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Chapter 93 - Management of Upper Urinary Tract Obstruction (Campbell Walsh Wein Urology)

Explained Simply - All Key Points

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1. What Is Upper Urinary Tract Obstruction?

• Definition: Obstruction is any blockage that impairs urine drainage AND damages kidney function if untreated. Simply having a dilated (wide) ureter or kidney pelvis does NOT always mean there is obstruction - the key is whether kidney function is being harmed.
• Hydronephrosis = swelling/dilation of the kidney due to backed-up urine. It can occur WITH or WITHOUT true obstruction.
• The ureteropelvic junction (UPJ) is the most common site of obstruction (where the kidney meets the ureter).

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2. How Common Is It? (Prevalence)

• Upper urinary tract obstruction is detected much more commonly now due to routine prenatal ultrasound screening.
• In children, UPJ obstruction is the most frequent cause of hydronephrosis.
• Can be congenital (present at birth) or acquired (develops later from stones, tumors, scarring, etc.)

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3. Clinical Presentation - How Do Patients Present?

In Adults:

• Flank pain / colicky pain (sharp, comes in waves, radiates to groin) - classic feature
• Nausea/vomiting with the pain
• Hematuria (blood in urine) - especially if caused by a stone
• Silent obstruction - some patients have no symptoms at all but slowly lose kidney function
• Urinary tract infections (UTI) - recurrent infections can be a clue
• Hypertension (high blood pressure)
• Palpable abdominal/flank mass (especially in children)

In Children:

• Abdominal mass (parents notice swollen abdomen)
• UTI
• Failure to thrive
• Often found on prenatal ultrasound before any symptoms develop

Progressive Renal Dysfunction:

• Obstruction - if left untreated - causes slowly progressive kidney failure even without symptoms
• One of the most important reasons to evaluate and treat even "silent" obstruction

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4. Definition of Obstruction (What Makes It "True" Obstruction?)

• A dilated collecting system (hydronephrosis) does NOT automatically = obstruction
• True obstruction means the blockage is impairing drainage AND causing or likely to cause kidney damage
• Diuresis renography (nuclear scan with a diuretic drug given during the test) is the most widely used way to decide if true obstruction exists
• The half-time (t½): After giving furosemide (a diuretic), if the radiotracer takes >20 minutes to clear half the radioactivity from the kidney = obstructed. 10-20 min = equivocal. <10 min = not obstructed.

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5. Diagnosis and Imaging

Lab Studies:

• Serum creatinine / BUN - assess overall kidney function
• eGFR - estimated glomerular filtration rate, tells you how well kidneys are filtering
• Urinalysis - look for blood, infection, casts
• Fractional Excretion of Sodium (FENa): <1% suggests pre-renal (reduced blood flow to kidney); >1% suggests intrinsic kidney damage or obstruction has already caused tubular injury

Biomarkers (newer research area):

• NGAL, KIM-1, L-FABP, Cystatin C - newer urine biomarkers that can detect kidney injury from obstruction earlier than creatinine
• Still being studied and not yet standard clinical practice

Imaging:

• Ultrasound first - finds hydronephrosis
• CT (non-contrast) if stone suspected
• MAG-3 renography to answer "is this causing real obstruction and how much function is left?"

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6. Pathological Changes of Obstruction (What Happens to the Kidney)

In the Mature (Adult) Kidney:

1. Tubular dilation - the tubules fill up and stretch
2. Tubular atrophy - cells die off
3. Glomerular damage - the filters of the kidney get damaged
4. Interstitial fibrosis - scar tissue replaces normal kidney tissue (irreversible damage)
5. Loss of nephrons - kidney shrinks over time

In the Developing (Fetal/Newborn) Kidney:

• Far more vulnerable to obstruction than adult kidneys
• Obstruction during fetal development disrupts normal kidney growth and differentiation
• Can lead to renal dysplasia (abnormal kidney development - the kidney looks abnormal under microscope)
• The earlier the obstruction occurs during fetal development, the worse the outcome

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7. Tubulointerstitial Fibrosis (The Core of Irreversible Damage)

Inflammatory Cells:

• Macrophages and T-cells invade the obstructed kidney
• These cells release cytokines and growth factors that drive fibrosis

Key Growth Factors and Cytokines:

Emerging Therapies (Research Phase):

• Angiotensin-converting enzyme (ACE) inhibitors - may reduce fibrosis by blocking angiotensin II
• Anti-TGF-β agents - experimental
• These are not yet standard treatment but are an active research area

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8. Hemodynamic Changes (Blood Flow Changes in the Kidney)

With Unilateral Ureteral Obstruction (UUO - one kidney blocked):

• After prolonged UUO, renin-angiotensin system kicks in and causes afferent arteriolar vasoconstriction, reducing GFR
• Blood flow shifts from outer cortex to inner cortex in UUO

With Bilateral Ureteral Obstruction (BUO - both kidneys blocked):

• Modest increase for ~2 hours, then profound and rapid decline
• Blood flow shifts in the opposite direction (toward outer cortex)
• More clinically dangerous because both kidneys are failing

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9. Kidney Tubular Function After Obstruction

Concentrating Ability:

• Obstruction disrupts aquaporin (AQP) water channels - these are the proteins that let the kidney concentrate urine
• AQP2 (the main vasopressin-regulated channel) is markedly reduced after 24 hours of bilateral obstruction
• AQP2 is still 50% below normal even 7 days after the obstruction is relieved
• Result: Post-obstructive polyuria (lots of dilute urine after the blockage is released) - especially after bilateral obstruction

Sodium Handling:

• NHE3 (sodium/hydrogen exchanger) and NaKATPase activity are reduced - kidneys can't reabsorb sodium well
• After relief of bilateral obstruction: kidneys dump large amounts of sodium and water = post-obstructive diuresis
• This diuresis is usually physiological (appropriate) - getting rid of accumulated fluid and solutes
• However, if patient's volume status is not managed, can lead to dangerous dehydration

Managing Post-Obstructive Diuresis:

• Replace half the urine output per hour with IV fluids (typically 0.45% saline)
• Avoid complete replacement (would perpetuate diuresis)
• Monitor electrolytes closely - especially sodium, potassium, bicarbonate

Potassium Handling:

• Obstruction impairs potassium excretion - can cause hyperkalemia (high potassium)
• After relief: potassium handling normalizes, can sometimes cause hypokalemia from excessive loss

Acid-Base:

• Obstruction → Type 4 renal tubular acidosis (hyperkalemic, hyperchloremic metabolic acidosis)
• Mechanism: reduced aldosterone effect in collecting duct

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10. Recovery of Renal Function After Relief of Obstruction

• Duration of obstruction - shorter = more recovery
• Degree/completeness of obstruction - partial vs. complete
• Presence of infection - infected obstruction causes faster and worse damage (pyonephrosis)
• Age - developing kidneys in children are particularly vulnerable but can also be resilient if obstruction relieved early
• Pre-existing kidney disease - baseline function matters

• Complete obstruction of 1 week → significant but largely recoverable function
• Complete obstruction of 2 weeks → ~70% function recovery possible
• Complete obstruction of 4 weeks → ~30% function recovery possible
• Complete obstruction of 6 weeks → minimal function recovery (<10%)
• These are estimates; individual variation is large

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11. Specific Causes of Upper Urinary Tract Obstruction

Intrinsic Causes (inside the urinary tract):

• Urinary stones (calculi) - most common cause of acute obstruction
• Transitional cell carcinoma of the ureter or renal pelvis
• Blood clots - after trauma or kidney procedure
• Fungal bezoars - in immunocompromised patients
• Ureteral stricture - narrowing from previous stone passage, surgery, radiation, or infection (TB, schistosomiasis)
• UPJ obstruction - congenital narrowing at ureteropelvic junction

Extrinsic Causes (outside the urinary tract pressing on ureter):

• Retroperitoneal fibrosis - fibrosis wraps around and compresses ureters
• Pelvic malignancy - cervical, ovarian, prostate, colorectal cancer
• Lymphoma/lymph node metastases
• Aberrant renal vessels crossing UPJ (common cause of congenital UPJ obstruction)
• Pregnancy - right-sided hydronephrosis in pregnancy is normal/physiological
• Aortic aneurysm

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12. Management Principles

Goals of Treatment:

1. Relieve the obstruction
2. Preserve/recover kidney function
3. Treat the underlying cause
4. Prevent complications (infection, sepsis, permanent kidney damage)

Emergency Decompression - When Needed IMMEDIATELY:

• Infected obstructed system (pyonephrosis) - this is a urological emergency
• Bilateral obstruction causing acute kidney injury
• Solitary kidney obstructed
• Uncontrolled pain despite medications
• Urosepsis - infected obstruction causing systemic sepsis

Methods of Decompression:

1. Ureteral Stenting (JJ Stent / Double-J Stent)

• A soft plastic tube placed inside the ureter from the kidney to the bladder
• Done cystoscopically (through the urethra) under anesthesia
• Bypasses the obstruction internally
• Pros: No external tube, patient can go home, good for temporary relief
• Cons: Bladder irritation, urinary frequency, flank discomfort with voiding (stent colic), needs periodic replacement every 3-6 months
• Good for: Stones <10mm likely to pass, strictures, malignant obstruction

2. Percutaneous Nephrostomy (PCN)

• A tube placed through the back/flank directly into the kidney under ultrasound/fluoroscopy guidance
• Drains urine externally into a bag
• Pros: Can be done quickly under local anesthesia, doesn't require patient to go to OR, excellent drainage even in infection
• Cons: External tube, risk of dislodgment, patient discomfort, infection risk
• Preferred in: Septic patients (faster, avoids anesthesia), when stenting fails, after failed retrograde access, need for culture-directed drainage

3. Medical Expulsive Therapy (MET) for Stones

• For ureteral stones ≤10mm: Alpha-1 blockers (tamsulosin 0.4mg daily) relax the ureteral smooth muscle and help stones pass
• NSAIDs for pain management
• Push fluids
• Can observe for 4-6 weeks if no fever, no infection, pain controlled

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13. Specific Management by Cause

UPJ Obstruction (Congenital):

• Anderson-Hynes dismembered pyeloplasty is the gold standard
• Done laparoscopically or robotically (open now uncommon)
• Success rate: ~90-95%
• The narrowed segment is excised and the ureter reconnected to the renal pelvis in a wider anastomosis
• Anterior crossing vessels (crossing renal vessel causing UPJ obstruction) are transposed

• Endoscopic incision of the UPJ stricture
• Can be done retrograde (ureteroscopy) or antegrade (percutaneous)
• Success ~65-75%, lower than pyeloplasty
• Best for: Secondary UPJ obstruction (recurrence after pyeloplasty), where crossing vessels are NOT the cause

Ureteral Stricture:

• Short, benign strictures (<1-2 cm): Endoscopic balloon dilation or endoureterotomy (incision)
• Longer strictures: Ureteral reimplantation, Boari flap, ileal ureter interposition, autotransplantation
• Malignant strictures: Metal stents for palliation; nephrostomy tube

Stone-Related Obstruction:

• <10mm, distal ureter: Medical expulsive therapy (tamsulosin), observe up to 4-6 weeks
• >10mm or proximal: Ureteroscopy with laser lithotripsy (break up stone with laser)
• Large stones in kidney (>2cm): PCNL (percutaneous nephrolithotomy)
• Infected/obstructed stone: EMERGENCY - drain first (PCN or stent), treat infection, THEN elective stone removal

Retroperitoneal Fibrosis:

• Steroids (prednisolone) - first-line to reduce inflammation and fibrosis
• Ureteral stenting - to relieve obstruction while steroids work
• Ureterolysis - surgical freeing of the ureter from the fibrous tissue, often with omentum wrapping to prevent re-encasement
• Biopsy to rule out malignancy (IgG4-related disease is an important cause)

Malignant Obstruction:

• Ureteral stent or nephrostomy for decompression
• Metal ureteral stents have longer patency than plastic stents for malignant obstruction
• Treatment of the underlying cancer is the definitive approach

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14. Special Considerations

Obstruction in Pregnancy:

• Right-sided hydronephrosis is physiological in pregnancy (due to uterus compressing right ureter)
• For symptomatic obstruction (stones) in pregnancy:
  • Conservative first (hydration, safe analgesia)
  • Ureteral stenting or PCN if conservative fails (both are safe)
  • CT avoided; use ultrasound or low-dose X-ray
  • Ureteroscopy is safe in 2nd trimester

Obstruction with Infection (Pyonephrosis):

• Most serious complication of upper tract obstruction
• Can progress to gram-negative urosepsis rapidly
• Treatment: IMMEDIATE drainage (PCN preferred - can be done at bedside/under local) + IV antibiotics
• Do NOT try to instrument the ureter in a septic patient through cystoscopy (manipulation can worsen bacteremia)

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15. KEY POINTS SUMMARY (as listed in the chapter)

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