Neurogenic Bladder

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R.SRIVATHSAN

NEUROGENIC BLADDER A REVIEW

Fn features of bladder

Normal capacity of 400–500 mL.  Sensation of fullness.  Ability to accommodate various volumes without a change in intraluminal pressure.  Ability to initiate and sustain a contraction until the bladder is empty.  Voluntary initiation or inhibition of voiding despite the involuntary nature of the organ. 

Neurogenic control

 Brain:

-

Master control Frontal lobe Tonically inhibitory signals to detrusor. Stroke,dementia,cancer, CP, parkinson, shy drager syndrome….

 Brain

-

stem: Pons- PMC. inborn excitatory nature. a relay switch in the voiding pathway. coordinates the urethral sphincter relaxation and detrusor contraction to facilitate urination. affected by emotions. brain takes over the control of the pons at age 3-4 years. the stretch receptors of the detrusor muscle send a signal to the pons, which in turn notifies the brain.

 Sacral

-

-

spinal cord: Primitive voiding center – sacral reflex center – bladder contractions. Important intermediary between the pons and the sacral cord. Spinal injury: urinary frequency, urgency and urge incontinence and are unable to empty bladder. [detrusor sphincter dyssynergia with detrusor hyperreflexia (DSD-DH)]. (multiple sclerosis). Or detrusor areflexia. (herniated disc/ tumor)

 Peripheral

nerves: - Sympathetic: constantly active. [T10-L2]. 1. Bladder to increase its capacity without increasing detrusor resting pressure (accommodation) and stimulates the internal urinary sphincter to remain tightly closed. 2.Sympathetic activity also inhibits para sympathetic stimulation [S2-4] (opposite action).



-

-

Somatic nervous system: External urinary sphincter and the pelvic diaphragm. Pudendal nerve [S2-3] originates from the nucleus of Onuf and regulates the voluntary actions of the external urinary sphincter and the pelvic diaphragm. Shy- drager synd : lesion in Onuf nucleus. Neuropraxia : after delivery- stress incontinence. Suprasacral-infrapontine spinal cord trauma can cause overstimulation of the pudendal nerve - urinary retention.

Storage & voiding reflexes

Urinary tract innervation

Control of micturition

Definitions Neurogenic bladder is a malfunctioning bladder due to any type of neurologic disorder.  Detrusor hyperreflexia: Overactive bladder [suprapontine upper motor neuron disease]. External sphincter functions normally. The detrusor muscle and the external sphincter function in synergy (in coordination).  DSD-DH - Overactive bladder symptoms suprasacral spinal cord. Paradoxically, the patient is in urinary retention- detrusor and the sphincter are contracting at the same time; they are in dyssynergy. 

Detrusor hyperreflexia with impaired contractility (DHIC) overactive bladder symptoms, but the detrusor cannot generate enough pressure to allow complete emptying. The external sphincter is in synergy with detrusorcontraction. The condition is similar to urinary retention, but irritating voiding symptoms are prevalent.  Detrusor instability -overactive bladder symptoms without neurologic impairment. External sphincter normal.  Overactive bladder - urinary urgency, with or without urge incontinence with frequency and nocturia-neurologic or nonneurologic 

Spinal above T6 Complete cord transection above T6 - detrusor

hyperreflexia, striated sphincter dyssynergia, and smooth sphincter dyssynergia.

Autonomic dysreflexia - exaggerated sympathetic response to any stimuli below the level of the lesion. Inciting event - instrumentation of the bladder/ rectum (visceral distention). Symptoms- sweating, headache, hypertension, and reflex bradycardia. Decompress the rectum or bladder - reverses the effects of unopposed sympathetic outflow. Terazosin/ spinal anesthetic may be used as a prophylaxis.

Below T6  Detrusor

hyperreflexia, striated sphincter dyssynergia, and smooth sphincter dyssynergia no autonomic dysreflexia.

 Mng:

catherisation & anticholinergics.

Peripheral neuropathy

 Diabetic

: sensory(first) & motor loss.  Tabetic : areflexic.  Herpetic : sacral nerve.  Herniated disc : sensory + & motor -ve

Investigations Voiding diary. Pad test. PVRV. Uroflo. Filling cystometrogram : 1.bladder capacity 2.compliance 3.presence of phasic contractions (detrusor instability).  Voiding cystometrogram (pressure-flow study). [Detrusor instability]  Cystogram – static/ voiding.  EMG.  Cystoscopy  Videourodynamics.     

Uroflowmetry Uroflowmetry is the study of the flow of urine from the urethra.  The normal peak flow rate for males is 20– 25 mL/s and for females 20–30 mL/s.  Lower flow rates - outlet obstruction or a weak detrusor.  Higher flow rates - bladder spasticity or excessive use of abdominal muscles to assist voiding.  Intermittent flow patterns generally reflect spasticity of the sphincter or straining to overcome resistance in the urethra 

Normal urodynamics 

Measure: Bladder pressure (Pves)

(< 30cmH2O)

Rectal (abdominal)

pressure (Pabd)



Calculate: Detrussor Pressure

Pdet = Pves - Pabd

Components of urodynamics

Classification International Continence Society: (urodynamic based)  Detrusor: Normal (N), hyperreflexic (+), hyporeflexic (–)  Striated sphincter: Normal (N), hyperactive (+),incompetent(–)  Sensation: Normal (N), hypersensitive (+), hyposensitive (–)

Neurogenic bladder types  Cerebral Detrussor instability due to loss of volitional

inhibition

 Suprasacral

spinal

Detrussor sphincter dyssynergia

 Sacral

& peripheral

Detrussor areflexia

 Supraspinal.  Spinal.  Suprasacral.  Sacral

& peripheral.

Neurogenic bladder types

DD  CYSTITIS.  Cystocoele.  Chr

urethritis.  BOO.  Psychiatric disturbances.  Interstitial cystitis.

Complications  Hydronephrosis  Infection.  Calculus.  Renal

amyloidosis.  Sexual dysfn.  Autonomic dysreflexia.

Spastic bladder (1) reduced capacity. (2) involuntary detrusor contractions. (3) high intravesical voiding pressures. (4) Marked hypertrophy of the bladder wall. (5) spasticity of the pelvic-striated muscle. (6) autonomic dysreflexia in cervical cord lesion.

Flaccid bladder 1) 2) 3) 4)

Large capacity. Lack of voluntary detrusor contractions. Low intravesical pressure Mild trabeculation (hypertrophy) of the bladder wall. 5) Decreased tone of the external sphincter.

Flaccid bladder 1) 2) 3) 4)

Large capacity. Lack of voluntary detrusor contractions. Low intravesical pressure Mild trabeculation (hypertrophy) of the bladder wall. 5) Decreased tone of the external sphincter.

Spinal shock syndrome

 Flaccid

spastic / flaccid (level).  Drain the bladder – overdistension causes detrusor smooth muscle dmg and limit functional recovery of the bladder.  Few principles: - foleys’< 16Fr - silicone -changed every 3 wks - taped to abd wall.

Goals in treatment Preservation of upper urinary tract  Maintain adequate bladder capacity with good compliance  Promote low-pressure micturition  Avoid bladder overdistension  Prevent urinary tract infection  Minimize use of Foley catheter  Choose therapy that minimizes patient risks while maximizing social, emotional, and vocational acceptability 

Management Stress incontinence - surgical and nonsurgical.  Urge incontinence - behavioral modification / bladder-relaxing agents.  Mixed incontinence - medications as well as surgery.  Overflow incontinence - catheter regimen.  Functional incontinence - treat the underlying cause, such as urinary tract infection, constipation. 

Anti incontinent measures  Pelvic

floor exercises.  Vaginal weights.  Biofeedback.  Electrical stimulation.  Bladder training.

New modalities OAB : Bladder denervation. bladder desensitisation. [Resiniferatoxin intravesically]. Latissimus dorsi muscle is harvested from the back and transplanted around the urinary bladder: nerves are coapted and blood vessels anastomosed

Thank you

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