UrinaryTract Obstruction¶

Chapter 331 | Harrison's 22e · Part 9 – Renal & Urinary Tract Disorders · Chapter 331

Key Clinical Points¶

Urinary tract obstruction (UTO) causes stasis and increased pressure, leading to impaired renal function, potential loss of renal mass (atrophy), hypertension, infection, and stone formation.
Acute UTO is characterized by increased renal blood flow and vasodilator-mediated responses; chronic UTO leads to decreased renal blood flow and significant GFR decline.
Postobstructive diuresis occurs upon release of obstruction, posing a risk for severe electrolyte imbalances (Na+, K+, PO43-, Mg2+).
Stone prevention strategies are specific to stone type: Calcium phosphate requires thiazides/alkalies; Uric acid requires alkalinization to pH 6.5; Cystine requires solubility enhancement and high urine volume; Struvite requires infection control.
Diagnostic workup for unexplained renal failure follows a structured logic: bladder catheterization, ultrasound for hydronephrosis, and CT scan to determine site/etiology.
Ureteric obstructions can be congenital (e.g., UPJ/UVJ narrowing, ureterocele) or acquired (e.g., calculi, inflammation, infection, extrinsic compression).
Bladder outlet obstructions include congenital defects (e.g., posterior urethral valves) and acquired issues (e.g., malignancy).

DEFINITION & PATHOPHYSIOLOGY¶

• Urinary Tract Obstruction (UTO): Obstruction to the flow of urine, with attendant stasis and elevation in urinary tract pressure. • Pathophysiological Impact: Impairs renal and urinary conduit functions. • Clinical Consequences: - Acute or chronic kidney disease (obstructive nephropathy). - Potential for permanent loss of renal mass (renal atrophy) and excretory capability. - Increased susceptibility to hypertension, infection, and stone formation.

ETIOLOGY & HEMODYNAMICS¶

Mechanical Causes of Obstruction (Table 331-1)¶

• Ureter: - Congenital: Ureteropelvic junction (UPJ) narrowing or obstruction; Ureterovesical junction (UVJ) narrowing or obstruction and reflux; Ureterocele; Retrocaval ureter. - Acquired Intrinsic: Calculi, Inflammation, Infection. - Acquired Extrinsic: Pregnant uterus; Retroperitoneal fibrosis; Aortic aneurysm; Uterine leiomyomata; Carcinoma of uterus, prostate, bladder, colon, rectum; Lymphoma; Pelvic inflammatory disease, endometriosis; Accidental surgical ligation. • Bladder Outlet: - Congenital: Ureterocele; Posterior urethral valves; Anterior urethral valves; Stricture; Meatal stenosis; Phimosis. - Acquired: Carcinoma of cervix, colon. • Urethra: - Acquired: Trauma.

Hemodynamics of Obstruction (Table 331-2)¶

• Acute Obstruction: - Hemodynamics: ↑ Renal blood flow, ↓ GFR, ↓ Medullary blood flow; ↑ Vasodilator prostaglandins, nitric oxide. - Tubule Effects: ↑ Ureteral and tubule pressures, ↑ Reabsorption of Na+, urea, water. - Clinical Features: Pain (capsule distention), Azotemia, oliguria, or anuria. • Chronic Obstruction: - Hemodynamics: ↓ Renal blood flow, ↓↓ GFR; ↑ Vasoconstrictor prostaglandins. • Release of Obstidence: - Tubule Effects: Slow ↑ in GFR (variable); ↓ Tubule pressure; ↑ Solute load per nephron (urea, NaCl); Natriuretic factors present. - Clinical Features: Postobstructive diuresis; potential for volume depletion and electrolyte imbalance due to losses of Na+, K+, PO43-, Mg2+, and water.

STONE PREVENTION STRATEGIES¶

• Calcium Phosphate: - Risk Factors: Higher urine phosphate; higher pH (≥6.5). Common in distal renal tubular acidosis and primary hyperparathyroidism. - Management: Thiazide diuretics (with sodium restriction) to reduce urine calcium; alkali supplements (potassium citrate or bicarbonate) for low urine citrate; reduction of dietary phosphate. • Uric Acid: - Risk Factors: Persistently low urine pH; higher uric acid excretion. Note: Serum uric acid levels do not reflect urine excretion as they depend on fractional excretion. - Management: Alkalinize urine to target pH 6.5 using potassium-based salts; reduce purine-containing foods; if alkalinization is insufficient, use xanthine oxidase inhibitors (allopurinol or febuxostat) to reduce urine uric acid excretion by 40–50%. • Cystine: - Management: Increase solubility via tiopronin (preferred) or penicillamine; maintain high urine volume. - Note: Use potassium citrate or bicarbonate to achieve a urine pH of 7.5; avoid sodium salts as they may increase cystine excretion. • Struvite: - Characteristics: "Infection stones" or triple phosphate; form in presence of urease-producing bacteria (e.g., Proteus mirabilis, Klebsiella pneumoniae, Providencia species); can grow quickly into staghorn calculi. - Management: Prevention of UTIs.

DIAGNOSTIC APPROACH¶

Initial Step: For unexplained renal failure → Insert bladder catheter.
Assessment of Diuresis:
If Diuresis is present → Obstruction below bladder neck → Urologic evaluation.
If No diuresis → Perform ultrasound.
Evaluation of Hydronephrosis (via Ultrasound):
If Hydronephrosis is present → Perform CT scan to identify site and etiology of obstruction.
Decision based on CT Scan & Clinical Suspicion:
High suspicion (or positive result with high suspicion) → Retrograde urography and ureteral stent considered.
Low suspicion → No further workup for obstruction.
Negative CT but clinical concern remains → Antegrade urography and percutaneous nephrostomy considered.

MANAGEMENT & TREATMENT¶

Immediate Intervention (Obstruction below bladder neck):
Identify obstruction via diuresis check → Urologic evaluation.
Advanced Imaging for High Suspicion:
If CT shows high suspicion of obstruction → Retrograde urography and ureteral stent.
Alternative Intervention for Low Certainty/Negative CT:
If CT is negative but clinical concern remains → Antegrade urography and percutaneous nephrostomy.
Stone Prevention Management:
Uric Acid: Target urine pH 6.5; use potassium-based salts; consider allopurinol/febuxostat if needed.
Cystine: Use tiopronin or penicillamine; maintain high urine volume; target pH 7.5 with potassium citrate/bicarbonate (avoid sodium salts).
Struvite: Focus on prevention of UTIs.

KEY PEARLS & HIGH-YIELD POINTS¶

• Acute vs. Chronic: Acute obstruction involves vasodilation/increased flow; chronic leads to vasoconstriction and significant GFR drop. • Postobstructive Diuresis: High risk of electrolyte loss (Na+, K+, PO43-, Mg2+) upon relief of obstruction. • Uric Acid: Serum uric acid levels do NOT reflect urine excretion because they depend on fractional excretion; use urine pH as the primary indicator. • Struvite Stones: These are "infection stones" that can grow rapidly into staghorn calculi and require complete removal. • Cystine Caution: Sodium salts must be avoided for alkalization in cystinuria to prevent increased cystine excretion.

Reference Tables¶

TABLE 331-1 Common Mechanical Causes of Urinary Tract Obstruction URETER Congenital Ureteropelvic junction narrowing or…¶

Harrison's 22e, p.2454

URETER	BLADDER OUTLET	URETHRA
Congenital
Ureteropelvic junction narrowing or obstruction Ureterovesical junction narrowing or obstruction and reflux Ureterocele Retrocaval ureter	Bladder neck obstruction Ureterocele	Posterior urethral valves Anterior urethral valves Stricture Meatal stenosis Phimosis
Acquired Intrinsic Defects
Acquired Extrinsic Defects
Pregnant uterus Retroperitoneal fibrosis Aortic aneurysm Uterine leiomyomata Carcinoma of uterus, prostate, bladder, colon, rectum Lymphoma Pelvic inflammatory disease, endometriosis Accidental surgical ligation	Carcinoma of cervix, colon Trauma	Trauma

TABLE 331-2 Pathophysiology of Bilateral Ureteral Obstruction¶

Harrison's 22e, p.2455

HEMODYNAMIC EFFECTS	TUBULE EFFECTS	CLINICAL FEATURES
Acute
↑ Renal blood flow ↓ GFR ↓ Medullary blood flow ↑ Vasodilator prostaglandins, nitric oxide	↑ Ureteral and tubule pressures ↑ Reabsorption of Na+, urea, water	Pain (capsule distention) Azotemia, oliguria, or anuria
Chronic
Release of Obstruction
Slow ↑ in GFR (variable)	↓ Tubule pressure ↑ Solute load per nephron (urea, NaCl) Natriuretic factors present	Postobstructive diuresis Potential for volume depletion and electrolyte imbalance due to losses of Na+, K+, PO2–, Mg2+, 4 and water