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Ovid: Oxford Handbook of Urology

Authors: Reynard, John; Brewster, Simon; Biers, Suzanne Title: Oxford Handbook of Urology, 1st Edition Copyright ©2006 Oxford University Press > Table of Contents > Chapter 14 – Neuropathic bladder Chapter 14 Neuropathic bladder P.492
Innervation of the lower urinary tract (LUT) Motor innervation of the bladder Parasympathetic motor innervation of the bladder Preganglionic, parasympathetic nerve cell bodies are located in the intermediolateral column of spinal segments S2–4. These preganglionic, parasympathetic fibres pass out of the spinal cord through the anterior primary rami of S2, S3, and S4 and, contained within nerves called the nervi erigentes, they head towards the pelvic plexus. In the pelvic plexus (in front of the piriformis muscle) the preganglionic, parasympathetic fibres synapse, within ganglia, with the cell bodies of the postganglionic parasympathetic nerves which then run to the bladder and urethra. 50% of the ganglia of the pelvic plexus lie in the the adventitia of the bladder and bladder base (the connective tissue surrounding the bladder) and 50% are within the bladder wall. The postganglionic axons provide cholinergic excitatory input to the smooth muscle of the bladder. Sympathetic motor innervation of the bladder In the male, preganglionic sympathetic nerve fibres arise from the intermediolateral column of T10–12 and L1–2. These preganglionic neurons synapse in the sympathetic chain and postganglionic sympathetic nerve fibres travel as the hypogastric nerves to innervate the trigone, blood vessels of the bladder and the smooth muscle of the prostate and pre-prostatic sphincter (i.e. the bladder neck). In the female, there is sparse sympathetic innervation of the bladder neck and urethra. In both sexes, some postganglionic sympathetic nerves also terminate in parasympathetic ganglia (in the adventitia surrounding the bladder and within the bladder wall) and exert an inhibitory effect on bladder smooth muscle contraction. Afferent innervation of the bladder Afferent nerves from receptors throughout the bladder ascend with parasympathetic neurons back to the cord and from there, up to the pontine storage and micturition centres or to the cerebral cortex. They sense bladder filling. Other receptors are located in the trigone and afferent neurons from these neurons ascend with sympathetic neurons up to the thoracolumbar cord, and thence to the pons and cerebral cortex. Other receptors are located in the urethra. The afferent neurons pass through the pudendal nerve and again ascend to the pons and cerebral cortex. All these neurons have local relays in the cord. Somatic motor innervation of the urethral sphincter: the distal urethral sphincter mechanism Anatomically, this is located slightly distal to the apex of the prostate in the male (between the verumontanum and proximal bulbar urethra) and P.493
in the mid-urethra in the female. It has 3 components:

  • Extrinsic skeletal muscle. This is the outermost layer, the pubourethral sling (part of levator ani). Composed of striated muscle and innervated by the pudendal nerve (spinal segments S2–4, somatic nerve fibres). It is activated under conditions of stress and augments urethral occlusion pressure.
  • Smooth muscle within the wall of the urethra. Cholinergic innervation. Tonically active. Relaxed by nitric oxide.
  • Intrinsic striated muscle (i.e. skeletal muscle within the wall of the urethra, hence known as the ‘intrinsic rhabdosphincter’). It forms a ‘U’ shape around the urethra, around the anterior and lateral aspects of the membranous urethra, and is absent posteriorly (i.e. it does not completely encircle the membranous urethra). It may produce urethral occlusion by kinking the urethra rather than by circumferential compression.

Preganglionic somatic nerve fibres (i.e. neurons which innervate striated muscle) are, along with parasympathetic nerve fibres (which innervate the bladder), derived from spinal segments S2–4, specifically from Onuf’s nucleus (also known as spinal nucleus X) which lies in the medial part of the anterior horn of the spinal cord. (Onuf’s nucleus is the location of the cell bodies of somatic motoneurons that provide motor input to the striated muscle of the pelvic floor—the external urethral and anal sphincters.) These somatomotor nerves travel to the rhabdosphincter via the perineal branch of the pudendal nerve (documented by direct stimulation studies and horseradish peroxidase tracing—HRP accumulates in Onuf’s nucleus following injection into either the pudendal or pelvic nerves). There also seems to be some innervation to the rhabdosphincter from branches of the pelvic plexus (specifically the inferior hypogastric plexus) via pelvic nerves. In dogs, complete silence of the rhabdosphincter is seen only if both the pudendal and pelvic efferents are sectioned. Thus, pudendal nerve block or pudendal neurectomy does not cause incontinence. The nerve fibres which pass distally to the distal sphincter mechanism are located in a dorsolateral position (5 and 7 o’clock). More distally, they adopt a more lateral position. Sensory innervation of the urethra Afferent neurons from the urethra travel in the pudendal nerve. Their cell bodies lie in the dorsal root ganglia, and they terminate in the dorsal horn of the spinal cord at S2–4, connecting with neurons which relay sensory information to the brainstem and cerebral cortex. P.494
The pudendal nerve—a somatic nerve derived from spinal segments S2–4—innervates striated muscle of the pelvic floor (levator ani—i.e. the pubourethral sling). Bilateral pudendal nerve block1 does not lead to incontinence because of maintenance of internal (sympathetic innervation) and external sphincter function (somatic innervation, S2–4, nerve fibres travelling to the external sphincter alongside parasympathetic neurons in the nervi erigentes). Clinical consequences of damage to the nerves innervating the LUT Bladder neck function in the female ~75% of continent young women and 50% of perimenopausal continent women have a closed bladder neck during the bladder filling phase. 25% of continent young women and 50% of perimenopausal continent women have an open bladder neck and yet they remain continent (because of their functioning distal sphincter mechanism, the external sphincter).2,3 Presacral neurectomy (to destroy afferent pain pathways) does not lead to incontinence because of maintenance of the somatic innervation of the external sphincter. Sympathetic motor innervation of the bladder Division of the hypogastric plexus of nerves during a retroperitoneal lymph node dissection for metastatic testis tumours results in paralysis of the bladder neck. This is of significance during ejaculation, where normally sympathetic activity results in closure of the bladder neck so that the ejaculate is directed distally into the posterior and then anterior urethra. If the bladder neck is incompetent, the patient develops retrograde ejaculation; they remain continent of urine because the distal urethral sphincter remains functional, being innervated by somatic neurons from S2–4. During pelvic fracture, the external sphincter and/or its somatic motor innervation may be damaged, such that it is incompetent and unable to maintain continence of urine. Preservation of bladder neck function (the sympathetic innervation of the bladder neck usually remains intact) can preserve continence. However, if in later life the patient undergoes a TURP or bladder neck incision for symptomatic prostatic obstruction, they may well be rendered incontinent because their one remaining sphincter mechanism (the bladder neck) will be divided during these operations. P.495
The physiology of urine storage and micturition Urine storage During bladder filling, bladder pressure remains low despite a substantial increase in volume. The bladder is thus highly compliant. Its high compliance is partly due to the elastic properties (viscoelasticity) of the connective tissues of the bladder and partly due to the ability of detrusor smooth muscle cells to increase their length without any change in tension. The detrusor is able to do this as a consequence of prevention of transmission of activity from preganglionic parasympathetic neurons to postganglionic efferent neurons—a so-called ‘gating’ mechanism within the parasympathetic ganglia. In addition, inhibitory interneuron activity in the spinal cord prevents transmission of afferent activity from sensors of bladder filling. Micturition A spino-bulbar-spinal reflex, co-ordinated in the pontine micturition centre in the brainstem (also known as Barrington’s nucleus or the M region), results in simultaneous detrusor contraction, urethral relaxation, and subsequent micturition. Receptors located in the bladder wall sense increasing tension as the bladder fills (rather than stretch). This information is relayed, by afferent neurons, to the dorsal horn of the sacral cord. Neurons project from here to the periaqueductal gray matter (PAG) in the pons. The PAG is thus informed about the state of bladder filling. The PAG and other areas of the brain (limbic system, orbitofrontal cortex) input into the PMC and determine whether it is appropriate to start micturition. At times when it is appropriate to void, micturition is initiated by relaxation of the external urethral sphincter and pelvic floor. Urine enters the posterior urethra and this, combined with pelvic floor relaxation, activates afferent neurons which results in stimulation of the pontine micturition centre (located in the brainstem). Activation of the PMC switches on a detrusor contraction via a direct communication between neurons of the PMC and the cell bodies of parasympathetic, preganglionic motoneurons located in the sacral intermediolateral cell column of S2–4. At the same time that the detrusor contracts, the urethra (the external sphincter) relaxes. The PMC inhibits the somatic motoneurons located in Onuf’s nucleus (the activation of which causes external sphincter contraction) by exciting GABA and glycine-containing, inhibitory neurons in the intermediolateral cell column of the sacral cord, which in turn project to the motoneurons in Onuf ‘s nucleus. In this way, the PMC relaxes the external sphincter. Micturition is an example of a positive feedback loop, the aim being to maintain bladder contraction until the bladder is empty. As the detrusor contracts, tension in the bladder wall rises. The bladder wall tension receptors are stimulated and the detrusor contraction is driven harder. One of the problems of positive feedback loops is their instability. Several inhibitory pathways exist to stabilize the storage–micturition ‘loop’. P.497

  • Tension receptors activate bladder afferents, which via the pudendal and hygastric nerves inhibit S2–4 parasympathetic motor nerve output. An ongoing detrusor contraction cannot be overriden.
  • Afferents in the anal and genital regions and in the distribution of the posterior tibial nerve stimulate inhibitory neurons in the sacral cord, and these neurons inhibit S2–4 parasympathetic motor nerve output. This pathway can override an ongoing detrusor contraction. It is hypothesized that this system prevents involuntary detrusor contraction during sexual activity, defaecation, and while walking, running, and jumping.

Excitatory neurotransmission in the normal detrusor is exclusively cholinergic, and reciprocal relaxation of the urethral sphincter and bladder neck is mediated by NO, released from postganglionic parasympathetic neurons. P.498
Bladder and sphincter behaviour in the patient with neurological disease A variety of neurological conditions are associated with abnormal bladder and sphincter function (e.g. spinal cord injury (SCI), spina bifida (myelomeningocele), MS). The bladder and sphincters of such patients are described as ‘neuropathic’. They may have abnormal bladder function or abnormal sphincter function or, more usually, both. The bladder may be overactive or underactive, as may the sphincter, and any combination of bladder and sphincter over or underactivity may coexist. ‘Activity’ here means bladder and sphincter pressure. In the normal lower urinary tract during bladder filling the detrusor muscle is inactive and the sphincter pressure is high. Bladder pressure is therefore low and the high sphincter pressure maintains continence. During voiding, the sphincter relaxes and the detrusor contracts. This leads to a short-lived increase in bladder pressure, sustained until the bladder is completely empty. The detrusor and sphincter thus function in synergy—when the sphincter is active, the detrusor is relaxed (storage phase), and when the detrusor contracts, the sphincter relaxes (voiding phase). An overactive bladder is one that intermittently contracts during bladder filling, so developing high pressures when normally bladder pressure should be low. In between these waves of contraction, bladder pressure returns to normal or near normal levels. In a patient with an underlying neurological problem, bladder overactivity is called detrusor hyperreflexia (DH). In other patients the bladder wall is stiffer than normal, a condition known as poor compliance. Bladder pressure rises progressively during filling, such bladders being unable to store urine at low pressures. Some patients have a combination of DH and poor compliance. The other end of the spectrum of bladder behaviour is the underactive bladder, which is low pressure during filling and voiding. This is called detrusor areflexia. An overactive sphincter generates high pressure during bladder filling, but it also does so during voiding, when normally it should relax. This is known as detrusor-external sphincter dyssynergia (DESD or DSD) (Fig. 14.1). During EMG recording, activity in the external sphincter increases during attempted voiding (the external sphincter should normally be ‘quiet’ during voiding) (Fig. 3.16). An underactive sphincter is unable to maintain enough pressure, in the face of normal bladder pressures, to prevent leakage of urine.

Fig. 14.1 Detrusor-external sphincter dyssynergia (DSD) seen during video-cystourethrography

The neuropathic lower urinary tract: the clinical consequences of storage and emptying problems Neuropathic patients experience two broad categories of problems— bladder filling and emptying—depending on the balance between bladder and sphincter pressures during filling and emptying. The effects of these bladder filling and emptying problems include incontinence, retention, recurrent UTIs, and renal failure. High-pressure sphincter High-pressure bladder If the bladder is overactive (detrusor hyperreflexia) or poorly compliant, bladder pressures during filling are high. The kidneys have to function against these chronically high pressures. Hydronephrosis develops and ultimately the kidneys fail (renal failure). At times the bladder pressure overcomes the sphincter pressure and the patient leaks urine (incontinence). If the sphincter pressure is higher than the bladder pressure during voiding (detrusor sphincter dyssynergia, DSD), bladder emptying is inefficient (retention, recurrent UTIs). Low-pressure bladder If the bladder is underactive (detrusor areflexia), pressure during filling is low. The bladder simply fills up—it is unable to generate enough pressure to empty (retention, recurrent UTIs). Urine leaks at times if the bladder pressure becomes higher than the sphincter pressure (incontinence), but this may occur only at very high bladder volumes or not at all. Low-pressure sphincter High-pressure bladder If the detrusor is hyperreflexic or poorly compliant, the bladder will only be able to hold low volumes of urine before leaking (incontinence). Low-pressure bladder If the detrusor is areflexic, such that it cannot develop high pressures, the patient may be dry for much of the time. They may, however, leak urine (incontinence) when abdominal pressure rises (e.g. when coughing, rising from a seated position, or when transferring to or from a wheelchair). Their low bladder pressure may compromise bladder emptying (recurrent UTIs). P.501
Bladder management techniques for the neuropathic patient A variety of techniques and procedures are used to treat retention, incontinence, recurrent UTIs, and hydronephrosis in the patient with a neuropathic bladder. Each of the techniques described below can be used for a variety of clinical problems. Thus, a patient with a high-pressure, hyperreflexic bladder which is causing incontinence can be managed with ISC (with intravesical botox injections if necessary), or a suprapubic catheter, or by sphincterotomy with condom sheath drainage, or by deafferentation combined with a sacral anterior root stimulator (SARS). Precisely which option to choose will depend on the individual patient’s clinical problem, their hand function, their lifestyle, and other ‘personal’ factors such as body image, sexual function, etc. Some patients will opt for a suprapubic catheter, as a simple, generally safe, generally very convenient and effective form of bladder drainage. Others wish to be free of external appliances and devices because of an understandable desire to look and ‘feel’ normal. They might opt for deafferentation with a SARS. Intermittent self-catheterization (ISC) See p.98. Indwelling catheters See p.108. External sphincterotomy Deliberate division of the external sphincter to convert the high-pressure, poorly emptying bladder due to DSD to a low-pressure, efficiently emptying bladder. Indications: retention, recurrent UTIs, hydronephrosis. Techniques

  • Surgical (with an electrically heated ‘knife’ or laser). Disadvantages: irreversible, post-operative bleeding, septicaemia, and stricture formation6.
  • Intra-sphincteric botox (botulinum toxin). Increasingly popular because minimally invasive and reversible. Disadvantage: repeat injection required every 6–12 months.
  • A third potential option is an oral or sublingual nitric oxide (NO) donor (e.g. nifedipine, GTN). NO is a neurotransmitter which relaxes the external sphincter. Hypothesized as a treatment for DSD, and preliminary studies support this hypothesis.7,8

Augmentation Technique of increasing bladder volume to lower pressure by implanting detubularized small bowel into the bivalved bladder (‘clam’ ileocystoplasty) (Fig. 14.2) or by removing a disc of muscle from the dome of the bladder (autoaugmentation or detrusor myectomy). Indications: incontinence, hydronephrosis.

Fig. 14.2 A ‘clam’ ileocystoplasty. (Reproduced with permission from McAninch 19969

Recently, intravesical botox injections at multiple sites in the bladder every 6–12 months have produced impressive reductions in bladder pressure and increases in volume, with minimal side-effects. This may replace traditional surgical augmentation. Deafferentation Division of dorsal spinal nerve roots of S2–4, to convert the hyper-reflexic, high-pressure bladder into an areflexic, low-pressure one. Can be used where the hyperreflexic bladder is the cause of incontinence or hydronephrosis. Bladder emptying can subsequently be achieved by ISC or implantation of a nerve stimulator placed on ventral roots (efferent nerves) of S2–4 to ‘drive’ micturition when the patient wants to void (a pager-sized externally applied radiotransmitter activates micturition (Figs. 14.3 and 14.4). Also useful for DSD/incomplete bladder emptying causing recurrent UTIs and retention.

Fig. 14.3 A sacral anterior root stimulator, used to ‘drive’ micturition following a deafferentation (external components)
Fig. 14.4 KUB X-ray showing the sacral electrodes positioned on the ventral roots of S2, 3, and 4

Catheters and sheaths and the neuropathic patient Many patients manage their bladders by intermittent catheterization (IC) done by themselves (intermittent self-catheterization, ISC) or by a carer if their hand function is inadequate, as is the case with most tetraplegics. Many others manage their bladders with an indwelling catheter (urethral or suprapubic). Both methods can be effective for managing incontinence, recurrent UTIs, and bladder outlet obstruction causing hydronephrosis. Intermittent catheterization Requires adequate hand function. The technique is a ‘clean’ one (simple handwashing prior to catheterization) rather than ‘sterile’. Gel-coated catheters become slippery when in contact with water, so providing lubrication. Usually done 3–4 hourly. Problems

  • Recurrent UTIs.
  • Recurrent incontinence: check technique (adequate drainage of last few drops of urine). Suggest increasing frequency of ISC to minimize volume of urine in the bladder (reduces bacterial colonization and minimises bladder pressure). If incontinence persists, consider intravesical botulinum toxin.

Long-term catheterization Some patients prefer the convenience of a long-term catheter. Others regard it as a last resort when other methods of bladder drainage have failed. The suprapubic route (suprapubic catheter, SPC) is preferred over the urethral because of pressure necrosis of the ventral surface of the distal penile urethra in men (acquired hypospadias—‘kippering’ of the penis) and pressure necrosis of the bladder neck in women, which becomes wider and wider until urine leaks around the catheter (‘patulous’ urethra) or frequent expulsion of the catheter occurs with the balloon inflated. Problems and complications of long-term catheters

  • Recurrent UTIs: colonization with bacteria provides a potential source of recurrent infection.
  • Catheter blockages are common: due to encrustation of the lumen of the catheter with bacterial biofilms. Proteus mirabilis, Morganella, and Providencia species secrete a polysaccharide matrix. Within this, urease-producing bacteria generate ammonia from nitrogen in urine, raising urine pH and precipitating magnesium and calcium phosphate crystals. The matrix-crystal complex blocks the catheter. Catheter blockage causes bypassing which soils the patient’s clothes. Bladder distension can cause autonomic dysreflexia, leading to extreme rises in blood pressure which can cause stroke and death! Regular bladder washouts and increased catheter size sometimes help. Impregnation of catheters with antibacterials (e.g. Triclosan) are under investigation.10 P.507
    Intermittent filling and emptying of the bladder using a ‘flip-flow’ valve may reduce frequency of catheter blockages.
  • Bladder stones: develop in 1 in 4 patients over 5 years.11

Bladder cancer: chronic inflammation (from bladder stones, recurrent UTIs, long-term catheterization) may increase the risk of squamous cell carcinoma in SCI patients. Some studies report a higher incidence of bladder cancer (whether chronically catheterized or not); others do not.12 Condom sheaths These are an externally worn urine collection device consisting of a tubular sheath applied over the glans and shaft of the penis (just like a contraceptive condom only without the lubrication to prevent it slipping off). Usually made of silicone rubber with a tube attached to the distal end to allow urine drainage into a leg bag. They are used as a convenient way of preventing leakage of urine, but are obviously only suitable for men. Detachment of the sheath from the penis is prevented by using adhesive gels and tapes. They are used for patients with reflex voiding (where the hyperreflexic bladder spontaneously empties, and where bladder pressure between voids never reaches a high enough level to compromise kidney function). They are also used as a urine collection device for patients after external sphincterotomy (for combined detrusor hyperreflexia and sphincter dysynergia where incomplete bladder emptying leads to recurrent UTIs and/or hydronephrosis). Problems The principal problem experienced by some patients is sheath detachment. Despite the fact that a man walked on the moon 30 years ago, we have been unable to design a condom sheath which will consistently prevent urine leakage in all men. This can be a major problem, and in some cases requires a complete change of bladder management. Skin reactions sometimes occur. P.508
Management of incontinence in the neuropathic patient Causes High-pressure bladder (detrusor hyperreflexia, reduced bladder compliance); sphincter weakness; UTI; bladder stones; rarely, bladder cancer (enquire for UTI symptoms and haematuria). Hyperreflexic peripheral reflexes suggest bladder may be hyperreflexic (increased ankle jerk reflexes, S1–2 and a +ve bulbocavernosus reflex indicating an intact sacral reflex arc—i.e. S2–4 intact). Absent peripheral reflexes suggest the bladder and sphincter may be areflexic (i.e. sphincter unable to generate pressures adequate for maintaining continence). Initial investigations Urine culture (for infection); KUB X-ray for bladder stones; bladder and renal ultrasound for residual urine volume and to detect hydronephrosis; cytology and cystoscopy if bladder cancer suspected. Empirical treatment Start with simple treatments. If the bladder residual volume is large, regular ISC may lower bladder pressure and achieve continence. Try an anticholinergic drug (e.g. oxybutynin, tolterodine). Many SCI patients are already doing ISC and simply increasing ISC frequency to 3–4 hourly may achieve continence. ISC more frequently than 3 hourly is usually impractical, particularly for paraplegic women who usually have to transfer from their wheelchair onto a toilet and then back onto their wheelchair. See Table 14.1. Management of failed empirical treatment Determined by VCUG, to assess bladder and sphincter behaviour. Detrusor hyperreflexia or poor compliance High-pressure sphincter (i.e. DSD). Treating the high-pressure bladder is usually enough to achieve continence.

  • Bladder treatments—intravesical Botulinum toxin, detrusor myectomy (autoaugmentation), bladder augmentation (ileocystoplasty). All will usually require ISC for bladder emptying
  • Long-term suprapubic catheter
  • Sacral deafferentation + ISC or Brindley implant (SARS—sacral anterior root stimulator)

Low-pressure sphincter. Treat the bladder first (as above). If bladder treatment alone fails, consider a urethral bulking agent, a transvaginal tape (TVT), or bladder neck closure in women or an artificial urinary sphincter in either sex (Fig. 14.5). Detrusor areflexia + low pressure sphincter

  • Urethral bulking agents
  • TVT
  • Bladder neck closure in women
  • Artificial urinary sphincter
Table 14.1 Summary of treatment for incontinence
  High bladder pressure Low bladder pressure
High sphincter pressure Lower bladder pressure by ISC + anticholinergics or botox or augmentation ISC*
Low sphincter pressure Lower bladder pressure by (ISC + anticholinergics or botox or augmentation) + urethral bulking agent TVT or bladder neck closure or artificial urinary sphincter Urethral bulking agent, TVT Bladder neck closure Artificial urinary sphincter
* High sphincter pressure is usually enough to keep patient dry.
Fig. 14.5 Artificial urinary sphincter implanted around the bulbar urethra

Management of recurrent urinary tract infections (UTIs) in the neuropathic patient Causes of recurrent UTIs

  • Incomplete bladder emptying
  • Kidney stones
  • Bladder stones
  • Presence of an indwelling catheter (urethral or suprapubic)

History What the patient interprets as a UTI may be different from your definition of UTI. The neuropathic bladder is frequently colonized with bacteria and often contains pus cells (pyuria). From time to time it becomes cloudy due to precipitation of calcium, magnesium, and phosphate salts in the absence of active infection. The presence of bacteria, pus cells, or cloudy urine in the presence of non-specific symptoms (abdominal pain, tiredness, headaches, feeling ‘under the weather’) is frequently interpreted as a UTI. Indications for treatment of UTI in the neuropathic patient It is impossible to eradicate bacteria or pus cells from the urine in the presence of a foreign body (e.g. a catheter). In the absence of fever and cloudy, smelly urine, we do not prescribe antibiotics, the indiscriminate use of which encourages growth of antibiotic-resistant organisms. We prescribe antibiotics to the chronically catheterized patient where there is a combination of fever, cloudy, smelly urine, and where the patient feels unwell. Culture urine and immediately start empirical antibiotic therapy with nitrofurantoin, ciprofoxacin, or trimethoprim (the antibiotics sensitivities of our local ‘bacterial flora’), changing to a more specific antibiotic if the organism is resistant to the prescribed one. Investigations For recurrent UTIs (= frequent episodes of fever, cloudy, smelly urine, and feeling unwell), organize the following:

  • KUB X-ray—looking for kidney and bladder stones.
  • Renal and bladder ultrasound to determine the presence/absence of hydronephrosis and to measure pre-void bladder volume and post-void residual urine volume.

Treatment In the presence of fever and cloudy, smelly urine, culture the urine and start antibiotics empirically (e.g. trimethoprim, nitrofurantoin, amoxicillin, ciprofloxacin), changing the antibiotic if the culture result suggests resistance to your empirical choice. ‘Response’ to treatment is suggested by the patient feeling better and their urine clearing and becoming non-offensive to smell. Persistent fever, with constitutional symptoms (malaise, rigors) despite treatment with a specific oral antibiotic in an adequate dose is an indication for admission for treatment with intravenous antibiotics. P.511
Management of recurrent UTIs See Table 14.2. If there is residual urine present, optimize bladder emptying by intermittent catheterization (males, females) or external sphincterotomy for DSD (males). Intermittent catheterization can be done by the patient (intermittent self-catheterization, ISC) if hand function is good (paraplegic), or by a carer if tetraplegic. An indwelling catheter is an option, but the presence of a foreign body in the bladder may itself cause recurrent UTIs (though in some it seems to reduce UTI frequency).

Table 14.2 Summary of treatment for recurrent UTIs
Low bladder pressure High bladder pressure + DSD*
External sphincterotomy—surgical, botox, stent
Remove stones if present—cystolitholapxy for bladder stones, PCNL for staghorn stones.
* A new potential option for DSD is augmentation of external sphincter nitric oxide (NO), a neurotransmitter which relaxes the external sphincter, thereby encouraging antegrade flow of urine and potentially, therefore, lowering residual urine volume. NO donors such as nifedipine or GTN can be used. There is theoretical and some experimental evidence to support this.13,14

Management of hydronephrosis in the neuropathic patient An overactive bladder (detrusor hypereflexia) or poorly compliant bladder is frequently combined with a high-pressure sphincter (detrusor-sphincter dysynergia—DSD). Bladder pressures during both filling and voiding are high. At times the bladder pressure may overcome the sphincter pressure and the patient leaks small quantities of urine. For much of the time, however, the sphincter pressures are higher than the bladder pressures and the kidneys are chronically exposed to these high pressures. They are hydronephrotic on ultrasound and renal function slowly, but inexorably, deteriorates. Treatment options for hydronephrosis Bypass the external sphincter

  • IDC (indwelling catheter)
  • ISC (intermittent self-catheterization) + anticholinergics

Treat the external sphincter

  • Sphincterotomy: surgical incision via a cystoscope inserted down the urethra (electrically heated knife or laser), botox injections into sphincter, urethral stent
  • Deafferentation1 + ISC or SARS

Treat the bladder

  • Intravesical botox + ISC
  • Augmentation + ISC
  • Deafferentation1 + ISC or SARS

Footnote 1 Deafferentation converts the high-pressure sphincter into a low-pressure sphincter and the high-pressure bladder into low-pressure bladder. P.513
Bladder dysfunction in multiple sclerosis, in Parkinson’s disease, after stroke, and in other neurological disease Multiple sclerosis (MS) ~75% of patients with MS have spinal cord involvement and, in these patients, bladder dysfunction is common. The most common symptom in patients with MS is urgency (due to DH). Bladder pressures are rarely high enough to cause upper tract problems (hydronephrosis). Parkinson’s disease (PD) PD is a cause of parkinsonism (tremor, rigidity, bradykinesis—slow movements) and is due to degeneration of dopaminergic neurons in the substantia nigra in the basal ganglia. Frequency, urgency, and urge incontinence are common. The most common urodynamic abnormality is DH (the basal ganglia may have an inhibitory effect on the micturition reflex). L-dopa seems to have a variable effect on these symptoms and DH, improving symptoms in some and making them worse in others. LUTS in Parkinson’s disease may simply be due to benign prostatic obstruction or may be due to the PD itself. Traditionally, patients with PD have had a poorer outcome after TURP than those without PD, but if the patient has urodynamically proven BOO, TURP is a treatment option. Multiple system atrophy (MSA; formerly Shy–Drager syndrome) A cause of parkinsonism characterized clinically by postural hypotension and detrusor areflexia. Loss of cells in the pons leads to DH (symptoms of bladder overactivity), loss of parasympathetic neurons due to cell loss in the intermediolateral cell column of the sacral cord causes poor bladder emptying, and loss of neurons in Onuf’s nucleus in the sacral anterior horns leads to denervation of the striated sphincter causing incontinence. The presentation is usually with DH (i.e. symptoms of bladder overactivity), followed over the course of several years by worsening bladder emptying. Cerebrovascular accidents DH occurs in 70%, DSD in 15%. Detrusor areflexia can occur.15 Frequency, nocturia, urgency, and urge incontinence are common. Retention occurs in 5% in the acute phase. Incontinence within the first 7 days after a CVA predicts poor survival.16 Other neurological disease Frontal lobe lesions (e.g. tumours, AVMs) May cause severe frequency and urgency (frontal lobe has inhibitory input to the pons). P.515
Brainstem lesions (e.g. posterior fossa tumours) Can cause urinary retention or bladder overactivity. Transverse myelitis Severe tetraparesis and bladder dysfunction, which often recovers to a substantial degree. Peripheral neuropathies The autonomic innervation of the bladder makes it ‘vulnerable’ to the effects of peripheral neuropathies such as those occurring in diabetes mellitus and amyloidosis. The picture is usually one of reduced bladder contractility (poor bladder emptying—i.e. chronic low pressure retention). P.516
Neuromodulation in lower urinary tract dysfunction This is the electrical activation of afferent nerve fibres to modulate their function. Electrical stimulation applied anywhere in the body preferentially depolarizes nerves (higher current amplitudes are required to directly depolarize muscle). In patients with LUT dysfunction, the relevant spinal segments are S2–4. Indications: urgency, frequency, urge incontinence, chronic urinary retention where behavioural and drug therapy has failed. Several sites of stimulation are available, the electrical stimulus being applied directly to nerves, or as close as possible:

  • sacral nerve stimulation (SNS)
  • pudendal nerve—direct pelvic floor electrical stimulation (of bladder, vagina, anus, pelvic floor muscles) or via stimulation of dorsal penile or clitoral nerve (DPN, DCN)
  • posterior tibial nerve stimulation (PTNS)18

PTNS PTN (L4,5; S1–3) shares common nerve roots with those innervating the bladder. PTNS can be applied transcutaneously (stick-on surface electrodes) or percutaneously (needle electrodes). Percutaneous needle systems include the SANS (Stoller) and the UrgentPC system. Stimulation is applied via an acupuncture needle inserted just above the medial malleolus with a reference (or return) electrode—30 min of stimulation per week, over 12 weeks. Thereafter, 30 min of treatment every 2–3 weeks can be used to maintain the treatment effect in those who respond. PTNS has not been compared with placebo (‘sham’ stimulation) and therefore reported efficacy may represent a placebo response. SNS A sacral nerve stimulator (Medtronic Interstim) delivers continuous electrical pulses to sacral nerve root 3 via an electrode inserted through the sacral foramina and connected to an electrical pulse generator which is implanted subcutaneously. A test stimulation (the peripheral nerve evaluation, PNE) is performed, under local anaesthetic, by a percutaneous test electrode placed in S3 foramina to confirm an appropriate clinical response (a reduction in urgency, frequency, or incontinence episodes). A permanent implant is offered if there is a 50% reduction in frequency and urgency. This is placed in a subcutaneous pocket and is connected to the sacral electrode. It can be switched on and off and the amplitude varied within set limits. ~50% of patients have a successful PNE, and of this 50% who undergo subsequent permanent implantation, 50% report resolution of their urge incontinence and 80% report >50% reduction in incontinence episodes, persisting for at least 3–5 years. Supported by NICE19 for patients with urge incontinence who have failed lifestyle modification, behaviour and drug therapy. References 1 Brindley GS (1974) The pressure exerted by the external sphincter of the urethra when its motor nerve fibres are stimulated electrically. Br J Urol 46:453–62. 2 Chapple CR et al. (1989) Asymptomatic bladder neck incompetence in nulliparous females. Br J Urol 64:357–59. 3 Versi E et al. (1990) Distal urethral compensatory mechanisms in women with an incompetent bladder neck who remain continent and the effect of the menopause. Neurourol Urodyn 9:579–90. 4 Gosling JA, Dixon JS (1998) Structure of the bladder and urethra. In: Whitfield et al. (ed) Textbook of Genitourinary Surgery. Blackwell Science, p. 456. 5 De Groat WC (1993) Anatomy and physiology of the lower urinary tract. Urol Clin NA 20:383–401. 6 JM Reynard (2003) Sphincterotomy and the treatment of detrusor-sphincter dyssynergia: current status, future prospects. Spinal Cord 41:1–11. 7 Keitz A et al. (2004) Oral nitric oxide donors: a new pharmacological approach to detrusor-sphincter dyssynergia in spinal cord injured patients. Eur Urol 45:516–20. 8 Mamas MA, Reynard JM, Brading AF (2001) Augmentation of external uretheral sphincter nitric oxide: a potential pharmacological treatment for detrusor-external sphincter dyssynergia in spinal cord injury. Lancet 357:1964–67. 9 McAninch JW (1996) Traumatic and Reconstructive Urology. W.B. Saunders/Elsevier, p. 301. 10 D Stickler et al. (2003) Control of encrustation and blocked Foley catheters. Lancet 361:1435–37. 11 Ord J, Lunn D, Reynard J (2003) Bladder management and risk of bladder stone formation in spinal cord injured patients. J Urol 170:1734–37. 12 K Subramonian et al. (2004) Bladder cancer in patients with spinal cord injuries. Br J Urol Int 93:739–43. 13 Mamas MA, Reynard JM, Brading AF (2001) Augmentation of external urethral sphincter nitric oxide: a potential pharmacological treatment for detrusor-external sphincter dyssynergia in spinal cord injury. Lancet 357:1964–67 14 Keitz A et al. (2004) Oral nitric oxide donors: a new pharmacological approach to detrusorspincter dyssynergia in spinal cord injured patients. Eur Urol 45:516–20. 15 Sakakibara R et al. (1996) Micturitional disturbance after acute hemispheric stroke: analysis of the lesion site by CT and MRI. J Neurol Sci 137:47–56. 16 Wade D et al. (1985) Outlook after an acute stroke: urinary incontinence and loss of consciousness compared in 532 patients. Quart Med J 56:601–8. 17 Chandiramani VA, Palace J, Fowler CJ (1997) How to recognise patients with prostatism who should not have urological surgery. Br J Urol 80:100–4. 18 Andrews B, Reynard J (2003) Transcutaneous posterior tibial nerve stimulation for the treatment of detrusor hyperreflexia in spinal cord injury. J Urol 170:926 19 NICE (June 2004) Interventional Procedure Guidance 64. http://www.nice.org.uk/ip082systematic review.

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