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MANAGEMENT OF UPPER
URINARY TRACT OBSTRUCTION
BABALOLA R N
SENIOR REGISTRAR,
UROLOGY UNIT, OAUTHC, ILE-IFE.
OUTLINE
INTRODUCTION
EPIDEMIOLOGY
AETIOLOGY
PATHOPHYSIOLOGY
CLINICAL FEATURES
DIAGNOSIS
TREATMENT
CONCLUSION
INTRODUCTION
Obstruction to the upper urinary tract, affecting the ureters, renal
pelvis and parenchyma
Could be acute or chronic, complete or incomplete, unilateral or
bilateral
Can result in sequelae like upper tract dilatation, impairment in renal
function, secondary hypertension as well as urinary tract infections
Prompt diagnosis and treatment is needed to preserve renal function
and improve quality of life
EPIDEMIOLOGY
A frequently encountered diagnosis in urology.
However, because of the fact its etiology is varied, reliable cumulative
incidence rates do not exist.
Antenatally hydronephrosis id detectable via ultrasonography and its
incidence is reported to be around 1%
The major cause in adults - intrinsic, intraluminal nephrolithiasis and
urolithiasis
CLASSIFICATION
Congenital vs acquired
Intraluminal vs extrinsic
Proximal vs distal
Unilateral vs bilateral(incl. solitary kidney)
AETIOLOGY
PATHOPHYSIOLOGY
EFFECT OF URETERIC OBSTRUCTION ON
URETERIC FUNCTION
Normal Pyelo-ureteric Peristalsis
Mechanisms poorly understood
During low urine output, renal pelvic contractions outnumber ureteric
contraction
During diuresis, renal pelvis contractility instigates myogenic transfer
of action potentials to the ureteric muscularis, leading to coordinated
pelvic/ureteric contractions
It is currently believed that the primary oscillator of ureteric
peristalsis is renal pelvic urine volume and its effect on pyelo-ureteric
pacemaker activity
Pacemaker coordination of pyelourteric peristalsis has been
suggested to depend primarily on the activity of atypical smooth
muscle cells and interstitial cells of Cajal-like cells which predominate
in the renal pelvis, have a low depolarization threshold and act to
drive depolarization (and peristalsis) in naturally more refractory
typical smooth muscle cells
OBSTRUCTIVE NEPHROPATHY
Animal models
With complete obstruction comes associated urinary pooling which,
in combination with changes in ureteric contractility, gives rise to
retrograde pressure transfer to the proximal kidney and
hydronephrosis
With increasing time post obstruction, the kidney becomes swollen
because of pooling of urine proximal to the site of obstruction. As the
renal pelvis expands, the renal parenchyma becomes affected.
Flattening of the renal papilla and back filling of the collecting system
occurs. This leads to compression of the renal cortex causing the
characteristic cortical thinning observed in obstruction
Unilateral obstruction:triphasic
Renal blood Collecting system Comment
flow pressure
1 Afferent arteriolar
0 90 min
vasodilation
(6.5 to 70 mmHg)
2 Afferent and
90 min 5h
Efferent arteriolar
(by 40 70%) vasoconstriction
(remains elevated)
3 Collecting system
5 18h
dilatation
Pyelotubular
reflux
(continued (towards resting)
Pyelovenous reflux
decrease)
Pyelolymphatic
reflux
UNILATERAL UUO
Phase I (0-90 mins).
Pre-glomerular vasodilatation
Increased RBF in response to increased ureteral pressure.
Phases II and III
Post-glomerular vasoconstriction, then pre- and post-glomerular
vasoconstriction
Phase II (90 mins 4/5 hours) characterised by a fall in RBF with a
continued rise in ureteral pressure. Due to post-glomerular
vasoconstriction. Further attempt by kidney to maintain GFR.
UNILATERAL UUO
Phase III (5 hours+)
Drop in RBF and ureteral pressure.
By 24 hours tubular pressure and ureteral pressure fall to 30% and
50% of control values respectively.
Vaso-constrictive mediators in Phase II and III:
o Eicosanoids, TXA2 and TXB2, Renin/ Angiotensin II
Decreased GFR due to
Reduced single-nephron renal blood flow and
Shunting of blood from outer to inner cortex, decreasing the total number of
perfused glomeruli.
Mechanism of shunting. Increased production of renin witnessed in outer vs.
inner cortex.
Fall in ureteral pressure due to;
Reduced GFR
Pelvicalyceal dilatation
Pyelolymphatic and pyelovenous backflow
Unilateral obstruction
The contralateral kidney
Compensatory Growth
Response proportional to degree of injury
Initial vasoconstriction, subsequent vasodilation
Hypertrophy
Increased blood flow and GFR
Compensatory growth is age dependent
The number of nephrons remains constant
Increase in proximal tubular length due to increase
in cell size
Bilateral obstruction
Similar to unilateral upper tract obstruction
Less pronounced rise in blood flow initially
Less afferent vasodilation
Lasts 90 mins
More substantial decline in blood flow
Greater vasoconstriction (thought to be due to no renal
clearance of vasoconstrictors from other kidney)
Renal pelvic and ureteric pressures remain raised
for longer, approaching pre-obstruction pressure
at 24 hrs
No other side to compensate
Macroscopic effects on kidney
Dilatation of pelvis/calyxes hydronephrosis
Dilation of ureter
Flattened papillae (42hrs)
Parenchymal oedema (7 days)
Cortical parenchymal thinning (21 days)
Microscopic effects
42 hrs lymphatic dilatation, interstitial oedema
MRI
Can identify
hydronephrosis
No radiation
Useful in the pregnant
patient
Imaging for obstruction
Renogram
A study of the uptake, transit and elimination by the
kidney of an intravenous dose of a radionucleotide
Gives drainage and relative function
Limited anatomical information
Use of diuretic improves discrimination between
obstructed and non-obstructed
Renography
3 phases
DOSE %
Vascular phase,
1 2 3 represents uptake
12 Transit phase, represents
Renal transit through kidney
Elimination phase,
8 Bladder
excretion from the
kidney and expulsion
4
down the ureter
TIME (minutes)
0
10 20 30
131I-Hippuran
in urology