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Diaa Mohammad Srahin
5th year Medical Student
Al-Quds University
Obstetrics & Gynecology
March / 2018
Dr. Mashoor Nasan
Introduction
 Urinary incontinence is the inability to hold urine,
producing involuntary urinary leakage.
 It is specially problematic because it is affects personal
hygiene as well as social life.
 It is increasingly prevalent as the ageing population
expands.
 The prevalence increases with age, with approximately
5 % of women between 15 and 44 years of age being
affected, rising to 10 % of those aged between 45 and
64 years, and approximately 20 % of those older than
65 years.
 It’s far beyond wetting clothes !!
 Social Impact
 Psychological impact
 Physical morbidity
Risk Factors
Physiology of continence
 Continence and micturition involve a balance between urethral closure and detrusor
muscle activity.
 Urethral pressure normally exceeds bladder pressure, resulting in urine remaining in the
bladder.
 The proximal urethra and bladder are normally both within the pelvis.
 Intraabdominal pressure increases (from coughing and sneezing) are transmitted to both
urethra and bladder equally, leaving the pressure differential unchanged, resulting in
continence.
 Normal voiding is the result of changes in both of these pressure factors: urethral
pressure falls and bladder pressure rises.
 Spontaneous bladder muscle (detrusor) contractions are normally easily suppressed
voluntarily.
Pharmacology of Incontinence
 a -adrenergic receptors.
These are found primarily in the urethra and when stimulated
cause contraction of urethral smooth muscle, preventing
micturition.
 b-adrenergic receptors.
These are found primarily in the detrusor muscle and when
stimulated cause relaxation of the bladder wall, preventing
micturition.
 Cholinergic receptors.
These are found primarily in the detrusor muscle and when
stimulated cause contraction of the bladder wall, enhancing
micturition.
Normal micturition
Cystometric studies
 Basic office cystometry begins with the patient emptying her bladder as
much as possible. A urinary catheter is first used to empty the bladder
and then left in place to infuse saline by gravity, with a syringe into the
bladder retrograde assessing the following:
 Residual volume. How much is left in the bladder?
 Sensation-of-fullness volume. How much infusion (in mL) until the
patient senses fluid in her bladder?
 Urge-to-void volume. How much infusion (in mL) until the patient feels
the need to empty her bladder?
 Involuntary bladder contractions. By watching the saline level in the
syringe rise or fall, involuntary detrusor contractions can be detected. The
absence of contractions is normal.
The following are parameters of normal bladder function:
 Residual urine of <50 mL.
 First desire to void between 150 and 200 mL.
 Capacity between 400 and 600 mL.
 Detrusor pressure rise of <15 cmH2O during filing and
standing.
 Absence of systolic detrusor contractions.
 No leakage on coughing.
 A voiding detrusor pressure rise of <70 cmH2O with a peak
flow rate of >15 mL/second for a volume >150 mL.
Classification of Incontinence
 Urinary incontinence is classified according to pathophysiological
concepts rather than symptomatology.
 but the following definitions of
symptoms are commonly used.
Urodynamic stress incontinence
 Urodynamic stress incontinence (USI), previously
called genuine stress incontinence.
 is defied as the involuntary leakage of urine during
increased abdominal pressure in the absence of a
detrusor contraction.
 This is the most common incontinence in young
women.
 Rises in bladder pressure because of intra-abdominal
pressure increases (e.g., coughing and sneezing) are
not transmitted to the proximal urethra because it is
no longer a pelvic structure owing to loss of support
from pelvic relaxation.
The etiology of USI is thought to be related to a number of factors:
 Damage to the nerve supply of the pelvic floor and urethral sphincter.
 Menopause and associated tissue atrophy may also cause damage to the
pelvic floor.
 A congenital cause may be inferred, This may be due to altered
connective tissue, particularly collagen.
 Chronic causes, such as obesity and chronic obstructive pulmonary
disease, raise intra-abdominal pressure, and constipation and
associated straining may also result in problems.
History
 Loss of urine occurs in small spurts simultaneously with coughing or sneezing.
It does not take place when the patient is sleeping.
Examination
 Pelvic examination may reveal a cystocele. Neurologic examination is normal.
 The Q-tip test is positive when a lubricated cotton-tip applicator is placed in
the urethra and the patient increases intra-abdominal pressure, the Q-tip will
rotate >30 degrees.
 Investigative studies. Urinalysis and culture are normal. Cystometric studies
are normal with no involuntary detrusor contractions seen.
Management
 Medical therapy includes Kegel exercises and estrogen replacement in
postmenopausal women.
 Surgical therapy aims to elevate the urethral sphincter so that it is again an
intra-abdominal location (urethropexy).
 This is done by attachment of the sphincter to the symphysis pubis, using the
Burch procedure as well as the Marshall Marchetti-Kranz (MMK) procedure.
 The success rate of both of these procedures is 85–90%.
 A minimally invasive surgical procedure is the tension-free vaginal tape
procedure in which a mesh tape is placed transcutaneously around and under
the mid urethra. It does not elevate the urethra but forms a resistant platform
against intra-abdominal pressure.
Bladder over-activity
 It’s a bladder contraction during filling phase (< 400ml
volume). So, it’s characterized by
 Urgency
 Frequency
 Nocturia
 Motor Urge (Hypertonic) Incontinence. This is the
most common incontinence in older women.
 It can be wet (there is urinary incontinence) or dry (no
urinary incontinence).
Etiology
 Involuntary rises in bladder pressure occur from idiopathic
detrusor contractions that cannot be voluntarily
suppressed.
History
 Loss of urine occurs in large amounts often without warning. This can
take place both day and night. The most common symptom is urgency.
Examination
 Pelvic examination shows normal anatomy. Neurologic examination is
normal.
Investigative studies
 Urinalysis and culture are normal.
 Cystometric studies show normal residual volume, but involuntary
detrusor contractions are present even with small volumes of urine in
the bladder.
Management
Anticholinergic medications (e.g., oxybutynin
[Ditropan]); non-steroidal anti-inflammatory drugs
(NSAIDs) to inhibit detrusor contractions; tricyclic
antidepressants; calcium-channel blockers.
Retention with over-flow
 It’s leakage secondary to over-distended bladder,
which becomes higher than urethral pressure. There
is no or poor bladder contraction
 Pathophysiology
 Detrusor muscle hypotonia
 Denervated bladder
 Medication like anti-cholinergic or alpha agonist
 Urethral obstruction
Overflow (Hypotonic) Incontinence
Etiology
 Rises in bladder pressure occur gradually from an over-
distended, hypotonic bladder. When the bladder pressure
exceeds the urethral pressure, involuntary urine
loss occurs but only until the bladder pressure equals
urethral pressure.
 The bladder never empties.
 Then the process begins all over. This may be caused by
denervated bladder (e.g., diabetic neuropathy, multiple
sclerosis) or systemic medications (e.g., anticholinergics).
History
 Loss of urine occurs intermittently in small amounts. This can take
place both day and night. The patient may complain of pelvic
fullness.
Examination
 Pelvic examination may show normal anatomy; however, the
neurologic
examination will show decreased pudendal nerve sensation.
Investigative studies
 Urinalysis and culture are usually normal, but may show an infection.
 Cystometric studies show markedly increased residual volume, but
involuntary detrusor contractions do not occur.
Management
 Intermittent self-catheterization may be necessary.
 Discontinue the offending systemic medications.
 Cholinergic medications to stimulate bladder
contractions and a-adrenergic blocker to relax the
bladder neck.
Sensory Irritative Incontinence
Etiology
 Involuntary rises in bladder pressure occur owing to
detrusor contractions stimulated by irritation from any
of the following bladder conditions: infection, stone,
tumor, or a foreign body.
History
 Loss of urine occurs with urgency, frequency, and
dysuria. This can take place day or night.
Examination
 Suprapubic tenderness may be elicited, but otherwise the pelvic examination is
unremarkable.
Investigative studies
A urinalysis will show the following abnormalities:
 bacteria and white blood cells (suggest an infection) or red blood cells (suggest
a stone, foreign body, or tumor).
 A urine culture is positive if an infection is present.
 Cystometric studies (which are usually unnecessary) would reveal normal
residual volume with involuntary detrusor contractions present.
Management
 Infections are treated with antibiotics.
 Cytoscopy is used to diagnose and remove stones, foreign bodies, and tumors.
Congenital causes
 Intra-urethral
 Epispidias, it’s due to failure of midline fusion of
mesoderm. It’s associated with widening of bladder
neck and short urethra.
Congenital causes
 Extra-urethral cause
 Bladder exstrophy is failure of mesoderm migration with
absence of anterior bladder wall, anterior bladder wall
 Ectopic ureter
Fistula
 Can be
 Gynecological cause like 95% due to pelvic surgery and
radiation. Pelvic tumor can cause fistula
 Obstetric cause like childbirth, in which bladder is
compressed between head of fetus and bony pelvis
 Can be uretrovaginal, vesicovaginal and urethrovaginal
History
 The patient usually has a history of radical pelvic surgery or pelvic radiation therapy.
 Loss of urine occurs continually in small amounts. This can take place both day and
night.
Examination
 Pelvic examination may show normal anatomy and normal neurologic findings.
Investigative studies
 Urinalysis and culture are normal.
 An intravenous pyelogram (IVP) will demonstrate dye leakage from a urinary tract
fistula. With a urinary tractvaginal fistula, intravenous indigo carmine dye will leak onto
a vaginal tampon.
Management
 can be treated by primary closure or by surgery and can be delayed until tissue
inflammation and edema have resolved at about 4 weeks.
" Urogynecology - Urinary Incontinence "
" Urogynecology - Urinary Incontinence "

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" Urogynecology - Urinary Incontinence "

  • 1. Diaa Mohammad Srahin 5th year Medical Student Al-Quds University Obstetrics & Gynecology March / 2018 Dr. Mashoor Nasan
  • 2. Introduction  Urinary incontinence is the inability to hold urine, producing involuntary urinary leakage.  It is specially problematic because it is affects personal hygiene as well as social life.  It is increasingly prevalent as the ageing population expands.
  • 3.
  • 4.  The prevalence increases with age, with approximately 5 % of women between 15 and 44 years of age being affected, rising to 10 % of those aged between 45 and 64 years, and approximately 20 % of those older than 65 years.  It’s far beyond wetting clothes !!  Social Impact  Psychological impact  Physical morbidity
  • 5.
  • 7. Physiology of continence  Continence and micturition involve a balance between urethral closure and detrusor muscle activity.  Urethral pressure normally exceeds bladder pressure, resulting in urine remaining in the bladder.  The proximal urethra and bladder are normally both within the pelvis.  Intraabdominal pressure increases (from coughing and sneezing) are transmitted to both urethra and bladder equally, leaving the pressure differential unchanged, resulting in continence.  Normal voiding is the result of changes in both of these pressure factors: urethral pressure falls and bladder pressure rises.  Spontaneous bladder muscle (detrusor) contractions are normally easily suppressed voluntarily.
  • 8.
  • 9.
  • 10.
  • 11. Pharmacology of Incontinence  a -adrenergic receptors. These are found primarily in the urethra and when stimulated cause contraction of urethral smooth muscle, preventing micturition.  b-adrenergic receptors. These are found primarily in the detrusor muscle and when stimulated cause relaxation of the bladder wall, preventing micturition.  Cholinergic receptors. These are found primarily in the detrusor muscle and when stimulated cause contraction of the bladder wall, enhancing micturition.
  • 12.
  • 14. Cystometric studies  Basic office cystometry begins with the patient emptying her bladder as much as possible. A urinary catheter is first used to empty the bladder and then left in place to infuse saline by gravity, with a syringe into the bladder retrograde assessing the following:  Residual volume. How much is left in the bladder?  Sensation-of-fullness volume. How much infusion (in mL) until the patient senses fluid in her bladder?  Urge-to-void volume. How much infusion (in mL) until the patient feels the need to empty her bladder?  Involuntary bladder contractions. By watching the saline level in the syringe rise or fall, involuntary detrusor contractions can be detected. The absence of contractions is normal.
  • 15.
  • 16.
  • 17. The following are parameters of normal bladder function:  Residual urine of <50 mL.  First desire to void between 150 and 200 mL.  Capacity between 400 and 600 mL.  Detrusor pressure rise of <15 cmH2O during filing and standing.  Absence of systolic detrusor contractions.  No leakage on coughing.  A voiding detrusor pressure rise of <70 cmH2O with a peak flow rate of >15 mL/second for a volume >150 mL.
  • 18. Classification of Incontinence  Urinary incontinence is classified according to pathophysiological concepts rather than symptomatology.  but the following definitions of symptoms are commonly used.
  • 19. Urodynamic stress incontinence  Urodynamic stress incontinence (USI), previously called genuine stress incontinence.  is defied as the involuntary leakage of urine during increased abdominal pressure in the absence of a detrusor contraction.  This is the most common incontinence in young women.
  • 20.  Rises in bladder pressure because of intra-abdominal pressure increases (e.g., coughing and sneezing) are not transmitted to the proximal urethra because it is no longer a pelvic structure owing to loss of support from pelvic relaxation.
  • 21.
  • 22. The etiology of USI is thought to be related to a number of factors:  Damage to the nerve supply of the pelvic floor and urethral sphincter.  Menopause and associated tissue atrophy may also cause damage to the pelvic floor.  A congenital cause may be inferred, This may be due to altered connective tissue, particularly collagen.  Chronic causes, such as obesity and chronic obstructive pulmonary disease, raise intra-abdominal pressure, and constipation and associated straining may also result in problems.
  • 23. History  Loss of urine occurs in small spurts simultaneously with coughing or sneezing. It does not take place when the patient is sleeping. Examination  Pelvic examination may reveal a cystocele. Neurologic examination is normal.  The Q-tip test is positive when a lubricated cotton-tip applicator is placed in the urethra and the patient increases intra-abdominal pressure, the Q-tip will rotate >30 degrees.  Investigative studies. Urinalysis and culture are normal. Cystometric studies are normal with no involuntary detrusor contractions seen.
  • 24.
  • 25.
  • 26.
  • 27.
  • 28. Management  Medical therapy includes Kegel exercises and estrogen replacement in postmenopausal women.  Surgical therapy aims to elevate the urethral sphincter so that it is again an intra-abdominal location (urethropexy).  This is done by attachment of the sphincter to the symphysis pubis, using the Burch procedure as well as the Marshall Marchetti-Kranz (MMK) procedure.  The success rate of both of these procedures is 85–90%.  A minimally invasive surgical procedure is the tension-free vaginal tape procedure in which a mesh tape is placed transcutaneously around and under the mid urethra. It does not elevate the urethra but forms a resistant platform against intra-abdominal pressure.
  • 29.
  • 30.
  • 31.
  • 32.
  • 33.
  • 34. Bladder over-activity  It’s a bladder contraction during filling phase (< 400ml volume). So, it’s characterized by  Urgency  Frequency  Nocturia
  • 35.  Motor Urge (Hypertonic) Incontinence. This is the most common incontinence in older women.  It can be wet (there is urinary incontinence) or dry (no urinary incontinence). Etiology  Involuntary rises in bladder pressure occur from idiopathic detrusor contractions that cannot be voluntarily suppressed.
  • 36. History  Loss of urine occurs in large amounts often without warning. This can take place both day and night. The most common symptom is urgency. Examination  Pelvic examination shows normal anatomy. Neurologic examination is normal. Investigative studies  Urinalysis and culture are normal.  Cystometric studies show normal residual volume, but involuntary detrusor contractions are present even with small volumes of urine in the bladder.
  • 37.
  • 38.
  • 39. Management Anticholinergic medications (e.g., oxybutynin [Ditropan]); non-steroidal anti-inflammatory drugs (NSAIDs) to inhibit detrusor contractions; tricyclic antidepressants; calcium-channel blockers.
  • 40. Retention with over-flow  It’s leakage secondary to over-distended bladder, which becomes higher than urethral pressure. There is no or poor bladder contraction  Pathophysiology  Detrusor muscle hypotonia  Denervated bladder  Medication like anti-cholinergic or alpha agonist  Urethral obstruction
  • 41. Overflow (Hypotonic) Incontinence Etiology  Rises in bladder pressure occur gradually from an over- distended, hypotonic bladder. When the bladder pressure exceeds the urethral pressure, involuntary urine loss occurs but only until the bladder pressure equals urethral pressure.  The bladder never empties.  Then the process begins all over. This may be caused by denervated bladder (e.g., diabetic neuropathy, multiple sclerosis) or systemic medications (e.g., anticholinergics).
  • 42. History  Loss of urine occurs intermittently in small amounts. This can take place both day and night. The patient may complain of pelvic fullness. Examination  Pelvic examination may show normal anatomy; however, the neurologic examination will show decreased pudendal nerve sensation. Investigative studies  Urinalysis and culture are usually normal, but may show an infection.  Cystometric studies show markedly increased residual volume, but involuntary detrusor contractions do not occur.
  • 43.
  • 44. Management  Intermittent self-catheterization may be necessary.  Discontinue the offending systemic medications.  Cholinergic medications to stimulate bladder contractions and a-adrenergic blocker to relax the bladder neck.
  • 45. Sensory Irritative Incontinence Etiology  Involuntary rises in bladder pressure occur owing to detrusor contractions stimulated by irritation from any of the following bladder conditions: infection, stone, tumor, or a foreign body. History  Loss of urine occurs with urgency, frequency, and dysuria. This can take place day or night.
  • 46. Examination  Suprapubic tenderness may be elicited, but otherwise the pelvic examination is unremarkable. Investigative studies A urinalysis will show the following abnormalities:  bacteria and white blood cells (suggest an infection) or red blood cells (suggest a stone, foreign body, or tumor).  A urine culture is positive if an infection is present.  Cystometric studies (which are usually unnecessary) would reveal normal residual volume with involuntary detrusor contractions present. Management  Infections are treated with antibiotics.  Cytoscopy is used to diagnose and remove stones, foreign bodies, and tumors.
  • 47. Congenital causes  Intra-urethral  Epispidias, it’s due to failure of midline fusion of mesoderm. It’s associated with widening of bladder neck and short urethra.
  • 48. Congenital causes  Extra-urethral cause  Bladder exstrophy is failure of mesoderm migration with absence of anterior bladder wall, anterior bladder wall  Ectopic ureter
  • 49. Fistula  Can be  Gynecological cause like 95% due to pelvic surgery and radiation. Pelvic tumor can cause fistula  Obstetric cause like childbirth, in which bladder is compressed between head of fetus and bony pelvis  Can be uretrovaginal, vesicovaginal and urethrovaginal
  • 50. History  The patient usually has a history of radical pelvic surgery or pelvic radiation therapy.  Loss of urine occurs continually in small amounts. This can take place both day and night. Examination  Pelvic examination may show normal anatomy and normal neurologic findings. Investigative studies  Urinalysis and culture are normal.  An intravenous pyelogram (IVP) will demonstrate dye leakage from a urinary tract fistula. With a urinary tractvaginal fistula, intravenous indigo carmine dye will leak onto a vaginal tampon. Management  can be treated by primary closure or by surgery and can be delayed until tissue inflammation and edema have resolved at about 4 weeks.

Editor's Notes

  1. Social impact: person become isolated and maps journey near bath facilities. Moreover, there will be decrease in ability for production Psychological impact: poor self esteem and depression with social withdrawal Physical morbidity: due to skin moisture, there is increase risk of perineum infection and cellulitis. Moreover there is sleep disruption from nocturia
  2. Leavator ani muscle and endo-pelvic fasica support proximal part of urethra and bladder neck. So, in case of increase intra-abdominal pressure, they ensure to equal transmission of pressure to bladder and proximal part of urethra. So, no urine leakage. However, when these muscle are weakened or relaxed  unequal pressure transmission urine leakage.
  3. It’s incontinence due to unequal transmission of pressure to bladder and urethra. So, leakage is associated with any cause of increase intra-abdominal pressure like cough, intercourse, sneezing, lifting heavy weight. It comes in episodes and bladder does not empty completely Most common cause of urinary incontinence
  4. Damage to the nerve supply of the pelvic flor and urethral sphincter caused by childbirth leads to progressive changes in these structures, resulting in altered function. In addition, mechanical trauma to the pelvic flor musculature and endopelvic fascia and ligaments occurs as a consequence of vaginal delivery. Prolonged second stage, large babies and instrumental deliveries cause the most damage. • Menopause and associated tissue atrophy may also cause damage to the pelvic flor. • A congenital cause may be inferred, as some nulliparous women suffer from incontinence. This may be due to altered connective tissue, particularly collagen. Stress incontinence is much less common in black women and differences in connective tissue are thought to be responsible. • Chronic causes, such as obesity and chronic obstructive pulmonary disease, raise interabdominal pressure, and constipation and associated straining may also result in problems.
  5. Anterior prolapse, also known as a cystocele (SIS-toe-seel), occurs when the supportive tissue between a woman's bladder and vaginal wall weakens and stretches, allowing the bladder to bulge into the vagina
  6. Estrogen replacement therapy (vaso-dilation of peri-urethral plexuses elevating resting urethral pressure