2. History
• CNE Essa 7 year old male, presented in ER with complaints of
acute urinary retention for last 12 hours. He was referred from
SIH, where his cystoscopy was done and Right sided DJ stent
was removed.
• According to my patient’s father he was in his general state of
health when he started having fever and abdominal pain in
October 2021 resistant to any medication, he took him to
Mansehra where USG KUB and abdomen was done along with
other essential tests, (documents were missing), and was
referred to PIMS Islamabad for further management. At PIMS
blood work up USG KUB, MCUG, CT Abdomen and KUB was
done.
3. USG KUB
13/10/2021
• Right sided pyonephrosis. With ipsilateral hydroureter.
• Non visualization of left kidney in left renal fossa.
• Retro-hepatic collection.
• Thick walled urinary bladder with internal echoes-cystitis
IV antibiotics were given and treatment was done but there was
no resulotion of the symptoms.
20/10/2021
• Right kidney shows gross dilatation of pelvicalyceal system
with thick internalechoes and renal cortical paper thinning
• Right sided gross pyonephresis
• Cystitis
4. • CT scan was done as well on 20/10/2021
RIGHT KIDNEY: Appears grossly enlarged in size due to gross
dilatation of the pelvicalyceal system with thinning of the renal
cortex predominantly in the upper pole. Cortical thickness
measures 12.5mm of lateral wall in upper pole region Fluid with
CT density of 4-10 HU is noted.
Right kidney measures 206 x 127 x 99mm in (CC x T x AP)
dimension. No stone or mass is noted. Right ureter is dilated and
tortuous throughout its course
Conclusion: Gross right sided hydronephroureter and dilated &
tortuous ureter with thinning of the renal cortex likely due to
reflux disease.
5. • Patient was diagnosed with right solitary kidney and Vesico
ureteric junction obstruction.
• Patient underwent Pyeloplasty and PCN in November at PIMS
and was discharged.
• It got obstructed in December and patient went SIH, and his
nephrostomy was removed and DJ Stenting was done and was
called for follow up after 3 months for removal of DJS and
Ureter reimplantation.
• In March 2022 his DJS was removed and was discharged but
patient again developed acute on chronic urinary retention
and was then referred to PKI for further management.
• We received patient in Acute pain abdomen, vomiting and
nausea and his Cystoscopy+ RPUG+ DJ stenting was done
again on 9th March 2022 and his obstruction was relieved.
6. • On admission baselines investigations were sent and then till
day of discharge his investigations were followed.
• He got discharged on 12th March 2022 and is on follow up in
OPD.
Further Plan is to remove DJS and ureter reimplantation.
7. • On admission baselines investigations were sent and then till
day of discharge his investigations were followed.
10. What is obstructive uropathy?
• Functional or anatomic obstruction of urine flow at any level
of the urinary tract.
• Obstructive nephropathy – when obstruction causes
functional or anatomic renal damage.
• Hydronephrosis – aseptic dilatation of the renal pelvis or
calyces.
11. Prevalence
• 3.1% of autopsy cases
• Until 20 yrs – no gender difference
• 20- 60 yrs – females more common
• >6o yrs – males more common
12. CAUSES
• Acute or chronic – duration
• Congenital or acquired
• Unilateral or bilateral
• Upper tract obstruction and lower tract obstruction – site of
obstruction
• Mechanical or functional
• Intraluminal
• Intramural
• Extra luminal
14. Pathophysiology of obstructive
uropathy
Unilateral ureteral occlusion
• Triphasic pattern of renal blood flow and ureteral pressure
changes
• during first 1-2 hrs - Renal blood flow increases and is
accompanied by a high pressure in tubule and collecting
system
• Another 3-4 hours – the pressures remains elevated but renal
blood flow begins to decline
• 6 hrs – further decline in RBF and decrease in PT and also the
collecting system.
15. • Alterations in flow dynamics within the kidney occur due to
changes in the biochemical and hormonal milieu regulating
renal resistance
• Phase I- The 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 vasodilation early in
UUO
• 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
preglomerular vasoconstriction during the 2nd and 3rd phase
of UUO
16. Hemodynamic Changes with
Bilateral Ureteral Occlusion
• Increase in RBF lasting 90 minutes followed by a 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 that
contributes to preglomerular vasodilation and postglomerular
vasoconstriction
• With UUO, these substances would be excreted by the
normal kidney
• When obstruction is released, GFR and RBF remain depressed
due to persisent vasoconstriction of the afferent arteriole
• The post-obstructive diuresis is much greater than with UUO
17. Partial Ureteral Occlusion
• Changes in renal hemodynamics and tubular function are
similar to complete models of obstruction
• Develop more slowly
• Animal Studies- Difficult to imitate partial obstruction
• 14 days- normal functional recovery
• 28 days- recover 31% of function
• 60 days- recovery 8% of function
18. Effects of Obstruction on
Tubular Function
• Dysregulation of aquaporin water channels in the proximal
tubule, thin descending loop and collecting tubule
• Lead to polyuria and impaired concentrating capacity
• Sodium Transport - Decreased which leads to a role in the
post-obstructed kidney’s impaired ability to concentrate and
dilute urine
• Much greater sodium and water excretion after release of
BUO than UUO
• Thought to be due to the retention of Na, water, urea nitrogen
and increased ANP, all which stimulate a profound natriuresis
19. • Potassium and phosphate excretions follow changes in sodium
• Decreased with UUO
• Increased transiently with BUO in parallel with the massive
diuresis
• Deficit in urinary acidification
• Magnesium excretion is increased after release of UUO or
BUO
• Changes in peptide excretion mark renal damage
20. Pathologic Changes of
Obstruction(porcine model)
• Gross Pathologic Changes
• 42 hours- Dilation of the pelvis and ureter and blunting of
the papillary tips. Kidney also become heavier
• 7days- Increased pelvi-ureteric dilation and weight.
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
21.
22. • 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
23. Compensatory Renal Growth
• Enlargement of the contralateral kidney with unilateral
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
24. 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 is 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
25. Management of Patients with
Obstruction
• 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
26.
27. • Excretory Urography
• Applies anatomic and functional information
• Limited use in patients with renal insufficiency
• Increased risk of contrastinduced nephropathy
• Cannot use in patients with contrast allergy
28. Diagnostic Imaging
• Retrograde Pyelography
• Gives accurate details of ureteral and collecting system
anatomy
• Good if renal insufficiency or other risks for contrast
• Loopogram- use for evaluation of patients with cutaneous
diversions
• Antegrade Pyelography - Can do if RGP is not possible and
other imaging doesn’t offer enough details
29. • 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
30. • Computed Tomography
Most accurate study to diagnose ureteral calculi
More sensitive to identify cause of obstruction
Helpful in surgical planning
• **Preferred initial imaging study in those with suspected
ureteral obstruction
• MRI
Can identify hydronephroureter but unable to identify calculi
and ureteral anatomy of unobstructed systems
• Diuretic MRU can demonstrate obstruction
• Especially accurate with strictures or congential abnormalities
31. • IV gadopentetate-DTPA allows functional assessment of
collecting system while providing anatomic detail
• GFR assessment
• Renal clearance
• Still several limitations in its use
32. Issues in Patient Management
• Hypertension
• Can be caused by ureteral obstruction
• Especially BUO or obstruction of a solitary kidney
• Less common with UUO
• Volume-mediated
• Increased ANP with obstruction which normalizes after
drainage
• Decreased plasma renin activity
33. Renal Drainage
• Endo-urologic or IR procedures allow prompt temporary and
occasionally permanent drainage
• Patients with extrinsic compression causing obstruction have
a high risk of ureteral stent failure
• 42-56.4 % failure rate at 3 months
• 43% failed within 6 days of placement in one study
• High failure rate at even getting placement(27%)
• Stent diameter did not predict risk of failure
• Ultrasound guided percutaneous drainage should be initial
consideration in pregnant patients
Percutaneous placement with suspected pyonephrosis
• Large diameter ureteral stents
34. Post-obstructive Diuresis
• Usually with BUO or solitary kidney
• Urine output > 200ml/hour
• A normal physiologic response to volume expansion and
solute accumulation
• Elimination of sodium, urea, and free water
• Diuresis ends when homeostasis returns
• Pathologic postobstructive diuresis
• Impaired concentating abilility or sodium absorption
• Down regulation of sodium transporters and sodium
reabsorption in the thick ascending loop of Henle
• Increased production and altered regulation of ANP
• Poor response of collecting system to ADH
35. Post-obstructive Diuresis
Monitor those with BUO or UUO in solitary kidney for POD
- Electrolytes, Mg, BUN, Cr
• Intensity of monitoring depends on clinical factors :
• If no signs of POD - If alert, no fluid overload, normal renal function,
normal electolytes then discharge and follow up
• If signs of POD - If alert, able to consume fluids, then continue in-
patient observation, free access to oral fluids, and daily labs until
diuresis resolves (No IV Fluids) •
• If signs of POD and signs of fluid overload, poor renal function,
hypovolemia, then Frequent BP TPR and u.o records, labs q 12 hrs
(or more), urinary osmolarity, restrict oral hydration (Minimal IV
fluid hydration)
• Most have self-limiting physiologic diuresis
• If pathologic diuresis occurs- very intense monitoring is indicated
36. Surgical Therapy
• The goal of surgical intervention is to completely relieve the
urinary tract obstruction.
• The recovery of renal function depends on the severity and
duration of the obstruction.
37. • Lower urinary tract obstruction (bladder, urethra) can be
relieved with the following:
• Urethral catheter – A urethral catheter (size 8F-24F) is a
flexible external catheter that extends from the bladder
through the urethra. – The catheter can be left indwelling, or,
as an alternative, the patient can perform clean intermittent
catheterization.
• – If blood is present at the urethral meatus after pelvic
trauma and suspicion of urethral injury exists, urethral
catheterization is contraindicated.
38. • Suprapubic catheter: If a Foley catheter cannot be passed, a
suprapubic catheter can be placed percutaneously (at the
bedside) or in an open fashion (in the operating room).
• The placement is in the lower anterior abdominal wall,
approximately 2 fingerbreadths above the pubic symphysis
39. • Upper urinary tract obstruction (ureter, kidney) can be
relieved with the following:
• Ureteral stent: A ureteral stent is a flexible tube that extends
from the renal pelvis to the bladder. It can be placed during
cystoscopy to relieve obstruction along any point in the ureter.
A ureteral stent generally needs to be changed every 3
months.
• Nephrostomy tube: A nephrostomy tube is a flexible tube that
is placed through the back directly into the renal pelvis.
40. Warning!
• The following are urologic emergencies that require
immediate attention and intervention:
• Complete urinary tract obstruction
• Any type of obstruction in a solitary kidney
• Obstruction with fever, infection, or both
• Renal failure
• Pain that is uncontrolled with oral medications
• Nausea and vomiting that causes dehydration