Physiology of Lower Urinary Tract Function (including Neurogenic Bladder) Eric S. Rovner, M.D....

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Transcript of Physiology of Lower Urinary Tract Function (including Neurogenic Bladder) Eric S. Rovner, M.D....

Physiology of Lower Urinary Tract Function (including

Neurogenic Bladder)

Eric S. Rovner, M.D.Professor of UrologyMedical University of South Carolina

Outline

Physiology of Micturition Micturition cycle Neurologic factors Pharmacology

Neurogenic Bladder Lesions above pons Lesions below pons above sacral SC Lesions of sacral SC and peripheral NS

Ideal Plumbing Requirements for a Terrestrial

Store a reasonable amount of urine at a pressure < kidney filtration pressure (25 to 40 cm H2O)

Rapid on-demand emptying

The micturition cycle:Filling/StorageEmptying

Micturition Cycle: Simplified*

*Wein

Bladder Filling and Urine Storage Requirements:

Reservoir: Accommodation of increasing volumes of urine

At a low intravesical pressure (compliance) With appropriate sensation

Absence of involuntary bladder contractions Overactivity

Outlet: A bladder outlet that is closed at rest and remains so

during increases in intra-abdominal pressure

Urine Emptying Requirements:

Reservoir: Coordinated bladder contraction of adequate magnitude (or

other increase in pressure)

Outlet: Absence of anatomic obstruction Concomitant lowering of resistance at the level of:

Smooth muscle of bladder neck and proximal urethra Striated muscle that surrounds urethra

Voiding Dysfunction*

Pathophysiology simplified All voiding dysfxn is sub-classified as abnormality of:

Filling/storage:• Bladder• Urethra• Both

Emptying:• Bladder• Urethra• Both

Key factors:BladderSmooth sphincterStriated sphincterSensation

*Wein

Voiding dysfunction

Because of urethra Too weak:

SUI (sphincteric) Too strong

BOO/retention/DESD

Because of the bladder Too weak

Detrusor underactivity (retention) Too strong

Detrusor overactivity (OAB/UUI)

Because of both (MIXED)

“I am not certain why humans or

animals are continent of urine and

feces and I am not convinced that

anyone really knows.”

J. Berry, 1961

(Berry Prosthesis)

Physiology of Urinary Continence

Continence = urethral closure forces > bladder expulsive forces

Bladder

Urethra

>>1. Sphincters2. Connective tissue3. Urethral mucosa

1. Intravesical (IBC’s, compliance)2. Extravesical (abdominal, etc.)

=Continence

Micturition reflex at sacral SC:Coordination/influenced by higher centers

What defines neurogenic voiding dysfunction?

Abnormality in storage or voiding function of the bladder as a result of a neurologic disturbance

Must be confirmed by objective evidence of a nervous system disorder

Patterns of Neurogenic dysfunction

Often predicted by level of injury/disease

However, limited by Complete/Incomplete Description of sx’s is often poor (sensory loss)

“….the bladder is an unreliable witness”

Other co-morbidities (diabetes, CHF, etc.) Other pelvic disease (POP, SUI, BPH, etc.)

Incidence of Bladder Dysfunction

Spinal cord injury (8k new/yr) 70%–80%

Multiple sclerosis (400k) 50%–80%

Lumbo-sacral DDD 27%-92% (60-90% overall prevalence with 5% sciatica)

Radical pelvic surgery 16%-20%

Parkinson’s disease 15%–35%

Diabetes (17,000,000) 10%–30%

CVA (540k new/yr) 10%–15%

Central Nervous SystemCortex, Basal Ganglia, Cerebellum

-Frontal lobes and cingulate gyrus

-Voluntary initiation of voiding

-Inhibition of reflex voiding activity

-Supra-pontine structures are generally inhibitory on the LUT

-Injuries (CVA, etc.) release this inhibition

-detrusor overactivity, and clinical sxs of urgency, frequency, incontinence

Central Nervous System: Pons

Coordination of sphincter and bladder

- Afferent input (ascending and descending)

-bladder wall and supra-pontine centers

• - Efferent outflow (descending)

-sacral spine

- somatic

- parasympathetic centers for voiding

-T-L spine

-sympathetic nerves for accomodation

Injuries separating Pons from LUT(SCI, MS) : reflex voiding patterns and uncoordinated voiding

Supra-sacral spinal injury/disease

Functional Abnormality Depends on

chronology, type of lesion completeness

Neurogenic Detrusor Overactivity Striated sphincter dysynergia

If above T6 (Sympathetic Outflow Tract)

• Smooth sphincter dysynergia

• Autonomic dysreflexia

Infrasacral Injury/Disease

Clinical Presentation Urge/frequency or urinary retention +/- straining to void Usually continent

Most common urodynamic abnormality Detrusor areflexia Normal innervation of the striated sphincter Normal smooth sphincter function Irritative lesions- detrusor overactivity

Goals of NGB Evaluation

Accurate diagnosis characterization of voiding dysfunction (NGB)

Reassess as needed

recognition of concomitant non-neurogenic VD BPH, SUI, etc.

Assess prognosis Urological

Neurological

Direct management

Neurourologic Evaluation

History Physical examination

neurologic examination PVR Creatinine U/A, C&S +/- Upper tract study +/- Urodynamic study +/- Cystoscopy

Urodynamics:Utility in prognosis and treatment in NGB

LUTS and PE do not correlate well with of type, extent or level of injury/disease…..or UDS findings

LUTS and PE do not correlate well with prognosis or “danger” to upper tracts (but UDS does!!!!)

In SCI/MS, level of injury not always predictive of UDS* Correlation of neuro imaging and UDS not exact

Therefore management often dictated by UDS

*Weld and Dmochowski, 2000

Detrusor overactivity with UI

Valsalva induced DO with UI

MS with sx’s of SUI with urge +/- UUI

SUI

Q

Vol

pVes

pAbd

pdet

EMG

47 y.o. with Sx’s of SUI after Rad Hyst. PVR=175cc

Treatment Issues in NGB

Assessing Safety 1st Upper tracts Risk factors: compliance, UTI’s, VUR, etc Other

Relieving Symptoms 2nd Incontinence Frequency, urgency Other

Goals of Management

Upper Tract Preservation (or improvement)

Absence or control of infection

Continence

Reduce or eliminate impact on QOL

Make an acceptable solution for the patient Physically Economically Socially Culturally

How to achieve goals

Adequate urine storage at low pressure

Adequate emptying in absence of obstruction

Adequate urethral closure forces (competence)

Selecting least invasive/expensive Rx option.

Individual management.

Rx of NGB

Bladder

Urethra

All Rx either All Rx either ΔΔ urethral or urethral or ΔΔ bladder pressure or both bladder pressure or both

Lesions above the ponsCVA, brain tumor, etc.

Usually:

Clinical presentation:1. frequency/urgency2. incontinence3. usually normal upper tracts

Urodynamics:1. detrusor overactivity2. synergic sphincters3. normal sensation4. normal emptying

Treatment: Lesions above pons

Strategy: Reduce detrusor overactivity Sphincters are OK usually

Management: Behavioral modification Antimuscarinics Sacral neuromodulation Botulinum toxin A Augmentation cystoplasty

Lesions between pons and sacral spinal cordMS, SCI, transverse myelitis, etc.

Clinical presentation:1. frequency/urgency (if sensation)

-overactivity vs. retention

2. incontinence (+/- awareness)3. beware upper tracts

Urodynamics:1. detrusor overactivity

-sometimes underactivity

2. dyssynergic sphincters3. +/- sensation4. abnormal emptying

Lesions between pons and sacral spinal cordMS, SCI, transverse myelitis, etc.

Strategy: 1. reduce detrusor overactivity (if present) 2. improve emptying (when problematic) 3. reduce storage pressure 4. protect upper tracts

Management: 1. Rx detrusor overactivity (drugs, Botox, etc.) 2. +/- CIC 3. +/- urinary diversion

Autonomic Hyperreflexia (Dysreflexia)

Autonomic Hyperreflexia (Dysreflexia)

THIS IS AN EMERGENCY

Lesions above T6-T8 Occurs after resolution of spinal shock

Often years later Must have viable distal SC

Assoc. with DSD

Autonomic Hyperreflexia(Dysreflexia)

Precipitating factors: Any distention of rectum or LUT LUT instrumentation (UDS) Urinary catheter issue

Tube change Obstructed catheter

• clot retention, etc. Long bone fracture Decubiti GI pathology Sexual activity Other

AH: Treatment

Find and reverse precipitating stimulus

Acute: Parenteral ganglionic blockers α blockers Others

Prophylaxis: Do procedures under spinal or general with careful

monitoring ?????? Nifedipine 10–20 mg orally 30 minutes prior; SL during Chronic α blockade (i.e. terazosin)

Lesions distal to the spinal cordDisc disease, radical pelvic surgery, diabetes etc.

Usually:

Presentation:1. frequency, urgency +/- incontinence2. +/- urinary retention, straining3. upper tracts at risk

Urodynamics:1. detrusor overactivity or underactivity2. impaired compliance, +/- contractility3. normal sensation4. no dyssynergia

Lesions distal to the spinal cordDisc disease, radical pelvic surgery, etc.

Strategy: 1. improve emptying (when problematic)2. reduce storage pressure3. protect upper tracts

Management:1. Rx poor emptying

+/- CIC2. improve compliance

Infrapontine lesions: Chronic Risk Factor

High intravesical storage pressure