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Pathophysioogy of urinary tract obstruction bassem presentation
1. Dr. Bassem W. Yani ,MD
Diploma of urology, FEBU urology, FCS
Cairo, EGYPT
CONSULTANT UROLOGIST
UTH LUSAKA ZAMBIA
2. Definitions
• Hydronephrosis- Dilation of the renal
pelvis or calyces
• Obstructive uropathy- functional or
anatomic obstruction of urine flow at
any level of the urinary tract
• Obstructive nephropathy- when
obstruction causes function or
anatomic renal damage
3. Prevalence
• 3.1% in autopsy series
• 2-2.5% of children at autopsy
• No gender differences until THE AGE
OF 20 years
– Females are more common 20-60 years
– Males are more common older than 60
years
4. classifications
1/onset :acute or chronic
2/ site: unilateral or bilateral
3/degree : partial or complete
4/aetiology :
mechanical or functional
congenital or acquired
7. Causes of Obstructive Nephropathy
• Bladder and Urethra
Congenital- Posterior
urethral valve,
Neoplastic- Bladder
carcinoma, Prostate
carcinoma, Carcinoma of
urethra, Carcinoma of
penis
Inflammatory- Para
urethral abscess, phimosis
Miscellaneous-Benign
prostatic hypertrophy
Functional Neurogenic
bladder
Metabolic stone bladder or
urethra
Traumatic stricture urethra
8. Global Renal Functional Changes
• Obstruction can affect hemodynamic variables and GFR
Degree of affect depends on extent and severity of
obstruction, whether UUO or BUO, and whether it has been
relieved or not
• GFR= Kf(PGC-PT-PGC)
– Kf glomerular ultrafiltration coeffecient related to the surface
area and permeability of the capillary membrane
– PGC glomerular capillary pressure. Influenced by renal plasma
flow and the resistance of the afferent and efferent arterioles
– PT Hydraulic pressure of fluid in the tubule
-P the oncotic pressure of the proteins in the glomerular capillary
and efferent arteriolar blood
9. Global Renal Functional Changes
• RPF= (aortic pressure-renal venous
pressure)
renal vascular resistance
– Influences PGC
– Constriction of the afferent arteriole
will result in a decrease of PGC and
GFR
– An increase in efferent arteriolar
resistance will increase PGC
10. Hemodynamic Changes with Unilateral
Ureteral Occlusion
Triphasic pattern of renal blood flow and
ureteral pressure changes
1.RBF increases during the first 1-2 hours and
is accompanied by a high PT and collecting
system pressure
2. For another 3-4 hours, the pres. remains
elevated but the RBF begins to decline.
3. 5 hours after obstruction, further decline in
RBF occurs. A decrease in PT and collecting
system pressure also occurs
12. Hemodynamic Changes with Unilateral
Ureteral Occlusion
Alterations in flow dynamics within the
kidney occur due to biochemical and
hormonal changes regulating renal
resistance
Phase I: increased PT is counterbalanced
by an increase in renal blood flow via
net renal vasodilation, which limits the
fall of GFR.
PGE2, NO. Contribute to net renal
vasodilatation early in UUO
13. Hemodynamic Changes with Unilateral
Ureteral Occlusion
Phase II and III- An increase in afferent
arteriolar resistance occurs causing a
decrease RPF. A shift in RBF from the
outer cortex to the inner cortex also
occurs all reducing GFR
Angiotensin II, TXA2, Endothelin - mediators of
the pre-glomerular vasoconstriction during
the 2nd and 3rd phase of UUO
14. Hemodynamic Changes with Bilateral
Ureteral Occlusion
Only a modest increase in RBF lasting 90 min.
followed by prolonged and profound decrease
in RBF that is even more than with UUO
• The intrarenal distribution of blood flow
changes from the inner to the outer cortex
(opposite from UUO)
• Accumulation of vasoactive substances (ANP)
in BUO, contributes to pre-glomerular
vasodilatation and post-glomerular
vasoconstriction
15. Hemodynamic Changes with Bilateral
Ureteral Occlusion
With UUO, these substances would be excreted
by the normal kidney.
• When obstruction is released, GFR and RBF
remain depressed due to persistent
vasoconstriction of the afferent arteriole
The post-obstructive diuresis is much greater
than with UUO
Partial Ureteral Occlusion: Changes in renal
hemodynamics and tubular function are similar
to complete models of obstruction, but it
Develops more slowly
16. Effects of Obstruction on Tubular
Function
• Dys-regulation of aquaporin water channels
in the proximal tubule, thin descending
loop, and collecting tubule. Lead to polyuria
and impaired concentrating capacity
• Sodium Transport
• Potassium and phosphate excretions follow
changes in sodium
• Deficit in urinary acidification
• Magnesium excretion is increased after
release of UUO or BUO
• Changes in pepetide excretion mark renal
damage
17. Cellular and Molecular Changes lead to
Fibrosis and Tubular Cell Death
• Obstruction leads to biochemical, immunologic,
hemodynamic, and functional Kidney's changes
• These changes lead to release of angiotensin II,
cytokines, and growth factors (TGF-B, TNF-a,
NFkB): Some mediators are produced directly
from the renal tubular and interstitial cells. Others
are generated by way of fibroblasts and
macrophages
• Progressive and permanent changes to the kidney
occur:
Tubulointerstitial inflammation, Tubular atrophy
and apoptosis, Interstitial fibrosis
18. Pathologic Changes of Obstruction
Gross Changes
42 hours- Dilation of the pelvis and ureter and
blunting of the papillary tips. Kidney is also
heavier
7days- Increased pelvi-ureteric dilation and the
Parenchyma is edematous
21-28 days- External dimensions of kidneys are
similar but the cortex and medullary tissue is
diffusely thinned
6 weeks- Enlarged, cystic appearing, weighs less
than non-obstructed kidney
Did not see such differences in partially obstruct. kidneys
19. Pathologic Changes of Obstruction
• Microscopic Pathologic Findings
– 42 hours- Lymphatic dilation, interstitial edema,
tubular and glomerular preservation
– 7 days- Collecting duct and tubular dilation,
widening of Bowman’s space, tubular basement
membrane thickening, cell flattening
– 12 days- Papillary tip necrosis, regional tubular
destruction, inflammatory cell response
– 5-6 weeks- widespread glomeular collapse and
tubular atrophy, interstitial fibrosis, proliferation
of connective tissue in the collecting system
20. Compensatory Renal Growth
• Enlargement of the contra lateral
kidney with unilateral advanced
hydronephrosis or renal agenesis
• A reduction in compensatory growth
occurs with age
• An increase in the number of
nephrons or glomeruli does not occur,
despite enlargement
21. Diagnosis
• History:
– Pain, renal colic
– Inability to void effectively
– Alteration in pattern of micturition (anuria,
polyuria, nocturia)
– Abdominal swelling
– Recurrent UTI
– New-onset or poorly controlled hypertension
– History of pelvic radiation
– Recent gynecologic or abdominal surgery
22. • Physical Examination
–Signs of uremia or acidosis
–Peripheral edema, hypertension, signs
of congestive heart failure
–Palpable kidney or bladder
–Enlargement of pelvic organs (eg.
Prostate, uterus)
–Examination of external urethra for
phimosis, meatal stenosis
Diagnosis
24. Diagnosis: Radiological
• Renal US
– Safe in pregnant and pediatric patients
– Good initial screening test
– No need for IV contrast
– May have false negative in acute obstruction (35%)
– Hydronephrosis= anatomic diagnosis
• Can have caliectasis or pelviectasis in an
unobstructed system
– Doppler- measures renal resistive index (RI), an
assessment of obstruction : RI= (PSV-EDV)/PSV
–RI > 0.7 is suggestive elevated resistance to
blood flow suggesting obstructive uropathy
25. • Excretory Urography
– Applies anatomic and
functional information
– disadvantages
1- Limited use in
patients with renal
insufficiency
2- Increased risk of
contrast-induced
nephropathy
3-Cannot use in patients
with contrast allergy
Diagnosis: Radiological
26. •CT
– Most accurate
study to diagnose
ureteral calculi
– More sensitive to
identify cause of
obstruction
• MRI
– Can identify
hydronephrosis but
unable to identify calculi
and ureteral anatomy of
unobstructed systems
– advantages
• Especially accurate with
strictures or congenital
abnormalities
• No contrast
• More safe
Diagnosis: Radiological
27. •voiding urethro cystogram
helpful in diagnosis of stricture urethra
•uroflow meter
Helpful in diagnosis of infra vesicle
obstruction
Diagnosis: Radiological
28. • Nuclear Renography
– Provides functional assessment without contrast
• Obstruction is measured by the clearance
curves
– Tc 99m DTPA- glomerular agent
– Tc 99m MAG3 – tubular agent
– Diuretic renogram- maximizes flow and
distinguishes true obstruction from dilated and
unobstructed
Normal = T ½ < 10 min Indeterminate = T ½ 10-20 min Obstructed T ½ > 20 min
Diagnosis: Radiological
29. Diagnostic Imaging
• Retrograde
Pyelography
– Gives accurate details of
ureteral and collecting
system anatomy
– Good if renal
insufficiency or other
risks for contrast
• Antegrade Pyelography
– Can do if RGP is not
possible and other
imaging doesn’t offer
enough details
30. Diagnostic Imaging
• Whitaker Test
– “True pressure” within the pelvis =
Collecting system pressure – intravesicle presure
• Saline or contrast though a percutaneous
needle or nephrostomy tube at a rate of 10mL/
min
• Catheter in bladder to monitor intravesicle
pressure
– Invasiveness and discordant results limit clinical usefulness
Normal < 15 cm H2O Indeterminate = 15-22 cm H2O Obstruction > 22 cm H2O
31. Management
• Relief of obstruction first followed by
Treatment of the cause of the
obstruction
• Or treatment of the obstruction and
the cause at the same time
• Treatment of the associated conditions
32. Management
• Depend on the following
• 1 /general condition of the patient
• 2 /facilities
• 3 /surgical experience
33. Management
1 relief of the obstruction
Infra vesicle obstruction
immediate Relief of the obstruction (urine
retention ) using urethral Foleys catheter or
supra pubic catheter in cases of
1/ acute urine retention
2/chronic urine retention with:
• impaired kid function
• urine incontinence
• unresolved infection
34. Management
1 relief of the obstruction
Vesicle or supra vesicle obstruction
– End urologic ureteric stents or percutaneous
nephrostomy procedures allow prompt
temporary and occasionally permanent
drainage .it Is mostly indicated in acute BUO
with anurea at the vesicle and supra vesicle
level.
35. Management
2/ Treatment of the cause and relief of
obstructive uropathy ,
We can start to treat the cause of
obstruction together with relief of the
obstruction it self in cases of
1/ partial or complete UUO.
2 / partial BUO .
36. 3/ management of associated
condition
• Pain
• Hypertension
• Urinary tract infection
• Post obstructive duresis
37. Renal Recovery after Obstruction
• Degree of obstruction, age of patient, and
baseline renal function affect chance of
recovery
– Two phases of recovery may occur
• Tubular function recovery
• GFR recovery
• Duration has a significant influence
– Full recovery of GFR seen with relief of acute
complete obstruction
– Longer periods of complete obstruction are
associated with diminished return of GFR
• DMSA scan is predicative of renal recovery
Notes de l'éditeur
Most acute obstructive uropathies are associated with significant pain or the abrupt diminution of urine flow that alerts the clinician to the need for further evaluation and treatment. However, the insidious nature of chronic urinary obstruction requires a careful history and a high index of suspicion, which prompt an appropriate evaluation that may confirm or rule out the presence of obstruction. A large (933 patients) prospective study by de la Rosette et al failed to correlate a wide range of symptoms of lower urinary tract obstruction with bladder outflow studies.Pain secondary to stretching of the urinary collecting system is the most common symptom in acute obstruction. Prevalence of pain is related more to acuity of obstruction than degree of distention. Acute obstruction of the ureter by a calculus commonly results in an excruciating pain, commonly referred to as renal colic. This pain is described as unrelenting, radiating from the flank to lower abdomen and testicles or labia on the affected side.By contrast, pathological processes that slowly obstruct, such as retroperitoneal tumors, are relatively pain free. Prostatic hypertrophy also may be associated with an obstructive uropathy that is relatively painless. It usually is identified when a superimposed acute obstruction occurs with the inability to void effectively; the resultant painful, distended bladder prompts a visit to an emergency physician.Alterations in patterns of micturition often associated with more distal obstructions are early but frequently missed symptoms. Although anuria is dramatic and specific for obstruction, nocturia and polyuria are much more common presenting symptoms associated with renal concentrating defects due to partial obstruction. Bladder outlet obstruction leads to the symptoms of prostatism (eg, frequency, urgency, hesitancy, dribbling, decrease in voiding stream, the need to double void).Acute and chronic renal failures are common complications of urinary obstruction. Obstructive nephropathy should be considered especially in uremic patients without a previous history of renal disease, hypertension, or diabetes.Gross or microscopic hematuria often is associated with renal calculi, papillary necrosis, and tumors, all of which can cause obstruction.Recurrent UTIs should always lead to an investigation for urinary obstruction.New-onset or poorly controlled hypertension secondary to obstruction and increased renin-angiotensin has been reported.Polycythemia secondary to increased erythropoietin production in the hydronephrotic kidney also has been reported.History of recent gynecologic or abdominal surgery can give important clues to the etiology of urinary obstruction.Pediatric patients may present with recurrent infections. Symptoms of voiding dysfunction such as enuresis, incontinence, or urgency should be sought.
Signs of dehydration and intravascular volume depletion can be seen as a result of urinary concentrating defects associated with partial obstruction. Peripheral edema, hypertension, and signs of congestive heart failure from fluid overload may be observed in obstruction from renal failure. Palpable kidney or bladder provides direct evidence of a dilated urinary collection system.Rectal and/or pelvic examination is essential in determining whether enlargement of pelvic organs (eg, prostate, uterus) is a possible source of urinary obstruction. Examination of the external urethra may disclose phimosis or meatal stenosis.