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Buddhist Tzu Chi General Hospital

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Presentation on theme: "Buddhist Tzu Chi General Hospital"— Presentation transcript:

1 Buddhist Tzu Chi General Hospital
The Spastic Sphincter Hann-Chorng Kuo Department of Urology Buddhist Tzu Chi General Hospital

2 Function of urethral sphincter
Provide adequate urethral resistance at filling phase to prevent incontinence Active relaxation during voiding phase for micturition Inhibition of detrusor nucleus to postpone voiding before threshold Release of inhibitory effect on detrusor nucleus at initiation of voiding (on-off switch)

3 Anatomy of male urethral sphincter

4 Anatomy of Female Urethral sphincter

5 Toilet training – A learning process influences voiding
Traditional voiding control by age 3 CNS plasticity and adaptation to sensory input of micturition process Retentive behavior of children Parent pushing of toilet training Behavioral stress to muscles and change in functional integrity of tissue

6 The overactive sphincter
Incorrect conditioning of voiding reflexes during CNS maturing Symptoms ranging from incontinence to retention Chronic LUT dysfunction is maintained by permanently up-regulated sacral reflex arcs Dysfunctional voiding develops

7 The Pelvic Floor Deep layer – Levator ani provide relaxation during micturition and defecation (S3,4), contraction to lift pelvic organ upward and compression Transverse perinealis, ischeocavernous, bulbocavernous, urethral sphincter, anal sphincter muscles (S2) provide squeezing effect on pelvic organs

8 Anatomy of Pelvic Floor

9 Innervation of Pelvic Floor
Perineal skin sensation from S2 nerve Skin sensation can be impaired unilaterally or bilaterally in S2 nerves Loss of skin sensation often reflects a loss of urethral sphincter integrity Deficits in S3,4 nerves are not associated with significant incontinence Hypersensitivity of bladder is often mirrored hypersensitivity of the levator (S3,4)

10 Neuroregulation of sacral nerves in micturition reflex
Loss of pudendal afferent input can dampen the detrusor reflex Enhanced afferent input to micturition center can augment detrusor reflex Supraspinal inhibition or increased inhibitory input to micturition center can suppress detrusor reflex Chronic anxiety or via behavioral pathway can cause loss of volitional or ability to relax the sphincter with void efforts

11 Pathophysiology of pelvic floor dysfunction
Changes in peptide release from nerve endings secondary to stress (supraspinal) Enhanced release of inflammatory or neural-sensitizing peptides into tissue (local inflammation) Inadequate pelvic floor control due to learned behavior (dysfunctional voiding)

12 Detrusor instability and Holding urine during involuntary DI

13 CNS Control of Pelvic floor
Medial part of dorsal pontine tegmentum (M-region) – sphincter relaxation and detrusor contraction Lateral part of pontine tegmentum – sphincter contraction and detrusor inhibition Onuf’s nucleus – spinal control center of pelvic floor – linkage to paraventricular nucleus

14 Micturition and Continence center in CNS

15 Central peptide pools linked to CNS centers regulating LUT function
Paraventricular peptide pool Vasopressin, oxytocin, substance P Somatostatin, dopamine, neurotensin Glucagon, renin Corticotropin-releasing factor Met- and leu-enkephalin Nucleus Onuf peptides (for sphincter control) Somatostatin, neuropeptide Y, serotonin Substance P (from paraventricular nucleus, dorsal and ventral roots) Met-and leu-enkephalin

16 Neurobiological background of pelvic floor dysfunction

17 Clinical assessment of a hypertonic pelvic floor
LUT Symptoms – frequency, urgency, suprapubic, perineal, deep pelvic pain, lower backpain, slow stream, intermittency, recurrent UTI, retention Constipation or difficult defecation Sexual dysfunction Insomnia and other somatic complaints

18 Important past history
Current symptoms? Since when? development over the last time? change in last time? Pain? Where?, character?, intensity (using visual analog scale 0-10), Change over time? Micturition? Any problems?, double voiding?, infections?m burning?, inability to void? Defecation? Frequency, consistency Sexual life? Dysfunction?, emotional problems?, female: vaginism? Childhood prolonged bedwetting?, excessive exercises to achieve early urinary continence?, punishment for bedwetting?, retentive voiding habits (I.e.,low micturition frequency?), sexual abuse (female)? Adolescence Female:painful menses?,frequent urinary tract infections? Male:urinary tract infections Adulthood Female: childbirths?, vaginal delivery?, pelvic surgery?, infections?, voiding habits over time,profession, personal satisfaction Male:voiding habits, profession,social life

19 Hypertonic pelvic floor = hypertonic urethral sphincter?
Urethral sphincter and external anal sphincter are mainly innervated by S2 Levator ani are innervated by S3,4 Reflex coordination to bladder sensory input is synchronized in most of cases Isolated denervation or impairment in conduction may occur

20 Hypertonic urethral sphincter Straining to initiate voiding

21 Hypertonic urethral sphincter Straining to open urethra

22 Hypertonic urethra = hyperactive urethra?
Hypertonic urethra indicates increased and sustained urethral pressure (tonic) during resting state Hyperactive urethra indicates increased activity of urethral sphincter during voiding state A spastic urethral sphincter causes difficulty in initiation of voiding

23 Hyperactive urethral sphincter during initiation & voiding

24 SCI with type 1 DESD and low detrusor contractility

25 States of dysfunctional voiding due to spastic sphincter
1. Fill phase (normally very stable pressure cmH2O) Pathology High sphincter pressure (>80) Hypersensitivity Clonic or hyperreflexic dynamic Spasms (pain)versus spontaneous relaxations (leakage episodes) 2.Transition phase (normally smooth) Nonrelaxation Hesitant/delayed relaxation Precipitous relaxation Aborted relaxation Rising sphincter pressures 3.Void phase (normally coordinated) Partial relaxations Intermittency of sphincter relaxation 4.Recovery stage (normally smooth) Intermittency (dribbling)

26 Clinical assessment of pelvic floor muscle function
Uterine prolapse or cystocele Sensation of perineal skin Anal tone measurement Volitional contraction of pelvic floor Search for inflammatory sources (hemorrhoid, prostatitis, vaginitis) Focal neurological findings (Bulbocavernous reflex, deep tendon reflex)

27 Digital rectal examination of Pelvic floor muscles
Deep and superficial sphincter muscle tone, weak, high, or normal? Hypersensitivity or tenderness of the levator or urethral sphincter Motor identity of sphincter muscles or levator ani muscles Voluntary repetitive contractions of sphincter and levator muscles

28 Tentative diagnosis of pelvic floor hypertonicity
Spastic urethral sphincter – a chronic hypertonic urethral sphincter causing functional bladder outlet obstruction Poor relaxation of pelvic floor muscles – inadequate relaxation during voiding causing hesitancy, low intermittent flow Non-relaxing pelvic floor or urethral sphincter –-- no relaxation during voiding efforts by abdominal straining or Valsalva maneuver

29 Diagnosis based on initial investigations
LUT symptoms Negative urinalysis or urine culture High pelvic floor muscle tone Low maximal flow rate and obstructive intermittent flow pattern No evidence of BPH or other pathology Voiding diary verified LUTS

30 VUDS Analysis in 112 Non-obstructive Men with LUTS
Normal bladder & urethra 25 (22.3%) Hypersensitive bladder 17 (15.2%) Detrusor instability 6 (4.5%) Detrusor failure 3 (2.7%) Poor relaxed external sphincter 61(54.5%)

31 Urodynamics Uroflowmetry & EMG Cystometrogram & EMG
Pressure flow study Videourodynamic study Urethral pressure profilometry Pudendal nerve latency time Evoke potential study

32 Intermittent Flow

33 Relaxation of urethral sphincter at initiation of voiding

34 Poor relaxation of urethral sphincter during voiding

35 Intermittency due to poor relaxation of ES

36 Pseudodyssynergia in CVA causing high voiding pressure

37 Inhibition of detrusor contraction by urethral sphincter during voiding

38 Stop test – volitional sphincter contraction and inhibition of voiding

39 Guarding reflex – during uninhibited detrusor contractions

40 Coordinated sphincter activity during filling phase in Enterocystoplasty

41 Increased sphincter activity causing isolated obstruction in detrusor areflexia

42 DHIC and increased sphincter activity during filling

43 Detrusor overactivity and overactive sphincter & pelvic floor

44 Type I DESD in C5,6 SCI

45 Type II DESD in Thoracic SCI

46 Urethral sphincter v Pelvic floor muscles – analogue?

47 Discoordinated urethral sphincter in dysfunctional voiding

48 Chronic pelvic floor spasticity – A cause of pelvic pain?
Increased muscle tone of pelvic floor muscles Spasticity of urethral sphincter Spasticity of external anal sphincter Hypertonicity of pyriformis muscles Fascitis of pubococcygeus or coccygeus muscles Physiotherapy and medication for pelvic floor spasticity can relieve pelvic pain Should search for tendered points or infection

49 Chronic prostatitis syndrome
Symptoms of frequency, urethral irritation, hesitancy, intermittency, residual urine sensation, perineal pain and lower back pain Spastic urethral sphincter might be a cause of chronic prostatitis or reflux abacterial prostatitis Treated as spastic sphincter may work

50 Spastic urethral syndrome and constipation
Chronic constipation causes hypertonic anal sphincter and hence, pelvic floor muscles Poor relaxation of pelvic floor muscles results in inhibition of detrusor contractions during voiding Concomitant treatment of constipation can relieve voiding symptoms

51 Treatment of spastic urethral sphincter
Behavioral therapy: hydration, laxatives, time voiding, changing voiding posture Physiotherapy: pelvic floor muscle exercises Electric stimulation : interferential current stimulation Biofeedback: visual or Uroflowmetry & EMG Medication: baclofen, alpha-adrenergic blockers, estrogen, combination therapy Urethral injection of botulinum A toxin

52 Therapeutic results of baclofen and terazosin in treatment of spastic urethral sphincter
IPSS Qmax Residual urine Baseline Trated Treated Baclofen (n=73) 15.2±6.7 10.4±5.7 14.3±9.7 16.7±8.1 65.7±33.9 37.5±21.7 % of change 31.6±21.5 16.87±12.7 42.9±34.1 Baclofen plus 12.7±7.9 61.±4.5 14.8±11.0 58.1±21.8 31.01±31.2 Terazosin (n=64) 51.7±27.4 52.7±31.1 46.5±29.3 Statistics* P<0.05 NS

53 Biofeedback pelvic floor muscle relaxation

54 Strengthened PFM after 3 M training

55 Botulinum A toxin

56 Identification of External Sphincter in Man

57 Preliminary Result in Reduction of MUCP

58

59 Results of Botulinum A Toxin in Patients with Voiding Dysfunction
Good Improved Failed Detrusor underactivity (n=27) 13 (48.2%) 8 (29.6%) 6 (22.2%) DESD (n=18) 3 (16.7%) 10 (55.6%) 5 (27.8%) Dysfunctional voiding (n=18) (33.3%) 2 (11%) Poor relaxation of urethral sphincter (n=12) (25%) 7 (58.3%) (16.6%) TOTAL (n=75) 25 35 (43.7%) 15 (20%) DESD=Detrsor external sphincter dyssynergia

60 Influence of Detrusor contractility and Urethral sphincter activity on Botox Effects
Good Improved Failed High pressure contractility (n=26) 8 (30.7%) 15 (57.6%) 3 (11.5%) Low pressure contractility (n=49) 17 (34.6%) 20 (40.8%) 12 (24.4%) No-relaxing sphincter (n=27) 13 (48.2%) (29.6%) 6 (22.2%) Hyperactive or poorly relaxed urethral sphincter (n=48) (25%) 27 (56.2%) 9 (18.7%) TOTAL (n=75) 25 (33.3%) 35 (43.7%) (20%)


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