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A
spinal injury, depending on the level and completeness of the lesion,
will result in a certain type of neuromuscular dysfunction of the lower
urinary tract (bladder and urethra). The resultant problem is the
inability (partial or total) to evacuate the bladder (retention) or to
store urine (incontinence). Apart from injury to the spinal cord or
cauda equinae, which causes impairment of the nervous supply to the
bladder and urethra, there are areas of the nervous system such as the
frontal lobes and pontine centers which can also cause disorders of
micturition. Spinal injury can also cause bowel and sexual
dysfunction.
Anatomy and physiology of the bladder and urethra:
The
body of the urinary bladder, including the trigone, is composed of layers
of smooth muscle (detrusor). The Detrusor contracts ‘as a whole’ and
is supplied by cholingergic (parsympathetic) fibres whose motor efferent
innervation is served by S2, S3, S4 roots, pelvic nerves and conus
medullaris through bladder wall ganglia. It is also innervated by and
b-adrenergic (sympathetic) motor efferents which are controlled by T11-12
myelotomes (via sympathetic ganglion chain and hypogastric nerves).
The sensation of the bladder (fullness, pain, tactile) is served both by
sacral and T11-12 cord, via the afferents of pelvic and hypogastric
nerves. Central conduction to the brain is mainly several via the
spinothalamic tract (bladder sensation) and posterior columns (pelvic
floor proprioceptive sensation).
At
the lower end of the bladder there are three related anatomical areas,
all of smooth muscle of similar embryological origin, which have a high
proportion of a-sympathetic receptors: a) the trigone, small triangular
area where the ureters enter. Its apex leads to internal urethral
orifice, b) the neck or posterior urethra which has been called the
internal (proximal) sphincter (concentric smooth muscle) and in the male
is continuous with the prostatic capsule, c)the internal longitudinal
layer of smooth urethral muscle.
The
anterior urethra is surrounded by the external (distal) urethral
sphincter (striated muscle). This complex has two groups of
muscles: a) the periurethral striated part which is continuous with
pelvic floor muscles. This can contract rapidly to interrupt the
stream and is innervated by the pudendal nerve (S2, S3, and S4). b) the
intrinsic striated sphincter or rhabdo sphincter which can maintain its
tone for long periods and is innervated by the pelvic nerve.
The
function of bladder and urethra is to store and evacuate urine and it is
imperative that these two anatomical structures are considered as one,
the vesico-urethral unit.
The
physiological basis of lower urinary tract performance is the continuous
and simultaneous bladder (detrusor) and urethra (sphincter) interaction
(facilitation or inhibition of vesico-urethral reflex).
Ultimately
the storage and evacuation of the bladder depend on brainstem/sacral cord
reflex mechanism controlled by cortical centers (superior frontal
gyrus, anterior cingulated gyrus) which are involved in the
awareness of bladder fullness and the socially acceptable way of voiding.
During storage the bladder smooth musculature remains relaxed whilst the
smooth sphincter is constricted. The opposite happens during micturition
with detrusor contraction, sphincter relaxation and subsequent voiding.
The storage phase is assisted by sympathetic mechanisms (hypogastric
nerve, thoracolumbar cord) via relaxation of detrusor (efferent
b-response). The voiding phase starts when the afferent pelvic nerve
stimulus reaches a certain threshold where the spontaneous inhibitory
control by higher centers stops or is overcome and bladder contraction/
sphincter relaxation occurs due to parasympathetic stimulation and
sympathetic inhibition. During this phase the external sphincter
(striated muscle innervated by pudendal nerve) is also relaxed. The final
control of micturition is mediated via pontine (proprioceptive
efferents), thalamic (pain) and frontal lobe (sensory and motor cortex)
centers.
Classification of neurogenic bladder:
Anatomical: Upper motor neuron, Lower motor neuron,
Cauda equine, Peripheral nerves. This classification is schematic and
does not necessarily correspond to the underlying functional
clinical problem.
Functional: Uninhibted
neuropathic bladder (bladder hyper-reflexia): It is caused
by suprasacral cord lesions and the associated lack of upper motor neuron
inhibition results in spontaneous bladder contractions. If the
damage is partial and sensation of the bladder intact the patient will
experience urgency. If the damage is partial, with preservation of
voluntary function, then the patient will be able to control the
hyperreflexic detrusor and manage to void in a socially acceptable way.
If the damage is complete with loss of bladder sensation and
external sphincter control then spontaneous detrusor activity
(hyperreflexia) will cause uncontrolled urine loss i.e. reflex
incontinence
Depending
on the level of injury, the patient may demonstrate detrusor-sphincter
dyssynergia, where simultaneous contraction of both muscles causes an
initial high-pressure retention and finally incontinence but only partial
bladder evacuation. This problem can cause ureteral reflux and subsequent
kidney damage, even in the absence of infection. It is more common in
the higher spinal cord lesion.
If
the level of injury is below the thoracic sympathetic outflow (T10-L2)
and the sympathetic centers are preserved, but without inhibition from
sacral parasympathetic cord, there may be additional sympathetic
dysreflexia, mediated smooth muscle urethral constriction.
Paralytic neuropathic bladder: This is caused
by sacral cord, cauda equine or plexus injury, where the contraction
activity of the detrusor is totally lost due to its motor and sensory
decentralization (detrusor areflexia). The bladder is enlarged and
continence depends on sphincter function and competence of the bladder
neck during the filling phase. In complete cord lesions the coexisting
loss of sphincter activity will result in total incontinence. In partial
lesions the preservation of sphincter function will prevent incontinence
if measures to empty bladder are taken before overflow incontinence occurs.
Clinical features:
The
degree of neurological impairment will determine the patient’s urologic
symptomatology, and those with gross neurological deficits may only
recognize their inability to remain continent or their inability to
void. However, those with more subtle neurological lesions may
present with symptoms that are not immediately identifiable as of
neurogenic etiology, and they may mimic bladder irritative or obstructive
problems.
Urinary
incontinence may
be of different forms. Stress incontinence may occur as a result
of sphincter incompetence due to sacral cord or peripheral nerve
lesions. Urgency incontinence is a manifestation of hyper-reflexic
bladder dysfunction. The patient with intact bladder sensation will
recognize the urge to void but will not reach the bathroom in time before
forceful involuntary urine loss occurs; however, in more complete
lesions, when sensation is lost, unconscious reflex incontinence
occurs. Overflow incontinence occurs in an areflexic bladder when
the bladder fills to the point where intravesical pressure exceeds the
urethral closing pressure and continuous dribbling loss of urine
results. Total urinary incontinence where the bladder and urethra
are converted into a virtual open conduit rarely occurs because of
neurogenic dysfunction.
Frequency
and incomplete emptying of the bladder may suggest
vesicourethral dysfunction as in upper motor neurone dysfunction. Bowel
dysfunction frequently accompanies.
Abdominal
discomfort and flank pain is a frequent warning symptom of
urologic disease in a neurogenic bladder. Depending on the level and
completeness of the neurological lesion, such pain may or may not be
perceived by the patient. Inflammatory changes in the bladder and
urethra usually manifest with pain.
Hematuria may suggest urinary infection and
calculus disease in a neurogenic bladder. In patients on intermittent
catheterization, however, catheter trauma may be responsible.
Autonomic dysreflexia occurs in
patients with cervical or high thoracic injury where stimulation of areas
below the lesion, e.g. bladder or bowel, causes a profuse autonomic
discharge (bradycardia, hypertension, pupillary dilatation, chest
tightness, perspiration, headache, flashing, nausea) due to
parasympathetic–sympathetic imbalance. Occasionally it might cause
cerebral hemorrhage and/or death.
Clinical Examination:
It should
include three parts: physical, neurological, and urological.
In
most cases the identification of the neurological deficit is a simple
matter; however, it is not uncommon for occult neurological lesions to
result in neurogenic bladder dysfunction before any other obvious
manifestations occur. Neurological examination can predict the
likely nature of the resultant bladder dysfunction, and also determine
the patient’s ability to accomplish planned urologic management.
The
urologic examination should include inspection and palpation of the
abdomen, inguinal region, and external genitalia and a rectal
examination. It should also include a pelvic examination in the
female.
Investigations:
The
planning of diagnostic tests and therapy will depend on the type of
neurologically injury (level and cause) and patient’s ultimate
handicap.
Urine microscopy and Culture is mandatory in
order to exclude underlying urinary tract infection, the single most
important cause of severe kidney damage and subsequent chronic renal
failure. Frequent microscopic urine examination and culture (every 2
months) is advised for all patients with neuropathic bladder. The
examination of serum creatinine and electrolytes will exclude an
underlying renal disease.
Plain
X-ray of the abdomen, including the areas of the kidneys, ureters, and
bladder (also called a scout film or KUB) is generally performed as an
initial study prior to subsequent radiographic examination. This is
also valuable as an isolated study for the identification of opaque
urinary calculi.
Excretory
Urography should be
performed as a baseline in all patients with neurogenic vesicourethral
dysfunction to look for the changes arising from chronic infection,
obstruction, reflux, and stone disease. In the uncomplicated case, it is
repeated every 3 years.
Voiding
Cystourethrography identifies the morphologic
characteristics of the bladder and the presence of vesicoureteral reflux,
and hints at the functional status of the urethral sphincters. The
indications for voiding cystourethrography (VCUG) in neurogenic bladder
dysfunction are controversial and usually reserved for such occasions or
for patients with recurrent urinary infections.
Renal
Ultrasound adequately
demonstrate even minor changes in upper tract dilatation, can identify
renal size accurately, will demonstrate opaque and nonopaque calculi, and
are indispensable in the evaluation of renal masses and avoids the danger
of exposure to high levels of radiation
Nuclear
Medicine Evaluation can not only assist by evaluating
total and differential renal function but may also, when combined with
fursemide, give an indication as to whether the upper tracts are
obstructed. Although these studies occasionally give inconclusive
results, they are associated with less radiation than conventional
intravenous urograms. Newer contrast agents are becoming
available.
Magnetic
Resonance Imaging has the ability to show spinal cord lesions
that may represent as urologic symptom complexes. Where available
this investigation may be performed first for investigation of such
complexes to rule out spinal cord pathology.
Cytoscopy has little to
offer in its identification. However, it is indicated for the
evaluation of other abnormal parameters in the neurogenic bladder
patient, such as hematuria, recurrent urinary tract infection or
unexplained pyuria, and voiding dysfunction unexplained by urodynamic
study.
Urodynamics permits
assessment of lower urinary tract function, identification of specific
functional abnormalities of bladder and/or urethra causing impaired
micturition, and accurate localization (detrusor, smooth muscle urethral
sphincter, ‘striated muscle urethral sphincter, sensation) of
problems. This is achieved by measurement of bladder and urethral
function during storage and voiding with methods such as abdominal
pressure and intravesical pressure measurements (the difference between
them is detrusor pressure), urine volume and flow rate, urethral pressure
and urethral length, EMG. These are recorded with the aid of special
equipment (multichannel recorder using data from several transducers,
flow meters and from X-ray or ultrasonic video-cysto-urethrography).
In some cases evoked responses and reflex conduction studies may be made.
Although
there seems to be a correlation between the location of injury and the
resultant type of neuropathic bladder this is not always the case. The
clinical neurological examination alone was not a sufficient predictor of
function and it is suggested that videourodynamic assessment should be
performed for accurate diagnosis of bladder/sphincter imbalance. It is
further suggested that failure of this correlation should raise the
suspicion of a second lesion e.g. the urodynamic detrusor areflexia or
hypocontractility, in a patient with suprasacral cord injury, may suggest
a second area of damage involving the sacral centres. Finally, it should
also be noted that the urodynamic assessment allows classification of the
problem as: a) Storage disorder caused by bladder or sphincter, b)
Voiding disorder caused by bladder or sphincter.
Management:
Neurourology
is a relatively new domain which examines the urinary and sexual dysfunctions
related to neurological disease and it involves many related specialties
such as urology, neurology, neurosurgery, gynecology, psychiatry, and
engineering. Normal renal function is the primary goal in the long term
management of the spinal injury patients.
In
the initial period of ‘spinal shock’ and loss
of bladder function (detrusor paralysis) the patient may be
catheterized continuously, mainly for convenience reasons. After the
acute period, depending on the level and completeness of injury, the catheterization
may continue on an intermittent basis. Commercially made disposable
plastic catheters are available at reasonable cost. When expense is
a consideration, however, the same catheter may be simply reused by
thoroughly washing it in soap and water after use and wrapping it in a
clean towel until the next use.
The level,
nature and completeness of cord damage, evaluated by clinical and
radiological diagnosis, usually predetermine the type of long term
therapeutic
management, although the final decision can only be made after a
comprehensive urodynamic assessment. It should also be kept in mind
that, after an injury to the cord, bladder behavior passes through
different stages and therefore before starting any bladder management, a
re-evaluation of pathophysiology and urodynamic results is mandatory.
The
therapeutic approach aims towards avoidance of residual urine, control of
infection and calculus formation, protection of kidneys, and preservation
of continence. The patient achieves this through low-pressure urine
storage, low pressure voiding and adequate bladder evacuation. Conservative management is indicated in
patients with potentially fatal neurological disease and for those with
potentially changeable problems such as multiple sclerosis.
A)
Therapy to Facilitate Urine Storage:
In
some patients storage may be improved, leaving volitional voiding
intact. However, therapy to improve storage generally compromises
emptying such that residual urine with the potential for infection
results. In this event, a clean intermittent catheterization
program must be added. Bacteria are obviously introduced into the bladder
during clean catheterization; but providing that complete emptying is
achieved, these organisms are neutralized by the host defence mechanisms
and infection is usually avoided. Over distension of the bladder
must be avoided, for it compromises the blood supply to the bladder wall
and impairs the host resistance. Using clean intermittent
catheterization, sterile urine is achieved in from 39 to 65 percent of
cases. Those patients who do not have sterile urine generally have
asymptomatic bacteriuria. Most go untreated unless recurrent
symptomatic infective episodes occur or anatomic reasons such as reflux
make treatment advisable. However, many physicians, uncertain of
the long-term adverse effects of chronic bacteriuria, advocate adjunctive
prophylactic antimicrobial treatment for all patients on a clean
intermittent catheterization program.
The
bladder storage capacity can be increased by either reducing detrusor
function or by enhancing the sphincter resistance. In a patient with
detrusor areflexia and a competent outlet, intermittent catheterization
alone will suffice. However, in many cases one or more of the
adjunctive procedures to inhibit bladder contractility may be necessary
to promote bladder storage.
Pharmacologic
Manipulation:
The agents most often used to inhibit bladder contractility are the
anticholinergic drugs and agents with a direct inhibitory effect on
smooth muscle. Oxybutynin is the most widely used agent for this
purpose. In addition to its anticholinergic activity it has an
independent musculotropic effect and also some moderate local anesthetic
effect on the bladder. It is customarily used in adults in a dosage
of up to 5mg four times daily and is also available in a pediatric
suspension. Its antimuscarinic side effects include drying of
salivary secretions, mydriasis, blurred vision, tachycardia, drowsiness,
and constipation. Alternative agents with the same effect include
propantheline, methantheline, flavoxate hydrochloride, dicyclomine
hydrochloride, and imipramine hydrochloride. Use of these agents requires
careful follow-up. In some cases, symptomatic improvement with
increase in bladder capacity and a decrease in incontinence is rapid,
without compromising voiding efficiency. In others, however, the
dosage required to reduce incontinence abolishes the micturition
contraction and makes the use of the clean intermittent catheterization
program necessary. All of these agents may be contraindicated in
patients who have glaucoma, and they must be used with great care in
patients with obstructive gastrointestinal disease, bladder outlet
obstruction, or tachycardia. A new anticholinergic, vamicacide, is
recently shown to be effective.
Electrical
Stimulation:
Devices designed to stimulate the afferent limb of the pudendal reflex
arc have been used for some years to treat urinary incontinence.
They were originally designed to improve the urethral closing function by
stimulation of the pelvic floor musculature. However, it appears
that there is a sacral pathway for the inhibition of detrusor reflex
activity, and electrical stimulation of the pudendal afferents has been
used clinically to achieve this end. Two different types of local
external electrical stimulation are in use, and they are distinguished by
the different time courses of treatment and by the different strengths of
electrical pulses used. The first is chronic (long-term)
stimulation; this is a weak stimulation characterized by prolonged
application of low-strength stimuli up to a maximum of 12 V for many
hours a day for a period of several months. Applied stimulation is
normally so weak it does not reach sensory threshold and is used predominantly
for improving bladder outlet resistance but has also been described for
increasing bladder functional capacity. The second method of
electrical stimulation, using acute maximal stimulation with several
20-min sessions using vaginal and/or anal probes with currents up to 100
mA, is used primarily to increase bladder functional capacity.
Outcomes of attempts to improve continence or cure incontinence with
these methods have been varied, with response rates ranging from 30 to 70
percent.
Bladder
over distension: This is performed under epidural anesthesia using a
specially constructed ballon catheter that is filled within the bladder
until the pressure within it approximates systolic blood pressure.
This pressure is maintained for four 30-mi periods, the bladder being
emptied at the end of each period. The procedure results in
degeneration in the unmyelinated nerve fibres in the bladder wall with a
resultant peripheral denervation and alteration of both sensory and motor
function. However, it is not without risk, and rupture of the
bladder can result.
Detrusor
Denervation:
These procedures are reserved for patients with intractable detrusor
hyper-reflexia unresponsive to other conservative modalities.
Central denervation involves interruption of S2, S3, or S4 nerve roots,
the particular roots selected depending on either preliminary diagnostic
nerve blocks using local anesthesia, or intraoperative testing by nerve
stimulation and the monitoring of the bladder’s contractile
response. Such selective sacral neurectomy may be performed
surgically or by percutaneous radiofrequency coagulation of the
nerve. In the patient with an incomplete neurological lesion it is
important that denervation procedures do not compromises other functions,
nor cause significant somatic sensory loss. Following denervation
the bladder becomes areflexic and may be managed by clean intermittent
catheterization.
Detrusor
Myomectomy:
This newer technique may replace augmentation cystoplasty in some
cases. The thickened, hyperactive bladder muscle is dissected off
the underlying bladder mucosa over a large surface area, providing for
increased distensibility and improved bladder compliance.
Increase
in Outlet Resistance:
Pharmacologic
Manipulation:
The innervation of the bladder outlet, detailed earlier, implies that
alpha-adrenergic drugs will have a facilitatory effect on the smooth
muscle sphincter mechanism. These agents find their major clinical
use in the treatment of pediatric neurogenic incontinence in the
myelodysplastic child, in the treatment of the patient with
postprostatectomy urinary incontinence, and in the treatment of very mild
stress urinary incontinence in the female. The agents most commonly
used are ephedrine, pseudoephedrine hydrochloride, and phenylpropanolamine
hydrochloride. These agents have limited capacity to improve the
urethral closing pressure and only mild incontinence will be corrected.
Artificial
Sphincter Prostheses: The Brantley Scott genitourinary sphincter
prosthesis has undergone remarkable development during recent years, and
providing that stringent implantation criteria are met, its success rate
in controlling urinary incontinence exceeds 85%. It is an
implantable hydraulically operated device composed of a
silicone-constructed cuff for occlusion of the urethra or bladder neck, a
pressure balloon that controls the amount of compression, a pump
implanted in the scrotum or labia (squeezing of which activates the
device), and a control assembly that is made up of resistors that control
fluid flow within the system. The device finds particular use in
the myelodysplastic child who has an incompetent outlet due to sphincter
denervation. Devices have also been implanted in adults with
acquired neurogenic bladder dysfunction. Most failures
following implantation are the result of sphincter erosion due to
ischemia of the urethral tissue beneath the occlusive cuff or to
prosthesis infection or mechanical malfunction. A prerequisite is
that the patient be able to empty the bladder efficiently when the device
is activated, and this frequently requires the performance of
sphincterotomy or other outlet procedures prior to sphincter prosthesis
implantation.
Bladder
Neck Surgery: Reconstructive
procedures at the level of the bladder neck have been used to improve the
competence of the bladder outlet in a variety of congenital and acquired
conditions. Inconsistent results have dulled the enthusiasm of most
urologists for these operations; however, the fascial sling
cystourethropexy does find a role in the myelodysplastic girl with outlet
incompetence. The procedure can produce urinary retention, allowing
the child to perform clean intermittent catheterization to empty the
bladder.
Periurethral
Bulking Agents
(Teflon and collagen) may be injected into the periurethral tissues to
improve urethral cooptation.
B)
Therapy to Facilitate Bladder Emptying:
Bladder
emptying may be facilitated either by methods designed to increase
bladder contractility or abdominal pressure, or by procedures designed to
decrease the outlet resistance. These procedures often achieve their end
only at the expense of continence, in which event they are only
appropriate for use in males who can use an external collecting device.
Urodynamic
studies will identify whether the bladder emptying failure is due to
problems of bladder contractility, failure of sphincter relaxation, or
structural outlet obstruction. The voiding cystourethrogram is also
invaluable in this regard.
Maneuvers
to Increase Bladder Contractility:
Pharmacologic
Manipulation:
The most widely used drug for this purpose is bethnechol hydrochloride.
It has acetylcholine-like activity and may be administered either
subcutaneously or orally. Although it is widely used, there is
little evidence that is improves voiding appreciably in the oral doses
currently used. In patients with detrusor areflexia the medication
will not produce a voiding contraction, although the tone of the detrusor
muscle may be increased.
Crede
and Valsalva Maneuvers: An increase in abdominal pressure
by the Valsalva maneuver or direct extrinsic bladder compression by the Crede
maneuver will improve bladder emptying efficiency in patients with
low outflow resistance. In patients with detrusor areflexia due to
a sacral or infrasacral spinal cord lesion, these maneuvers are rarely
successful, for the sphincter mechanisms remain competent and no amount
of extrinsic bladder compression will effect complete emptying. In
fact, under such circumstances, the procedure may be hazardous. It
is contraindicated in patients with vesicoureteric reflux. In
effect, it finds its main use in a select group of women with detrusor
areflexia and in males who have previously undergone sphncterotomy.
Triggering
reflex Bladder Contractions: The areflexic bladder due to
sacral or infrascral spinal cord lesions cannot be triggered to contract
by this method; however, suprapubic percussion and pubic hair
stimulation, among other maneuvers, may trigger contractions in the
hyper-reflexic neurogenic bladder, facilitating complete emptying.
One must be certain that there is no striated sphincter dys-synergia
because this could result in high-pressure obstructed voiding
contractions with potentially damaging effects on the upper urinary tracts.
Electrical
stimulation:
This has been an area of considerable advance in the management of the
neurogenic bladder. Brindley and coworkers developed the sacral
anterior root stimulator, an intradural implant that is controlled by an
external radiofrequency device and may selectively stimulate three nerve
roots, usually S2, S3 and S4. Concurrently, Schmidt and Tanagho have
developed an extradural implant that can directly stimulate specific
sacral nerves at the level of the sacral foramina. The sacral anterior
root stimulator is specifically designed for management of spinal cord
injured patients, whereas the Schmidt and Tanagho stimulator has been
used for not only spinal cord-injured patients but patient with voiding
dysfunction and pelvic pain syndrome. The aim of the implanted
sacral anterior root stimulator is to provide implant-driven voiding with
low residuals, reducing the incidence of urinary tract infections.
Also, with differential nerve stimulation implant-driven erections and
defecation may be possible. The indications for implant require
that a patient has a stable neurological lesion and an intact S3 efferent
nerve, with associated detrusor contraction. It also requires a
motivated and intelligent patient who is capable of handing the stimulation
device. Anterior root stimulators are specifically indicated in
female spinal cord-injured patients in whom no adequate external urinary
collecting device exists, and in men with complete neurological
lesions. Implantation is a combined neurosurgical-urologic
operation, in which via a laminectomy approach, intraoperative
stimulation of the ventral sacral nerve roots is performed while bladder
pressure is measured. Stimulation of the S2 nerve roots appears to
give gluteal contraction and plantar flexion, erections in 90 percent of
men, and detrusor contractions in 60 percent. Stimulation of S4
occasionally gives bladder contraction and may have a role in
antierectile function. Stimulation of the various sacral nerve
roots, however, gives a variable response and intraoperative testing is
warranted to determine that a bladder contraction can be facilitated by
nerve root stimulation. Stimulation is provided with bursts of
intermittent electrical energy so that the detrusor smooth muscle, which
contracts slowly, develops adequate pressure for complete emptying and
the urethral striated muscle contracts in short bursts giving short
elevation in urethral resistance and subsequent dys-synergic voids.
However, dorsal rhizotomies of S2, S3 and S4 are recommended at the time
of implantation to abolish that detrusor sphincter dys-synergia.
They also eliminate the detrusor hyper-reflexia, increase functional
bladder capacity, and abolish autonomic dysreflexia; however, in males
they also abolish reflex erection, which may contraindicate dorsal
rhizotomies in some men. Three nerve roots are encased within the
electrical stimulator, and the cables and receiving device are tunneled
subcutaneously to lie in the superficial tissue, usually in the left
lower quadrant of the abdomen. Good results have been reported. Further
information is being gathered on the results of the sacral anterior root
stimulators and as the technology continues to improve, implantation may
begin to be performed outside specialized centers.
Maneuvers to
Decrease Outlet Resistance:
Pharmacologic
Manipulation
Drugs with alpha-adrenergic blocking activity tend to inhibit the
proximal smooth muscle sphincter, and striated muscle relaxants may
inhibit pelvic floor striated muscle sphincter activity. Prazosin,
terazosin and, phenoxybenzamine are common alpha blockers;
terazosin has the advantage of being given only once a day.
Striated muscle relaxants include dantrolene sodium, baclofen, and
diazepam. None of these agents acts specifically on the urinary
sphincter mechanisms, and other muscular functions are also
affected. Although there are some enthusiastic reports of their
use, we have not achieved any dramatic improvement in emptying
efficiency.
Bladder Outlet
Surgery
Procedures that have been advocated to decrease outlet resistance
surgically include bladder neck incision or resection, radical
transurethral resection of the prostate and external
sphincterotomy. Each of these procedures may be performed
endoscopically, and selection of the appropriate operation is based upon
urodynamic features and voiding cystourethrography. These
operations frequently compromise continence and occasionally potency, and
are only appropriate in the male. In the patient for whom bladder
emptying into an external collecting device is deemed more appropriate
than a clean intermittent catheterization program, these procedures are
the optimal way to facilitate bladder emptying and thereby reduce the
risk of upper tract deterioration and infection.
A newer method of reducing
bladder outlet resistance is the implantation of intraurethral stents
to hold open the urethral sphincter. The Wall-stent has been
implanted in a number of patients with detrusor sphincter dys-synergia,
with encouraging early results. However, there have been some
complications with early dislodgement of the stent, and late
complications associated with fibrosis and urethral obliteration.
At present, intraurethral stents are experimental in reducing bladder
outlet resistance.
Dys-synergic obstruction to urine
flow by the striated muscle of the pelvic floor may be blocked by pudendal
nerve interruption. The main disadvantage of this procedure is
its invariable adverse effect on erectile potency in the male. In
addition, it does not always improve bladder emptying, and before the
nerve is surgically or chemically interrupted, the likelihood of success
should be checked by a local anesthetic nerve block. This procedure
has been largely abandoned in most centers.
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