5. Pathophysiology
High resistance caused by an obstructive
lesion in the urethra or bladder neck,
Detrusor muscle contractions become
stronger to overcome the high resistance
Detrusor muscle contractions become
stronger to overcome the high resistance
Progressive hypertrophy of the
detrusor muscle bundles
Hypertrophied muscle bundles protrude
significantly and are called trabecula
Strong detrusor contractions
Increased
intravesical pressure
Herniation of the bladder
mucosa at these weak points
A diverticulum is a bigger herniation that
extends beyond the bladder wall
A “cellule” is a small herniation
within the bladder wal
Small diverticulum is harmless and
does not require to be removed.
Huge diverticulum is surgically
removed to avoid complications.
6. Cont.Pathophysiology
● A bladder that completely empties its urine content, in spite of
high infravesical resistance, is known as a “Compensated
bladder”.
● A bladder that is chronically fatigued from sustained strong
detrusor contractions against high resistance is known as a
“Decompensated bladder”.
● With incomplete bladder emptying in a decompensated bladder,
“residual urine” starts to collect in the bladder.
.
7. Cont.Pathophysiology
● As the detrusor contractions get weaker, the volume of residual
urine increases progressively.
● In an advanced stage, the volume of residual urine becomes
equal to the bladder capacity. At this stage, urine entering the
full bladder from the ureters escapes involuntarily through the
urethra: “Overflow incontinence”.
● High volumes of residual urine will hinder urine flow from the
ureters to the bladder causing Bilateral hydroureters and
bilateral hydronephroses. If neglected, renal failure and
Uremia occur
8. Diagnosis
● Palpation: a fully distended bladder is felt as a
midline suprapubic swelling
● Cystoscopy: shows bladder trabecula and necks
of bladder diverticula.
● Detection of residual urine:
post-voiding ultrasound of the bladder
post-voiding catheterization
post-voiding cystogram
9. ● Cystogram: shows bladder diverticula.
● Detection of a lesion that caused obstructive uropathy:
e.g. urethral stricture, BPH.
10. SymptomsandTreatment
● Partial obstruction:
the patient can micturate (void), but will experience obstructive urinary
symptoms (hesitancy, difficulty, straining, weak and narrow urine
stream, interruption and bifurcation of the urine stream, terminal
dribbling or sense of incomplete bladder emptying).
The lesion causing the obstruction should be treated to correct the
urine stream.
11. SymptomsandTreatment
● Complete obstruction:
The patient cannot micturate (acute retention).
A filled bladder causes severe suprapubic pain.
Urethral catheterization is required to relieve the retention.
If urethral catheterization fails (e.g. if there is urethral stricture), an
emergency suprapubic cystostomy is done.
At a later stage, the lesion causing the obstruction should be treated to
correct the urine stream.
12. SUPRAVESICALOBSTRUCTIVEUROPATHY
• Ureterocele
• Vesico-ureteric reflux
• Pelvi-ureteric junction
obstruction.
Congenital
lesions
• Stone
• Stricture
• Tumor
Acquired
lesions
• Bladder decompensation and
massive volumes of residual
urine that fill the bladder and
cause back pressure on both
ureters and kidneys.
Neglected
infravesical
uropathy
13. Pathophysiology
● Complete obstruction
Caused by:
o A small stone impacted in the ureter from muscle spasm and edema
o Iatrogenic ligation of the ureter during a difficult hysterectomy or colonic
surgery.
The completely obstructed kidney stops producing urine.
Bilateral complete obstruction of the ureters leads to “obstructive anuria”
14. Pathophysiology
● Partial obstruction
Hydroureter: dilated, elongated and tortuous ureter.
Hydronephrosis: progressive aseptic dilatation of the pelvicalyceal
system with ischemic atrophy of the renal parenchyma. The normal
“cupping” of the calyces turns to “clubbing” (ballooning of the calyces).
In advanced cases, the completely atrophied renal parenchyma becomes
as thin as a paper, and even transparent, with the renal pelvis and calyces
hugely dilated
15. Symptoms
● Renal colic with acute complete obstruction:
The colic is caused by reflex ureteral muscle spasm around the stone.
It is usually severe and may require hospitalization.
● Dull aching renal pain with chronic partial obstruction:
The pain is caused by irritation of the sensory nerves in the renal capsule.
The pain is persistent, and is usually mild to moderate in intensity.
16. Diagnosis
● Detection of the lesion that caused the obstructive uropathy; e.g. stone, tumor or
stricture in the ureter are seen by
○ Ultrasound
○ IVU
○ CT scan.
17. Complications
● In case of acute complete bilateral obstruction:
Obstructive anuria: both kidneys stop producing urine. The patient has no
desire to void and the bladder is empty for more than 24 hours. Acute
progressive uremia develops. It is fatal if the obstruction is not rapidly
relieved
● In case of neglected partial chronic obstruction:
progressive hydroureter and hydronephrosis, up to complete parenchymal
atrophy.
Uremia occurs if partial obstruction is bilateral and neglected.
18. Treatment
● Complete obstruction is an emergency that requires
immediate kidney drainage by introduction of a
ureteric catheter.
● If ureteric catheterization is not technically possible,
percutaneous nephrostomy is done.
● The lesion causing obstruction must be removed to
avoid complications.
19. ● Advanced unilateral hydronephrosis with complete parenchymal
atrophy and renal pain is managed by nephrectomy (only if the
kidney is not functioning and symptomatic)
● Advanced bilateral hydronephroses with complete parenchymal
atrophy and uremia is managed by hemodialysis or renal
transplantation.