Normal Bladder Function
CNS voiding components
- Periaqueductal gray (PAG): midbrain, receives stretch signals from bladder, activates PMC
- Pontine micturition center (PMC) aka Barrington's nucleus: stimulates parasympathetics to bladder to initiate voiding
- Onufrowicz's (Onuf's) nucleus: control external urethral sphincter contraction, inhibited by PMC
Neural pathways
- Parasympathetic: S2-S4 nerves travel via pelvic nerve, release acetylcholine to M3 bladder receptors to cause contraction, release NO to stimulate guanylate cyclase in penis and cause erection
- Somatic: S2-S4 nerves travel via pudendal nerve, release acetylcholine to nicotinic sphincter receptors causing contraction and nicotinic penile muscle receptors causing rhythmic contraction/ejaculation
- Sympathetic: T10-L2 nerves travel via hypogastric nerves, release norepinephrine to B3 bladder receptors to cause relaxation, a1 sphincter receptors to cause contraction, a penile receptors to cause detumescence, and a vas/SV receptors to cause emission
Voiding reflexes
- Supraspinal vesicovesical (vesicobulbovesical): bladder stretch receptors, activate PAG, activate PMC, activate parasympathetics, initiate bladder contraction
- Vesicospinalvesical: spinal lesions interrupt the vesicobulbovesical pathway, loss of voluntary control, result in detrusor/sphincteric dyssynergia (DSD)
- Sympathetic storage (pelvic/hypogastric) reflex: bladder stretch receptors, activate L1-L3, inhibits parasympathetic efferents, allows bladder filling
- Somatic storage (pelvic/pudendal) reflex: increased intraabdominal pressure, bladder stretch receptors, activates Onuf's nucleus, stimulates external urethral sphincter contraction to prevent leakage
- Post-stroke: loss of voluntary suppression of PMC results in reflex voiding and urge incontinence
General incontinence evaluation
History
- Precipitating factors: cough, sneeze, laugh, strain, lifting, alcohol/caffeine, constipation
- Severity: degree of bother, pad usage, pad wetness
- Associated voiding symptoms: frequency, urgency, nocturia, weak stream, hesitancy
- Obstetric history: # pregnancies (gravida), results/type of birth (vaginal, C-section, miscarriage/abortion)
- Other GU conditions: stricture, diverticulum, STI, UTI, BPH
- Hx pelvic surgery: hysterectomy, prolapse repair, abdominopelvic resection, prostate surgery, stricture repair
- Neurologic diseases/symptoms: stroke, MS, Parkinson, congenital disorders, weakness/numbness/tingling
- Fluid intake: amount, timing
Reversible incontinence causes (DIAPPERS)
- Delirium: improves once underlying cause removed
- Infection: UTI may not present with classic symptoms in older patients
- Atrophic urethritis/vaginitis: vaginal dryness/friable, treat with estrogen
- Pharmacologic: can be due to irritation or overflow incontinence
- Psychologic: depression or dementia worsen ability to void appropriately
- Excess urine: diuretics, diabetes, peripheral edema
- Restricted mobility: difficulty to reach bathroom in time
- Stool impaction: impairs adequate voiding
Medications that can increase incontinence risks
- Anticholinergics: increase risk for retention and constipation, includes antipsychotics, antidepressants, antihistamines
- Diuretics: increases urine output, includes caffeine and alcohol
- Narcotics: increase retention risk, can cause delirium, cause constipation
- a-agonists: increase sphincter tone leading to retention, includes decongestants and imipramine
- a-antagonists: decrease sphincter tone leading to SUI
- Sedatives: increased delirium risk
- Ca-channel blockers: can impair bladder contraction, leading to retention
- ACE inhibitors: cough side effect can increase SUI
- Alcohol: acts as bladder irritant and diuretic, can also increase risk of delirium and retention
References
- AUA Core Curriculum
- Newman, D. and K. Burgio. "Conservative Management of Urinary Incontinence." Campbell-Walsh Urology 12 (2020).
- Wieder JA: Pocket Guide to Urology. Sixth Edition. J.Wieder Medical: Oakland, CA, 2021.