Neuropathic Bladder Disorder

NEUROPATHIC BLADDER DISORDERS

ANATOMY & PHYSIOLOGY

The Bladder Unit

The functional features of the bladder include
(1) a normal capacity of 400–500 mL,
(2) a sensation of fullness,
(3) the ability to accommodate various volumes without
a change in intraluminal pressure,
(4) the ability to initiate
and sustain a contraction until the bladder is empty.
(5) voluntary initiation or inhibition of voiding
despite the involuntary nature of the organ.

The Sphincteric Unit

In both males and females, there are 2 sphincteric elements:
(1) an internal involuntary smooth-muscle sphincter at the
bladder neck.
(2) an external voluntary striated-muscle
sphincter from the prostate to the membranous urethra in
males and at the mid urethra in females.


The uretrovesical junction

The function of the ureterovesical junction is to prevent backflow of urine from the bladder to the upper urinary tract. Longitudinal muscle from the ureter contributes to the makeup of the trigone. Stretching of the trigone has an occlusive effect on the ureteral openings.
Nerve supply

The lower urinary tract receives afferent and efferent innervation from both the autonomic and somatic nervous systems.
The parasympathetic innervation originates in the second to fourth sacral segments. The cholinergic postganglionic fibers supply both the bladder and smooth-muscle
sphincter.
The sympathetic nerves originate at T10–L2. The noradrenergic postganglionic fibers innervate the smooth muscles of the bladder base, internal sphincter, and proximal urethra.
Somatic motor innervation originates in S2–3 and travels to the striated urethral sphincter via the pudendal nerve. Some motor neurons to the tonic small muscle fibers of the striated sphincter may also project through the pelvic nerve .
There are both somatic and visceral afferents from the bladder and urethra. The somatic afferent is carried by the pudendal nerve, while the visceral afferent projects through
the sympathetic and parasympathetic nerves to their respective spinal areas.

The Micturition Reflex

Intact reflex pathways via the spinal cord and the pons are required for normal micturition. Afferents from the bladder are essential for the activation of the sacral center, which then causes detrusor contraction, bladder neck opening, and sphincteric relaxation.
The pontine center, through its connection with the sacral center, may send either excitatory or inhibitory impulses to regulate the micturition reflex.
Cerebral (Suprapontine) Control

Although micturition and urine storage are primarily functions

of the autonomic nervous system, these are under voluntary control from suprapontine cerebral centers, so that other groups of muscles (arm, leg, hand, bulbocavernosus) can be integrated to assist in urination at the appropriate time and place.
Cerebral lesions (eg, from tumor,Parkinson’s disease, vascular accident) are known to affect the perception of bladder sensation and result in voiding dysfunction.


URODYNAMIC STUDIES

Urodynamic studies are techniques used to

obtain graphic recordings of
activity in the urinary
bladder,Urethral sphincter, and pelvic musculature.
Figure . Classic normal flow rate,

Uroflowmetry

Uroflowmetry is the study of the flow of urine from the urethra.
BECAUSE URINARY FLOW RATE IS THE PRODUCT OF DETROSAL ACTION AGAINST OUTLET RESISTANCE variation from the normal flow rate might reflect dysfunction .
The normal peak flow rate for males is 20–25 mL/s and for females 20–30 mL/s.
A flow rate less than 10 ml / sec is definitive evidence of obstruction.
THE NORMAL UROGRAPH IS BELL SHAPED , IN OBSTRUCTED PROSTATE WE WILL HAVE INTERUPTTED MULTIPLE BELL SHAPES.

BLADDER FUNCTION

The basic factors of normal bladder function are bladder capacity, accommodation, sensation, contractility, voluntary control, and response to drugs. All of them can be
evaluated by cystometry. If all are within the normal range, bladder physiology can be assumed to be normal.
Cystometry can be done by either of 2 basic methods:
(1) allowing physiologic filling of the bladder with secreted urine and continuously recording the intravesical pressure throughout a voiding cycle (starting the recording when
the patient’s bladder is empty and continuing it until the bladder has been filled—at which time the patient is asked to urinate—and voiding begins) or (2) by filling the bladder
with water and recording the intravesical pressure against the volume of water introduced into the bladder.
The cystometrogram is obtained during the phase of bladder filling; the volume of fluid in the bladder is plotted against the intravesical pressure to show
bladder wall compliance to filling.
SPHINCTERIC FUNCTION
Urinary sphincteric function can be evaluated either by recording the electromyographic activity of the voluntary component of the sphincteric mechanism or by recording
the activity of both smooth and voluntary components by measuring the intraurethral pressure of the sphincteric unit. The latter method is called pressure profile measurement (profilometry).


CLASSIFICATION OF NEUROPATHIC BLADDER
1.Spastic Neuropathic Bladder(Neuropathic Bladder Due to Lesions Above the Sacral Micturition Center)
Most lesions above the level of the cord where the micturition
center is located will cause bladder spasticity. Sacral
reflex arcs remain intact, but loss of inhibition from
higher centers results in spastic bladder and sphincter
behavior on the segmental level.
The sphincter will behave according to the level of lesion as one of the following three :
• Normal sphincter pressure - the pt. have frequency
• High intraurethral (sphincter)pressure - will have retention
• Low sphincter pressure - incontinence

Atiology

SPASTIC NEUROPATHIC BLADDER RESULT FROM PARTIAL OR EXTENSIVE NEURAL DAMAGE ABOVE THE CONUS MEDULARIS (T12)
Common lesion includes dementia ,vascular accidents , multiple sclerosis ,tumurs,and inflammatory disorder such as encephalitis or menengitis .

Features :

• reduced capacity,
(2) involuntary detrusor contractions,
(3) high intravesical voiding pressures,
(4) markedhypertrophy of the bladder wall,
(5) spasticity of the pelvic striated muscle.
(6) autonomic dysreflexia in cervical cord lesions.

Clinical Findings

A. SYMPTOMS
The severity of symptoms depends on the site and extent
of the lesion as well as the length of time from injury.
Symptoms include involuntary urination, which is often
frequent, spontaneous, scant, and triggered by spasms in
the lower extremities also urge incontinence
The major nonurologic symptoms are those of spastic paralysis and objective sensory deficits.
B. SIGNS
A complete neurologic examination is most important.The sensory level of the injury needs to be established, followed by assessment of the anal, bulbocavernosal, knee, ankle, and toe reflexes. These reflexes vary in degree of Hyperreflexia With high thoracic and cervical lesions, distention of the bladder (due to a plugged catheter or during cystometry or cystoscopy) can trigger a series of responses, including hypertension, bradycardia, headache, piloerection, and sweating. This phenomenon is known as autonomic dysreflexia. Bladder volumes in established lesions are usually less than 300 mL (not infrequently, <150 mL) and cannot be detected by abdominal percussion.

C. LABORATORY FINDINGS

Virtually all patients experience one or more urinary tract
infections during the recovery phase of spinal shock.
D. X-RAY FINDINGS
Periodic excretory urograms and retrograde cystograms are
essential because complications are common. A trabeculated
bladder of small capacity is typical of this type of neuropathic
dysfunction. The bladder neck may be dilated.
The kidneys may show evidence of pyelonephritic scarring,
hydronephrosis, or stone disease. The ureters may be
dilated from obstruction or reflux.
E.Cystoscopy and Pandoscopy
Bladder capacity, stones, competency of the ureteral
orifices, changes secondary to chronic infection or indwelling
catheters, and the integrity of the bladder neck and
external urethral sphincter can be assessed.


F. URODYNAMIC STUDIES
Combined recording of bladder and urethral sphincter
activity during filling will reveal a low-volume bladder
with spastic dyssynergy of the external sphincter (Figure
27–4). High voiding pressures in the bladder are not
unusual. Ureteral reflux or obstruction is more likely if
voiding pressures exceed 40 cm of water.

3. Flaccid (Atonic) Bladder

Direct injury to the peripheral innervation of the bladder
or sacral cord segments S2–4 results in flaccid paralysis of
the urinary bladder. Characteristically, the capacity is large,
intravesical pressure low, and involuntary contractions
absent. Because smooth muscle is intrinsically active, fine
trabeculations in the bladder may be seen. Common
causes of this type of bladder behavior are trauma, tumors,
tabes dorsalis, and congenital anomalies (eg, spina bifida,
meningomyelocele).

Clinical Findings

A. SYMPTOMS
The patient experiences flaccid paralysis and loss of sensationaffecting the muscles and dermatomes below the level of injury. The principal urinary symptom is retention with overflow incontinence. Male patients lose their erections.
B. SIGNS
Neurologic changes are typically lower motor neuron.Extremity reflexes are hypoactive or absent. Sensation is diminished or absent.a palpable bladder might be felt
C. LABORATORY FINDINGS
Repeated urinalysis at regular intervals is no less important in this group than in others. Infection with white blood cells (leukocytes) and bacteria may occur because of the need for bladder catheterization.
D. X-RAY FINDINGS
A plain film of the abdomen may reveal fracture of the lumbar spine or extensive spina bifida.
Calcific shadows compatible with urinary stone may be seen. Excretory
urograms should be performed initially to check for calculus, hydronephrosis, pyelonephritic scarring, or ureteral obstruction secondary to an overdistended bladder.
A cystogram may detect morphologic changes in the
detrusor (it is usually large and smooth walled)


E. INSTRUMENTAL EXAMINATION
Cystoscopy and urethroscopy performed some months
or weeks after the injury will confirm the laxity and
areflexia of the sphincter and pelvic floor; the bladder neck
is usually funneled and open and the bladder should be
large and smooth walled.
F. URODYNAMIC STUDIES
The urethral pressure profile reflects low smooth and striated
sphincter tone. Bladder filling pressures are low;
detrusor contractions are weak or absent; voiding is accomplished
by straining or by the Crede maneuver, if at all;
and there is a large volume of residual urine.
Crede maneuver : appling sustaned pressure over the bladder

DIFFERENTIAL DIAGNOSIS OF NEUROPATHIC BLADDER

Cystitis
Chronic urethritis
Vesical irritation secondary to psychic disturbance
Myogenic damage
Interstitial cystitis
Cystocele and
Infravesical obstruction
TREATMENT OF NEUROPATHIC BLADDER
The treatment of any form of neuropathic bladder is
guided by the need to restore low-pressure activity to the
bladder. In doing so, renal function is preserved, continence
restored, and infection more readily controlled.
We are always afraid from the effect on the upper U. tract so the spastic bladder is more serious .


1. Spinal Shock
Intermittent catheterization using strict aseptic technique has proved to be the best form of management of bladder rehabilatation. This avoids urinary tract infection as well as the complications of an indwelling catheter (eg, urethral stricture, abscess, erosions, stones).
If a Foley catheter becomes necessary, a few principles need to be followed. The catheter should not be larger than 16F and preferably should be made of silicon, and it should be taped to the abdomen.
Some urologists advocate the use of suprapubic cystostomy rather than a urethral catheter to avoid the risks associated with permanent indwelling catheters.
A cystogram is needed to rule out reflux ,The urodynamic study should be repeated every 3 months as long as spasticity is improvingand then annually to check for complications of the
upper urinary tract.
To control infection, a fluid intake of at least 2–3 L/ day should be maintained (100–200 mL/h) if at all possible.
Renal and ureteral drainage are enhanced by moving the patient frequently, with ambulation
in a wheelchair as soon as possible, and even by raising the head of the bed. These measures improve ureteral transport of urine, reduce stasis, and lower the risk of infection.
Additional measures aid in prophylaxis for calculus formation (eg, reduction of intake of calcium and oxalate and elimination of vitamin D in the diet).

Spastic Neuropathic Bladder

A. PATIENT WITH REASONABLE BLADDER CAPACITY
To consider a bladder rehabilitated to a functional state, a patient should be able to go 2–3 hours between voiding and not be incontinent during this interval.
Voiding is initiated using trigger techniques—tapping the abdomen suprapubically , tugging on the pubic hair, squeezing the penis, or scratching the skin of the lower abdomen, genitalia,
or thighs. They may be helped by low dose
anticholinergic medication (to decrease intravesicl pressure)or by neural stimulation.

B. PATIENT WITH MARKEDLY DIMINISHED FUNCTIONAL VESICAL CAPACITY

If the functional capacity of the bladder is under 100 mL, involuntary voiding can occur as often as every 15 minutes.
Satisfactory training of the bladder cannot be achieved, and alternative measures must be taken
One of the following treatment regimens can then be administered:
1. A permanent indwelling catheter with or without anticholinergic medication.
2. A condom catheter and a leg bag in males if residual urine volumes are small and the patient does not have bladder pressures above 40 cm of water on
urodynamic evaluation.
3. Performance of a sphincterotomy in males. It is incontinence
4. Conversion of the spastic bladder to a flaccid bladder
through sacral rhizotomy. Retention
5. Neurostimulation of sacral nerve roots to accomplish bladder evaluation .
6. Urinary diversion for irreversible, progressive upper
urinary tract deterioration. A variety of procedures are
available, including the standard ileal conduit, cutaneous
ureterostomies, transureteroureterostomy.


C. PARASYMPATHOLYTIC DRUGS
Commonly used drugs and dosages are as follows: oxybutynin chloride (Ditropan), 5 mg 2–3 times daily; Ditropan XL, once daily; dicyclomine hydrochloride (Bentyl), 80 mg in 4 equally divided doses daily
D. BOTULINUM-A TOXIN
Several centers have investigated injection of 85–300 Units of botulinum-A toxin into 30–40 sites in the detrusor muscle in both children and adults who have detrusor hyperreflexia.
E. INTRAVESICAL INSTILLATION OF CAPSAICIN OR RESINIFERATOXIN
Capsaicin and resiniferatoxin are specific C-fiber afferent neurotoxins. After spinal cord injury, C-fiber afferents proliferate proliferate in the bladder mucosa and are involved in detrusor hyperreflexia.
F. NEUROSTIMULATION (BLADDER PACEMAKER)
Neuroprosthetics are becoming an established alternative to managing selective neuropathic bladder disorders.
Patients are evaluated for a bladder pacemaker primarily by urodynamic monitoring of bladder and sphincter responses to trial stimulation of the various sacral nerve roots.
Sacral nerve stimulation(SNS) by the interstim procedure is performed in two stages :stage one , a clinical trial of temporary or permanent lead for external stimulation and stage two , implantation of a subcutaneous implantation plus generator (IPG)للاطلاع

3 . Flaccid Neuropathic Bladder

If the neurologic lesion completely destroys the micturition center, volitional voiding cannot be accomplished
without manual suprapubic pressure, that is, the Crede maneuver. Bladder evacuation can be accomplished by
straining, using the abdominal and diaphragmatic muscles to raise intra-abdominal pressures.

A. BLADDER TRAINING AND CARE

In partial lower motor neuron injury, voiding should be tried every 2 hours by the clock to avoid embarrassing
leakage. This helps protect the bladder from over distention due to a buildup of residual urine.

B. INTERMITTENT CATHETERIZATION

Any patient with adequate bladder capacity can benefit from regular intermittent catheter drainage every 3–6
hours. This technique eliminates residual urine, helps prevent infection, avoids incontinence, and protects against
damage to the upper urinary tract. It simulates normal voiding and is easily learned and adapted by patients.


C. SURGERY
Transurethral resection is indicated for hypertrophy of the bladder neck or an enlarged prostate, either of which may
cause obstruction of the bladder outlet and retention of residual urine.

D. PARASYMPATHOMIMETIC DRUGS

The stable derivatives of acetylcholine are at times of value in assisting the evacuation of the bladder. Although they do
not initiate or effect bladder contraction, they do provide increased bladder tonus. They may be helpful in symptomatic treatment of the milder types of flaccid neuropathic bladder
Bethanechol chloride is the drug of choice. It is given orally, 25–50 mg every 6–8 hours.

COMPLICATIONS OF NEUROPATHIC BLADDER

1.Infection
Infection is virtually inevitable with the neuropathic bladderSterile intermittent catheterization is recommended at thisstage. Episodic renal infection should be treated aggressively with appropriate antibiotics to prevent renal loss. The source and cause of infection should be eliminated if possible.
2.Hydronephrosis
Two mechanisms lead to back pressure on the kidney. Early, the effect of trigonal stretch secondary to residual urine and detrusor hypertonicity becomes compounded by evolving trigonal hypertrophy. When ureteral reflux is detected by cystography, previous methods of bladder care must be radically adjusted. An indwelling catheter may manage the problem temporarily.
However, if the reflux persists after a reasonable period of drainage, antireflux surgery must be considered.
3. Calculus
A number of factors contribute to stone formation in the bladder and kidneys. Bed rest and inactivity cause demineralization of the skeleton, mobilization of calcium, and
subsequent hypercalciuria. Recumbency and inadequate fluid intake both contribute to urinary stasis, possibly with increased concentration of urinary calcium. Catheterization of the neurogenic bladder may introduce bacteria. Subsequent infection is usually due to a urea-splitting organism, which causes the urine to become alkaline, with reduced solubility of calcium and phosphate.

4.Renal Amyloidosis

Secondary amyloidosis of the kidney is a common cause of death in patients with neuropathic bladder. It is a result of
chronic debilitation in patients with difficult decubitus ulcers and poorly controlled infection. Fortunately, due to
better medical care, this is an uncommon finding today.

5.Sexual Dysfunction

Men who have had traumatic cord or cauda equina lesions experience varying degrees of sexual dysfunction.

6.Autonomic Dysreflexia

Autonomic dysreflexia is sympathetically mediated reflex behavior triggered by sacral afferent feedback to the spinal cord. The phenomenon is seen in patients with cord
lesions above the sympathetic outflow from the cord. As a rule, it occurs in rather spastic lesions above T1 but on occasion in lesions of mild spasticity or those as low as T5.
Symptoms include dramatic elevations in systolic or diastolic blood pressure (or both), increased pulse pressure, sweating, bradycardia, headache, and piloerection. Symptoms are brought on by overdistention of the bladder.

PROGNOSIS

The greater threat to the patient with a neuropathic bladder is progressive renal damage (pyelonephritis, calculosis , and hydronephrosis). Advances in the management of the
neuropathic bladder, together with better follow-up of patients at regular intervals, have substantially improved the outlook for long-term survival.

The end

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