Urology

Obstructive Uropathy

Obstruction is one of the most important obstruction of the urinary tract, since it eventually leads to decompensation of the muscular conduits and back preserve, and atrophy of several parenchyma. Invites infection and stone formation, which cause additional damage and can ultimately end in complete unilateral on bilateral destruction of the kidneys.

Both the level and degree of obstruction are important to an understanding of the pathologic consequences. Any obstruction at a distal to the bladder neck may lead to back preserve affecting both kidneys. Obstruction at a proximal to the urethral orifice leads to cenilateral damage urilene the lesion involves both ureters simultaneously. Complete obstruction leads to rapid decompensation of the system proximal to the side of obstruction, with immediate muscular failure. For example, acute retention occurs if the obstruction is distal to the bladder, and anemia occurs if obstruction involves both ureters. Partial obstruction leads to gradual progressive muscular hypertrophy followed by gradual dilation, decompensation, and hydronephrosis changes. Vericozetezal reflux may develop in some cases.

Etiology

Occupied urinary tract obstruction may be due to inflammatory or traumatic urethral structures, bladder outlet obstruction (benign prostatic hypertrophy , a cancer of the prostate), vesicle tumors, neuropathic bladder, extrinsic ureteral compression (tumor, retroperitoneal fibrosis, on enlarged lymph nodes), ureteral on pelvic stones, ureteral structure, or ureteral or pelvic tumors.

Pathogenesis

            Regardless of its cause, acquired obstruction leads to similar changes in the urinary tract, which vary depending on the security and duration of obstruction.

  1. Ureteral changes: Proximal to the obstruction, the urethra dilates and balloons. A urethral diverticulum may develop, and dilatation and gaping of the prostatic and ejaculatory ducts may occur.
  2. Vertical changes: Early, the dextroses and trifocal thickening and hypertrophy compensate for the outlet obstruction, allowing complete bladder emptying. This change leads to progressive development of bladder tribulation, cellules, saccades, and then, diverticulitis. Subsequently, bladder, decompensation and residual wrine accumulation, there is stretching of the hypertrophic trigone, which appreciable increase ureteral obstruction. This is the mechanic of back preserve on the kidney in the presence of vertical outlet obstruction (while the ureterovesical junction maintains its competence). Catheter drainage of the bladder relieves trigonal stretch and improves drainage from the upper tract.
  3. Ureteral changes: The filet noted change is a gradually progressive increase in ureteral  dietention. This increases ureteral wall stretch, which in turn increases contractile power and produces ureteral hyperactivity and hypertrophy. Because the ureteral musculature runs in an irregular helical pattern, stretching of its muscular elements leads to lengthening as well as widening. This is the start of ureteral decompensation, where tortuosity and dilatation become apparent, These changes progress until the ureter become atonic, with infrequent and ineffective or completely a burst peristalsis.
  4. Pelricaliceal changes: The renal pelvis and calices, being subjected to progressively increasing volume of retained urine, progressively distend. The pelvis first shows evidence of hyperactivity and hypertrophy and then progressive dilatation and atony. The calices show the same changes to a variable degree, depending on whether the renal pelvis is interregnal or extrarenal. On the latter, calicoes dilatation may be minimal in spite of marked pelvis dilatation. On the intrarenal pelvis, calicoes dilatation and srenal parenchymal damage are maximal. The successive phases seen with obstruction are sounding of the fornices-followed by flattening of the papillae and finally cliffing of the minion calices.
  5. Renal parenchymal chages: with progressive pelricaliceal dietention, there is parenchymal compression against the renal capsule, This, plus the more important factor of compression of the arcuate vessels as a result of the expanding dietended calices, results in a marked drop in renal bloodflow. This leads to progressive parenchymal compression and in chemic atrophy. Lateral groups of rephrons and affected more than central ones, leading to patchy atrophy with variable degree of severity. The glomeruli and proximal convoluted tubules suffer moot from this ischemia. Associated with the increased intrapelric pressure, there is progressive dilation of the collecting and distal tubules, with compression and atrophy of tubular cells.

Clinical Findings

  1. Symptoms and signs: The findings vary according to the site of obstruction:

Intravesical obstruction-intravesical obstruction leads to difficulty in initiation of voiding, a weak stream, and a diminished flour rate with terminal driffling. Burning and frequency are common associated symptoms. A distended or thickened bladder wall may be palpable. Urethral incluration of a structure, benign prostatic hypertrophy , or cancer of the prostate may be noted on rectal examination, meatal stenosie and impacted urethral stones are readily diagnosed by physical examination. Supravesical obstruction- Renal pain or renal colic and gastrointestinal symptoms are commonly associated. Supravesical obstruction may be completely asymptomatic when it develops gradually over a period of several weeks or months. An enlarged kidney may be palpable. Costorentebral angle tenderness may be present.

  1. Laboratory Findings: Evidence of coronary infection, hematuria, or crystalluria may be seen, impaired kidney function is noted by elevated blood urea nitrogen and serum creatinine, with the ratio will above the normal 10:1 because of urea reabsorption.
  2. Special Examination

Antegrade urography via percutaneous needle or take nephrostomy is of particular value when the obstructed kidney fails to excrete the radiopaque material on excretory urography. This procedure allows application of the whitaker text, during which fluid is introduced into the renal pelvis at varying rates. The fluid transport can be measured and the degree of obstruction estimated by the use of a preserve monitor.

Ultrasonography-This will reveal the degree of dilatation of the renal pelvis and calices and allows for diagnoses of hydronephrosis in the prenatal period.

Isotope stadice-A technetium to qqm DMSA scan portrays the degree of hydronephrosis, as well as renal function. Use of diuretics during the scan can provide information similar to that obstained with Whitaker text.

CT scan-This may be of value in revealing the degree and site of obstruction as well as the cause in many cases. The use of continual agents will allow estimation of residual renal function.

Complications

The most important complication of urinary tract obstruction is renal parenchyma as a result of back pressure. Obstruction also predisporoses to infection and stone formation, and infection occurring with obstruction leads to rapid kidney destruction.

Treatment

The aim of therapy is relief of the obstruction (e.g., catheterization for relief of acute urinary retention). Surgery is of ten necessary. Simple urethral structure may be managed conservatively by dilation or urethrotomy. However, urethroplasty may be required. Benign prostatic hypertrophy and obstructing bladder tumors require surgical removal.

Impacted stones must wither be removed or bypassed by a catheter if it is thought that they may pass spontaneously, if they do not pass spontaneously, the stone must be removed surgically later.

Ureteral or ureteropelric junction obstruction requires surgical recision and plastic repair, either by ureterovesicoplasty, ureteroureteral anastomosis, bladder flaps to bridge a gap in the lower ureter, transureterourotoral anastomosis, or ureteropyeloplasty. Renal stones may be removed instrumentally via percutaneous nephrostomy or by irrigation through a tube placed directly into the kidney.

Preliminary drainage above the obstruction is sometime needed to improve kidney function occasionally, permanent drainage and diversion loop diversion, or permanent nephrostomy is required. If damage is advanced, nephrostomy mat be indicated.

Prognosis

The prognosis depends on the cause, site, duration, and degree of kidney damage and renal decompensation. In general, relief of obstruction leads to improvement in kidney function except in seriously damaged kidneys, especially those destroyed by inflammatory scaring.

  • Benign Prostatic Hyperplasia
  • Tumors of the testis
  • Uraemia
  • Cystitis, acute pyelonephritic, Urethral Syndrome
  • Kidney Transplantation
  • STD
  • ED
  • TCC
  • RCC
  • Hematuria
  • Renal Ureteral calculi