URINARY TRACT OBSTRUCTION

Definition of terms Obstructive uropathy Obstructive nephropathy Hydronephrosis Any Structural impedance to the flow of urine anywhere along the tract can be described as obstructive uropathy The term obstructive nephropathy should be reserved for the damage to the renal parenchyma that results from an obstruction to the flow of urine along the urinary tract Hydronephrosis from Greek word hydor (water), nephros (kidney) and osis (condition), and is generally defined as dilatation of the pelvis and calyces regardless of the cause of obstruction. Thus the term obstructive uropathy and hydronephrosis should not be used interchangeably.

Obstruction of the urinary tract can occur during -fetal development, -childhood, or -adulthood. *The point of obstruction can be as proximal as the calyces and as distal as the urethral meatus. * Classification according to the : ~cause (congenital or acquired) ~duration (acute or chronic) ~degree (partial or complete) ~level (upper or lower urinary tract) .

Pathologic consequences: infravesical Level of obstruction supravesical complete Degree of obstruction partial Nature of obstruction infection,injury,stone, tumor…… Duration of obstruction

The conseqences include Incresed intraluminal pressure urinary stasis infection stone formation loss of renal function

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 -external meatus in boys (meatal stenosis) or just inside the external meatus in girls (distal urethral stenosis), posterior urethral valve, urethral stricture. -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 (infection, injury) 2-BPH or ca of the prostate 3-vesical tumor ( bl. neck or ureteric orifices) 4-local extension of ca. of the prostate or cx. 5-ureteral or pelvic stones, tumor or stricture. 6-retroperitoneal fibroses. 7-pregnancy. ~neurogenic dysfuncton –ureterovesical obstruction or reflux. ~sever constipation sp. In children.

According to the level A-lower tract (urethral stricture) Hydrostatic pressure proximal to the obstruction causes dilation of the urethra. The wall of the urethra may become thin, and a diverticulum may form. If the urine becomes infected, urinary extravasation may occur, and periurethral abscess can result. The prostatic ducts may become widely dilated

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. individual muscle bundle taut & give coarsly interwoven appearance to the mucosal surface *the trigon & interureteral ridge hypertrophy & become prominent increase resistant to urine flow in the intravesical ureteral segment--obstruction

the obstruction increase the presence of significant residual urine –further stretch of the ureterotrigonal complex. B-cellules normal intravesical pressure 30cm water at the beginning of micturition. 2-3 times as great may be reached by trabeculated (hypertrophied) bl. In an attempt to force urine past the obstruction. this pressure tend to push mucosa between the superficial ms. bundles, causing the formation of small pockets (cellules)

C- diverticula. If the cellule force their way entirely through the ms. They become saccules, then actual diverticula (embedded in perivesical fat or covered by peritoneum. ~diverticula have no ms. wall –unable to expel their content into the bl. efficiently even after obstruction removed. ~if secondary infection occur difficult to eradicate. ~if its on the anterior wall of the ureter (weakest area) lead to ureterovesical incomptence. (reflux)

Stage of decompensation The compensatory power of the bladder musculature varies greatly. One patient with huge prostatic enlargement may have only mild symptoms of prostatism; 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, resulting in the presence of residual urine after voiding. The amount may range up to 500 mLor more.

C- Upper tract Ureter progressive back pressure on the ureter & kidney by ureteral obstruction in early (compensation) & reflux late (decompensation) –ureteral dilatation & hydronephrosis ~Elongation & tortuosity of ureteral ms. bands of fibrous tissue develop –secondary ureteral obstruction (persist after removal the obstruction)

The causes of hydrocalycosis

The causes of hydronephrosis

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. Which is unusual type of pathologic changes. 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 (pyelointerstitial),lymphatic (pyelolymphatic) or venous (pyelovenous). -as unilateral hydronephrosis progress the normal kidney undergo compensatory hypertrophy. Therefore successful anatomic repair of ureteral obstruction may fail to improve power of waste elimination. *if both kidneys or solitary kidney obstructed strong stimulus exerted to maintain maximum function

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 *Although filtered fluid is not completely free of small proteins, for practical purposes, its oncotic pressure is negligible

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 of obstruction *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

Triphasic pattern of UUO 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 pressures 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

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, lessened force &size of 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. ~A cystometrogram can differentiate between the 2 conditions.

B- Upper tract Enlarge kidney may be discovered by palpation or percussion. Renal tenderness. Large pelvic mass (tumor, pregnancy). Laboratory finding. -microscopic hematuria (infection, stone or tumor), -Anemia, secondary to ch. infection or renal f. -Leukocytosis (infection), -urea-creatinine ratio well above the normal 10:1. (urea is significantly reabsorbed but creatinine is not)

Diagnostic Imaging As the clinical signs and symptoms of obstructive uropathy are so widely variable, prompt and accurate diagnosis is dependent upon appropriate imaging ultrasonography Is the mainstay in evaluation of suspected urinary tract obstruction not associated ionizing radiation, safe in pediatric and pregnant patients. no need for iodinated contrast material, can be utilized in those with azotemia or contrast allergy

Plain film– enlargement of renal shadow, calcified body suggest renal or ureteric stone metastasis in the spine (neuropathic bl.) if they are osteoplastic usually ca. prostate. Excretory urograms (EXU) usually diagnostic but has been gradually supplanted by other modalities should not be performed in subjects with renal insufficiency, 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 because of its speed, safety, and accuracy, this modality has now replaced EXU as an initial imaging study in those with suspected ureteral obstruction, especially in an acute setting such as stone-induced colic 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)