Bladder and Sexual Dysfunction

Fig. 5.1

Template of a bladder diary, complete over at least 48 hrs

The complete diagnostic work-up of urological autonomic failure is summarized in Fig. 5.2.

Fig. 5.2

Neurogenic bladder: diagnostic work-up

5.1.1.5 Investigations

Post-void urine volume can be assessed by means of in-out catheterization or, noninvasively, by bladder ultrasound. Uroflowmetry is particularly indicated in men: in case of reduced urine flow, prostatic enlargement needs to be excluded.

The gold standard for a detailed evaluation of urinary storage and/or voiding dysfunction in patients with suspected neurogenic bladder is the urodynamic evaluation. Sterile urine is a prerequisite for performing this examination safely and minimizing the risk of pyelonephritis. For detailed description of urodynamic assessment, see Text Box 5.1 “Focus on Neuro-urological Investigations.”

Urodynamic assessment includes a multichannel registration, which combines cystometrogram (CMG) with pressure flow study and electromyography (EMG). During the examination, the patient is in his/her usual voiding position. A transurethral and a rectal balloon catheter detect intravesical (Pves) and abdominal pressure (Pabd). Based on measured pressures, detrusor pressure (Pdet) can be calculated (pdet = Pves – Pabd). EMG surface electrodes are used to assess external urethral sphincter activity throughout urodynamic testing. Combination of multichannel urodynamic testing with radiographic imaging, also known as videourodynamic study (or VUDS), provides further morphological information and can be performed in selected cases. Sterile water or saline is used as fluid medium for the bladder filling phase during standard urodynamic evaluation, while Cystografin and fluoroscopy table tilted to 45–60° are used in case of videourodynamic study.

During the filling phase, bladder storage is assessed by asking the patient about sensation of bladder filling and is quantified by means of the bladder wall elasticity (compliance, C = ΔV/Δ Pdet). The “leak point pressure,” that is, the pressure at which urinary loss is experienced without detrusor contraction, is measured for evaluation of neurogenic bladder and stress urinary incontinence. Voiding dysfunction, including detrusor sphincter dyssynergia, is detected via EMG, and urine evacuation is quantified by pressure flow study recording flow rate, voided volume, and related pressures (Pabd, Pves, Pdet). Provocative maneuvers including cough or Valsalva maneuver may be performed to elicit detrusor overactivity and to unmask stress urinary incontinence [31].

Kidney ultrasound and functional renal assessment (creatinine clearance and blood urea) are recommended to exclude, or eventually monitor for, hydronephrosis, reflux, and secondary renal failure.

Electrophysiological studies may be added in single cases (see Text Box 5.1).

Text Box 5.1 Focus on Neuro-urological Investigations

Urodynamic assessment: it includes a multichannel registration, which combines cystometrogram (CMG) with pressure flow study and electromyography (EMG). During the examination, the patient is in his/her usual voiding position. A transurethral and a rectal balloon catheter detect intravesical (Pves) and abdominal pressure (Pabd). Sterile water or saline is used as fluid medium for the bladder filling phase. Based on measured pressures, detrusor pressure (Pdet) can be calculated (pdet = Pves – Pabd). EMG surface electrodes are used to assess external urethral sphincter activity throughout urodynamic testing. Bladder storage capacity is assessed by asking the patient about sensation of bladder filling. The “leak point pressure,” that is, the pressure at which urinary loss is experienced without detrusor contraction, is measured for evaluation of neurogenic bladder and stress urinary incontinence. Voiding dysfunction, including detrusor sphincter dyssynergia, is detected via EMG, and urine evacuation is quantified by pressure flow study. Provocative maneuvers including cough or Valsalva maneuver may be performed to elicit detrusor overactivity and to unmask stress urinary incontinence [31].
Videourodynamic assessment: based on the combination of multichannel urodynamic testing with radiographic imaging, it provides further morphological information and can be performed in selected cases. In this case, Cystografin and a fluoroscopy table, tilted to 45–60°, are used.

Concentric needle anal sphincter electromyography (EMG): can be used to investigate muscle reinnervation following axonal damage to the sacral spinal segments S2–S4. In the setting of suspected neurodegenerative disorders, the test is useful to evaluate the integrity of the motor neurons of these segments, known as Onuf’s nucleus. Neuronal loss in Onuf’s nucleus is a characteristic, but not exclusive, feature of MSA, therefore limiting the role of this investigation in the differential diagnosis of parkinsonian syndromes [26, 34, 35, 42, 45, 47].
Transanal pudendal motor terminal latency: may help to evaluate a distal lesion of pudendal motor fibers.
Pudendal somatosensory evoked potentials: to investigate for lesions of pudendal somatosensory afferent fibers.
Cortical evoked potentials of the vesicourethral junction: evaluate viscerosensory afferent pathways in patients with lower urinary tract dysfunction. Combined with evaluation of pudendal somatosensory evoked potentials, it distinguishes between intraspinal and extraspinal (e.g., sacral plexus) lesions of the bladder afferent pathways, if the site of lesion is unknown [22].

5.1.2 Sexual Dysfunction

Male erectile dysfunction (ED) is defined as the inability to achieve or maintain an erection sufficient for satisfactory sexual performance [7]. Prevalence of ED is 2% in the third decade of life and may increase up to 53% in the seventh decade [5].

ED may be of organic, psychogenic, or, in most of cases, multifactorial origin. A psychogenic cause is suspected in case of sudden onset, previous or ongoing stressful events, situation-dependent disturbs (contact with a partner versus masturbation), absence of relevant organic risk factors, young age, and preserved spontaneous nocturnal erections. Organic causes of ED encounter vascular origin (arterial, venous, or mixed), structural penile abnormalities, and endocrine or neurogenic causes. Erectile dysfunction may be the presenting feature of primary autonomic disorders like multiple system atrophy [13] and pure autonomic failure [1], frequently occurs in patients with spinal cord injuries [44] and multiple sclerosis [25], and may complicate diabetes mellitus or polyneuropathies of diverse etiologies.

History taking is essential for a proper diagnostic work-up of erectile complaints: even if a putative cause for ED is suspected (e.g., previous diagnosis of polyneuropathy), a careful history taking should be aimed at pointing out further, eventually modifiable, contributing factors. Patients’ psychosocial, lifestyle, and pharmacological aspects, as well as comorbidities, should be taken into account during the first diagnostic assessment (see also Table 5.1 – History taking in males referring erectile dysfunction). Sexual anamnesis should be carefully documented, if possible also with the bed partner in order to define disease burden and plan tailored interventions. Several rating scales have been developed for research purposes in order to stratify severity degree of male ED: the most frequently used is the “International Index of Erectile Function – 5 items” (IIEF-5 scale), which is reported in Table 5.2 [32] and may be used on a routine basis for follow-up purposes as well. In case a psychogenic ED is suspected, a multidisciplinary evaluation, including psychopathological assessment, is recommended.

Table 5.1

History taking in patients referring erectile dysfunction

Comorbidities	Arterial hypertension Hyperlipidemia Diabetes mellitus (for both vascular and neurogenic erectile dysfunction) Depression Parkinsonism Multiple sclerosis Polyneuropathy of any etiology Spinal stenosis Hyperprolactinemia Hypothyroidism Hypogonadism Obesity
Risk factors	Smoking Sedentary lifestyle Increased alcohol intake Recreational drug use (e.g., cocaine, by inducing hyperprolactinemia) Previous pelvic or perineal surgery, trauma, or radiotherapy
Drugs	Thiazide type diuretics Aldosterone receptor blockers β-blockers Benzodiazepines SSRI Antiepileptic drugs

Table 5.2

The IIEF-5 questionnaire

Over the past 6 months:	1	2	3	4	5
1. How do you rate your confidence that you could get and keep an erection?	Very low	Low	Moderate	High	Very high
2. When you had erections with sexual stimulation, how often were your erections hard enough for penetration?	Almost never/never	A few times (much less than half the time)	Sometimes (About half the time)	Most times (much more than half the time)	Almost always/always
3. During sexual intercourse, how often were you able to maintain your erection after you had penetrated (entered) your partner?	Almost never/never	A few times (much less than half the time)	Sometimes (About half the time)	Most times (much more than half the time)	Almost always/always
4. During sexual intercourse, how difficult was it to maintain your erection to completion of intercourse?	Extremely difficult	Very difficult	Difficult	Slightly difficult	Not difficult
5. When you attempted sexual intercourse, how often was it satisfactory for you?	Almost never/never	A few times (much less than half the time)	Sometimes (about half the time)	Most times (much more than half the time)	Almost always/always

Reprinted from Rosen et al. [32], with permission from the Nature Publishing Group

The IIEF-5 questionnaire is the sum of the ordinal responses to the five items (range, 5–25)

Physical examination of the abdomen, penis, testicles, secondary sexual characteristics, and leg arterial pulses should be performed at first visit. Digital rectal examination of the prostate and serum PSA are recommended in men above 40 years of age: this is particularly important in case ED is due to hypogonadism and testosterone replacement therapy is planned.

Laboratory testing is also recommended at first visit and should include blood glucose, HbA1c, HDL and LDL cholesterol, liver enzymes, creatinine, and blood count. In patients with gynecomastia, androgen hormone measurement should be also performed.

Provocative erection test (intracavernous prostaglandin E1 injection – Alprostadil), alone or in combination with Doppler ultrasound, can be considered if penile artery disease is suspected. In case of penile arteriopathy, further investigations should be prompted to exclude an ongoing coronary artery disease.

Electrophysiological studies can be considered if a neurogenic cause of ED is suspected. Autonomic ɣ-fibers inducing vasodilation of cavernous vessels cannot be tested, but anal sphincter electromyography, pudendal nerve terminal motor latency, and somatosensory evoked potentials of pudendal nerve may provide indirect clues for a neurogenic etiology in unclear cases (Fig. 5.3).

Fig. 5.3

Male erectile dysfunction: diagnostic work-up *[30]

In women, sexual dysfunction may manifest with decreased vaginal lubrication and dryness, anorgasmia, and low sexual drive. Any kind of lesion affecting neural pathways subserving sexual function may cause neurogenic sexual dysfunction, but like in men, a multifactorial origin is more often the case, with both organic and psychosocial aspects playing a key role (see above). In particular, age- or delivery-related perineal laxity, endocrine changes (i.e., age-related/drug-induced/iatrogenic menopause, contraceptive pill), concomitant bladder or bowel dysfunction, spasticity, or depression may influence libido and sexual function to a great extent. Hence, these aspects need to be considered when evaluating female patients with hypoactive sexual complaints. Questionnaire can be used for initial assessment and follow-up of female neurogenic sexual dysfunction: the most frequently used are the “sexual function questionnaire (SFD)” and the “female sexual function index – FSFI” [27].

5.2 Therapeutics of Bladder and Sexual Dysfunction

5.2.1 Neurogenic Bladder Dysfunction

Management of lower urinary tract autonomic dysfunction contemporarily aims at optimizing quality of life, by reducing incontinence episodes and increasing voiding control and protecting upper urinary tract from secondary damage. Therapeutic options need to be individualized, by taking into account objective findings, comorbidities, global health status, and personal expectations of the patient [36].

5.2.1.1 Storage Dysfunction

Overactive Bladder

Non-pharmacological treatment of detrusor overactivity by means of bladder training may be pursued in patients with milder symptoms or as add-on to pharmacological measures: patients are trained to resist urge symptoms for a stepwise longer interval until urine volume and frequency do not normalize [46].

Antimuscarinic agents are the first-line therapy for treatment of detrusor overactivity. Oxybutynin, tolterodine, solifenacin, darifenacin, and trospium relieve urge and incontinence. Possible side effects are increased post-void residual volumes, xerostomia, constipation, and blurred vision [48]. Delirium, confusion, and worsening of cognitive impairment are further side effects due to central anticholinergic activity, limiting their use in patients with overt dementia. To this end, trospium, said not to pass the blood-brain barrier, and darifenacin, more selective for the peripheral M3 muscarinic receptor subtype, should induce cognitive side effects less frequently [21, 43]. Four to 6 weeks after beginning an antimuscarinic therapy, therapeutic outcome as well eventual side effects should be monitored. Post-void urine volume should be monitored during the titration phase and after dose changes, as this may rise due to drug-induced hypoactive bladder [2].

In refractory cases, more invasive options can be considered. Botulinum toxin A intravesical injection may reduce incontinence episodes due to detrusor overactivity. The treatment reduces detrusor contractility, impairing voluntary voiding and resulting in urinary retention. Therefore, this procedure is indicated only in patients able to perform clean intermittent self-catheterization and not, for instance, in patients with a severe cognitive of motor impairment [8, 16, 38].

Other invasive options for treatment of therapy-resistant detrusor overactivity include sacral neuromodulation or, in selected cases and depending on disease prognosis and life expectancy, bladder augmentation through partial detrusor myectomy or ileal transplant [24]. Recent evidence suggests that percutaneous posterior tibial nerve stimulation may improve lower urinary tract symptoms and urodynamic findings in patients with Parkinson’s disease suffering from overactive bladder [20].

Stress Incontinence

Conservative measures for treating stress incontinence due to hypoactive sphincter and/or pelvic floor laxity include pelvic floor training and behavioral therapy by means of biofeedback [17]. Invasive procedures include implantation of an artificial urethral sphincter [11, 15] or, in single cases, transurethral infiltration with bulking agents (i.e., fat, collagen, silicon, Teflon) but are to be considered on the basis of the patient’s life expectancy.

Nocturia

In patients reporting nocturia, it is essential to distinguish, on the basis of the bladder diary records, whether this is due to (I) increased nocturnal urine output (i.e., more than 1/3 of the 24 h total urine volume is excreted overnight, e.g., in case of pressure natriuresis in patients affected by nocturnal hypertension), (II) generally increased urine output (>40 mL/kg body weight, e.g., in case of uncontrolled diabetes), and (III) reduced bladder capacity (e.g., in case of overactive bladder). A combination of more than one cause is frequent, and a number of other contributing factors need to be taken into account at first evaluation. These are uncontrolled arterial hypertension with nocturnal blood pressure rise, diuretics scheduled in the evening, sleep apnea, psychogenic polydipsia, and insufficient antidiuretic hormone secretion (either idiopathic, drug-induced, or due to neuropituitary lesions).

Only gold members can continue reading. Log In or Register to continue