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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

Physical exam in a woman

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

Bladder training programs, from Campbell's

Behavioral management pathways for LUTS, from Campbell's

General non-surgical management of voiding issues

Lifestyle changes

• Weight loss: 8kg loss results in average 58% reduction in SUI
• Fluid management: maintain 1.5L minimum intake, minimize fluids before bed, alter diuretic timing, minimize caffeine intake
• Bowel management: encourage regular BMs and fiber intake, constipation worsens OAB symptoms
• Behavioral training: works on urge suppression, timed voiding

Pelvic floor interventions

• Physical therapy: improvements as long as exercises are continued, work on both relaxation and contraction
• Biofeedback: allows patients to monitor symptoms and responses in real time to understand how to modify and improve their responses, can also use electrostimulation
• Vaginal weights: contract pelvic floor to keep weight inside vagina, use for 10-15min BID

Anti-incontinence devices (pessary)

• Placed transvaginally, variety of shapes/sizes, prevents prolapse and SUI
• Common side effects: discharge, odor
• Rare side effects: vesicovaginal fistula, rectovaginal fistua, erosion, impaction, bleeding
• Contraindications: active infection, severe ulceration, silicone/latex allergy, noncompliance with follow up

Nocturia workup, from Campbell's

Nocturia

Workup

• OSA may cause patients to wake up more frequently and subsequently urinate - treating OSA may treat nocturia
• Nocturia index (Ni): total nocturnal urine volume (including first morning void) divided by maximum voided volume, if > 1 then either nocturia or enuresis occurs
• Nocturnal bladder capacity index: # nocturnal voids minus (Ni-1), if > 0 then nocturia is related to decreased bladder vvolumes
• Nocturnal polyuria: elevated nocturnal urine production with a subsequent daytime decrease, NPi 0.14 if 21-35yo vs 0.34 for > 65yo
• Global polyuria: 24hr UOP > 40mL/kg
• Overnight water deprivation test (OWDT): UOsm expected to be > 800mOsm/kg if no nocturnal water intake (normal secretion of ADH) - normal = primary polydipsia, abnormal = diabetes insipidus
• Renal concentrating capacity test (RCCT): 40ug desmopressin IN or 0.4mg PO and empty bladder, measure uOsm 3-5hrs later, uOsm > 800 indicating central DI, vs < 800 indicating nephrogenic DI

Treatments

• Nocturnal polyuria: minimize fluids 4hr before bed, use compression stockings, use diuretics, treat insomnia
• Desmopressin: consider for nocturnal polyuria, monitor hyponatremia at 7 days, 28 days, and q6mo
• BOO: nocturia improves in 18% with tamsulosin and 32% after TURP (decreases average 1.3 voids/night)
• Patients with most frequent nocturia secondary to severe urgency respond best to medical management

Symptomatic presentation of DUA, from Campbell's

Spectrum of DUA pathophys, from Campbell's

DUA Causes, from Campbell's

Detrusor Underactivity

Presentation/Causes

• Symptoms: similar to BOO - straining, hesitancy, frequency, incontinence, nocturia
• DUA can be myogenic, neurogenic, or both
• Diabetic cystopathy: decreased bladder sensation (neuropathy) + myocyte dysfunction
• Iatrogenic: common after GYN/CR surgery, but most regain function within 1yr
• Rule out underlying neurologic diagnoses
• UDS is only way to definitively diagnose DUA

Treatment

• Behavioral: timed voiding, double voiding
• PFPT: 24% demonstrate improvement
• Valsalva/Crede: not recommended, can lead to prostatic/upper tract reflux
• CIC: preferred over indwelling catheter, offer SPT if unable/unwilling to self-catheterize
• Bethanechol: parasymathomimetic agent, no proven benefit, significant side effects (nausea, bronchospasm, GI distress), rarely cause cardiac arrest, not recommended
• a-blockers: may show some improvement in some patients (~30%)
• Sacral neuromodulation: FDA-approved for non-neurogenic DUA, offer to motivated patients without severe comorbidities
• BOO surgery: no benefit as symptoms are not due to underlying obstruction