Section 15.2: Urinary Incontinence, Nephrolithiasis, and GU Trauma

Why This Matters for the PANCE

Urinary incontinence, nephrolithiasis, and genitourinary (GU) trauma are high-yield topics on the PANCE blueprint. The exam frequently tests your ability to distinguish types of incontinence based on history and select the correct initial and long-term treatments. For nephrolithiasis, you must know the unique properties of each stone type, the management pathways dictated by stone size, and the identification of obstructed infections as surgical emergencies. In GU trauma, recognizing the signs of urethral injury and knowing to perform a retrograde urethrogram (RUG) before placing a Foley catheter is a critical safety concept that is heavily tested.

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Urinary Incontinence

Urinary incontinence is the involuntary leakage of urine. It is categorized into four primary types based on pathophysiology and clinical features:

1. Stress Incontinence

• Pathophysiology: Caused by urethral hypermobility (weakness of the pelvic floor muscles and vaginal support) or intrinsic sphincter deficiency (often due to pelvic surgery or trauma). This leads to urine leakage when intra-abdominal pressure exceeds urethral closure pressure.
• Clinical Presentation: Involuntary leakage of urine during activities that increase intra-abdominal pressure, such as coughing, sneezing, laughing, lifting, or exercising.
• Clinical Management:
  • First-line: Pelvic floor muscle training (Kegel exercises) and lifestyle modifications (weight loss, fluid restriction).
  • Devices: Vaginal pessaries or urethral inserts.
  • Surgical: Midurethral sling procedures are the gold standard for refractory cases, providing support to the urethra.

2. Urge Incontinence (Overactive Bladder)

• Pathophysiology: Detrusor muscle overactivity, leading to involuntary detrusor contractions during the bladder filling phase. Often idiopathic, but can be triggered by neurological disorders or bladder irritants.
• Clinical Presentation: A sudden, intense urge to urinate followed by involuntary bladder contraction and immediate leakage. Nocturia and urinary frequency are common.
• Clinical Management:
  • First-line: Bladder training (timed voiding) and lifestyle modifications (avoiding caffeine, alcohol, and carbonated beverages).
  • Pharmacotherapy:
    • Anticholinergics (e.g., Oxybutynin, Tolterodine): Block muscarinic (M3) receptors on the detrusor muscle, preventing contraction. Contraindications: Narrow-angle glaucoma, gastroparesis, and urinary retention. Side effects include dry mouth, constipation, blurry vision, and cognitive impairment (especially in elderly patients).
    • Beta-3 Adrenergic Agonists (e.g., Mirabegron): Relax the detrusor muscle during filling. Contraindications: Severe, uncontrolled hypertension (as it can increase blood pressure). It has a lower incidence of anticholinergic side effects.

3. Overflow Incontinence

• Pathophysiology: Detrusor muscle underactivity (atonic bladder due to neuropathy, such as in diabetes or spinal cord injury) or bladder outlet obstruction (such as BPH, urethral stricture, or pelvic organ prolapse). The bladder becomes chronically distended, and pressure eventually exceeds urethral resistance.
• Clinical Presentation: Continuous dribbling of urine, urinary hesitancy, a weak stream, and a sensation of incomplete emptying.
• Diagnostic Workup: Post-Void Residual (PVR) volume is elevated, typically >200-300 mL.
• Clinical Management:
  • Treat Obstruction: Alpha-blockers or surgical intervention (e.g., TURP) if caused by BPH.
  • Atonic Bladder: Intermittent self-catheterization is the gold standard. Cholinergic agonists (e.g., Bethanechol) can be used to stimulate detrusor contraction.

4. Neurogenic Bladder

• Pathophysiology: Bladder dysfunction caused by neurologic damage.
  • Spastic (Hyperreflexic) Bladder: Caused by upper motor neuron lesions (e.g., spinal cord injury above T12, multiple sclerosis, stroke). The bladder contracts automatically when full, leading to urge incontinence.
  • Flaccid (Atonic) Bladder: Caused by lower motor neuron lesions (e.g., cauda equina syndrome, diabetic neuropathy, spinal cord injury below T12). The bladder fails to contract, leading to overflow incontinence.
• Management: Intermittent catheterization, anticholinergics (for spastic), or bethanechol (for flaccid).

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Nephrolithiasis (Renal Calculi)

Nephrolithiasis is the formation of stones in the urinary tract. The type of stone is determined by urinary pH, solute concentration, and predisposing risk factors.

Kidney Stone Characteristics

• Calcium Oxalate (80% of cases - most common): Radiopaque on X-ray. Crystals are envelope-shaped. Associated with hypercalciuria, hyperoxaluria, dehydration, and acidic/neutral urine. Prevention: Hydration, thiazide diuretics (which decrease urinary calcium excretion).
• Uric Acid (10% of cases): Radiolucent (invisible on plain KUB radiographs; requires CT). Crystals are rhomboid-shaped. Associated with acidic urine (pH <5.5), gout, hyperuricemia, and high-purine diets. Treatment/Prevention: Urine alkalinization with potassium citrate.
• Struvite / Magnesium Ammonium Phosphate (10% of cases): Radiopaque. Crystals are coffin-lid-shaped. Formed in alkaline urine (pH >7.2) caused by urease-producing bacteria (e.g., Proteus mirabilis, Klebsiella). These stones grow rapidly and can fill the renal pelvis, forming staghorn calculi. Management: Surgical removal (percutaneous nephrolithotomy) and antibiotic therapy.
• Cystine (<1% of cases): Faintly radiopaque. Crystals are hexagonal-shaped. Caused by a congenital defect in renal transport of dibasic amino acids (COLA: cystine, ornithine, lysine, arginine). Prevention: Massive hydration, urine alkalinization.

Management by Stone Size

• Stones <5 mm: 80% pass spontaneously.
  • Management: Aggressive oral hydration, NSAIDs (e.g., Ketorolac - first-line for renal colic pain due to reduction of ureteral spasm), and alpha-1 blockers (Tamsulosin) to relax the distal ureteral smooth muscle (medical expulsive therapy).
• Stones 5-10 mm: 50% pass spontaneously.
  • Management: Hydration and tamsulosin. If stone fails to pass in 4-6 weeks, or if there is intractable pain or persistent vomiting, proceed to Shock Wave Lithotripsy (SWL) or Ureteroscopy.
• Stones >10 mm: Highly unlikely to pass spontaneously.
  • Stones 10-20 mm: Treated with ureteroscopy with laser lithotripsy or SWL.
  • Stones >20 mm or Staghorn Calculi: Requires Percutaneous Nephrolithotomy (PCNL) as first-line treatment.
• Urologic Emergency: Any obstructing stone with signs of active infection (fever, chills, pyuria, hemodynamically unstable, or urosepsis) is a surgical emergency. Requires immediate urologic consultation for urgent decompression via retrograde ureteral stenting or percutaneous nephrostomy. Do not attempt lithotripsy or conservative management.

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Genitourinary (GU) Trauma

GU trauma can involve the kidneys, bladder, or urethra, and is classified by the mechanism of injury and anatomical site.

1. Renal Trauma

• Mechanism: Most commonly due to blunt trauma (motor vehicle collisions, falls, sports).
• Clinical Presentation: Flank pain, ecchymosis over the flank (Grey Turner sign), and hematuria (gross or microscopic).
• Diagnostic Workup: CT of the abdomen and pelvis with intravenous contrast (specifically with delayed excretory phase) is the gold standard imaging choice.
• Management: Hemodynamically stable patients are managed conservatively with bed rest and serial hematocrits. Unstable patients or those with expanding hematomas require surgical intervention.

2. Bladder Trauma

• Mechanism: Blunt trauma, often associated with pelvic fractures or direct blows to a distended bladder.
• Types of Rupture:
  • Extraperitoneal Rupture (most common): Rupture of the bladder base or neck. Urine leaks into the pelvic space. Managed conservatively with Foley catheter drainage for 10-14 days.
  • Intraperitoneal Rupture: Rupture of the dome of the bladder (weakest part). Urine leaks into the peritoneal cavity, causing chemical peritonitis. Requires urgent surgical repair.
• Diagnostic Workup: Retrograde cystogram (plain film or CT) demonstrating extravasation of contrast.

3. Urethral Trauma

• Mechanism:
  • Posterior Urethra (membranous/prostatic): Associated with pelvic fractures (shearing forces).
  • Anterior Urethra (bulbous/pendulous): Associated with straddle injuries (e.g., falling astride a fence or bicycle crossbar) or direct trauma.
• Clinical Presentation:
  • Blood at the urethral meatus (most common and classic sign).
  • Inability to void.
  • High-riding prostate on digital rectal exam (posterior injury).
  • Perineal ecchymosis ("butterfly" pattern in anterior injury).
• Critical Diagnostic and Safety Rule:
  • DO NOT place a Foley catheter in a patient with suspected urethral trauma (blood at the meatus, high-riding prostate, pelvic fracture) before obtaining a Retrograde Urethrogram (RUG). Inserting a catheter blindly can convert a partial urethral tear into a complete transection.
  • RUG Findings: Extravasation of contrast confirms urethral injury.
• Management: Suprapubic catheterization to drain the bladder, followed by delayed surgical repair.

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Key Differentiating Features of Incontinence Types

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Classic PANCE Traps & Clinical Pearls

• Urethral Trauma Foley Contraindication: If a trauma vignette describes pelvic fracture, blood at the meatus, or a high-riding prostate, the answer is always Retrograde Urethrogram (RUG), and blindly placing a Foley catheter is a major error.
• Struvite Stone Urease Link: Struvite stones are caused by urease-producing bacteria (Proteus and Klebsiella, NOT E. coli). Urease splits urea into ammonia, raising the urine pH (>7.2) and facilitating magnesium ammonium phosphate precipitation.
• Anticholinergic Glaucoma Contraindication: Never prescribe anticholinergics like oxybutynin for urge incontinence in patients with narrow-angle glaucoma. Blocking muscarinic receptors prevents pupillary constriction, which can precipitate acute angle-closure glaucoma.