urinary obstruction & stasis
DESCRIPTION
Urinary Obstruction & Stasis. Group 1 3-C Navarro - Nuevo. Classification & Etiology. Classification. Cause Congenital Acquired Duration Acute Chronic Degree Partial Complete Level Upper Lower. Congenital. Generally cause obstruction C ommon sites of narrowing: - PowerPoint PPT PresentationTRANSCRIPT
Urinary Obstruction & StasisGroup 1 3-C
Navarro - Nuevo
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.
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