2. INTRODUCTION
MICTURITION CYCLE:
Micturition cycle involves two relatively discrete
processes:
1. bladder filling and urine storage and
2. bladder emptying or voiding
3. Bladder filling and urine storage :
Accommodation of increasing volumes of urine at a
low intravesical pressure (normal compliance) and
with appropriate sensation.
A bladder outlet that is closed at rest and remains
so during increases in intra-abdominal pressure.
Absence of involuntary bladder contractions
(detrusor overactivity).
4. Bladder emptying/voiding :
A coordinated contraction of bladder smooth
musculature of adequate magnitude and duration.
A concomitant lowering of resistance at the level of
the smooth and striated sphincter (no functional
obstruction).
Absence of anatomic (as opposed to functional)
obstruction.
5. NEURAL CONTROL OF THE LOWER URINARY
TRACT
Peripheral Nervous System: The lower urinary tract is
innervated by 3 sets of peripheral nerves involving
parasympathetic, sympathetic, & somatic nervous
systems.
1. Pelvic parasympathetic nerves arise at the sacral level
of the spinal cord, excite the bladder, and relax the
urethra.
2. Lumbar sympathetic nerves inhibit the bladder body
and excite the bladder base and urethra.
3. Pudendal nerves excite the external urethral
sphincter.
6. Mechanism of storage and voiding reflexes
A) Storage reflexes.
During urine storage, distention of bladder
produces low-level bladder afferent firing.
This stimulates (a)sympathetic outflow to the
bladder outlet (base and urethra), and (b)pudendal
outflow to the external urethral sphincter.
These responses occur by spinal reflex pathways &
represent “guarding reflexes,” which promote
continence.
Sympathetic firing also inhibits detrusor muscle
and transmission in bladder ganglia.
7. B) Voiding reflexes.
At the initiation of micturition, intense vesical
afferent activity activates brainstem micturition
center(PMC), which inhibits spinal guarding
reflexes (sympathetic and pudendal outflow to the
urethra).
PMC also stimulates parasympathetic outflow to
bladder & internal sphincter smooth muscle.
8. Smooth sphincter :
Smooth musculature of the bladder neck and
proximal urethra.
A physiologic (but not anatomic )sphincter.
Not under voluntary control.
9. Striated sphincter:
1. Striated musculature that is a part of the outer
wall of the proximal urethra in both male and
female. a/k/s intrinsic or intramural striated
sphincter or rhabdosphincter, &
2. bulky skeletal muscle group that closely
surrounds the urethra at the level of the
membranous portion in the male and primarily
the middle segment in the female a/k/s extrinsic
or extramural striated sphincter.
The extramural portion is the classically described
external urethral sphincter and is under
voluntary control.
11. Bladder storage & emptying requires continual
coordination of detrusor & external urinary
sphincter (EUS), mediated by central & peripheral
nervous systems.
Neurological conditions, lesions or trauma can cause
disturbances in urinary storage and voiding,
resulting in bladder dysfunction.
12. DEFINITION
Dyssynergia:
Kinesiologic disassociation of two groups of muscles that
generally work in harmony.
Sphincter dyssynergia:
An involuntary contraction or lack of relaxation of either
the striated sphincter (the striated muscle surrounding
the proximal urethra and the striated muscle that forms a
part of the urethra for a variable distance from the
“urogenital diaphragm” to the bladder neck) or the
smooth sphincter (the smooth muscle of the bladder neck
and proximal urethra).
13. Detrusor sphincter dyssynergia (DSD):
defined by the ICS as
Impaired coordination between detrusor and
sphincter during voiding due to a neurologic
abnormality (i.e. detrusor contraction synchronous
with contraction of the urethral and/or
periurethral striated muscles).
unless specified otherwise, refers to dyssynergia of
the striated sphincter.
detrusor striated-sphincter dyssynergia and
detrusor external-sphincter dyssynergia.
14. Smooth sphincter dyssynergia or Proximal
sphincter dyssynergia occurs in an individual with
autonomic hyperreflexia/dysreflexia (Spinal cord
injury above T6 level).
True DESD: only in patients who have an
abnormality in pathways between sacral spinal
cord & brainstem PMC.
Detrusor sphincter dyssynergia (DSD) is the most
common cause of neurogenic sphincteric
obstruction.
15. ETIOLOGY
Common causes:
traumatic SCI,
multiple sclerosis,
Spinal dysraphism, and
various forms of transverse myelitis.
16. PATHOPHYSIOLOGY
During normal filling, pelvic nerve afferents are
modulated by sympathetic output to cause relaxation
of the detrusor while maintaining the tone of the
bladder neck sphincter.
There is tonic activity of EUS facilitated by input
from PMC.
17. During voluntary micturition, inhibitory
signals from frontal cortex to PMC are removed
thus allowing activation of micturition reflex.
The PMC inhibits spinal guarding reflexes and
transmits excitatory signals to bladder.
The EUS relaxes with synergistic contraction of the
detrusor for a coordinated decrease in urethral
pressure and rise in detrusor pressure to allow the
outflow of urine.
18. DSD occurs in the setting of neurological
abnormalities b/w PMC and sacral spinal cord.
This interruption of the spinobulbospinal pathways
→ failed inhibition of spinal guarding reflexes +
erroneous excitation of Onuf’s nucleus causing
EUS contraction to occur during detrusor
contraction, generating elevated detrusor
pressures.
19. CLASSIFICATION
BLAIVAS CLASSIFICATION:
Type 1:
concomitant increase in both detrusor pressure &
EMG activity;
at the peak of detrusor contraction, sphincter
suddenly relaxes & unobstructed voiding occurs.
Type 2:
Sporadic/clonic contractions of striated
sphincter intermittently during detrusor
contraction.
Intermittent urinary stream.
20. Type 3:
Crescendo-decrescendo pattern of sphincter
contraction that results in outlet obstruction
throughout entire detrusor contraction.
Urinary obstruction & Inability to urinate.
24. CORRELATION b/w DSD type & degree of
SCI lesions:
Incomplete sensory and motor lesion → type 1
DESD.
Complete sensory and motor lesions → type 2 and
type 3.
WELD CLASSIFICATION:
Continuous DESD.
Intermittent DESD.
25. PSEUDO DYSSYNERGIA:
Pseudodyssynergia is the presence of EUS
contraction occurring during micturition that may
be misinterpreted for DSD.
Sphincter EMG activity increases simultaneously
with intravesical or detrusor pressure.
26. Common causes of pseudodyssynergia include
(1) abdominal straining to either initiate or augment a
bladder contraction or in response to discomfort
and
(2) attempted inhibition of a bladder contraction
either because of its involuntary nature or because
of discomfort.
27. Pseudodyssynergia can reliably be differentiated
from true DESD urodynamically by analyzing the
patterns of detrusor and EMG activity.
28. EPIDEMIOLOGY
The precise incidence of DSD is unknown given the
variability in neurological disease.
SCI contributes to a significant portion of cases of
DSD.
≈ 75% of patients with suprasacral SCI have DSD.
Incidence of DSD in MS and spinal dysraphism is
estimated at 25 – 50%.
29. CLINICAL PRESENTATION
Mixed storage and voiding symptoms,
Urinary incontinence or
Complications of DSD, i.e. UTIs and bladder calculi.
Neurological symptoms may predominate and
trigger initial neurourological investigation.
30. DIAGNOSTIC EVALUATION
HISTORY AND PHYSICAL EXAMINATION:
Aim to diagnose the cause & nature of bladder
dysfunction, &
To identify associated complications.
assess for changes in urinary, bowel and neurological
symptoms,
Disease duration, severity, prior investigations and
treatments.
31. Screening for occult neurological disease: inquiry
regarding visual changes, back or neck pain,
weakness, paraesthesia, urinary or bowel
symptoms.
Abdominal examination: assess for palpable
bladder, constipation, tenderness and previous
incisions.
Genitalia: inspected for abnormality and skin
irritation
32. DRE is necessary to assess anal sphincter tone at
rest and during voluntary contraction.
Testing perineal sensation, bulbocavernosus reflex
and cremasteric reflexes.
33. BASIC INVESTIGATIONS:
Urine culture and sensitivity, if there is a suspicion
of UTI.
Serum electrolytes, urea & creatinine.
Voiding diaries helpful in characterising voiding
dysfunction.
Ultrasonography helpful for assessment of
hydronephrosis, urinary calculi & post-void
residual urine volumes.
34. URODYNAMICS
Urodynamics: critical role in detection of DSD and
monitoring for associated complications.
DSD can be diagnosed using electromyography
(EMG), voiding cystourethrogram (VCUG) and/or
urethral pressure profilometry.
35. Diagnosis of DSD by EMG requires elevated ‘EMG
activity during detrusor contraction, in the absence
of Valsalva and Crede manoeuvres .’
Typical VCUG findings: a closed bladder neck
during filling and subsequent dilation of bladder
neck & proximal urethra to the level of EUS during
micturition.
36.
37. Paediatric patient with SCI with DSD showing dilated posterior urethra
&
bladder neck during bladder contraction on VCUG.
38. EMG Vs VCUG
Diagnostic discrepancy between EMG & VCUG
ranges from 40% to 46%.
Males more often diagnosed with EMG whereas
females more often diagnosed by VCUG.
Diagnosis of DSD in males by VCUG may be
impaired due to anatomical BOO by prostate and
that in the female diagnosis by EMG may be
impaired due to increased electrode artefact.
39. Role of urethral pressure profilometry in diagnosis
of DSD is controversial.
Unfortunately, a perfect test for DSD does not
exist.
Detection of DSD can be improved by using both
EMG and VCUG.
Pathology such as BOO, Parkinson’s disease and
dysfunctional voiding should be considered before
diagnosis, as they may have similar
symptomatology.
40. COMPLICATIONS
DESD results in a high bladder pressure with
subsequent back pressure effects.
The rate of urological complications from DESD with
no intervention is 50%.
Complications are much less common in females
because of decreased detrusor pressures generated.
41. If left untreated, DESD can result in:
• UTI/Urosepsis
• VUR
• Hydronephrosis
• Upper tract deterioration
• Renal insufficiency
• Urolithiasis
42. TREATMENT
Goals of treatment:
Adequate storage at low intravesical pressure.
Adequate emptying at low intravesical pressure.
Absence or control of infection.
Upper urinary tract preservation or improvement.
Social acceptability and adaptability.
43. Type 1 DESD: observation alone unless there is
persistent reflux, hydronephrosis, or autonomic
hyperreflexia.
Types 2 and 3: treated.
DLPP>40 cm water- significantly higher incidence
of upper tract damage and persistent DESD, hence
warrants treatment.
44. Current approaches:
1-Chronic indwelling catheterization.
2-Intermittent self catheterization.
3-Pharmacological therapy.
4-Bladder reconstruction and urinary diversion.
5-External sphincterotomy.
6- Stent placement(Urolume)across the sphincter.
7-Sphincter ablation with Botulinum toxin inj.
8-Intrathecal continuous baclofen infusion.
9-Balloon dilatation.
10-Laser sphincter ablation
45. C.I.S.C.
Intermittent catheterisation combined with
anticholinergics to reduce detrusor pressures is the
most common treatment for DSD.
Pharmacotherapy has a limited role in the
management of DSD.
46. Surgical Sphincterotomy
Therapeutic destruction of the external urethral
sphincter.
A surgical incision into the sphincter muscle to open
it, then urine drains out and collected by condom
drainage.
Female anatomy does not allow for condom drainage
as an alternative.
47. The 12-o’clock sphincterotomy (Madersbacher and
Scott), remains the procedure of choice for a number
of reasons:
Main bulk of the sphincter is anteromedial.
With the blood supply primarily lateral, a 12-o’clock
incision is least likely to cause hemorrhage.
The rate of postoperative erectile dysfunction with
this incision is approximately 5%.
48. Early failure due to
an inadequate surgical procedure (either not deep
enough or not extensive enough),
inadequate detrusor function, and
bladder neck or prostatic obstruction.
Late failure may occur because of
fibrosis somewhere along the extent of the
sphincterotomy,
a change in detrusor function,
development of prostatic obstruction, or
a change in neurologic status such that smooth sphincter
dyssynergia develops.
49. Failure defined as
1. presence of large PVRU associated with UTI
2. autonomic hyperreflexia symptomatology
associated with bladder overdistention or high
voiding pressures, and/or
3. progressive upper tract deterioration from
persistent reflux or poor bladder emptying.
51. Urethral Stenting
Use of a urethral stent to bypass the striated
sphincter.
A significant decrease in
1. detrusor leak point pressure
2. residual urine volume
3. Mean voiding pressure
4. symptoms of autonomic dysreflexia.
One obvious advantage: sphincteric stent is
potentially reversible.
54. Complications include
obstruction by urothelial ingrowth,
stent encrustation,
stricture,
stent migration,&
UTI.
55. Pharmacologic Sphincterotomy
Periurethral injections of botulinum A toxin.
Acts by inhibiting acetylcholine release from
presynantic cholinergic nerve terminals, thereby
inhibiting striated & smooth muscle contractions.
Use remains uncommon & unclear.
56. Urethral Overdilatation
Urethral overdilatation through the use of urethral
sounds or balloon procedures may improve
compliance and decrease outlet resistance.
Urethral overdilatation to 40 to 50 Fr in females &
22 to 28 Fr in 11 myelodysplastic children with high
intravesical pressures refractory to traditional forms
of treatment.
An ineffective long-term treatment for striated
sphincter dyssynergia.
57. Neuromodulation
Pudendal nerve interruption is seldom performed
today due to potential complications, including
impotence and significant fecal and stress urinary
incontinence.
Dorsal root rhizotomy with sacral anterior nerve root
stimulation.
