Urinary bladder

1. Urinary bladder, physiology,
pathological types &it's
clinical implications
guided by
Dr Manoj Lakhotia
Sr. Prof
Presented by
Dr Umesh Yadav

2. URINARY BLADDER
• Hollow pelvic organ
• Strong muscular walls
• Part of the lower urinary tract
• Characterised by distensibility(Transitional
epithelium)
• Primary function is to store urine
• Normal bladder lies in lesser pelvis but As bladder
fills it ascends into pelvis major, and very full bladder
may ascend up to level of umbilicus.

3. NERVE SUPPLY
• VISCERAL MOTORS FIBERS
• 1. Parasympathetic
• preganglionic fibers from S2 to S4 spinal segments via
pelvic splanchnic nerves and through inferior
hypogastric plexus to ganglion near the wall of urinary
bladder to make contraction of detrusor muscle.
• 2. Sympathetic Outflow: from T12, L1, L2 spinal
segments via lumbar splanchnic nerves to ganglia in the
hypogastric plexuses to the internal urethral sphincter.
• 3.Voluntary fibers /Somatic fibers: from S2 to S4 spinal
segments via the pudendal nerve to the external
urethral sphincter.

4. SENSORY FIBERS
• Visceral sensory (afferrents) fibers passes along the
pelvic splanchnic nerves/parasympathetic.
• Some fibers travel with the sympathetic nerves via
hypogastric plexuses and enters the T12,L1 and L2
segment

5. Nerve supply

6. Sympathetic effect
• A.It has little or no effect on bladder wall.
• B. Supply mainly to blood vessels
• C. Its effect on sphincter vesicae to maintain the
urinary continence is also very minor.
• D. Its main role is active contraction of sphincter
vesicae during ejaculation.
• Parasympathetic Effect:
• stimulates contraction of detrusor muscle and
inhibits the action of the sphincter vesicae.

7. Afferent pathway
• A-delta fibers responds to bladder distension & c
fibers responds to pain
• Traverse through pelvic nerve
• Enters numerous cord levels S2,S3,S4
• Ascends through lateral spinothalamic tract and
posterior columns
• Pontine Micturition Centre
• thalamus
• cortex

8. EFFERENT SYSTEM
• 1.Parasympathetic (S2-S4)- Pelvic nerves
• - Excitatory to bladder, relaxes internal urethral
sphincter.
• 2.Sympathetic (T10-L2)
• - Hypogastric nerves to pelvic ganglia
• - Inhibitory to bladder body, excitatory to bladder
base/urethra.
• 3.Somatic (S2-S4)
• - Pudendal nerve
.Excitatory to external sphincter

9. Receptors

10. MICTURITION PHYSIOLOGY
• Micturition is a reflex action in toilet trained person,
controlled by higher center of brain.
• The reflex initiated by stretch receptors in bladder wall.
• Most afferents travel through the pelvic splanchnic nerve to
the S2, S3, S4 segments to the spinal cord.
• Some of afferents reaches L1, L2 segments by sympathetic
fibers
• Parasympathetic Efferents : by pelvic splanchnic nerves.-
Causes contraction of detrusor muscle and relaxation of the
sphincter vesicae
• The pudendal nerve supplies the external urethral sphincter
and perineal muscles to relax

11. CONTROL OF MICTURITION
• In children, micturition is a simple reflex and take place whenever
the bladder distended
• In adult, this simple stretch reflex is inhibited by the activity of the
cerebral cortex and pons until the time and place are favorable
• The pontine micturition center( PMC) modulate the opposing
action of parasympathetic and sympathetic system.
• The inhibitory fibers pass downward with cortico-
spinal tract to S2, S3, S4 segments of cord.
• Voluntary control of micturition is accomplished by contracting
the external sphincter urethrae, which closes the urethra.

12. 1.bladder emptying stage,
• (PMC )sends excitatory influence to the sacral
spinal cord that produces detrusor contraction
while simultaneously sending inhibitory influence
to the thoracolumbar cord and suppression of
sympathetic supply and internal urinary sphincter
relaxation. The overall effect is to allow evacuation
of the bladder contents.

13. 2.bladder storage phase
• PMC inhibition causes suppression of sacral spinal
cord that produces detrusor relaxation
[parasympathetic] while simultaneously sending
excitatory influence to the thoracolumbar cord
sympathetic that produces internal urethral
sphincter contraction.
• The overall effect is to allow filling/storage of urine
in the bladder.

14. How micturition takes place?
• Bladder tone is derived from the volume and pressure
exerted on the inside of the bladder(interavesical
pressure).
• Increasing bladder volume by 50 ml increases pressure.
As volume increases further, the interavesical pressure
increases, but not much until you get above 300 ml.
then the pressure rises steeply with additional volume.
• 1st urge to void occurs at 150cc.But Marked sense of
fullness at 400-600cc
• So at This volume and pressure there is sudden ries in
intravesical pressure bladder "tone" triggering the
micturition reflex.

16. Neuro-physiology of micturition

17. PONTINE MICTURITION CENTER
(PMC)/BARRINGTON'S NUCLEUS
• Located at the level of pontine mesencephalic
reticular formation. Higher centers cerebral cortex
exert inhibitory or facilitatory influence on the
PMC.
• Pontine micturition center :(medial)
• Stimulation results in decrease in urethral pressure
followed by a rise in detrusor pressure.
• Pontine storage center :(lateral)
• Stimulation results in increase in urethral pressure
followed by a fall in detrusor pressure.

18. STRESS INCONTINENCE
• The urethral sphincter is weakened so that transient
increases in intra-abdominal pressure raise the bladder
pressure to levels that exceed urethral resistance.
• Pelvic floor weakness and inadequate muscular and
ligamentous support of the bladder neck and proximal
urethra change the angle between the bladder and the
urethra
• CAUSES
• In Female -child birth & surgery, postmenopausal
atrophy of the mucosa.
• Male -prostate surgery

19. SYMPTOMS
• Momentary leakage of small amounts of urine with
coughing, laughing, and sneezing while the person
is in an upright position.
• Urine loss is unrelated to a conscious urge to
urinate.
• Bladder distention is absent.

20. URGE INCONTINENCE
• Detrusor contractions are stronger than normal
and overcome the normal urethral resistance.
• The bladder is typically small.
• Machenism-Decreased cortical inhibition of
detrusor contractions from UMN LESION [stroke,
brain tumor, demential and lesions of the spinal
cord above the sacral level.]
• Hyperexcitability of sensory pathways, as in bladder
infections, tumors, and fecal impaction.

21. SYMPTOMS
• Involuntary urine loss preceded by an urge to void.
• Urgency, frequency, and nocturia with small to
moderate volumes.
• If acute inflammation is present, pain on urination.

22. OVERFLOW INCONTINENCE
• Detrusor contractions are insufficient to overcome
urethral resistance, causing urinary retention.
• The bladder is typically flaccid and large, even after an
effort to void
• Obstruction of the bladder outlet, as in benign prostatic
hyperplasia or tumor. Weakness of the detrusor muscle
associated with LMN LESION [peripheral nerve disease at
S2–4 level. Impaired bladder sensation that interrupts the
reflex arc, as in diabetic neuropathy.]

23. SYMPTOMS
• When intravesicular pressure overcomes urethral
resistance, continuous dripping or dribbling
incontinence ensues. Decreased force of the
urinary stream.
• Exam.- enlarged, sometimes tender, bladder. Other
signs include prostatic enlargement, motor signs of
peripheral nerve disease, a decrease in sensation
(including perineal sensation), and diminished to
absent reflexes.

24. CLINICAL IMPLICATIONS OF
URINARY BLADDER
• 1 UNINIHIBITED NEUROGENIC BLADDER
/CORTICAL BLADDER
• 2 UMN /SPINAL/HYPER REFLEXIC /SPASTIC
BLADDER/AUTOMATIC BLADDER
• 3 LMN/AREFLEXIC / FLACCID/AUTONOMOUS
BLADDER

26. CORTICAL BLADDER
• Physiologic: Newborns and infants - periodic complete
evacuation.
• Pathologic:
• a Lesion in paracentral lobule (cerebral palsy, multiple
sclerosis, trauma, infarcts) Uncontrolled evacuation in
socially unacceptable situations.
• Since pontine arc is intact- evacuation is complete, no
residual urine and coordination is good, no detrusor
sphincter dyssynergia.
• No VUR, "'Safe bladder."
• Associated with dementia (frontal lobe).

27. UNINHIBITED NEUROGENIC
BLADDER
• There is a loss of the cortical inhibition of reflex
voiding, although bladder tone remains normal.
• Bladder distention causes contraction in response
to the stretch reflex.
• Bladder sensation is usually normal. There is no
residual urine.

28. CAUSE OF UNINHIBITED BLADDER
• Most common causes include:
• Anterior circulation Stroke
• Multiple Sclerosis
• Intracranial space occupying lesions
• Cerebral palsy
• Fronto-temporal dementia
• Alzheimers disease
• Normal pressure hydrocephalus

29. PATHOGENESIS
• The uninhibited neurogenic bladder or infantile
bladder is characterized by uncontrolled contractions
of bladder smooth muscle.
• In the infant up to two to three years of age, filling of
the bladder stimulates proprioceptive endings in the
bladder wall ,which in turn elicit a micturition reflex
and resultant detrusor contraction.
• In the adult an acquired defect in the
corticoregulatory tract may result in an uninhibited
bladder.

30. SYMPTOMS
• Acute onset of urge incontinence
• Increased urinary frequency and enuresis
• Inappropriate urination (no social inhibition)

31. 2-AUTOMATIC BLADDER

32. SPINAL/UMN/HYPER REFLEXIC
BLADDER
• Transection above the level of cord and below the level
of pons (transverse myelitis, trauma)
• 1:Acute spinal shock stage: [ immediately after
transection ]Bladder remains toneless with large
volume of urine.
• Urinary bladder- becomes flaccid, and have overflow
incontinence
• 2: Post spinal shock stage: Bladder tone recovers, [after
few weeks to months ]Spinal arc is established
• Hypertonic bladder with small capacity which empties
suddenly and reflexly with the help of spinal center
(Automatic bladder)

33. POST SPINAL SHOCK STAGE
• Residual urine due to incomplete evacuation
• VUR - infections, renal damage "Unsafe bladder"
• ⁃ Detrusor sphincter dyssynergia

34. CAUSES
• Most common causes in adults include:
• cord injury (excluding sacral spine)
• Posterior circulation Stroke
• In children:
• Sacral agenesis
• Spina bifida (Myelomeningocele)

35. PATHOGENESIS
• Pontine center regulates voiding by synergizing the
contraction of detrusor muscles and relaxation of
the urethral sphincter.
• Thus pontine lesions (and spinal cord lesions above
the sacral spinal segments) are characterized by
detrusor-sphincter dyssynergia (DSD)

36. SYMPTOMS OF DSD
• Lower abdominal pain, abdominal spasms
• Increased urgency, frequency of urination, leaking
of urine (urge incontinence)
• Urinary retention
• Difficulty voiding voluntarily
• Patient will need to strain(valsalva maneuvre) or
compress the lower abdomen (Crede maneuvre) to
pass urine.

37. 3-AUTONOMOUS BLADDER

38. LMN/AREFLEXIC/FLACCID
BLADDER
• Lesion in at/below spinal level (anterior horn
cell,nerve)
• No spinal reflex - areflexic, huge capacity bladder
• Overflow incontinence
• High residual volume – infections
• Similar to acute spinal shock stage of UMN

39. AUTONOMOUS NEUROGENIC
BLADDER
• There is destruction of the parasympathetic supply.
Sensation is absent, and there is no reflex or
voluntary control of the bladder; contractions occur
as the result of stimulation of the intrinsic neural
plexuses within the bladder wall. The amount of
residual urine is large, but the bladder capacity is
not greatly increased.

40. AUTONOMOUS BLADDER
• Combined involvement of both sensory and motor
limbs (Cauda equina lesions, spina bifida)
• Local vesical plexus takes over the control and
functions as autonomous bladder
• Continuous dribbling
• Incomplete evacuation
• High residual volumes

41. CAUSES
• Most common causes include
• 1) Sacral spine/nuclear lesions: Conus Medullaris
syndrome traumatic injury to sacral spinal segments
• 2-Spinal shock
• 3 Lower motor Neuron lesions
• May include compressive neuropathy (cauda equina
syndrome)
• Demyelination neuropathies (Diabetic Neuropathy)
• latrogenic causes: Damage to pudendal nerve during
pelvic procedures

42. CLINICAL FEATURES
• Overflow incontinence is the main presenting
symptom. Other
• symptoms include abdominal distention and
bloating sensation.
• Difficulty initiating stream of urine
• Involuntary dribbling of urine
• No pain on urination, no urgency

43. DIFFERENTIAL DIAGNOSIS
• Other common causes of over flow incontinence
are:
• BPH
• Pelvic organ prolapse (POP)
• Epidural analgesia
• Spinal anesthesia

44. COMPLICATIONS OF FLACCID
BLADDER
• 1) Recurrent UTI's
• 2) Bladder calculi due to stagnation of urine
• 3) Maceration and secondary infection of skin of
the groin
• 4) vaginitis/cervicitis leading to Pelvic Inflammatory
Disease
• 5) Myogenic bladder: chronic overdistention of
bladder leads to permanent detrusor muscle
damage leading to irreversible distended bladder.

45. SENSORY PARALYTIC BLADDER
• A is found with lesions that involve the posterior
roots or posterior root ganglia of the sacral nerves,
or the posterior columns(tabes dorsalis)of the
spinal cord. Sensation is absent, and there is no
desire to void.
• Symptoms:-There may be distention, dribbling, and
difficulty both in initiating micturition and in
emptying the bladder. There is a large amount of
residual urine( overflow Incontinence).

46. MOTOR PARALYTIC BLADDER
• A develops when the motor nerve supply to the
bladder is interrupted.
• The bladder distends and decompensates, but
sensation is normal.
• The residual urine and bladder capacity vary.
• May be seen transiently in Guillain Barrie
Syndrome, poliomyelitis.

47. MIXED TYPE A NEUROGENIC
BLADDER
• The more common of the mixed type bladders
• Detrusor nucleus damaged: detrusor nucleus damage
renders the detrusor flaccid (also referred to as
detrusor areflexia)
• Pudendal nucleus intact: the intact pudendal nucleus is
spastic producing a hypertonic external urinary
sphincter
• The bladder is distended and has low pressure due to
detrusor hypotonia
• Spastic external sphincter produces urinary retention
• The detrusor pressure is low so upper urinary tract
damage does typically not occur.

48. MIXED TYPES B NEUROGENIC
BLADDER
• Detrusor nucleus intact: the bladder is spastic due
to the disinhibited detrusor nucleus.
• Pudendal nucleus damaged: external urethral
sphincter is flaccid.
• Therefore bladder volume is low (no urinary
retention)
• Due to flaccid external urethral sphincter
incontinence occurs.

49. Step to diagnose neurogenic
bladder
• A) Identify type(Spastic, flaccid, mixed) of bladder
dysfunction:
• Testing modalities
• 1) Postvoidal residual volume Used to detect- Bladder
volume
• 2) Cystometrography-Bladder pressure
• 3) Peak urinary flow-rate testing to determine -
Urethral sphincter pressure
• 4) Pressure flow video -Detrusor sphincter dyssynergy

50. B) Etiology of bladder dysfunction
• 1) Urine analysis/culture & CBC with differential
count for -Presence of UTI
• 3) HbA1c-Risk of Diabetic neuropathy
• 4) USG KUB -Urethral outflow obstruction
• 5) CT/MRI brain & spine - CNS lesions

51. Treatment of neurogenic
bladder
• Goals of therapy:
• 1) achieve or maintain continence
• 2) prevent upper urinary tract damage
• 3) minimize risk of UTI's
• 4) prevent bladder overdistention

52. 1. Non Pharmacological
• a) Fluid intake time table
• b) Voiding stimulation techniques (Crede technique, valsalva)
• 2. Medications:
• First line agent: anti-muscarinic (oxybutynin, tolterodine)
• Trospium is a M-3 specific anti-muscarinic agent that has lower
ADR profile than oxybutynin
• Adjuvant agents: alpha 1 adrenergic blocker (prazosin), Tri-
cyclic antidepressant (imipramine)
• Alpha-2 agonists (clonidine) can be used for internal urethral
sphincter spasm.
• Benzodiazepines can be used for external urethral sphincter
spasm

53. 3. Minimally invasive techniques
• A) clean intermittent self catheterization
• B) Injection of BOTOX into detrusor muscle and
internal urethral sphincter to relieve spasm.
• Refractory cases of urinary retention
• Invasive Surgical techniques:
• Sacral nerve root stimulation
• Last resort measure: Enterocystoplasty

54. Treatment of flaccid
neurogenic bladder
• Flaccid bladder: Treatment of flaccid bladder often
involves
• invasive modalities associated with more
complications than spastic bladder.
• Invasive modalities:
• Indwelling Foley's catheter
• Lower risk of
• 1) UTI
• Suprapubic catheter has Lower risk of
• 1) Urethral damage
• 2) Urethral strictures