Urinary Obstruction & Stasis

1. Urinary Obstruction & Stasis Group 1 3-C Navarro - Nuevo

2. Classification & Etiology

3. Classification • Cause • Congenital • Acquired • Duration • Acute • Chronic • Degree • Partial • Complete • Level • Upper • Lower

4. Congenital • Generally cause obstruction • Common sites of narrowing: • External Meatus • Distal Urethra • Posterior Urethral Valves • Ectopic Ureters • Ureteroceles • Ureterovesical Junction • Ureteropelvic Junction

5. Congenital • Damage to Sacral Roots 2 to 4 • SpinaBifida • Myelomeningocele • Vesicoureteral Reflux

6. Acquired • Primary • Secondary • Stricture – infection • BPH or Cancer of the Prostate • Vesicaltumor • 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

7. Pathogenesis & Pathology

8. Pathogenesis & Pathology • Urinary Tract • Lower Tract - Distal to the Bladder neck • Middle tract - Bladder • Upper Tract - Ureter and Kidney

9. Lower Tract (Urethral Stricture) ↑Hydrostatic Pressure Infected Urine

10. Midtract(Prostatic Hyperplasia) • 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

11. 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

12. 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

13. Upper Tract (Prostatic Hyperplasia) Ureter • Early – competent valves • Back Pressure - Dilatation & Hydronephrosis • Residual urine adds stretch to the trigoneincreasing 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)

14. Upper Tract (Prostatic Hyperplasia) Kidneys • Higher obstruction = ↑ effect on kidney • IntrarenalPelvis • back pressure exerted on parenchyma • ExtrarenalPelvis • only part of the pressure exerted on parenchyma • embedded on FAT & easily dilates Intrarenal Pelvis Extrarenal Pelvis

15. Upper Tract (Prostatic Hyperplasia) HYDRONEPHROTIC ATROPHY 1 • 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)

16. Upper Tract (Prostatic Hyperplasia) 2 • Spotty atrophy • “end arteries” • Ischemia most marked in areas farthest from the interlobular arteries • Pressure is transmitted up the tubules, becoming dilated & atrophy from ischemia • Unilateral= advanced stages • Kidney destroyed; thin walled sac filled with clear fluid or pus • Suppression of renal function as intra-renal pressure ↑ 3 4

17. In unilateralyhydronephrosis, 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) • 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-Creatinineconcentration 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*

19. Physiologic Explanation of Symptoms of Bladder Neck Obstruction

20. A. Compensation Phase • Bladder neck and vesical musculature begins to hypertrophy • The force and size of urinary stream still remains normal • Bladder 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 1 (Stage of Irritability) Stage 2 (Stage of Compensation) • Further hypertrophy of muscle fibers • In addition to: Urgency + Frequency + Hesitancy • There 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

21. B. Decompensation Phase • 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 1 (Acute Decompansation) Stage 2 (Chronic Decompensation) • As the degree of obstruction ↑ progressive imbalance between bladder muscle power and urethral resistance occurs • There 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

22. Clinical Findings

23. 1. Hesitancy in starting urination A. Symptoms: Lower and Midtract (urethra and bladder) obstruction 2. Lessened force and size of the stream, and terminal dribbling 3. Hematuria 4. Burning on urination 5. Cloudy urine

24. Flank pain radiating along the course of the ureter A. Symptoms: Upper tract ( ureter and kidney) obstruction 2. Gross total hematuria (from stone) 3. Chills, Fever, Burning on urination and cloudy urine

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

26. B. Signs: Lower and midtract (urethra and bladder) obstruction • 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 atonicneurogenic bladder or with urethral stricture or prostatic obstruction

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

28. C. Laboratory Findings • Anemia • Leukocytosis • Microscopic hematuria • Urea-Creatinine ratio well above the normal 10:1

29. D. X- Ray Findings • Excretory urograms • Plain film of the abdomen

30. D. X- Ray Findings • Retrograde cystography • Cystogram

31. D. X- Ray Findings • Retrograde Urography

32. Instrumental Examination • 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 vesicalatony. • Inspection of the urethra and bladder by means of cystoscopy and panendoscopy may reveal the primary obstructive agent.

33. Differential Diagnosis & Symptoms

35. Complications • Infection • 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

36. Renal insufficiency • Both kidneys are affected Pyonephrosis • End stage of severylinected 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)

37. Treatment

38. Treatment • Relief of Obstruction • Eradication of Infection

39. Relief of Obstruction • 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

40. Relief of Obstruction 2. Upper tract obstruction (above the bladder) • Drainage • Nephrostomy or ureterostomy • Tortuous, kinked, dilated, or atonic ureters have developed secondary to lower tract obstruction • Ureteroileal conduit • Permanent urinary diversion • Surgery ( Nephrectomy) • If one kidney is irreversibly damaged

41. Eradication of infection • Done after obstruction is removed • Give proper antibiotics to treat the infection

42. 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.

43. Thank you!