Urinary Tract Obstruction
Lecture given:
Objectives
Define the term hydronephrosis and provide a differential diagnosis
Definitions
- Uremia: clinical signs and symptoms seen as a result of renal failure (fluid overload, hyperkalemia, impaired mentation, pericarditis, etc)
- azotemia: elevation of BUN
- Obstructive uropathy: reversible or irreversible renal dysfunction due to effects of impaired urine drainage
- Hydronephrosis: dilation of the renal pelvis and calyces (not the same as obstruction)
Hydronephrosis :
- Can occur with or without obstruction (e.g. vesico-ureteral reflux, megaureter)
- Identify by ultrasound, intravenous pyelogram, CT
List the potential causes of obstructive renal failure
- Congenital - e.g. uretheral pelvic junction obstruction by blood vessel compressing; or due to aperistaltic segment
- Horseshoe kidneys are prone to UPJ and stones
- Acquired
- Benign or Malignant
- Calyceal
- Renal pelvis
- Ureteral (unilateral or bilateral)
- Renal colic: classically described pain associated with acute ureteral obstruction due to an obstructing stone
- Very severe
- Persistent with waves of increasing pain
- Unilateral, begins in flank area and may radiate into the scrotum or labial areas (dermatones T12-L2 "Loin to groin" pain)
- 85% of stones will show up on xray
- Renal colic: classically described pain associated with acute ureteral obstruction due to an obstructing stone
- Bladder outlet
- Urinary retention: inability to void urine; can be acute (painful) or chronic (not painful)
- Most commonly seen in bladder outlet obstructure due to BPH
- Can also occur due to prostate cancer, urethral strictures, neurogenic causes
- Obstructure can cause stones and frequent UTIs
- Intrinsic or extrinsic
Outline the principles of treating obstructive renal failure and post obstructive diuresis
Urinary tract obstruction
- Pathophysiology - Ischemic event causes the renal injury
- results initially in increase in collecting system pressures (from 6-7 to 50-70mmHg)
- renal blood flow (RBF) initially increase due to pre-glomerular vasodilation to maintain GFR
- Persistent elevation in RBF causes shunting of blood to the vasa recta, causing a washout of the countercurrent exchange gradient in the renal medulla. Ability to concentrate urine is lost
- After 6 hours of obstructure, RBC drops below baseline level due to pre-glomerular vasoconstriction, and ureteral pressures fall
- Reduced blood flow produces cellular atrophy (tubular damage)
- It will take 4-6 weeks before long term damage occurs, if there is no infection
Renal impairment
- Pathophysiology
- First derangement is the loss of renal concentrating ability
- Inability to excrete K, and maximally acidifying the urine
- Glomerular function is spared until late
- Eventually, all renal functions (including endocrine) are affected
Factors influencing severity of renal dysfunction
- Degree: Complete or partial obstruction
- Time: >6 weeks of complete obstruction results in irreversible loss of renal function
- 50% or 100%: Unilateral or bilateral
- Infection: Will accelerate nephron loss
Major sequelae
- Loss of renal function
- UTI/sepsis (urine stasis leading to ecoli growth, abx ineffective)
- Stones (stasis, infection)
Diagnosis
- Clinical features
- Flank pain/renal colic (Loin to Groin)
- Urinary retention/overflow incontinence
- Anuria/Oliguira
- Uremia
- Stones
- Recurrent UTI
- Lab investigations
- Elevated BUN & Cr (bilateral ureteral or bladder outlet obstruction)
- Abnormal urinary indices (higher Na than in prerenal or renal causes of AKI)
- Imaging
- Ultrasound: often used to screen
- IVP: CI if SeCr > 200
- Retrograde pyelogram
- Lasix renogram (distinguish dilation from physiologically significant obstruction)
Management
- Supportive care: acid-base, electrolyte balance, dialysis PRN
- Temporizing measures to relieve source of obstruction
- Bypass the cause of obstruction
- Catheter (for bladder outlet obstruction)
- Stent or nephrostomy tube (renal or ureteral obstruction)
- Definitive treatment
- Remove the cause
- BPH - TURP, drugs
- Stone - ESWL (Extracorporeal shock wave lithotripsy), ureteroscopy, percutaneous stone removal
Post obstructive diuresis
- following relief of complete bilateral ureteral or bladder outlet obstruction
- Large volume diuresis
- Usually mild and self-limiting, but may be life threatening
- Causes:
- Impaired Na reabsorption/urinary concentrating ability, retention of urea and water. Upon relieving obstruction, diuresis of excess urea and water, and continued loss of electrolytes and water until concentrating mechanism is regained
- Nephrogenic diabetes insipidus (rare) when DCT doesn't respond to ADH, lead to salt losing nephropathy (water and salt wasting). Very rapid hypovolemia and electrolyte disturbances
- Wash out concentration gradient of the loop of henle by the vasa recta
- Patient is at first volume overloaded, and will try to get rid of water on relief
- Management:
- Hourly monitoring of urine output
- frequent vital signs (esp postural BP - sensitive for picking up dehydration)
- daily weight
- check serum lytes, esp K
- UO may exceed 150cc/h, but most patients able to replenish losses by drinking
- if UO>200cc/h, or if patient not capable of drinking, IV fluid is necessary (IV NS 50% of previous hour UO +/- K)
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page revision: 19, last edited: 27 Apr 2012 02:57