The document describes the anatomy and physiology of the urinary bladder. It discusses the normal micturition reflex and how it can become dysfunctional. Specifically, it covers three types of abnormal bladder function: irritative symptoms like urgency and frequency, obstructive symptoms like hesitancy, and incontinence. It also discusses various neurological disorders that can cause bladder disturbances, including multiple sclerosis and spinal cord injuries.
2. Anatomy
• The urinary bladder is a smooth muscle chamber
composed of two main parts:
– (1) the body, the major part, collects urine
– (2) the neck, a funnel-shaped extension of the body,
passing inferiorly and anteriorly into the urogenital
triangle and connecting with the urethra
3. • On the posterior wall of the
bladder, lying immediately above
the bladder neck, is a small
triangular area called the
trigone.
• The trigone can be identified by
the fact that its mucosa, the
inner lining of the bladder, is
smooth, in contrast to the
remaining bladder mucosa,
which is folded to form rugae.
• At the lowermost apex of the trigone,
the bladder neck opens into the
posterior urethra, and the two ureters
enter the bladder at the uppermost
angles of the trigone.
• Each ureter, as it enters the bladder,
courses obliquely through the detrusor
muscle and then passes another 1 to 2
centimeters beneath the bladder
mucosa before emptying into the
bladder
4. The bladder neck (posterior urethra) is 2 to 3 centimeters
long, and its wall is composed of detrusor muscle interlaced
with a large amount of elastic tissue. The muscle in this area is
called the internal sphincter.
5. • Its natural tone normally keeps the bladder neck and posterior urethra empty
of urine and, therefore, prevents emptying of the bladder until the pressure in
the main part of the bladder rises above a critical threshold.
• Beyond the posterior urethra, the urethra passes through the urogenital
diaphragm, which contains a layer of muscle called the external sphincter of
the bladder.
• External sphincter muscle is a
voluntary skeletal muscle, in contrast
to the muscle of the bladder body and
bladder neck, which is entirely smooth
muscle.
• The external sphincter muscle is under
voluntary control of the nervous
system and can be used to consciously
prevent urination even when
involuntary controls are attempting to
empty the bladder.
6. Blood supply
• The bladder is supplied by the superior and
inferior vesical arteries which are branches of
anterior trunk of internal iliac artery.
• The veins that drain the bladder form a plexus on
the infero-lateral surface before ending in the
internal iliac vein.
• Most of the lymph from the urinary bladder ends
in the external iliac nodes.
7. Innervation of the Bladder
• The principal nerve supply of the bladder is by way of the pelvic
nerves, which connect with the spinal cord through the sacral
plexus, mainly connecting with cord segments S-2 to S-4.
• Coursing through the pelvic nerves are both sensory nerve fibers
and motor nerve fibers.
• The sensory fibers detect the degree of stretch in the bladder wall.
Stretch signals from the posterior urethra are especially strong and
are mainly responsible for initiating the reflexes that cause bladder
emptying.
• The motor nerves transmitted in the pelvic nerves are
parasympathetic fibers. These terminate on ganglion cells located
in the wall of the bladder.
• Short postganglionic nerves then innervate the detrusor muscle.
8. • In addition to the pelvic nerves, two other types of innervation are
important in bladder function. Most important are the skeletal
motor fibers transmitted through the pudendal nerve to the
external urethral sphincter. These are somatic nerve fibers that
innervate and control the voluntary skeletal muscle of the
sphincter.
•
• Also, the bladder receives sympathetic innervations from the
sympathetic chain through the hypogastric nerves, connecting
mainly with the L-1,L-2 segments of the spinal cord.
• These sympathetic fibers stimulate mainly the blood vessels and
have little to do with bladder contraction.
• Some sensory nerve fibers also pass by way of the sympathetic
nerves and may be important in the sensation of fullness and, in
some instances, pain.
10. Micturition Reflex
• As the bladder fills, many superimposed
micturition contractions begin to appear. They are
the result of a stretch reflex initiated by sensory
stretch receptors in the bladder wall, especially by
the receptors in the posterior urethra when this
area begins to fill with urine at the higher bladder
pressures.
11. • Sensory signals from the bladder stretch receptors are
conducted to the sacral segments of the cord through
the pelvic nerves and then reflexively back again to the
bladder through the parasympathetic nerve fibers by
way of these same nerves.
12.
13. • When the bladder is only partially filled, these
micturition contractions usually relax spontaneously
after a fraction of a minute, the detrusor muscles stop
contracting, and pressure falls back to the baseline.
• As the bladder continues to fill, the micturition reflexes
become more frequent and cause greater contractions
of the detrusor muscle.
• Once a micturition reflex has occurred but has not
succeeded in emptying the bladder, the nervous
elements of this reflex usually remain in an inhibited
state for a few minutes to 1 hour or more before
another micturition reflex occurs.
• As the bladder becomes more and more filled,
micturition reflexes occur more and more often and
more and more powerfully.
14. • Once the micturition reflex becomes powerful
enough, it causes another reflex, which passes
through the pudendal nerves to the external
sphincter to inhibit it.
• If this inhibition is more potent in the brain than
the voluntary constrictor signals to the external
sphincter, urination will occur. If not, urination
will not occur until the bladder fills still further
and the micturition reflex becomes more
powerful.
15. Facilitation or Inhibition of
Micturition by the Brain
• The micturition reflex is a completely autonomic
spinal cord reflex, but it can be inhibited or
facilitated by centers in the brain.
• These centers include
– (1) strong facilitative and inhibitory centers in the
brain stem, located mainly in the pons, and
– (2) several centers located in the cerebral cortex that
are mainly inhibitory but can become excitatory
16. • The micturition reflex is the basic cause of micturition, but
the higher centers normally exert final control of
micturition as follows:
– 1. The higher centers keep the micturition reflex partially
inhibited, except when micturition is desired.
– 2. The higher centers can prevent micturition, even if the
micturition reflex occurs, by continual tonic contraction
of the external urethral sphincter until a convenient time
presents itself.
– 3. When it is time to urinate, the cortical centers can
facilitate the sacral micturition centers to help initiate a
micturition reflex and at the same time inhibit the
external urethral sphincter so that urination can occur.
17. • cortical activation with
bladder filling, brain activity
increased with increasing
bladder volume in the
periaqueductal gray- PAG
matter in the midline pons,
in the mid–cingulate
cortex, and bilaterally in
the frontal lobe area.
• Inhibition of micturition
was related to activation
of parietal cortex,
cerebellum, putamen.
and supplementary
motor area
• insular, posterior
parietal, and prefrontal
activation during urinary
storage.
20. Irritative Voiding Symptoms
• Urgency
– is the sudden desire to void
– in inflammatory conditions such as cystitis or in hyperreflexic neuropathic
conditions such as neurogenic bladders resulting from upper motor neuron
lesions.
• Dysuria
– painful urination
– associated with inflammation.
– The pain is typically referred to the tip of the penis in men or to the urethra in
women.
• Frequency
– is the increased number of voids during the daytime, and
– nocturia is nocturnal frequency.
– Adults normally void five or six times a day and once at most during the
nighttime hours.
– Increased frequency may result from increased urinary output or decreased
functional bladder capacity
21. Obstructive Voiding Symptoms
• Hesitancy
– is a delay in the initiation of micturition.
– results from the increased time required for the bladder to attain the high
pressure necessary to exceed that of the urethra in the obstructed setting.
• Decreased force of stream results from the high resistance the bladder faces
and is often associated with a decrease in caliber of the stream.
• Intermittency is the interruption of the urinary stream
• Postvoid dribbling the uncontrolled release of the terminal few drops of
urine.
• Obstructive symptoms are most commonly due to benign prostatic
hyperplasia, urethral stricture, or neurogenic bladder disorders, prostatic or
urethral carcinoma and foreign body are other causes.
22. Incontinence
• Urinary incontinence is the involuntary loss of urine.
• Total incontinence, patients lose urine at all times and in all
positions.
• Stress incontinence is the loss of urine associated with activities
that result in an increase in intra-abdominal pressure (coughing,
sneezing, lifting, exercising).
• Uncontrolled loss of urine preceded by a strong urge to void is
known as urge incontinence.
• Chronic urinary retention may result in overflow incontinence.
• The evaluation and treatment vary with each of the categories.
23. Uncontrolled Contraction of the
Bladder Muscle
Normal bladder Patients with
urge
incontinence
Patients with
urge or
frequency
Urethral resistance Uncontrolled bladder
muscle contractions
23
24. Bladder sphincter dyssynergia (detrusor sphincter dysynergia
(DSD), neurogenic detrusor overactivity (NDO)
• It is a consequence of a neurological pathology such as
spinal injury or multiple sclerosis that disrupts central
nervous system regulation of the micturition reflex
resulting in dys-coordination of the bladder
musculature and the external urethral sphincter.
• Instead of the urethral muscle relaxing completely
during voiding, it dys-synergically contracts causing the
flow to be interrupted and the bladder pressure to rise.
• On cystography there is an irregular appearance of the
bladder outline due to muscular contraction against
the unrelaxed bladder sphincter.
25.
26. Symptoms
• Symptomatically, people with this condition
generally experience daytime and night time
wetting, urinary retention, and often have a
history of urinary tract and bladder infections.
Constipation and encopresis are often associated
with this condition.
Diagnosis
• Strictly DSD can only be diagnosed from an CMG
trace
27. Neurologic disorders causing urinary
disturbences:
With regard to the neurologic diseases that cause
bladder dysfunction,
• multiple sclerosis, usually with urinary urgency, is
by far the most common.
• degenerative diseases (Parkinson disease and
multiple system atrophy) for 14 percent,
• spinal cord disorders account for 12 percent of
cases,
• and frontal lobe lesions for 9 percent.
28. Complete destruction of the cord below T12
– conus lesions
– trauma, myelodysplasias, tumor, venous angioma, and necrotizing myelitis.
– bladder is paralyzed for voluntary and reflexactivity
– no awareness of the state of fullness;
– voluntary initiation of micturition is impossible;
– the tonus of the detrusor muscle is abolished and the bladder distends as
urine accumulates until there is overflow incontinence;
– voiding is possible only by the Crede´ maneuver, i.e.,lower abdominal
compression and abdominal straining.
• Usually the anal sphincter and colon are similarly affected, and there is
“saddle” anesthesia and abolition of the bulbocavernosus and anal
reflexes as well as the tendon reflexes in the legs.
• The cystometrogram shows low pressure and no emptying contractions.
• Management: catherisation & anticholinergics
29. Disease of the sacral motor neurons in the spinal
gray matter
– autonomic bladder , autonomous bladder
– the anterior sacral roots, or peripheral nerves innervating the
bladder
– lumbosacral meningomyelocele and the tethered cord
syndrome.
– a lower motor neuron paralysis of the bladder.
– sacral and bladder sensation are intact.
• Various causes pertain in cauda equina disease, the
most frequent being compression by epidural tumor or
disc, neoplastic meningitis, and radiculitis from herpes
or cytomegalovirus.
• a hysterical patient can suppress motor function and
suffer a similar distention of the bladder.
30. Interruption of sensory afferent fibers
– atonic bladder
– as in diabetes and tabes dorsalis (tabetic bladder).
– motor nerve fibers unaffected
• Although a flaccid (atonic) paralysis of the bladder may be
purely motor or sensory, as described above, in most clinical
situations there is interruption of both afferent and efferent
innervation, as in cauda equina compression or severe
polyneuropathy.
• Neuropathies affecting mainly the small fibers are the ones
usually implicated (diabetes, amyloid, etc.), but urinary
retention also occurs in certain acute neuropathies such as
Guillain-Barre´ syndrome.
• Treatment includes intermittent self catheterisation
31. Upper spinal cord lesions, above T12
– reflex neurogenic (spastic) bladder, automatic bladder
– multiple sclerosis and traumatic myelopathy, which are the
commonest causes; myelitis, spondylosis, arteriovenous
malformation (AVM), syringomyelia, and tropical spastic
paraparesis
– If the cord lesion is of sudden onset, the detrusor muscle suffers
the effects of spinal shock. At this stage, urine accumulates and
distends the bladder to the point of overflow.
– As the effects of spinal shock subside, the detrusor usually
becomes reflexly overactive (detrusor hyperreflexia), and since
the patient is unable to inhibit the detrusor and control the
external sphincter, urgency, precipitant micturition, and
incontinence result.
– Incomplete lesions result in varying degress of urgency in voiding.
32. • With slowly evolving processes involving the upper cord, such as
multiple sclerosis, the bladder spasticity and urgency worsen with
time and incontinence becomes more frequent.
• In addition, initiation of voluntary micturition is impaired and
bladder capacity is reduced.
• Bladder sensation depends on the extent of involvement of sensory
tracts.
• Bulbocavernosus and anal reflexes are preserved.
• The cystometrogram shows uninhibited contractions of the
detrusor muscle in response to small volumes of fluid.
33. • Some patients can still control urination in this
condition by stimulating the skin (scratching or
tickling) in the genital region, which sometimes
elicits a micturition reflex.
• Management:
– Decompress the rectum or bladder - reverses the
effects of unopposed sympathetic outflow.
– Terazosin/ spinal anesthetic may be used as
prophylaxis.
34. Mixed type of neurogenic bladder.
• In diseases such as multiple sclerosis, subacute
combined degeneration, tethered cord, and
syphilitic meningomyelitis, bladder function may be
deranged from lesions at multiple levels, i.e., spinal
roots, sacral neurons or their fibers of exit, and
higher spinal segments.
• The resultant picture is a combination of sensory,
motor, and spastic types of bladder paralysis.
35. • Stretch injury of the bladder wall, as occurs with anatomic
obstruction at the bladder neck and occasionally with voluntary
retention of urine, as in hysteria.
• Repeated overdistention of the bladder wall often results in
varying degrees of decompensation of the detrusor muscle and
permanent atonia or hypotonia, although the evidence for this
mechanism is uncertain.
• The bladder wall becomes fibrotic and bladder capacity is greatly
increased.
• Emptying contractions are inadequate, and there is a large
residual volume even after the Crede´ maneuver and strong
contraction of the abdominal muscles.
• As with motor and sensory paralyses, the patient is subject to
cystitis, ureteral reflux, hydronephrosis and pyelonephritis, and
calculus formation.
36. • Frontal lobe incontinence
Often the patient, because of his confused mental
state, ignores the desire to void and the subsequent
incontinence. There is also a supranuclear type of
hyperactivity of the detrusor and precipitant
evacuation.
• Nocturnal enuresis
or urinary incontinence during sleep, due presumably
to a delay in acquiring inhibition of micturition.
37. Urodynamic Studies
1.Noninvasive Bladder
Investigations
voiding diary may be kept by either
the patient or the caregiver of the
approximate amount drunk,
frequency of micturition, and
episodes of incontinence, recorded
over the course of several days.
This gives a useful indication of the
severity of the bladder complaints
on which management decisions
can be based.
38. a.Urinary flowmetry:
• noninvasive investigation, valuable
particularly when combined with an
ultrasound measurement of the
postmicturition residual volume.
• It as a base of the collecting system is a
spinning disk, and flow of urine onto this disk
tends to slow its speed of rotation, which a
servomotor holds constant.
• Urine flow is derived from measurement of
the power necessary to maintain rotation
speed, and the machine usually produces a
graphic printout, together with an analysis,
for the time taken to reach maximal flow,
maximum and average flow rates, and the
voided volume
A, Urinary flow meter. The side of the uroflow transducer
has been cut away to show the disk at the base of the
funnel, which rotates as urine passes into the collecting
vessel. B, Typical (normal) printout from the uroflowmeter.
A total of 290 mL was voided (upper trace), with a
maximum flow rate of 30 mL per second (lower trace).
b.simple ultrasound
machines are now available
that require little operator
training and make it easy to
determine whether the
postmicturition residual is
negligible or in excess of 100
mL
39. Investigations Requiring
Catheterization
• Cystometry, the registration of bladder
pressure, can be performed during filling
and voiding .
• Detrusor pressure is derived by subtraction
of the abdominal pressure (measured using
a rectal line) from the intravesical pressure
(measured using a vesical line). The
efficiency of the subtraction usually is
checked at the beginning of cystometry by
asking the subject to cough.
• This produces an increase in abdominal
pressure and hence in intravesical pressure,
but no increase in detrusor pressure.
Cystometry during bladder filling. The bladder was filled (top trace) at 50 mL per minute (Vinfus) to a total of
300 mL. Detrusor pressure (Pdet) is derived by subtracting pressure in the rectum (Pabd) from the measured
intravesical pressure (Pves). At the beginning of the trace, these two values can be seen to be subtracting
effectively because on coughing there is an abrupt increase in intravesical pressure but no increase in detrusor
pressure. The detrusor pressure did not exceed 10 cm H2O, which is normal.
40. VIDEOCYSTOMETRY :
When cystometry is carried out using a contrast filling medium and the
procedure is visualized radiographically, the technique is known as
videocystometry.
CATHETER-MOUNTED TRANSDUCER:
Urethral pressure profile is measured using a catheter-mounted
transducer that is drawn slowly through the urethra by a motorized
armature.
The test is called static if no additional maneuver such as coughing or
straining is performed.
If intravesical pressure is measured simultaneously while the patient
coughs repeatedly during withdrawal of the catheter, the
transmission of the cough impulse in the urethra and bladder can be
measured and expressed as a ratio—the transmission pressure ratio.
measurements of the urethral pressure profile and parameters
derived from it would be useful in assessing genuine stress
incontinence
41. Neurophysiological Investigations
Electromyography:
To assess the extent of relaxation of the urethral
sphincter during voiding.
Interruption of the neural pathways between the
pons and the sacral cord results in loss of
coordination of sphincter and detrusor muscle
activity, a condition known as detrusor-sphincter
dyssynergia.
Neuroimaging: MRI
42. Therapy of Disordered Micturition
Goals in treatment:
• Preservation of upper urinary tract
• Maintain adequate bladder capacity with good
compliance
• Promote low-pressure micturition
• Avoid bladder over-distension
• Prevent urinary tract infection
• Minimize use of Foley catheter
• Choose therapy that minimizes patient risks while
maximizing social, emotional, and vocational
acceptability
43. MANAGEMENT OF BLADDER
DISORDERS
1.Detrusor Overactivity:
Antimuscarinic medications are the mainstay of
treatment
44. • main side effect is dry mouth, with less common
effects of blurred vision, drowsiness, and
constipation. Darifenacin and solifenacin are newer
anticholinergics, with greater specificity for the M3
receptor.
• Botulinum A toxin (BoNT/A):
introduced in the treatment of bladder overactivity by
injection into the detrusor smooth muscle under
cystoscopic guidance.
46. Desmopressin spray:
• First introduced to treat DI,
• Widely prescribed for children with nocturnal enuresis,
• patients with MS and nighttime frequency also have
used it.
• Disabled patients and their caregivers, the difficulties
of the patient having to get up to go to the toilet
several times in the night can be considerable.
• One or two nasal puffs of desmopressin from a
metered-dose spray administered on retiring reduces
urine output for the following 6 to 8 hours and may
significantly lessen nighttime urinary frequency.
• An oral preparation of desmopressin is now available.
• Used once in 24 hours
• Not be given to the elderly, in whom its use may
precipitate congestive heart failure.
47. 2.Incomplete Bladder Emptying or Urinary
Retention
Sterile intermittent catheterization
• Most patients are advised initially to perform
the technique at least twice a day
• Although bacteriuria is noted in 50% of
patients doing clean intermittent self-catheterization,
the incidence of symptomatic
urinary tract infections fortunately is low .
48. • In spinal cord disease, a combination
of intermittent self-catheterization
and an oral anticholinergic deals
effectively with both aspects of
bladder malfunction.
• In a borderline significant residual
volume, starting an anticholinergic
may have the effect of increasing it .
• This should be suspected if the
medication has some initial beneficial
effect for several days that then
disappears.
• This combined approach works well
in patients with spinal cord disease
such as MS, provided that the patient
is not too severely disabled. recommended management of neurological
incontinence. CISC, clean intermittent self-catheterization;
PVR, postvoid residual
49. Permanent Indwelling Catheters:
• When the patient is no longer able to perform self-catheterization,
or when urge incontinence and
frequency are unmanageable.
• No longer weight-bearing and is chair-bound.
• Suprapubic catheter is a better long-term
alternative to an indwelling urethral catheter and
often is the method of choice in managing
incontinence in patients for whom other means are
no longer effective.
50. The bladder symptoms in multiple sclerosis (MS) become increasingly difficult to manage with
progression of spinal cord disease. This diagram summarizes the various measures that may be
effective at each stage. BoNT/A, botulinum toxin A; CBME, cannabis-based medicinal extract,
CISC, clean intermittent self-catheterization; DDAVP, trademark for preparation of
desmopressin; IDC, indwelling catheter
51. External Device:
Urge incontinence is the main problem and the bladder
empties completely, some men are able to wear an
external device attached around the penis.
The simplest and least obtrusive is a self-sealing latex
condom sheath, which can be put on each night or kept in
place for up to 3 days.
Sacral Nerve Stimulators
• An extradural sacral nerve stimulator can be highly
effective in lessening detrusor overactivity that is
resistant to anticholinergic medication.
• It seems highly likely that the mechanism of action of
this device is stimulation in the presacral region of the
pelvic afferents, which are known to have an inhibitory
effect on the detrusor.
52. • Surgery :
• range from minimally invasive procedures, (TVT,
TOT) to increase bladder outflow resistance, or
implantation of an artificial urethral sphincter, to
the surgical techniques of increasing bladder
capacity by cystoplasty or urinary diversion into a
conduit or catheterizable reservoir
53. REFERENCES
• Neurology in Clinical Practice e-dition, 5th
Edition Bradley, Daroff, Fenichel & Jankovic.
• ADAMS AND VICTOR’S PRINCIPLES OF
NEUROLOGY Eighth Edition.