Bladder

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, S 3, S 4 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.

15. Neuro-physiology of micturition

16. 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.

17. 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

18. 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.

19. 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.

20. 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.

21. 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.]

22. 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.

23. 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

24. 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).

25. 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.

26. 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

27. 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 .

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

29. 2-AUTOMATIC BLADDER

30. 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)

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

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

33. 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)

34. 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.

35. 3-AUTONOMOUS BLADDER

36. 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

37. 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.

38. 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

39. 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

40. 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

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

42. 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.

43. 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).

44. 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.

45. 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.

46. 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.

47. 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

48. 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

49. 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

50. 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

51. 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

52. 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