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Urinary bladder dysfunction in neurosuregry

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Urinary bladder dysfunction in neurosuregry

  1. 1. DR. AJAY KUMAR SINGH DNB Neurosurgery VPIMS
  2. 2. ANATOMY OF BLADDER  The lower part of the bladder neck is also called the posterior urethra because of its relation to the urethra  The smooth muscle of the bladder is called the detrusor muscle
  3. 3.  The bladder neck (posterior urethra) is a 2 to 3 cm long, and its wall is composed of detrusor muscle interlaced with a large amount of elastic tissue  The muscle in this area is called the internal sphincter  Involuntary
  4. 4.  Beyond the posterior urethra, the urethra passes through the urogenital diaphragm, which contain a layer of muscle called the external sphincter of the bladder  Voluntary  Tonicaly contracted normaly
  5. 5.  The bladder outlet: trigone, ureterovesical junction, bladder neck, and proximal urethra.  α-Adr receptors predominate in this area, and stimulation of postganglionic α-adr receptors provides excitatory input to bladder outlet that results in increased bladder outlet closure force.
  6. 6. Sphincteric mechanisms  Proximal/internal (smooth muscle sphincter)‐formed by circular smooth muscle fibers at bladder neck and proximal prostatic urethra.  Distal/external (striated sphincter)‐ ‐‐Slow twitch fibers responsible for baseline tonic activity ‐‐Fast twitch responsible for voluntary contractions
  7. 7. Innervation  Parasympathetic innervation (pelvic nerve) mediates- Detrusor muscle contraction (ACh, M3 muscarinic receptors) Relaxation of IUS (NO)  Sympathetic innervation (hypogastric nerve) mediates- Relaxation of detrusor β3-adrenoceptors). contraction of IUS (NA α1-adrenoceptors) Somatic innervation: Arises from the spinal motoneurones of Onuf’s nucleus(S2–S4). During storage, pudendal nerve keeps the striated urethral sphincter closed.
  8. 8.  Preganglionic neurons (PGNs) of  Parasympathetic----Sacral segment. Iintermediate grey matter (laminae V–VII) of spinal cord.  Sympathetic ---- Lumbar segment. Iintermediate grey matter (laminae V– VII) of spinal cord.  Parasympathetic PGNs send dendrites into the dorsal commissure and into the lateral funiculus and lateral dorsal horn of the spinal cord and exhibit an extensive axon collateral system that is distributed bilaterally in the cord.
  9. 9.  The somatic motor neurons that innervate the EUS are located in the ventral horn (lamina IX) in Onuf's nucleus.  Interneurons in the lumbo-sacral spinal cord that are involved in LUT function are located in the dorsal commissure, the superficial dorsal horn and the parasympathetic nucleus.
  10. 10.  Some of these interneurons send long projections to the brain, whereas others make local connections in the spinal cord and participate in segmental spinal reflexes.
  11. 11.  In the brain, some neurons are specific for micturition:  The neurons of Barrington's nucleus (also called the pontine micturition centre (PMC)  The periaqueductal grey (PAG),  Cell groups in the caudal and preoptic hypothalamus.  The neurons of several parts of the cerebral cortex, in particular the medial frontal cortex.
  12. 12. Physiology of micturition MICTURITION REFLEX.  As the bladder fills with urine, the wall stretches, impulse are initiated by stretch receptors in the bladder wall causing sensory signals to convey to the dorsal nerve root S2,3,4 segments of spinal cord through pelvic nerves and then back to the urinary bladder through parasympathetic fibres in the same nerve.  During this reflex sympathetic effrents are reflexly inhibited. In brain  PONS: Facilitatory  FRONTAL LOBE: Inhibitory
  13. 13. Storage reflexes -Distention of bladder produces low-level bladder afferent firing. -This in turn stimulates the symp outflow to outlet and pudendal outflow to EUS. -These responses occur by spinal reflex pathways and represent “guarding reflexes,” which promote continence. -Sympathetic firing also inhibits detrusor muscle and transmission in bladder ganglia.
  14. 14. Voiding reflexes At the initiation of micturition, intense vesical aff activity activates spinobulbospinal reflex pathway, then, • Activation PMC via PAG, which inhibits pudendal outflow to EUS and sympathetic outflow to detrusor, and later it stimulates parasympathetic outflow to detrusor and urethra leading to voiding.
  15. 15. Neuroanatomy of bladder control Cortical control  Antero medial frontal lobes involved in voluntary initiation and inhibition of micturition, delay of reflex voiding.  Sends inhibitory signals to detrusor  To avoid voiding till an appropriate location is found  Has connection with pons; and corticospinal fibres synapse with motor nuclei controlling striated sphincter
  16. 16. Pontine micturition centre  At pontomesencephalic reticular formation (barrington nucleus)  Dorsomedial tegmental region – center for micturiton ( M-region )  Ventrolateral pontine tegmentum - center for storage (L-region)  Affected by emotions, some people may experience incontinence when they are excited or scared
  17. 17. Pontine Micturition Center  Bladder filling  detrusor muscle stretch receptors  signal to the pons  Frontal lobe  Perception of this signal (bladder fullness) as a sudden desire to go to the bathroom  Normally, the brain sends an inhibitory signal to the Pons to inhibit the bladder from contracting until a bathroom is found.  Urge to urinate disappears  When urination appropriate, brain sends excitatory signals to the Pons, allowing voiding.
  18. 18. Spinal control  Somatic (S2‐S4), Pudendal nerves(Excitatory to external sphincter)  Parasympathetic (S2‐S4) (Excitatory to bladder)  Sympathetic (T10‐L2) --Hypogastric nerves to pelvic ganglia --Inhibitory to bladder body, excitatory to bladder base/urethra
  19. 19. Neurogenic bladder dysfunction This has been classified by Lapides into : 1. Uninhibited bladder 2. Reflex neurogenic bladder 3. Sensory paralytic bladder 4. Motor paralytic bladder 5. Autonomous bladder
  20. 20. Dysfunctions in Neurological Disorders  Suprapontine lesions  Spinal or Suprasacral lesions  At or distal to Sacral lesion
  21. 21. Filling/Storage symptoms  Urgency: “the complaint of a sudden compelling desire to void, which is difficult to defer”  Nocturia: when he/she wakes at night one or more times to void.  Frequency: 8->8 void/24 hour  Incontinence: inability to hold urine  Urge incontinence: sudden, intense urge to urinate followed by an involuntary loss of urine.
  22. 22. Voiding symptoms  Hesitancy: difficulty in begining a urination reflex.  Straining to void  Dysuria
  23. 23. Lesion Older terminolog Newer terminolgy Pathogenesis Sens ation Tone & cap F/ U H Residual urine Supraponti ne Uninhibited bladder Nuero detrusor overactivity Loss of cortical inhibition of reflex voiding P Normal + Var iabl e No Infrapontie/ spinal (UMN) Reflex neurogenic bladder or automatic (spastic) bladder Neurogenic D- overactivity w detrusor dys- synergia Interruption of descending autonomic tract and ascending sensory pathway leading to reflex and involuntary micturition P/A (++) Small bladder capacity + + ++ Conus, S2-4 roots in cauda or N (LMN) Autonomus bladder Detrusor areflexia Interrutption of sensory and motor supply leading to loss of reflex and volutary control A Reduced (increasd capacity) No + +++ Sensory root ganglia, post column - Sensory paralytic bladder Interruption of sensory supply A (no desie to void) Reduced (increasd capacity) No + +++ Dribbling Motor nerve root - Motor paralytic Interruption of motor supply P Reduced (variable) No + +++
  24. 24. Mixed type A bladder: that damage the detrusor nucleus but spare the pudendal nucleus.  Renders the detrusor flaccid (also referred to as detrusor areflexia), while the intact pudendal nucleus is spastic producing a hypertonic EUS.  The bladder is large and has low pressure, so the spastic EUS produces urinary retention. Mixed type B bladder: that spare the detrusor n. but damage the pudendal n.  Flaccid EUS and spastic bladder.  The bladder capacity is low but vesicular pressures are usually not elevated since there is little outflow resistance.
  25. 25. SUPRAPONTINE LESIONS :  Uninhibited bladder  Decreased descend inhibitory input to pons.  Coordinated activity of the sphincter and the detrusor  Urgency, frequency, nocturia, and occasionally urge incontinence.  Filling upto a normal threshold of 300‐350ml  Bladder emptying too quickly and too often, with relatively low volumes of urine.  CVA, Brain tumors, Hydrocephalus.
  26. 26. SPINAL LESION SPINAL CORD INJURY 3 types: (1) above spinal segment T6, (2) below T6 to the sacral cord (3) distal to the sacral cord (cauda equina).  Bladder contractility and reflex contraction are dependent on an intact sacral cord and sacral reflex arcs, with injury to the sacral segments of the spinal cord resulting in detrusor areflexia and fixed EUS tone.
  27. 27. Spinal shock:  Initially, flaccid muscle paralysis and absent somatic activity as well as suppressed autonomic activity below the lesion.  Absence of sensation and motor function, loss of voluntary control and sphincter compromise.  The bladder is acontractile and areflexic.  But, b/c of preservation of EUS tone, urinary incontinence is usually secondary to poor emptying and overflow incontinence.
  28. 28. Suprasacral cord injury (UMN)  Detrusor overactivity, smooth sphincter synergy (if below T6), and striated sphincter dyssynergy.  The dyssynergic striated sphincter causes a functional obstruction with poor bladder emptying and high detrusor pressure.  Smooth sphincter dyssynergy is present with lesions above T6.
  29. 29.  Functionally, the m/c problem in patients with suprasacral SCI is failure of both filling/storage (because of detrusor overactivity) and emptying (because of striated or smooth sphincter dyssynergia, or both).
  30. 30. Autonomic dysreflexia.  Lesions above the T6 sympathetic outflow tract, response to specific stimuli can cause a massive disordered autonomic discharge.  Pounding headache, hypertension, bradycardia, and flushing with sweating above the zone of the lesion.  Cervical injury.  The stimulus for autonomic dysreflexia is most often distention or manipulation of the bladder or rectum.
  31. 31. Neurospinal Dysraphism  90% incidence.  An areflexic bladder with an open bladder neck, inconsistent.  There is a fixed EUS, with 10% to 15% of patients having detrusor–striated sphincter dyssynergia.  Patients usually suffer from incontinence as a result of filling pressures overcoming the low fixed sphincter pressures and transient increases in intra-abdominal pressure (stress incontinence).
  32. 32. DISEASED AT OR DISTAL TO SACRAL SPINAL CORD SACRAL SPINAL CORD INJURY  Detrusor areflexia  Over time, decreased bladder compliance and elevated storage pressure may develop.  The bladder outlet is classically described as a competent but non- relaxing smooth sphincter with a fixed EUS not responsive to voluntary control.
  33. 33. EVALUATION OF NEUROLOGIC DISORDER  History  Neurologic examination  Laboratory testing  Radiologic studies  Upper urinary tract imaging  Lower urinary tract imaging  Urodynamic testing of LUT  CYSTOMETRY  PRESSURE FLOW STUDIES AND UROFLOWMETRY  ELECTROMYOGRAPHY  VIDEOURODYANAMICS
  34. 34. Neurological examination: Sensory examination of  Anterior abdominal wall: thoracic  Genitalia: sacral  Lower extremities: lumbar lumbar nerve roots.  The anterior portions of the scrotum and labia majora derive innervation from the thoracolumbar spinal cord.  The sacral nerve roots innervate the posterior portion.  Saddle area of the perineum evaluate the afferent limb of pudendal n.
  35. 35. Basic motor and muscular tone—specifically, the tibialis anterior, gastrocnemius, and toe extensors, innervated by the lower lumbar and upper sacral nerves.  P/R to evaluate the external anal sphincter is important for evaluation of the pelvic floor musculature.  Voluntary contraction of the external anal sphincter confirms innervation of the pelvic floor and integrity of the corticospinal tract.  Preserved sphincter tone in the absence of voluntary contraction is consistent with a suprasacral lesion, whereas diminished tone is consistent with a sacral or peripheral nerve abnormality.
  36. 36. Neurological examination: to evaluate the integrity of sensorimotor pathway known as the segmental reflex arcs
  37. 37. Laboratory testing  Serum Creatinine  Urine routine  Urine culture and sensitivity  Serum electrolytes  Input-Output chart
  38. 38. Radiologic Upper UTI  Hydronephrosis  Chronic pyelonephritis  Renal scarring  Vesicouretric reflux  Renal calculi Lower UTI  Cystoscopy : detrusor overactivity as trabeculation and diverticula, urethral strictures and prostatic obstruction.  Voiding cystourethrogram: vesicoureteric reflux morpholgic changes
  39. 39. Urodyanamic testing: Non invasive  Assesment of PVR and urolflowmetry  No absolute volume above which PVR is universally considered to be abnormal. (<100ml), ideally <50 ml.  PVR indicates poor bladder contractility or BOO or both,
  40. 40. Uroflowmetry: provides the data on the rate of urinary flow over time from the urethra.  A low flow rate indicates poor bladder contractility or BOO or both.  Normal uroflow rate : 25ml/sec  Obstructed : < 5ml/sec  Reliable only when voided volumes is 200‐400ml
  41. 41. Cystometry  Invasive  Evaluate the compliance of bladder during filling and voiding.  Detrusor pressure is measured.  At 50 and 100 ml/min.  1st sensation: 100 ml  Full: b/w 400 and 600 ml
  42. 42. Normal • Low detrusor pressures at initiation • Normal bladder sensations • No detrusor contraction during filling • Rapid rise in detrusor pressure just prior to voiding • Voiding at detrusor pressure below 40 cm in males & 20 cm in females. 3 Voiding States  Low detrusor pressure and high flow rate (unobstructed)  High detrusor pressure and low flow rate (obstructed)  Low detrusor pressure with low flow rate (poor detrusor contractility).
  43. 43. Electromyography.  Sphincter EMG is used to record bioelectric potentials generated by the striated sphincter complex during bladder filling, storage, and micturition.  It provides information on voluntary control of the pelvic floor musculature and coordination between the detrusor and pelvic floor.  During bladder filling, EMG activity should gradually increase and reach a maximum before voiding.  This so-called guarding reflex is also present during the Valsalva maneuver, coughing, or other maneuvers that increase abdominal pressure.
  44. 44. TREATMENT Failure to store urine  Management of detrusor overactivity or impaired compliance  Timed voiding and pelvic floor exercises  Medications  Sacral neuromodulation  Augmentation cystoplasty
  45. 45. Timed voiding and pelvic floor exercises  Decreased fluid intake  Avoidance of dietary irritants such as caffeine, bowel regulation and avoidance of constipation and timed voiding.  Bladder retraining and pelvic floor muscle exercises
  46. 46. Medications: Anticholinergic: Oxybutynin (5mg TDS), Flavoxate, tolterodine. By blockage of muscarinic Ach receptors to inhibit unstable detrusor contraction.  Detrusor inastability  Incontinence  Urgeny  Cathter induced bladder spasm,
  47. 47. Beta agonist: Mirabegron Activation of beta-3 adrenargic receptors relaxes the detrusor smooth muscle during the storage phase. Alpha blocker: BOO. Phenoxybenzammine (10-20 mg BD), prazocin (0.5-2 mg BD Tricyclic antidepressant: imipramine Anticholinergic and sympathetic action Decrease bladder contractality and increase sphincter resistance Botulinum toxin A: (blocks NMJ presynaptic vesicle fusion, which prevent Ach release. Ideopathic or neurogenic detrusor overactivity (200 U) and decreased bladder compliance(100 U).
  48. 48. Management of outlet deficiency Intrinsic sphincter deficicncy, poorly functioning EUS, bladder outlet injury. Iinjectable bulking agents Sling procedure Artificial urinary sphincters Bladder neck closure Urinary diversion
  49. 49. Failure to empty urine  Managment of detrusor acontractility  Clean intermittent catheterization  Indwelling catheters  Voiding with valsalva maneuvers  Cholinergic agonists  Sacral neuromodulation  Urinary diversion
  50. 50. Management of detrusor-external sphincter dyssynergia  External spincterotomy  Urethral stenting  Botulinum toxin A injection Management of Detrusor-internal sphincter dyssynergia  Alpha adrenargic blocker  Cystoscopic incision with electrocautery
  51. 51. THANK YOU
  52. 52.  Urgencey : sudden urge to urinate  Frequency: frequent urination (> 8 voids/24 hour) or > 1 void in night.  Nocturia:  Hesitency: difficulty in beginning the voiding reflex  Urge incontinence: sudden urge to micturate  Incontinence: involuntary loss of urine per urethra  Overflow incontinence: frequent dribbling  Dysuria: painful sensation of micturition