Urinary Obstruction & Stasis

Urinary Obstruction & StasisGroup 1 3-C

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Classification & Etiology

ClassificationI. Cause

Congenital Acquired

II. Duration Acute Chronic

III. Degree Partial Complete

IV. Level Upper Lower

Congenital Generally cause obstruction

Common sites of narrowing:

External Meatus

Distal Urethra

Posterior Urethral Valves

Ectopic Ureters

Ureteroceles

Ureterovesical Junction

Ureteropelvic Junction

Congenital Damage to Sacral Roots 2 to 4

Spina Bifida

Myelomeningocele

Vesicoureteral Reflux

Acquired Primary

Secondary Stricture – infection

BPH or Cancer of the Prostate

Vesical tumor

Local extension of cancer of prostate or cervix

Metastatic nodes from cancer of prostate or cervix

Ureteral Stone

Retroperitoneal fibrosis or malignant tumor

Pregnancy

Severe Constipation

Pathogenesis & Pathology

Pathogenesis & Pathology Urinary Tract

Lower Tract- Distal to the Bladder

neck

Middle tract

- Bladder Upper Tract

- Ureter and Kidney

Lower Tract (Urethral Stricture)Obstruction

Dilation of the Proximal Urethra

Thinning of Wall or Formation of a Diverticulum

Urinary Extravasation & Periurethral Abscess

↑Hydrostatic Pressure

Infected Urine

Midtract (Prostatic Hyperplasia)I. Stage of Compensation

Bladder musculature hypertrophies for complete emptying (To balance the ↑outlet resistance)

Infection – edema of submucosa, infiltrated with plasma cells, lymphocytes and polymorphonuclear cells

Evidences:

Trabeculation of the bladder wall

Cellules

Diverticula

Changes in the Mucosa

Bladder Musculature Hypertrophy

Trabeculation of the bladder wall• Muscle bundles become taut• Coarsely interwoven appearance• Trigonal muscle & interureteric ridge

hypertrophies and becomes prominent

• ↑ resistance to urine flow resulting to functional obstruction of ureterovesical junctions, back pressure on kidneys & hydroureteronephrosis

• Obstruction ↑ with residual urine

Cellules – small pockets• Trabeculated bladder reaches pressures 2-4 times greater

than normal to force urine past the obstruction• Pushes mucosa between superficial muscle bundles

Diverticula• When cellules force their way

entirely through the musculature of the bladder wall → saccules → diverticula

• Unable to expel contents (no muscle wall)

Mucosa• With Infection – red & edematous• Leading to vesicoureteral reflux

(temporary)• Thin and pale (chronic inflammation)

II. Stage of Decompensation• Less contractile• Weak• Residual urine > 500ml

Upper Tract (Prostatic Hyperplasia)Ureter Early – competent valves

Back Pressure - Dilatation & Hydronephrosis

Residual urine adds stretch to the trigone increasing further the resistance to flow and further hydroureteronephrosis

Secondary to back pressure the muscle thickens in its attempt to push urine downward by ↑ peristaltic activity

Elongaton & Tortuosity

Bands of fibrosis develops

On contraction, they angulate the ureter, thus obstruction

Walls become attenuated & loses contractile powers (decompensation)

Kidneys

Higher obstruction = ↑ effect on kidney

Intrarenal Pelvis

back pressure exerted on parenchyma

Extrarenal Pelvis

only part of the pressure exerted on parenchyma

embedded on FAT & easily dilates

Upper Tract (Prostatic Hyperplasia)

Intrarenal Pelvis

Extrarenal Pelvis

Earliest changes = seen on calyces

Fornices blunt and rounded

Papilla becomes flattened & clubbed

Parenchyma b/w calyces is less affected

Changes in parenchyma are due to:

• Compression atrophy ↑intrapelvic pressure

• Ischemic atrophy from hemodynamic changes (arcuate vessels)

HYDRONEPHROTIC ATROPHY

1

Upper Tract (Prostatic Hyperplasia)

Spotty atrophy

“end arteries”

Ischemia most marked in areas farthest from the interlobular arteries

2

Upper Tract (Prostatic Hyperplasia)

3 Pressure is transmitted up the tubules, becoming dilated & atrophy from ischemia

4 Unilateral= advanced stages

Kidney destroyed; thin walled sac filled with clear fluid or pus

Suppression of renal function as intra-renal pressure ↑

As the intra-pelvic structure approaches the GF pressure (6-12 mmHg): ↓ Urine is secreted

↓GFR

Renal plasma flow concentrating power is gradually lost

↓Urea-Creatinine concentration ratio

Kidney still continue to secrete urine; fluid and soluble substances are reabsorbed in the tubules or lymphatics

Cessation of Filtration:

Safety Mechanism = Break in the surface lining of the collecting structure at the fornices (weakest point) → Pyelointerstitial Backflow*

In unilateraly hydronephrosis, the normal kidney undergoes compensatory hypertrophy of its nephrons (assuming function of diseased kidney)

4 weeks to recover function

Irreversible loss of function can begin as early as 7 days (dilatation and necrosis of proximal tubules)

Physiologic Explanation of Symptoms of Bladder Neck Obstruction

A. Compensation PhaseStage 1 (Stage of Irritability)

Bladder neck and vesical musculature begins to hypertrophyThe force and size of urinary stream still remains normalBladder appears Hypersensitive

In hypertrophied detrussor the contraction is so strong that it virtually goes into spasm causing irritable bladder

Earliest symptoms therefore are: 1. Urgency 2. Frequency

Stage 2 (Stage of Compensation)Further hypertrophy of muscle fibersIn addition to: Urgency + Frequency + HesitancyThere is a loss in the force and size of the urinary stream

the stream becomes slower as vesical emptying nears completion because of exhaustion of the detrusor as it nears the end of the contraction phase

B. Decompensation Phase Stage 1 (Acute Decompansation)

Tone of the compensated vesical muscle is temporarily embarassed Happens when there is : 1. rapid filling of the bladder (high fluid intake)

2. overstretching of the detrusor (postponement of urination though the urge is felt)

There may be: 1. increase difficulty of urination 2. marked hesitancy 3. need for straining to initiate urination 4. residual urine (due to termination of stream before

bladder completely empties)

Stage 2 (Chronic Decompensation) As the degree of obstruction ↑ progressive imbalance between bladder muscle power and urethral resistance occursThere may be: 1. marked difficulty to expel urine

2. amount of residual urine gradually increases 3. functional capacity of the bladder diminishes 4. progressive frequency 5.loss power of contraction & overflow incontinence

Clinical Findings

A. Symptoms: Lower and Midtract (urethra and bladder) obstruction2. Lessened force and size of the stream, and terminal dribbling

1. Hesitancy in starting urination

3. Hematuria 4. Burning on urination 5. Cloudy urine

A. Symptoms: Upper tract ( ureter and kidney) obstruction1. Flank pain radiating along the course of the ureter

2. Gross total hematuria (from stone)

3. Chills, Fever, Burning on urination and cloudy urine

4. Nausea, Vomiting, Loss of weight and strength, and pallor

Palpation of urethra reveal induration about a stricture Rectal examination may show atony of the anal sphincter or

benign or malignant enlargement of the prostate. Urine flowmeter measurement

* flow rate under 10ml/s= indicative of obstruction or weak detrussor function

* flow rate as low as 3-5ml/s= associated with atonic neurogenic bladder or with urethral stricture or prostatic obstruction

B. Signs: Lower and midtract (urethra and bladder) obstruction

Enlarged kidney by palpation or percussion Renal tenderness if infection is present Children with advanced urinary tract obstruction may develop

ascites Rupture of renal fornices= leakage of urine retroperitoneally Rupture of the bladder= urine pass into the peritoneal cavity

through a tear in the peritoneum

B. Signs: Upper tract ( ureter and kidney) obstruction

C. Laboratory Findings

Anemia

Leukocytosis

Microscopic hematuria

Urea-Creatinine ratio well above the normal 10:1

Plain film of the abdomen

D. X- Ray Findings• Excretory urograms

Cystogram

D. X- Ray Findings

• Retrograde cystography

D. X- Ray Findings Retrograde Urography

Exploration of the urethra with a catheter or other instrument is a valuable diagnostic measure. Passage may be blocked by stricture or tumor.

Spasm of the external sphincter may make passage difficult. Passage of the catheter immediately after voiding allows

estimation of the amount of residual urine in the bladder. Measurement of vesical tone by means of cystometry is helpful

in diagnosing neurogenic bladder and in differentiating between bladder neck obstruction and vesical atony.

Inspection of the urethra and bladder by means of cystoscopy and panendoscopy may reveal the primary obstructive agent.

Instrumental Examination

Differential Diagnosis & Symptoms

Obstructive Benign Prostatic Hyperplasia, Pelvic Organ Prolapse

urinary retention,weak stream of urineinterrupted streamblood in the urine

Infectious/ Inflammatory

Acute Prostatitis, Urethritis, Vulvovaginitis

constitutional urinary symptoms,urinary retention, urethral edema, painful urination

Vesicourethral Reflux

Anatomic abnormalities of the urinary tract, Infected Urinary

Tract

almost always asymptomatic unless it has led to a kidney infection (febrile UTI)

Neurologic Spinal Cord Injury, Pelvic Trauma

Severity of symptoms depends on site and extent of lesions

Foreign Body Contraceptive devicesCystitis, Hematuria, Infection, Stone Formation, Colonization causing urinary tract obstruction

ComplicationsInfection

• Stagnation of urine leads to infection, which then may spread throughout the entire urinary sytem

• Often the invading organisms are urea-splitting (proteus, staphylococci)

• Calcium stones precipitate and form kidney or bladder stones

Renal insufficiency

• Both kidneys are affected

Pyonephrosis

• End stage of severy linected obstructed kidney.

• Kidney is functionless and filled with thick pus

• Air urogram is caused by gas liberated by infecting organisms.(plain film of the abdmen)

Treatment

TreatmentA. Relief of Obstruction

B. Eradication of Infection

Relief of Obstruction1. Lower tract obstruction (distal to the bladder)

Correction of obstruction

Patients with minimal secondary renal or ureterovesical damage.

Drainage (eg, loop ureterostomy)

To preserve or improve renal function

Surgical Repair

Significant reflux is demonstrated and does not subside spontaneously after relief of obstruction

Considerable hydronephrosis in addition to reflux

Relief of Obstruction2. Upper tract obstruction (above the bladder)

Drainage

Nephrostomy or ureterostomy

o Tortuous, kinked, dilated, or atonic ureters have developed secondary to lower tract obstruction

Ureteroileal conduito Permanent urinary diversion

Surgery ( Nephrectomy)

If one kidney is irreversibly damaged

Eradication of infection Done after obstruction is removed

Give proper antibiotics to treat the infection

Prognosis No simple statement can be made about the prognosis in this group of

patients.

Outcome depends on the cause, site, degree, and duration of obstruction.

Prognosis is definitely influenced by complicating infection and duration of the inkfection.

If renal function is good, obstrution and oher causes of stasis can be corrected, and if complicating infection can be eradicated, prognosis is generally excellent.

Thank you!