Eval/treatment of female urinary incontinence Flashcards
Define Urinary Incontinence
Involuntary loss of urine that is objectively demonstrable and is a social or hygenic problem. It has been reported to affect 15-50% women- prevalence increases with age, reaching >50% in elderly in nursing homes
Normal bladder function/phase
- Filling/storage phase + Emptying phase
Filling/Storage
- highly elastic detrusor smooth muscle bundles stretch to keep pressure low as bladder fills. Urethral sphincter under high pressure to maintain constant intra-vesical pressure
- 100 cc volume = first sensation of bladder fullness
- 250 mL - first desire to void (bladder at 1/2 filling capacity)
- 500 cc - max cystometric bladder capacity achieved– strong desire to void and beginning of emptying phase.
- Chose to void: urethral sphincter voluntarily relaxed, pelvic floor relaxes, detrusor contracts —> Micturition
- nl post void residual
Normal Innervation
Lower UT under parasympathetic and sympathetic innervation
- Parasympathetic (Pelvic nerve) from S2-4. Stimulation = detrusor contracts. Anticholinergic drugs reduce bladder pressure/increase capacity
- Sympathetic: fibers from T10-L2 of spinal cord with alpha and beta components. (hypogastric)
- Beta fibers: mainly in detrusor: stimulation relaxes urethra and detrusor.
- alpha mostly in urethra
- beta adrenergic stimulation – relaxes urethra and detrusor
- Pudendal nerve (S2-4) provides motor innervation to striated urethral sphincter
Vaginal axis
Vagina is midline with freedom in distensibility from both bladder and rectum. Attached to sidewall via connective tissue
- connective tissue in lateral to lower 1/3 of vagina attached to fibers of pubococcygeal muscle adn to fibers fixing it to perineal membrane
Urethra and sphincter
Urethra = muscle tube with transitional epithelium; continuous with bladder epithelium internally and vaginal epithelium externally. Smooth muscle mostly longitudinal and oblique – under alpha-adrenergic control (intrinsic sphincter)
External sphincter (rhabdosphincter)= striated muscle surrounding distal 2/3 of urethra; contributes ~50% of total resistance & secondary defense against incontinence. Responsible for urinary flow at end of micturition
3 things holding up pelvic structures (bladder, vagina, urethra)
- Levator Ani
- Arcus tendinous fasciae pelvis
- Endopelvic fascia (pillow on top of hammock)
Steps of Storage phase of urination
Beta receptors on detrusor sense stretch – send message to sacral spinal cord to activate pudendal nerve – constricts external sphincter (alpha)
Hypogastric nerve allows detrusor to relax/expand (beta receptors)
Need higher pressure in urethra than bladder to maintain continent
Neurotransmitters:
- NE and serotonin released
- signals detrusor to relax and urethra to contract
Emptying Phase
controlled by Pontine micturition center
- input from bladder to Pontine center sending message to cerebral cortex to devide if good place to urinate
- Message via hypogastric to detrusor to relax and pudendal nerve relaxes external urethral sphincter –> urination
Neurotransmitters
- ACh released to detrusor to contract
Genuine Stress incontinence
involuntary loss of urine when bladder pressure > urethral pressure
- usually with cough/sneeze
- accounts for almost half of all cases of urinary incontinence
- most commonly accepted theory = urethral hypermobility due to vaginal wall relaxation, displacing bladder neck and proximal urethra downward. When this happens, increased intra-abd pressure from cough/seeze/etc no longer transmitted equally to bladder and proximal urethra. Normal urethral resistance overcome– leakage
- 2nd possible mechanism = intrinsic sphincter deficiency - urethra fails to close in response to increases in intra-abd pressure
SYMPTOMS
- leak occurs in spurt
- usually with predictable activity (laugh, cough, sneeze, jumping jacks)
- Rarely when supine, usually while upright
- leak occurs while intra-abdominal pressure increased
Risk factors
- childbirth, prior UG surgery, pelvic radiation, estrogen deficiency (nenopause) and medications such as diuretics/alpha blockers
Detrusor instability/overactive bladder/urge incontinence
- all characterized by overactive detrusor, usually with strong urge to void and inability to defer voiding
SXS
- urgency
- nocturia
- frequency (nl person:
Mixed incontinence
combo of stress incontinence and detrusor instability
What to ask when working up pt for urinary incontinence
- Type of leakage
- Triggers
- Onset of symptoms
- Severity
- Pad usage
- Impact on quality of life
- Past medical history
- Past surgical history
- Medication
What receptors are on the bladder
M2 and M4 receptor found in bladder and cause detrusor contraction when stimulated
M3 specifically directly evoke bladder smooth muscle contraction, and M2 receptors indirectly reverse sympathetic mediated smooth muscle relaxation
Pharmacology for incontinence
- Antimuscarinic agents usefyl but can antagonize muscarinic receptors on other body parts– side effects (dry mouth, constipation, blurred vision, drowsiness)
- Antispasmodics (oxybutynin, Tolterodine, Fesoterodine)
- Antimuscarinics (trospium, Solifenacin, Darifenacin)
What supports the urethra/holds it in place
– these 2 posterior pubo-urethral ligaments provide suspensory mechanism for urethra and serve to hold it forward close to pubis during stressful conditions
- urethra held in place by 2 systems. Suspended by perineal membrane and its attachment to the pubic bone for most of its length by arched, bilaterally symmetric, anterior, posterior, and intermediate pubo-urethral ligaments