Surgery Urinary Tract Obstruction Dr.Ali abd Baqi
Classification
according to the :
~cause (congenital or acquired)
~duration (acute or chronic)
~degree (partial or complete)
~level (upper or lower urinary tract)
According to cause
A-congenital anomalies more common in the U.T than any other organ system. (generally
obstructive)
*the common sites of cong. narrowing
- meatal stenosis ,posterior urethral valve
-ectopic ureters, uretrocele,and the ureterovesical & ureteropelvic junctions
~Damage to the sacral roots 2-4 (spina bifida & meningomyelocele)
~vesicoureteral reflux cause both vesical & renal stasis.
B-Acquired causes
numerous & primary or secondary
1-urethral stricture
2-BPH or ca of the prostate
3-vesical tumor
4-local extension of ca. of the prostate or cx.
5-ureteral stones
6-retroperitoneal fibroses or malignant tumor.
7-pregnancy.
~neurogenic dysfuncton –ureterovesical obstruction or reflux.
~sever constipation sp. In children.
According to the level
A-lower tract (urethral stricture)
Ieading to :
• dilation of the urethra.
• The wall of the urethra may become thin
• diverticulum may form.
• periurethral abscess can result.
B- mid tract (BPH)
Stage of compensation:
hypertrophy of detrusor ms. to overcome the urethral resistance.
Complete emptying of the urinary bladder is possible.
*In cystocope, autopsy or surgery we find
A-Trabeculation of the bladder wall
B-cellules normal intravesical pressure 30cm water at the beginning of micturition.
2-3 times as great may be reached by trabeculated
this pressure tend to push mucosa between the superficial ms. bundles, causing the formation of
small pockets (cellules)
C- diverticula.
~diverticula have no ms. wall –unable to expel their content into the bl. efficiently even after
obstruction
removed.
Stage of decompensation
The compensatory power of the bladder musculature varies greatly. One patient with huge
prostatic may have only mild symptoms of another may suffer acute retention and yet have a gland
of normal size
In the face of progressive outlet obstruction, possibly
aggravated by prostatic infection with edema decompensation of the detrusor may occur
C- Upper tract
Ureter
in early (compensation) & reflux
late (decompensation)
–ureteral dilatation & hydronephrosis
~Elongation & tortuosity of ureteral ms.
Kidney
pressure in the renal pelvis normally close to zero.
If its increase (obstruction or reflux) –dilatation of the pelvis & calyces (hydronephrosis) which
depend on duration, degree & site of obstruction.
-the higher the obstruction the greater effect on the kidney.
-intrarenal pelvis all the pressure exerted on parenchyma, while only part of the pressure in
extrarenal pelvis.
-the pelvic ms. Also have compensation & decompensation phases.
Hydronephrotic changes;
1-the earliest changes in the calyces the papilla become flattened, then convex (clubbed).
-the parenchyma; compression atrophy from increase intrapelvic pressure & ischemic atrophy
pressure on arcuate artery.
2-only in unilateral hydronephrosis advance stage of hydronephrotic atrophy seen.
Unlike other secretory organs (which cease secreting when their duct obstructed) the completely
obstructed kidney continue to secret urine
-fluid &soluble substance reabsorbed from the pelvis through the tubule ,lymphatic or venous .
-as unilateral hydronephrosis progress the normal kidney undergo compensatory hypertrophy.
Pathophysiology of urinary tract obstruction
GFR influenced by
-renal plasma flow and the resistances of the afferent and efferent arterioles
-The hydraulic pressure driving fluid into Bowman's space is resisted by the hydraulic pressure of
fluid in the tubule
-the increasing oncotic pressure of the proteins remaining in higher concentration in the late
glomerular capillary
Hemodynamic Changes
A number of vasoactive substances are thought to play a role in the changes in RBF and GFR
occurring with both UUO & BUO
*With UUO,
1-RBF increases during the first 1 to 2 hours and is accompanied by a high tubular pressure
and collecting system pressure because of the obstruction
2-In a second phase lasting 3 to 4 hours, these pressure parameters remain elevated but RBF
begins to decline
3-A third phase beginning about 5 hours after obstruction is characterized by a further decline in
RBF, now paralleled by a decrease in tubular pressure and collecting system pressure
These changes are explained by physical alterations in flow dynamics within the kidney and are
modified by changes in the biochemical and hormonal milieu regulating renal resistance
-increase in tubular pressure would counterbalanced by an increase in RBF related to afferent
arteriolar vasodilation, its likely that both PGE2 and NO contribute to the net renal vasodilation
that occurs early following UUO
-the vasodilation effect of the PGE2could be blocked by NSAIDs, a prostaglandin synthesis inhibitor
*with BUO
The changes with BUO or obstruction of a solitary kidney are different
In contrast to the early robust renal vasodilation with UUO, there is a modest increase in RBF with
BUO lasting approximately 90 minutes followed by a prolonged and profound decrease in RBF that
is greater than that found with UUO
*Although in both cases ureteral and tubular pressure is increased for the first 4 to 5 hours, the
ureteral pressure remains elevated for at least 24 hours with BUO
This difference between the two pathophysiologic conditions has been hypothesized to be due to
an accumulation of vasoactive substances in BUO that could contribute to preglomerular
vasodilation and postglomerular vasoconstriction.
Such substances would not accumulate in UUO as they would be excreted by the contralateral
kidney. Atrial natriuretic peptide (ANP) appears to be one of these substances
Urinary tract obstruction leads to progressive and eventually permanent changes in the structure
of the kidney including the development of tubulointerstitial fibrosis, tubular atrophy and
apoptosis, and interstitial inflammation
Management of urinary tract obstruction
Clinical feature
A-symptom;
1-Lower & mid tract (urethra &bladder)
(Urethral stricture, BPH, neurogenic bl., ca bl,)
The principle symptom are
-hesitancy, weak stream &terminal dribbling.
-hematuria in BPH & ca bladder
-burning micturition &cloudy urine if there is infection.
-Occasionally urine retention.
Upper tract (ureters & kidneys)
Ureteral strictures or stone & renal stone
-Pain in the flank radiating along the course of the ureter,
-gross total hematuria (stone)
-GIT symptom,
-chills, fever, burning micturition & cloudy urine (infection).
-Nausea. vomiting, loss of weight & strength due to uremia (bilat. hydronephroses) .
Signs.
A-lower &mid tract
-induration in the urethra
-DRE atony of anal sphincter, benign or malig. enlargement of the prostate.
-Distended bladder by suprapubic exam.
-Observation of urinary stream afford rough estimate of max. flow rate, accurately measured by
flowmeter.
N 20-25 ml/sec in m. & 25-30 in f.
~A flow rate under 10ml/sec. indicate either obstruction or weak detrusor function.
B- Upper tract
Enlarge kidney may be discovered by palpation or percussion.
Renal tenderness.
Large pelvic mass (tumor, pregnancy).
Laboratory finding.
-microscopic hematuria
-Anemia, secondary to ch. infection or renal f.
-Leukocytosis
-urea-creatinine ratio well above the normal 10:1. (urea is significantly reabsorbed but creatinine is
not)
Diagnostic Imaging
ultrasonography
Safe ,non invasive, cheep, available
Plain film–
calcified body suggest renal or ureteric stone metastasis in the spine
Excretory urograms (EXU)
Limited in those who are at higher risk for developing contrast-induced nephropathy, or those with
history of contrast allergy
Retrograde cystography.
Trabeculation, diverticula, BPH, ca bladder, reflux.
CT & MRI
CT is the most accurate radiologic study for the diagnosis of ureteral calculi
-all urinary calculi can be demonstrated in CT even the radiolucent in KUB film except indinavir
stone
Instrumental exam.
Passage of catheter– stricture, or estimate residual urine.
Cystoscopic inspection of urethra &bladder may reveal the primary cause, retrograde
ureteropyelograms may be obtained
Complications
Stagnation– infection difficult to eradicate.
urea splitting organism (proteus, staph.) cause alkaline urine –stone formation.
Pyonephrosis –severely infected & obstructed
Treatment
A-relief of obstruction: (stone, tumor, stricture)
catheterization, nephrostomy, ureterostomy
or surgery.
B-eradication of infection.
Progx. depend on cause, site, degree, & duration of obstruction. If renal function good obstruction
released, infection treated (excellent)
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