FeatureStress IncontinenceUrge Incontinence (Overactive Bladder)Overflow Incontinence
EtiologyMultiparous women (pelvic floor weakness), post-prostatectomy in men.Often idiopathic. Can be associated w/ neurologic d/o (MS, stroke, Parkinson’s).BPH (men), diabetic neuropathy, spinal cord injury, anticholinergic meds.
PathophysiologyUrethral hypermobility or intrinsic sphincter deficiency (ISD). ↑ intra-abdominal pressure > urethral resistance.Detrusor overactivity/instability. Involuntary bladder contractions.Impaired detrusor contractility (underactive bladder) or bladder outlet obstruction (e.g., BPH).
Classic PresentationLeaks small amounts of urine with coughing, laughing, sneezing, lifting. No urge beforehand.Sudden, overwhelming urge to urinate, followed by involuntary loss of a large volume of urine. Associated w/ frequency & nocturia.Constant dribbling, incomplete bladder emptying, weak stream. High post-void residual (PVR) volume.
Dx EvaluationCough stress test: direct observation of leakage from urethra with coughing. Normal/low PVR.Often a clinical diagnosis. Urodynamic studies show detrusor contractions during filling. Normal/low PVR.↑ Post-void residual (PVR) volume on bladder US or catheterization is key finding.
1st Line ManagementPelvic floor muscle exercises (Kegel); lifestyle mods (weight loss).Bladder training (timed voiding); lifestyle mods (↓ caffeine/alcohol).Intermittent or indwelling catheterization to relieve obstruction/retention.
PharmacotherapyLimited role. Pessaries can be used. Surgery (mid-urethral sling) is definitive.Antimuscarinics (e.g., oxybutynin, tolterodine) or β3-agonists (e.g., mirabegron).α-blockers (e.g., tamsulosin) for BPH. Bethanechol for atonic bladder (rarely used).
Buzzwords/Key Differentiators”Leaks when I laugh/cough.""Gotta go NOW!""Constantly wet,” “can’t empty.” High PVR.

Mixed Incontinence: Features of both stress and urge incontinence. Very common, especially in older women. Treatment is directed at the more predominant symptom first.

Functional Incontinence: Patient has normal bladder control but cannot reach the toilet in time due to physical or cognitive impairment (e.g., dementia, severe arthritis). Management involves treating the underlying condition and using scheduled/prompted voiding.

Epidemiology


Etiology

urethritis/vaginitis, Pharmaceutical, Psychiatric causes (especially depression), Excessive urinary output (hyperglycemia, hypercalcemia, CHF), Restricted mobility, Stool impaction.

To remember the reversible causes of acute urinary incontinence, think DIAPPERS: Delirium/confusion, Infection, Atrophic


Classifications

Overflow incontinence

Mechanism

  • Impaired (weak) detrusor contractility
  • Bladder outlet obstruction (e.g., BPH)
  • Both mechanisms can lead to incomplete bladder emptying → bladder overfilling → chronically distended bladder with ↑ bladder pressure → dribbling of urine (leak) when intravesical pressure > outlet resistance

Clinical features

  • Frequent, involuntary intermittent/continuous dribbling of urine in the absence of an urge to urinate
  • Occurs only when the bladder is full
  • Postvoid residual urine volume (seen on ultrasound or with catherization)
    • Assess for urinary retention via bladder scan (≥200 mL) or straight catheterization yielding ≥200 mL urine output.

Treatment

  • Intermittent catheterization: for scheduled bladder emptying
    • Intermittent prevention of catheter-associated UTIs and is favored by most patients; indwelling catheters may be considered if necessary.

Stress incontinence

Epidemiology

Prevalence increases with age.


Etiology

  • Pathomechanism: outlet incompetence
    • Urethral hypermobility: loss of pelvic floor musculature and/or connective tissue support → weak pelvic floor → inability of the urethra to completely close
    • Intrinsic sphincter deficiency
  • Risk factors
    • Multipara
    • Pregnancy and vaginal deliveries
    • High-impact activity (e.g., jumping, running, hopping)
    • Menopause
    • Obesity
    • Smoking
    • Chronic cough (e.g., COPD)
    • Prostate or pelvic surgery

Pathophysiology


Clinical features

  • Physical activity that causes increased intra-abdominal pressure (e.g., laughing, sneezing, coughing, exercising) leads to loss of urine
  • Frequent, predictable, small-volume urine losses with no urge to urinate prior to the leakage

Diagnostics


Treatment

Conservative treatment

  • Kegel exercises
    • Strengthen Levator ani
  • Lifestyle changes (e.g., weight loss, avoiding alcohol and caffeine, smoking cessation)
  • Vaginal pessary

Surgical procedures

  • Indicated if conservative treatment does not provide sufficient improvement of symptoms
  • Procedure of choice: midurethral sling to elevate the urethra

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Urge incontinence

Epidemiology

Prevalence increases with age


Etiology

The condition is caused by sensory or motor dysfunction.

  • Idiopathic (most common)
  • Neurological conditions

Pathophysiology

Inflammatory conditions (e.g., UTI) or neurogenic disorders → sphincter dysfunction, detrusor overactivity, or overactive bladder → autonomous contractions of the detrusor muscle and premature initiation of a normal micturition reflex


Clinical features

  • Urinary urgency: sudden urge to urinate
  • Loss of urine without exertion, with urinary tenesmus → frequent episodes, with variable volumes of urine voided each time

Diagnostics


Treatment

Mnemonic

Oxybutynin treats Overactive bladder.


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Neurogenic bladder dysfunction

Mechanism

detrusor sphincter dyssynergia

  • Simultaneous contractions of the detrusor muscle and involuntary activation of the urethral sphincter → blockage of bladder outlet → small amounts of urine are pressed through the contracted sphincter muscle → high intravesical pressure along with inappropriate contraction of the urethral sphincter
  • Commonly seen in multiple sclerosis and spinal cord injury

Clinical features

  • Voiding and/or storage dysfunction, intermittent voiding, urinary retention
  • Irregular, small volume incontinence without an associated urge to void (sometimes referred to as reflex incontinence)

Total incontinence

Complete loss of sphincter function (due to previous surgery, nerve damage, metastasis) → Urinary leakage occurs at all times


Clinical features


Diagnostics


Treatment

Autonomic & Somatic Innervation

  • Sympathetic (Storage/“Sympathetic Stores”): Hypogastric nerve (T11-L2).
    • Relaxes detrusor muscle (via β3 receptors) → allows filling.
    • Contracts internal urethral sphincter (via α1 receptors) → prevents leakage.
  • Parasympathetic (Peeing/Voiding): Pelvic splanchnic nerves (S2-S4).
    • Contracts detrusor muscle (via M3 receptors) → initiates emptying.
    • Relaxes internal urethral sphincter (via M3 receptors).
  • Somatic (Voluntary Control): Pudendal nerve (S2-S4).
    • Contracts external urethral sphincter (via Nicotinic receptors) → allows voluntary holding of urine.

Overview of pharmacotherapy

Warning

The use of muscarinic agonists may lead to urinary urgency, while the use of sympathomimetics or muscarinic antagonists may lead to urinary retention, especially if there is an untreated outlet obstruction.

Tip

No pharmacological therapies are FDA-approved for stress incontinence; treatment is primarily conservative with surgery.