Definition and Incidence

Detrusor underactivity is defined as a contraction of reduced strength or duration, resulting in prolonged bladder emptying or a failure to achieve complete bladder emptying within a normal time span [7]. Detrusor failure or atonic bladder is the worst situation in this spectrum, whereby no detrusor activity can be demonstrated.

23.3.2.1.2 Aetiology

Detrusor underactivity or failure may be idiopathic or related to age, neurogenic bladder dysfunction, or associated with BOO and chronic retention.

A degree of detrusor underactivity can be reversible, and this is likely related to the length of time with the condition and the degree of overstretching of the bladder that has occurred. Complete detrusor failure is not reversible.

Detrusor underactivity is often associated with reduced bladder sensation and large voided volumes or large PVR.

23.3.2.1.3 History, Examination, and Investigations

Presenting symptoms may be infrequent bladder emptying and retention, straining to pass urine, or indeed frequency and urgency with small voided volumes and a feeling of incomplete emptying. Symptoms may not be evident to the patient until significant bother is caused by the symptoms or until retention occurs, seemingly suddenly. A poor urine flow rate may suggest detrusor underactivity, but normal flow does not exclude it. The diagnosis is confirmed during pressure or flow urodynamics because only then that specific information about the detrusor becomes available. The relative contribution of any type of BOO and detrusor underactivity can only be assessed during invasive urodynamics. Equally, the relative contribution to urine flow rate from detrusor pressure and abdominal straining are only distinguished during invasive urodynamics.

23.3.2.1.4 Treatment

1. Conservative treatment or lifestyle modification

The bladder must be allowed to drain without resistance, using CIC, urethral catheter, or suprapubic catheter. Any underlying pathology or causes of associated LUTS should be treated. The bladder can then be reassessed as to whether reasonable function has returned. This is done by measuring PVR over a period of time. Timed voiding (e.g. every two hours can be successful in idiopathic detrusor underactivity.

2. Medical and surgical treatment

There is currently no specific medical or surgical treatment for detrusor underactivity. Establishing bladder drainage by catheterisation of some variety (CIC, long‐term catheterisation [LTC], or suprapubic catheterisation [SPC]) is usually the most effective strategy.

23.4.4.1.1 Definition and Aetiology

Any central or peripheral neurological disorder can affect the lower urinary tract. These can be classified by describing the actions of the detrusor and sphincter separately as either overactive, underactive, or normo‐active.

Neurological urology encompasses both static conditions, such as spinal cord injury and stroke, as well as progressive disorders, such as multiple sclerosis and Parkinson disease. It also includes congenital disorders, such as spina bifida.

23.4.4.1.2 History and Examination

Early and regular diagnostic evaluation and treatment are essential to prevent the ultimate endpoint of renal failure due to poor bladder compliance, the pressure rises progressively during filling phase leading to a high pressure system. Some situations are inherently ‘safe’ (e.g. bladder pressure always low throughout the micturition cycle), whilst others are not. These do not necessarily correlate with symptoms. The only symptom may be incontinence, yet almost any possible combination of detrusor and sphincter dysfunction can occur. Furthermore, as neurological conditions evolve, the situation with regard to the LUTS may change. Bladder dysfunction can be the presenting symptom of a neurological disorder.

The history needs to include details of any known neurological disorder, and if so, which part is affected (e.g. brain, spinal cord, systematic), disease progression, and prognosis. History of urinary function, bowel function, sexual function, and neurological function is also vital. Any pain, UTIs, or haematuria need to be considered carefully.

Examination can be divided into general, neurological, and urological. The neurological examination needs to determine detailed neurological function in the urogenital area, anal sphincter, bulbocavernosal reflex (absent in spinal cord injuries in the acute shock phase, and returns once shock phase over), and lower limb neurology. Assessment of overall mobility and hand function will be important to choose appropriate management options. History of any allergies, specifically latex allergy because there is a higher incidence in patients with neuropathy.

Symptomatic consideration:

• Suprapontine lesions will cause DO and inappropriate voiding.
  
• Suprasacral lesions will cause DO, poor compliance, DSD, and autonomic dysreflexia.
  
• Sacral lesions: Detrusor underactivity or areflexia.

Autonomic dysreflexia is potentially life threatening and seen in patients with spinal lesions above the T6 spinal cord level. It is caused by overstimulation of the autonomic nervous system. Triggers are those that would normally cause a painful stimulus, such as bladder distention, catheterisation, or even cystoscopic, rectal, and vaginal examinations; other triggers include constipation, distal skin infections, or UTIs. It is characterised by sympathetic overactivity of the cord below the lesion leading to vasoconstriction and compensatory vasodilation of the normally innervated sympathetic areas above the spinal cord lesion. This manifests as significantly high blood pressure associated with headaches, profuse sweating, nasal congestion, flushing of the skin above the level of the lesion, with bradycardia. If left untreated, can lead to convulsions, intracranial bleeds, strokes, and death. Treatment is aimed to stop the triggering factor and reduce the blood pressure. Sublingual glyceryl trinitrate (GTN) spray, or captopril, nifedipine, or intravenous labetalol is recommended.

23.4.4.2.1 Definitions and Aetiology

Anterior wall prolapse (50%) results from herniation of the bladder (cystocele) or urethra (urethrocele) through the vaginal wall.

Posterior wall prolapse (30%) results from herniation of the rectum (rectocele) or bowel or omentum (enterocele) through the vaginal wall.

Middle compartment prolapse (20%) occurs when the the uterus or the vaginal vault descends.

Nearly half of all prolapses are causes by normal vaginal deliveries. Other causes include old age (due to lack of oestrogen), obesity, constipation, smoking, and chronic obstructive pulmonary disorder (regular coughing causes chronic strain), previous pelvis or vaginal surgery, or radiotherapy.

POP is commonly associated with UI and LUT symptoms, although there is no established causative relationship either way.

23.4.4.2.2 History and Examination

The history should be aimed to look for causative factors as well as LUTS and bowel and sexual dysfunction.

The examination is best performed in three positions: lithotomy, left lateral position, and standing. Pressure test to demonstrate prolapse (e.g. coughing, straining, or bearing down) and UI. POP can be classified either by the classical Baden‐Walker system or the more detailed POP‐Q system.

23.4.4.2.3 Baden‐Walker

By degree of descent of prolapsing structure in relation to the hymen.

• Grade 0 – no prolapse
  
• Grade 1 – halfway to hymen
  
• Grade 2 – up to hymen
  
• Grade 3 – halfway past hymen
  
• Grade 4 – maximum descent or complete prolapse (procidentia)

23.4.4.2.4 POP‐Q

The POP‐quantification (POP‐Q) system is a detailed anatomical representation of a prolapse.