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Neuroanatomical aspects of urinary incontinence
1.
2. Urinary incontinence is defined as
objectively demonstrable involuntary
loss of urine so as to cause hygienic
and/or social inconvenience for day
to day activity.
3. Female >> Male
Most prevalent in young and middle aged
women
Pure SUI occurs primarily in age group of 29-
49yrs
Prevalence of urge and mixed incontinence
increases with age
Int J Gynecol Obstet 2004;86: S1-S5 Drugs 2004:64;1503-16
6. Stress urinary incontinence:
› Urine leakage on effort , exertion , sneezing or coughing
› Occur when bladder pressure exceed urethral pressure
under a condition of increase abdominal pressure
Urge urinary incontinence:
› Leakage accompanied by, or immediately precede by
urgency (a sudden strong desire to void)
› A function of uncontrolled detrusor contraction that
overcome urethral resistance
Mixed urinary incontinence:
› Leakage associated with urgency , and also with effort of
exertion , sneezing or coughing
› Treatment should focus on predominant symptom
Overflow incontinence:
› Leakage of urine when bladder is abnormally distended
with large residual volume
› Especially in men with chronic retention
7. Bladder
› Detrusor Muscle
Smooth muscle – thin and highly distensible
3 layers – run in different directions
› Internal Sphincter
A component of detrusor muscle
Involuntary
At bladder base
8. Female Urethra
3-4 cm – muscular, short tube
Striated Sphincter
Poorly defined outer circular layer
Longitudinal layer shortens with
voiding
Submucosal vasculature—rich
vascular plexus
Forms a seal at rest
Squamous epithelium – distal
urethra
Sensitive to estrogen
12. Attaches midurethra to inferior side of pubic symphysis
Prevents downward rotational descent of mid urethra
It works in conjunction with the pubourethralis muscle, a subdivision
of the levator ani muscle that forms a sling around the proximal
urethra. Together they form the midurethral complex
Elongation of posterior pubourethral ligaments may be a significant
contributory factor to loss of urethral support seen in stress
incontinence.
13.
14. ATFP is a fascia that originates from pubic bone anteriorly
as fibrous bands, broaden out as aponeurotic structures ,
move dorsally, insert into ischial spine.
Tensile structures, located b/l on either side of urethra and
vagina
Act like ropes of a suspension bridge
Provide necessary support needed to hang urethra on
anterior vaginal wall.
15. Lateral view of pelvic floor- Reconstruction of urethra , vagina, & fascial tissue
transected at the level of vesical neck
16. Comprised of puborectalis, pubococcygeus,
& iliococcygeus muscle
Act as support in urinary control
Type 1 fibers- for constant muscle tone
compress vagina & urethra anteriorly toward
pubic bone & keep hiatus closed at rest
Type 2 (fast twitch) fibers- that, under
stress, maintain urethral closure & prevents
stretching of pelvic ligaments
17.
18. The bladder neck and upper third or half of the
urethra are above the level of the pelvic floor
With increased intra-abdominal pressure,
the pressure is equally transmitted to the
bladder and upper urethra and urine will not
escape.
19.
20.
21. Internal-Is an involuntary muscle which
surrounds the bladder neck and urethra
External- is a voluntary muscle found
between the superficial and deep perineal
membranes and surrounds the middle
part of the urethra
22. It empties the urethra after the act of micturition,
Interrupts the flow of urine on desire
It acts as a secondary defensive mechanism against
escape of urine.
At rest the urethra makes an angle of 90-100 degrees
with the base of the urinary bladder called the
:posterior urethrovesical angle.
The urethra also makes an angle of less than 30
degrees with the vertical line.
23.
24.
25.
26.
27. Sympathetic – Hypogastric Nerve
› T10-L2
› Forms the pelvic plexus with the parasympathetic
NS.
› Beta & alpha receptors- mainly concerned with
filling & storage phase of micturition
28. receptors located mainly in the body of
bladder, es bladder tone & bladder
relaxes & stores urine
receptors located in the urethra &
bladder neck, es urethral tone,
promoting closure & urine storage
29.
30. Parasympathetic Nervous system
1. S2-S4
2. Causes Detrusor contraction,
3. Also supply Bladder neck & Levator ani
34. – Afferent stretch input from
detrusor (S2,3,4)
– Efferent cortical input from
frontal lobes – inhibitory
– Cerebral control is under
control of Pontine centre
– Cerebellar input for
coordinated voiding
35.
36.
37.
38. STORAGE PHASE:
Bladder usually fills@ 0.5-5ml/min from
ureters
Normal intravesical pressure- 10 cm H2O
(lower than that of intraurethral pressure)
39. AT REST
Apposition of longitudinal mucosal folds
Submucosal vascular plexus ( hermetic seal)
Collagen & elastic tissues throughout the urethra circumference
Tonically contracted proximal urethral musculature
40. Stretching of detrusor reflexly contracts the sphincter muscles of
bladder neck
inhibition of the cholinergic system responsible for detrusor
contraction
Stimulation of β symp. Fibre (relax detrusor) & α symp.
Fibre(contracts internal urethral sphincter- First line guard)
External sphincter mechanism- slow fibres of periurethral muscle
innervated by pelvic efferent nerves and fast fibres of levator ani
innervated by pudendal nerve- Second line guard)
41. During stress— additional factors work like
Centripetal force of intraabdo. Pressure transmitted to proximal
urethra as long as bladder neck remains above the pelvic
diaphragm
Reflex contraction of urethral striated sphincter & periurethral
striated musculature
Kinking of urethra d/t:
1. Bladder base rocks downwards & backwards
2. Bladder neck is pulled upwards & forwards
42. When bladder fills about 250 ml- sensation passes up the spinal
roots S2,3,4
In untrained bladder( children), motion reflex automatically
contracts detrusor voiding
In trained adults-when time place is not convenient urge
supressed (reflex arc is under control of hypothalamus &
anterior frontal lobe & pontine centre)
43. When time & place is convenient- higher
inhibitory centres supressed
The detrussor contracts to raise the intravesical
pressure to 30-50 cm of H2O
Pressure is further raised to about 100 cm of H2O
via voluntary contraction of abdominal muscles
44. Diaphragm fixes, abdo muscle contract, pelvic floor relaxes
Drop of intraurethral pressure d/t skeletal muscle relaxation & sympathetic
blockade
Bladder base descends with obliteration of posterior urethrovesical angle ( N-
100 )
Detrusor contraction starts
Funneling of the bladder neck & upper urethra( Dilation of urethra from above
down
Urine leaks into upper urethra, external urethral sphincter opens voluntarily,
overwhelmed by the raised intravesical pressure
VOIDING
At the end of micturition the proximal urethral contracts from distal end to the
urethrovesical junction, milking back the last drop of urine into the bladder
47. In this case, urine escapes continuously
by day and by night.
It is caused by:
1. Urinary fistulae as vesicovaginal
fistula
2. Ectopia vesica.
48. It presents clinically as the involuntary loss of small
amount of urine during coughing, sneezing,
laughing, or other physical activities that increase
intra-abdominal pressure.
In the absence of a detrusor contraction or an
overdistended bladder.
50. 1.Congenital weakness of the internal urethral sphincter, seen in the
young nullipara.
2. Congenital defects such as:
Epispadias
Short urethra (less than 1 cm)
Wide bladder neck
Separation of symphysis pubis.
3. Trauma to the region of the bladder neck due to vaginal delivery or
operation. In fact vaginal delivery is the commonest cause of stress
incontinence
51. EFFECTS OF CHILDBEARING: Connective tissue
disruption
Stress Urinary Incontinence:
Advances of Surgical Management
DeLancey J., Clinical Obstet and Gynecol, Vol 33, No.2, June 1990
Peschers U., DeLancey J., Urethral Support and Child birth: Obstet & Gynecol, Vol. 88, No 6, December 1996
52. Stress Urinary Incontinence:
Advances of Surgical Management
EFFECTS OF CHILDBEARING: Levator Ani muscle
disruption
- 20% of women develop defect in Levator Ani muscle after NSVD
DeLancey J O, Appearance of levator ani muscle abnormalities in magnetic resonance images after vaginal delivery:Obstet &
Gynecol, 2003;101: 46-53
53. 4. Menopause: Lack of oestrogen leads to atrophy of
bladder neck supports.
5. Pregnancy and continuous administration of oestrogen-
progestogen preparation to induce psuedopregnancy
state to treat endometriosis.
The hormonal imbalance with increased progesterone
weakens the internal urethral sphincter
54. 6. Genital prolapse:
If the bladder neck descends below the
level of the pelvic floor, the increased
intra-abdominal pressure will be
transmitted to the bladder and not to the
upper urethra leading to escape of urine.
7. Organic nervous diseases as
disseminated sclerosis.
55. 1. Descent of the bladder neck with
complete loss of the posterior
urethrovesical angle.
2. Opening (funneling) of the bladder neck
and upper urethra.
3. Descent of the urethra leading to
increase in the angle between it and
vertical line, so the angle becomes more
than 30 degrees.
56. The basic pathology is urethral incompetence.
This can be either due to:
A) Urethral hypermobility (80 - 90% )
B) Intrinsic Sphincter Dysfunction (10 - 20%)
57. This results from loss of the normal
pelvic anatomical support mechanism of
the bladder and urethra due to:
1. Trauma and stretching during vaginal
delivery
2. Hysterectomy
3. Hormonal changes ( Menopause)
4. Pelvic denervation
5. Congenital weakness
58. CONGENITAL
1. Myelomeningocele
2. Epispadias
3. pelvic denervation
ACQUIRED
1. Trauma
2. radiation therapy
3. or a sacral cord
lesion.
4. In women (ISD) is
commonly associated
with multiple
incontinence surgical
procedures, as well as
with
hypoestrogenism,
aging, or both.
59. The urethra maintains continence
through the combination of
1. Urethral mucosal coaptation- The
underlying urethral vascular plexus,
2. The combined viscous and elastic
properties of the urethral epithelium,
3. Contraction of intrinsic sphincter
60. The urethral sphincter is unable to
generate enough resistance to retain
urine in the bladder, especially during
stress
Patients with ISD often leak continuously
or with minimal exertion.
61.
62. Type 0
› History of stress incontinence without
objective incontinence on urodynamic testing
› Bladder neck and urethra closed at rest
› Bladder neck and urethra open during stress
63. Type I
› Bladder neck and
urethra closed at
rest
› Bladder neck and
urethra open and
descend during
stress
› Descent less then 2
cm
› No evidence of
cystocele
64. Type IIA
› Bladder neck and
urethra open and
descend during
stress
› Descent greater
then 2 cm
› Evidence of
cystocele
65. Type IIB
› Bladder neck and
urethra closed and
below the
symphysis pubis at
rest
› May or may not
descend during
stress, but urethra
opens
66. Type III: ISD
› Bladder neck and
uretha open at rest
› Occurs in the
absence of detrusor
contraction
67. Urethral hypermobility Sphincteric dysfunction
Most patients with SUI
Staskin DR. Classification of voiding dysfunction. In: Cardozo L, Staskin DR, eds.
Textbook of Female Urology and Urogynaecology. London: Isis Medical Media;2001:84-89.
Stress Urinary Incontinence:
Advances of Surgical Management
MAKING A DIAGNOSIS: Cystoscopy
68. Involuntary loss of large amount of urine associated with a
strong desire to void (urgency).
Usually associated with the urodynamic finding of
involuntary detrusor contractions or detrusor instability
(DI).
Although DI can be associated with neurologic disorders,
it also occurs in individuals who appear to be normal
69. The uninhibited bladder contractions
associated with DI can cause UI with and
without symptoms of urgency.
When a causative neurologic lesion is
established, the DI is called detrusor
hyperreflexia (DH) .
70. Stroke is associated with DH.
Suprasacral spinal cord lesions/multiple
sclerosis: DH is commonly accompanied
by detrusor sphincter dyssynergia (DSD)
(inappropriate contraction of the external
sphincter with detrusor contraction).
This can result in the development of
urinary retention, vesicoureteral reflux,
and subsequent renal damage
71. It is involuntary loss of urine following
overdistension of the bladder.
short-term
It may have a variety of presentations,
including frequent or constant
dribbling, or urge or stress
incontinence symptoms.
Overflow UI may be caused by an
underactive or acontractile detrusor,
or to bladder outlet or urethral
obstruction leading to overdistension
and overflow
72. can occur after vaginal delivery—especially if epidural
anesthesia was used.
Other causes include
I. Diabetes
II. neurological diseases
III. severe genital prolapse
IV. post surgical obstruction.
V. Secondary to drugs (alpha1-adrenoceptor antagonists,
antipsychotics, benzodiazepines, antidepressants, and drugs used
for hormone replacement therapy)
73. 5. Functional/Transient
incontinence
It occurs in situations in
which a woman cannot reach
a toilet in time because of
physical, psychological, or
mentation limitations. It is
medically reversible
conditions.
74. Urine loss may be caused by factors outside the lower
urinary tract such as chronic impairment of physical
or cognitive functioning, or both.
This diagnosis should be one of exclusion, however,
because some immobile and cognitively impaired
individuals have other types and causes of UI that may
respond to specific therapies
75. UI can often be improved or "cured" by
improving the patient's functional status,
treating other medical conditions,
discontinuing certain types of medication,
adjusting the hydration status, reducing
environmental barriers, or all of the above --
even if a lower urinary tract abnormality is
present.
76. First desire & strong desire – to void =150-250ml
Bladder capacity = 400 – 600ml
Normal residual volume = 0-50 ml
Intravesical pressure on filling & standing= 0-15 cm H2O
No leakage on coughing
Able to interrupt the urine flow on command
Maximum detrussor pressure during voiding= <70cm H2O
Peak urinary flow >15ml/sec