Urinary tract obstrution
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Urinary tract obstruction can cause acute and chronic kidney injury by impairing renal function and urine flow. It has various etiologies like congenital abnormalities, tumors, infections, and trauma. Clinically, it presents with flank pain, azotemia, hypertension, and electrolyte abnormalities. Long-term obstruction leads to structural kidney damage through tubulointerstitial fibrosis and inflammation. Early diagnosis and treatment are important to minimize effects on kidney structure and function.
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Urinary tract obstrution
- 1. URINARY TRACT OBSTRUCTION Dr. Mukesh Sah Because of their damaging effect on renal function, urinary tract obstruction are among the most important of urologic disorders. 2/26/2023 Dr. Mukesh 1
- 2. Objectives â˘Define urinary tract obstruction â˘Incidence â˘Etiology/pathophysiology â˘Clinical presentation â˘Diagnosis â˘Treatment and Management 2/26/2023 Dr. Mukesh 2
- 3. 2/26/2023 Dr. Mukesh 3
- 4. Urine production ⢠Pressure gradient from glomerulus to Bowman capsule ⢠Peristalsis of renal pelvis and ureters ⢠Effects of gravity 2/26/2023 Dr. Mukesh 4
- 5. â˘Normal urine production in an adult is about 1.5-2 L/day. Urine flow depends on 3 factorsâa pressure gradient from the glomerulus to the Bowman capsule, peristalsis of the renal pelvis and ureters, and the effects of gravity (ie, hydrostatic pressure). 2/26/2023 Dr. Mukesh 5
- 6. Urinary tract obstruction ⢠Restricted flow of urine from the kidneys through the urinary tract to the external urethral orifice ⢠Common cause of acute and chronic renal failure ⢠Potentially curable form of kidney disease â˘Obstruction to the flow of urine impairs renal and urinary conduit functions and is a common cause of acute/chronic kidney injury (Obstruction nephropathy) esp if with stasis and elevation of urinary tract pressure. â˘But is potentially curable form if kidney disease so â˘Early dx and prompt therapy are essential to minimize the devastating effects of obstruction on kidney structure and function. 2/26/2023 Dr. Mukesh 6
- 7. Definition of terms ⢠Hydronephrosis- Dilation of the renal pelvis or calyces ⢠Obstructive uropathy- functional or anatomic obstruction of urine flow at any level of the urinary tract ⢠Obstructive nephropathy- when obstruction causes function or anatomic renal damage 2/26/2023 Dr. Mukesh 7
- 8. 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. 2/26/2023 Dr. Mukesh 8
- 9. Incidence â˘Frequency ⢠No data available in unselected populations ⢠20-35% prevalence in large survey among elderly men ⢠3.8% (adults); 2.0% (children) postmortem examinations â˘Sex ⢠No gender difference until 20 years ⢠Women 20-60; Men > 60 ⢠Age ⢠Special considerations in pediatric patients 2/26/2023 Dr. Mukesh 9
- 10. In an autopsy series of 59,064 patients aged 0-80 years ď§ Hydronephrosis - Frequency was 3.1%. ďź Women with uterine prolapse, 5% with first-degree prolapse 40% with third-degree prolapse. Develop during the third to seventh decade of life, secondary to pregnancy and gynecologic malignancies. ďź Men after age 60 years secondary to prostatic obstruction. ďź Children Hydronephrosis is found in of 2-2.5% 2/26/2023 Dr. Mukesh 10
- 11. In an autopsy series of 59,064 patients aged 0-80 years, the frequency of hydronephrosis was 3.1%. In women with uterine prolapse, hydronephrosis occurs in approximately 5% with first-degree prolapse and in 40% with third- degree prolapse. In women, hydronephrosis is more likely develop during the third to seventh decade of life secondary to pregnancy and gynecologic malignancies. In men, hydronephrosis is most likely after age 60 years secondary to prostatic obstruction. Hydronephrosis is found in 2-2.5% of children.ss 2/26/2023 Dr. Mukesh 11
- 12. Etiology â˘Types of obstruction ⢠Mechanical blockade ⢠Intrinsic ⢠extrinsic ⢠Functional defects ⢠Congenital 2/26/2023 Dr. Mukesh 12
- 13. ⢠Obstruction to urine flow can result from intrinsic or extrinsic mechanical blockade as well as from functional defects not associated with fixed occlusion of the urinary drainage system. ⢠Mechanical obstruction can occur at any level of the urinary tract, from the renal calyces to the external urethral meatus. ⢠Normal points of narrowing, such as the ureteropelvic and ureterovesical junctions, bladder neck, and urethral meatus, are common sites of obstruction. ⢠When blockage is above the level of the bladder, unilateral dilatation of the ureter (hydroureter) and renal pyelocalyceal system (hydronephrosis) occur; lesions at or below the level of the bladder cause bilateral involvement. 2/26/2023 Dr. Mukesh 13
- 14. Common Mechanical Causes of Urinary Tract Obstruction Ureter Bladder Outlet Urethra CONGENITAL Ureteropelvic junction narrowing or obstruction Bladder neck obstruction Posterior urethral valves Ureterovesical junction narrowing or obstruction and reflux Ureterocele Anterior urethral valves Ureterocele Damage to S2-4 Stricture Retrocaval ureter Meatal stenosis VUR VUR Phimosis 2/26/2023 Dr. Mukesh 14
- 15. ⢠Childhood causes include congenital malformations, such as narrowing of the ureteropelvic junction and anomalous (retrocaval) location of the ureter. ⢠Vesicoureteral reflux is a common cause of prenatal hydronephrosis and, if severe, can lead to recurrent urinary infections and renal scarring in childhood. ⢠⢠Posterior urethral valves are the most common cause of bilateral hydronephrosis in boys. ⢠Bladder dysfunction may be secondary to congenital urethral stricture, urethral meatal stenosis, or bladder neck obstruction. 2/26/2023 Dr. Mukesh 15
- 16. Ureter Bladder Outlet Urethra Acquired Intrinsic Defects Calculi Benign prostatic hyperplasia Stricture Inflammation Cancer of the prostate Tumor Infection Cancer of the bladder Calculi Trauma Calculi Trauma Sloughed Papillae Diabetic neuropathy Phimosis Tumor Spinal cord disease Blood Clots Anticholinergic drugs and alpha adrenergic antagonists Uric acid crystals 2/26/2023 Dr. Mukesh 16
- 17. ⢠In adults, urinary tract obstruction (UTO) is due mainly to acquired defects. Pelvic tumors, calculi, and urethral stricture predominate. 2/26/2023 Dr. Mukesh 17
- 18. Ureter Bladder Outlet Urethra Acquired Extrinsic Defects Pregnant uterus Carcinoma of cervix, colon Trauma Retroperitoneal fibrosis Trauma Aortic aneurysm Uterine leiomyomata Carcinoma of uterus, prostate, bladder, colon, rectum lymphoma Pelvic inflammatory disease, endometriosis Accidental surgical ligation 2/26/2023 Dr. Mukesh 18
- 19. ⢠Ligation of, or injury to, the ureter during pelvic or colonic surgery can lead to hydronephrosis which, if unilateral, may remain relatively silent and undetected. ⢠Schistosoma haematobium and genitourinary tuberculosis are infectious causes of ureteral obstruction. ⢠Obstructive uropathy may also result from extrinsic neoplastic (carcinoma of cervix or colon) or inflammatory disorders. ⢠Retroperitoneal fibrosis, an inflammatory condition in middle-aged men, must be distinguished from other retroperitoneal causes of ureteral obstruction, particularly lymphomas and pelvic and colonic neoplasms. 2/26/2023 Dr. Mukesh 19
- 20. 2/26/2023 Dr. Mukesh 20
- 21. Pathophysiology ⢠Unilateral (UUO)? ⢠Bilateral (BUO)? ⢠Obstruction relieved or not? ⢠Time 2/26/2023 Dr. Mukesh 21
- 22. Hemodynamic Changes with Unilateral Ureteral Occlusion ⢠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 2/26/2023 Dr. Mukesh 22
- 23. ⢠Alterations in flow dynamics within the kidney occur due to changes in the biochemical and hormonal milieu regulating renal resistance ⢠Phase I- The increased PT is counterbalanced by an increase in renal blood flow via net renal vasodilation, which limits the fall of GFR ⢠PGE2, NO â Contribute to net renal vasodilation early in UUO ⢠Phase II and III- An increase in afferent arteriolar resistance occurs causing a decrease RPF. A shift in RBF from the outer cortex to the inner cortex also occurs all reducing GFR ⢠Angiotensin II, TXA2, Endothelin - mediators of the preglomerular vasoconstriction during the 2nd and 3rd phase of UUO 2/26/2023 Dr. Mukesh 23
- 24. Hemodynamic Changes with Bilateral Ureteral Occlusion ⢠Only a modest increase in RBF lasting 90 minutes followed by a prolonged and profound decrease in RBF that is even more than with UUO ⢠The intrarenal distribution of blood flow changes from the inner to the outer cortex (opposite from UUO) ⢠Accumulation of vasoactive substances (ANP) in BUO that contributes to preglomerular vasodilation and postglomerular vasoconstriction ⢠With UUO, these substances would be excreted by the normal kidney ⢠When obstruction is released, GFR and RBF remain depressed due to persistent vasoconstriction of the afferent arteriole ⢠The post-obstructive diuresis is much greater than with UUO 2/26/2023 Dr. Mukesh 24
- 25. ⢠Only a modest increase in RBF lasting 90 minutes followed by a prolonged and profound decrease in RBF that is even more than with UUO ⢠The intrarenal distribution of blood flow changes from the inner to the outer cortex (opposite from UUO) ⢠Accumulation of vasoactive substances (ANP) in BUO that contributes to preglomerular vasodilation and postglomerular vasoconstriction ⢠With UUO, these substances would be excreted by the normal kidney ⢠⢠When obstruction is released, GFR and RBF remain depressed due to persisent vasoconstriction of the afferent arteriole ⢠The post-obstructive diuresis is much greater than with UUO 2/26/2023 Dr. Mukesh 25
- 26. Summary of UUO and BUO 2/26/2023 Dr. Mukesh 26
- 27. Clinical features ⢠Pain - Acute - steady and continuous, with little fluctuation in intensity, and often radiates to the lower abdomen, testes, or labia (Renal colic) - Chronic - narrowing of the ureteropelvic junction, may produce little or no pain and yet result in total destruction of the affected kidney. Retroperitoneal tumors/ Prostatic hypertrophy also may be associated with an obstructive uropathy are relatively pain free. - Flank pain that occurs only with micturition is pathognomonic of vesicoureteral reflux. 2/26/2023 Dr. Mukesh 27
- 28. Clinical features ⢠Azotemia - excretory function is impaired ⢠bladder outlet obstruction, ⢠bilateral renal pelvic or ureteric obstruction ⢠solitary functioning kidney ďź Complete bilateral obstruction should be suspected when acute renal failure is accompanied by anuria. ďź Anuria is dramatic and specific for obstruction, nocturia and polyuria are much more common presenting symptoms associated with renal concentrating defects due to partial obstruction. ďź Any patient with renal failure otherwise unexplained, or with a history of nephrolithiasis, hematuria, diabetes mellitus, prostatic enlargement, pelvic surgery, trauma, or tumor should be evaluated for UTO 2/26/2023 Dr. Mukesh 28
- 29. Clinical features ďź Wide fluctuations in urine output in a patient with azotemia should always raise the possibility of intermittent or partial UTO which is associated with increase urine ďźPartial bilateral UTO often results in acquired distal renal tubular acidosis, hyperkalemia, and renal salt wasting often accompanied by renal tubulointerstitial damage. ďźUTO must always be considered in patients with urinary tract infections or urolithiasis. Urinary stasis encourages the growth of organisms. Urea-splitting bacteria are associated with magnesium ammonium phosphate (struvite) calculi. 2/26/2023 Dr. Mukesh 29
- 30. Clinical features ďźHypertension is frequent in acute and subacute unilateral obstruction and is usually a consequence of increased release of renin by the involved kidney (Chronic Hydrnephrosis) ďźErythrocytosis, an infrequent complication of obstructive uropathy, is probably secondary to increased erythropoietin production. 2/26/2023 Dr. Mukesh 30
- 31. Consequences of urinary tract obstruction ⢠Reduced glomerular filtration rate ⢠Reduced renal blood flow (after initial rise) ⢠Impaired renal concentrating ability ⢠Impaired distal tubular function ⢠Nephrogenic diabetes insipidus ⢠Renal salt wasting ⢠Renal tubular acidosis ⢠Impaired potassium concentration ⢠Postobstructive diuresis 2/26/2023 Dr. Mukesh 31
- 32. Consequences of urinary tract obstruction ⢠Progressive and permanent changes to the kidney occur ⢠Tubulointerstitial fibrosis ⢠Tubular atrophy and apoptosis ⢠Interstitial inflammation 2/26/2023 Dr. Mukesh 32
- 33. Effects of Obstruction on Tubular Function ⢠Sodium Transport ⢠Decreased which leads to a role in the postobstructed kidneyâs impaired ability to concentrate and dilute urine ⢠Much greater sodium and water excretion after release of BUO than UUO ⢠Thought to be due to the retention of Na, water, urea nitrogen and increased ANP, all which stimulate a profound naturesis ⢠Potassium and phosphate excretions follow changes in sodium ⢠Decreased with UUO ⢠Increased transiently with BUO in parallel with the massive diuresis ⢠Deficit in urinary acidification ⢠Magnesium excretion is increased after release of UUO or BUO 2/26/2023 Dr. Mukesh 33
- 34. Pathophysiology of Bilateral Ureteral Obstruction Hemodynamic Effects Tubule Effects Clinical Features Acute Renal Blood Flow ureteral and tubular pressures pain GFR azotemia Medullary Blood Flow reabsorption of Na, urea, water Oliguria or anuria Vasodilator PGs Chronic Renal Blood Flow medullary osmolarity azotemia GFR concentrating ability hypertension vasoconstrictor PGs Structural damage; parenchymal atrophy ADH-insensitive polyuria renin-angiotensin pdn transport fxn for Na,K, H Hyperkalemic, hyperchloremic acidosis 2/26/2023 Dr. Mukesh 34
- 35. Pathophysiology of Bilateral Ureteral Obstruction Release of Obstruction Slow in GFR (variable) Tubular pressure Postobstructive diuresis solute load per nephron (urea, NaCl) Potential for volume depletion and electrolyte imbalance due to losses of Na, K, PO4, Mg and water Natriuretic factors present 2/26/2023 Dr. Mukesh 35
- 36. Diagnosis ⢠History âPain, renal colic âInability to void effectively (Sx Prostatism) âAlteration in pattern of micturition (anuria, polyuria, nocturia) âRecurrent UTI âNew-onset or poorly controlled hypertension âPolycythemia âRecent gynecologic or abdominal surgery 2/26/2023 Dr. Mukesh 36
- 37. 2/26/2023 Dr. Mukesh 37
- 38. ⢠History âMedication history ⢠Antihistamines, antipsychotics, antidepressants ⢠Ethylene glycol, indinavir, methotrexate, phenylbutazone, or sulfunamides ⢠Methysergide or other natural-occurring ergotamines âOccupational exposure history ⢠Textile manufacturers, shipyard workers, roofers or asbestos miners (retroperitoneal fibrosis) ⢠Textile workers, rubber manufacturing workers, leather workers, painters, hairdressers, drill press workers (bladder cancer) 2/26/2023 Dr. Mukesh 38
- 39. ⢠Physical Examination ⢠Signs of dehydration and intravascular volume depletion ⢠Peripheral edema, hypertension, signs of congestive heart failure ⢠Palpable kidney or bladder ⢠Enlargement of pelvic organs (eg. Prostate, uterus) ⢠Examination of external urethra for phimosis, meatal stenosis 2/26/2023 Dr. Mukesh 39
- 40. Management of Patients with Obstruction Diagnostic Imaging ⢠Renal US ⢠Safe in pregnant and pediatric patients ⢠Good initial screening test ⢠No need for IV contrast ⢠May have false negative in acute obstruction (35%) ⢠Hydronephrosis â anatomic diagnosis ⢠Can have caliectasis or pelviectasis in an unobstructed system ⢠Doppler- measures renal resistive index (RI), an assessment of obstruction ⢠RI= (PSV-EDV)/PSV ⢠RI > 0.7 is suggestive elevated resistance to blood flow suggesting obstructive uropathy 2/26/2023 Dr. Mukesh 40
- 41. Diagnostic Imaging ⢠Excretory Urography ⢠Applies anatomic and functional information ⢠Limited use in patients with renal insufficiency ⢠Increased risk of contrast-induced nephropathy ⢠performed in patients with a normal creatinine value (<1.5 mg/dL) for visualization of the upper urinary tract. ⢠Cannot use in patients with contrast allergy 2/26/2023 Dr. Mukesh 41
- 42. Diagnostic Imaging ⢠Retrograde Pyelography ⢠Gives accurate details of ureteral and collecting system anatomy ⢠Good if renal insufficiency or other risks for contrast ⢠Loopogram- use for evaluation of patients with cutaneous diversions ⢠Antegrade Pyelography ⢠Can do if RGP is not possible and other imaging doesnât offer enough details 2/26/2023 Dr. Mukesh 42
- 43. Diagnostic Imaging â˘Whitaker Test ⢠âTrue pressureâ within the pelvis = Collecting system pressure â intravesicle presure ⢠Saline or contrast though a percutaneous needle or nephrostomy tube at a rate of 10mL/ min ⢠Catheter in bladder to monitor intravesicle pressure ⢠Invasiveness and discordant results limit clinical usefulness Normal < 15 cm H2O Indeterminate = 15-22 cm H2O Obstruction > 22 cm H2O 2/26/2023 Dr. Mukesh 43
- 44. Diagnostic Imaging ⢠Nuclear Renography ⢠Provides functional assessment without contrast ⢠Obstruction is measured by the clearance curves ⢠Tc 99m DTPA- glomerular agent ⢠Tc 99m MAG3 â tubular agent ⢠Diuretic renogram- maximizes flow and distinguishes true obstruction from dilated and unobstructed Normal = T ½ < 10 min Indeterminate = T ½ 10-20 min Obstructed T ½ > 20 min 2/26/2023 Dr. Mukesh 44
- 45. Diagnostic Imaging ⢠CT ⢠Most accurate study to diagnose ureteral calculi ⢠More sensitive to identify cause of obstruction ⢠Helpul in surgical planning ⢠**Preferred initial imaging study in those with suspected ureteral obstruction ⢠MRI ⢠Can identify hydro but unable to identify calculi and ureteral anatomy of unobstructed systems ⢠Diuretic MRU can demonstrate obstruction ⢠Especially accurate with strictures or congential abnormalities ⢠IV gadopentetate-DTPA allows functional assessment of collecting system while providing anatomic detail ⢠GFR assessment ⢠Renal clearance ⢠Still several limitations in its use 2/26/2023 Dr. Mukesh 45
- 46. Diagnostic Imaging ⢠Voiding cystourethrography - diagnosis of vesicoureteral reflux and bladder neck and urethral obstruction. Postvoiding films reveal residual urine. ⢠Endoscopic visualization â permits precise identification of lesions involving the urethra, prostate,bladder and urethral orifice. 2/26/2023 Dr. Mukesh 46
- 47. Treatment and management â˘Prehospital Care ⢠Pulmonary edema ⢠Salt and water retention ⢠hypovolemia 2/26/2023 Dr. Mukesh 47
- 48. Treatment and management â˘Emergency department care ⢠Investigate and begin treatment of potentially life- threatening complications ⢠Pulmonary edema ⢠Hypovolemia ⢠Urosepsis ⢠Hyperkalemia 2/26/2023 Dr. Mukesh 48
- 49. Treatment and management ⢠Large PVR = obstruction below the bladder ⢠Fractionating urine removal (?) ⢠Christensen, et al. concluded that fractionating urine removal in bladder obstruction is unjustified ⢠Hematuria and bladder spasm ⢠Gould, et al. : hematuria correlated strongly with degree of bladder wall damage prior to relief of obstruction and not with rate of bladder emptying ⢠Urine should be drained completely and rapidly from an obstructed bladder ⢠Prolonged urine stasis only predisposes to UTI, urosepsis and renal failure 2/26/2023 Dr. Mukesh 49
- 50. Treatment and management ⢠Calculi â most common causes of unilateral ureteral obstruction ⢠90% pass spontaneously (calculi <5.0-7.0 mm) ⢠Surgical drainage necessary if with unrelenting pain, UTI, persistent obstruction, progressive loss of renal function ⢠Position of stone determines preferred method of removal 2/26/2023 Dr. Mukesh 50
- 51. Treatment and management ⢠Urgent management - Intervention maybe required when the stone is: ď§ too large ( > 8 mm is a rough guide, but and contour must be consedired) ď§ too painful (recurrent colic) ď§ too dangerous ( there is total obstruction or infection) ď§ too slow ( a small, non obstruction stone can be left for many months to pass spontaneously) 2/26/2023 Dr. Mukesh 51
- 52. Treatment and management ⢠Bilateral ureteral obstruction â always asymmetric process ⢠mid to proximal ureter â percutaneous nephrostomy ⢠Distal obstruction â cystoscopic placement of ureteral stent ⢠Intrarenal obstruction secondary to crystals or protein casts - hydration 2/26/2023 Dr. Mukesh 52
- 53. Prognosis ⢠With relief of obstruction ⢠Reversible or irreversible damage? ⢠Obstruction NOT relieved ⢠Complete or incomplete? ⢠Bilateral or unilateral? ⢠Presence or absence of infection 2/26/2023 Dr. Mukesh 56
- 54. Summary ⢠UTO is an important urologic disorder and a common cause of acute and chronic renal failure ⢠Multiple causes, high clinical suspicion and acumen necessary ⢠UTO is a potentially reversible process ⢠Prompt recognition ⢠Prompt treatment ⢠Prompt consultation/referral 2/26/2023 Dr. Mukesh 57
- 55. 2/26/2023 Dr. Mukesh 58
Editor's Notes
- Pain, the symptom that most commonly leads to medical attention, is due to distention of the collecting system or renal capsule. Acute supravesical obstruction, as a stone lodge in a ureter, is associated with excruciating pain, known as renal colic. This pain is relatively steady and continuous, with little fluctuation in intensity, and often radiates to the lower abdomen, testes, or labia. By contrast, more insidious causes of obstruction, such as chronic narrowing of the ureteropelvic junction, may produce little or no pain and yet result in total destruction of the affected kidney. Flank pain that occurs only with micturition is pathognomonic of vesicoureteral reflux.
- Azotemia develops when overall excretory function is impaired, often in the setting of bladder outlet obstruction, bilateral renal pelvic or ureteric obstruction, or unilateral disease in a patient with a solitary functioning kidney. Complete bilateral obstruction should be suspected when acute renal failure is accompanied by anuria. Any patient with renal failure otherwise unexplained, or with a history of nephrolithiasis, hematuria, diabetes mellitus, prostatic enlargement, pelvic surgery, trauma, or tumor should be evaluated for UTO
- Partial obstruction may be with increased rather than decreased urine output. Indeed, wide fluctuations in urine output in a patienPartial bilateral UTO often results in acquired distal renal tubular acidosis, hyperkalemia, and renal salt wasting. These defects in tubule function are often accompanied by renal tubulointerstitial damage. Initially the interstitium becomes edematous and infiltrated with mononuclear inflammatory cells. Later, interstitial fibrosis and atrophy of the papillae and medulla occur and precede these processes in the cortex.t with azotemia should always raise the possibility of intermittent or partial UTOâŚIn acute setting, bilateral obstruction may mimic prerenal azotemia. However, with more prolonged obstruction, symptoms of polyuria and nocturia commonly accompany partial UTO and result from impaired renal concentrating ability. This defect usually does not improve with administration of vasopressin and is therefore a form of acquired nephrogenic diabetes insipidus. Disturbances in sodium chloride transport in the ascending limb of the loop of Henle and, in azotemic patients, the osmotic (urea) diuresis per nephron lead to decreased medullary hypertonicity and, hence, a concentrating defect.. If fluid intake is inadequate, severe dehydration and hypernatremia may develop. Hesitancy and straining to initiate the urinary stream, postvoid dribbling, urinary frequency, and incontinence are common with obstruction at or below the level of the bladder. Partial bilateral UTO often results in acquired distal renal tubular acidosis, hyperkalemia, and renal salt wasting. These defects in tubule function are often accompanied by renal tubulointerstitial damage. Initially the interstitium becomes edematous and infiltrated with mononuclear inflammatory cells. Later, interstitial fibrosis and atrophy of the papillae and medulla occur and precede these processes in the cortex. UTO must always be considered in patients with urinary tract infections or urolithiasis. Urinary stasis encourages the growth of organisms. Urea-splitting bacteria are associated with magnesium ammonium phosphate (struvite) calculi.
- Hypertension is frequent in acute and subacute unilateral obstruction and is usually a consequence of increased release of renin by the involved kidney. Chronic hydronephrosis, in the presence of extracellular volume expansion, may result in significant hypertension.
- Acute supravesical obstruction, as from a stone lodged in a ureter (Chap. 281), is associated with excruciating pain, known as renal colic. This pain is relatively steady and continuous, with little fluctuation in intensity, and often radiates to the lower abdomen, testes, or labia. By contrast, more insidious causes of obstruction, such as chronic narrowing of the ureteropelvic junction, may produce little or no pain and yet result in total destruction of the affected kidney. Flank pain that occurs only with micturition is pathognomonic of vesicoureteral reflux. Azotemia develops when overall excretory function is impaired, often in the setting of bladder outlet obstruction, bilateral renal pelvic or ureteric obstruction, or unilateral disease in a patient with a solitary functioning kidney. Complete bilateral obstruction should be suspected when acute renal failure is accompanied by anuria. Any patient with renal failure otherwise unexplained, or with a history of nephrolithiasis, hematuria, diabetes mellitus, prostatic enlargement, pelvic surgery, trauma, or tumor should be evaluated for UTO. In the acute setting, bilateral obstruction may mimic prerenal azotemia. However, with more prolonged obstruction, symptoms of polyuria and nocturia commonly accompany partial UTO and result from impaired renal concentrating ability. This defect usually does not improve with administration of vasopressin and is therefore a form of acquired nephrogenic diabetes insipidus. Disturbances in sodium chloride transport in the ascending limb of the loop of Henle and, in azotemic patients, the osmotic (urea) diuresis per nephron lead to decreased medullary hypertonicity and, hence, a concentrating defect. Partial obstruction, therefore, may be associated with increased rather than decreased urine output. Indeed, wide fluctuations in urine output in a patient with azotemia should always raise the possibility of intermittent or partial UTO. If fluid intake is inadequate, severe dehydration and hypernatremia may develop. Hesitancy and straining to initiate the urinary stream, postvoid dribbling, urinary frequency, and incontinence are common with obstruction at or below the level of the bladder.Partial bilateral UTO often results in acquired distal renal tubular acidosis, hyperkalemia, and renal salt wasting. These defects in tubule function are often accompanied by renal tubulointerstitial damage. Initially the interstitium becomes edematous and infiltrated with mononuclear inflammatory cells. Later, interstitial fibrosis and atrophy of the papillae and medulla occur and precede these processes in the cortex.UTO must always be considered in patients with urinary tract infections or urolithiasis. Urinary stasis encourages the growth of organisms. Urea-splitting bacteria are associated with magnesium ammonium phosphate (struvite) calculi. Hypertension is frequent in acute and subacute unilateral obstruction and is usually a consequence of increased release of renin by the involved kidney. Chronic hydronephrosis, in the presence of extracellular volume expansion, may result in significant hypertension. Erythrocytosis, an infrequent complication of obstructive uropathy, is probably secondary to increased erythropoietin production.
- Most acute obstructive uropathies are associated with significant pain or the abrupt diminution of urine flow that alerts the clinician to the need for further evaluation and treatment. However, the insidious nature of chronic urinary obstruction requires a careful history and a high index of suspicion, which prompt an appropriate evaluation that may confirm or rule out the presence of obstruction. Pain secondary to stretching of the urinary collecting system is the most common symptom in acute obstruction. It usually is identified when a superimposed acute obstruction occurs with the inability to void effectively; the resultant painful, distended bladder prompts a visit to an emergency physician. Alterations in patterns of micturition often associated with more distal obstructions are early but frequently missed symptoms. Bladder outlet obstruction leads to the symptoms of prostatism (eg, frequency, urgency, hesitancy, dribbling, decrease in voiding stream, the need to double void. Recurrent UTIs should always lead to an investigation for urinary obstruction. New-onset or poorly controlled hypertension secondary to obstruction and increased renin-angiotensin has been reported. Polycythemia secondary to increased erythropoietin production in the hydronephrotic kidney also has been reported History of recent gynecologic or abdominal surgery can give important clues to the etiology of urinary obstruction. Pediatric patients may present with recurrent infections. Symptoms of voiding dysfunction such as enuresis, incontinence, or urgency should be sought.
- Renal pain arises because of rapid stretching or inflammation of renal capsule Pain from the renal pelvis / ureter is caused by distention & excessive peristaltic contractions Any back / retroperitoneal structure may give rise to back pain.
- A thorough medication history should be elicited. A variety of drugs and toxins affect renal function. Bladder dysfunction is seen with a variety of xenobiotic drugs with antimuscarinic anticholinergic activity such as antihistamines, antipsychotics, and antidepressants. A variety of xenobiotics such as ethylene glycol, indinavir, methotrexate, phenylbutazone, or sulfonamides will induce crystal deposition throughout the tubulointerstium obstructing urine output. Additionally, drug-induced retroperitoneal fibrosis may obstruct ureteral function such as methysergide or other natural-occurring ergotamines. In cases of both acute and chronic obstructive uropathy, occupational exposure history may be beneficial. For example, in textile manufactures, shipyard workers, roofers, or asbestos miners, retroperitoneal fibrosis due to asbestos-induced mesothelioma should be considered. Bladder cancerâinduced outlet obstruction may occur in textile workers, rubber manufacturing workers, leather workers, painters, hairdressers, or drill press workers exposed to alpha- or beta-naphthylamine, 4-aminobiphenyl, benzidine, chlornaphazine, 4-chlor-o-toluidine, 2-chloroaniline, phenacetin compounds, benzidine azo dyes, or methylenedianiline.
- Signs of dehydration and intravascular volume depletion can be seen as a result of urinary concentrating defects associated with partial obstruction. Peripheral edema, hypertension, and signs of congestive heart failure from fluid overload may be observed in obstruction from renal failure. Palpable kidney or bladder provides direct evidence of a dilated urinary collection system. Rectal and/or pelvic examination is essential in determining whether enlargement of pelvic organs (eg, prostate, uterus) is a possible source of urinary obstruction. Examination of the external urethra may disclose phimosis or meatal stenosis.
- Is useful imaging modality as an initial study . It is a noninvasive inexpensive study that does involve radiation exposure or depend on renal function and a study of choice in pregnant women. In children, this is often part of the initial workup for obstructive processes. It is 90% sensitive in revealing hydronephrosis, renal parenchymal masses, distended bladder and renal calculi. The accuracy depends on the experience of the ultrasonographer.
- R P is performed in the operating room with a cystoscope in the bladder. A radiographic dye is injected into each ureteral orifice and with the use of fluoroscopy, any ureteral or renal pelvis filling defects or abnormalities can be visualized. The dyes does not interfere with renal function and can be used in patients with elevated creatinine, or in patient with allergy to dyes⌠why? Because the contrast remains extravascular. A P necessitates percutaneous placement of a catheter into the renal pelvis.
- NR gives a very detailed representation of the function and drainaige of the kidneys. It is highly accurate at measuring kidney functions but the images are low resolution.
- CT is very useful in providing anatomic detail of the urinary tract or any possible retroperitoneal or pelvic pathology that can affect the urinary tract via direct extension or external compression or to r/o any intraabdominal processes eg app, chole, aaa, ovarian cyst âŚ..(read slide) MRI â In patients who cannot tolerate a ct scan with contrast, an MRI with gadolinium can be performed to reveal any enhancing renal lesion as well as in evaluating the presence or extent of a renal vein or IVC thrombus in case of renal tumorsâŚ(read slide)
- Voiding cystourethrography is of value in the diagnosis of vesicoureteral reflux and bladder neck and urethral obstruction. Postvoiding films reveal residual urine. Endoscopic visualization â permits precise identification of lesions involving the urinary structure.
- Pulmonary edema as a consequence of renal failure from complete urinary obstruction should be treated conventionally. Partial obstruction can cause significant defects in salt and water retention, resulting in hypovolemia, which responds to standard fluid administration protocols
- Prior to addressing the specific therapy for obstruction, the ED physician must investigate and begin treatment of the life-threatening complications of obstructive uropathy (eg, pulmonary edema, hypovolemia, urosepsis, hyperkalemia). Narcotic analgesic for pain relief. NSAIDs should be avoided in patient with renal impairment. Correction of fluid and electrolyte balances Intravenous antibiotics Relief obstruction
- If a large PVR volume is noted, obstruction below the bladder should be investigated. Catheter drainage should then be maintained until the etiology of the obstruction is treated appropriately. Intermittent clamping of the Foley is recommended to prevent symptoms of hypotension and hematuria often ascribed to rapid bladder decompression.Hypotension after bladder decompression is thought to be due to a vagolytic response from a rapid change in bladder-wall tension. In a series of patients with obstruction, Christensen et al found a 50% decrease in intravesical pressure after only the first 100 mL of urine was removed.[2] Since the major drop in bladder pressure occurred with the early removal of relatively small amounts of urine, they concluded that fractionating urine removal in bladder obstruction was unjustified. Hematuria and bladder spasm is another well-known complication of bladder decompression. Gould et al compared the incidence of hematuria in rapidly emptied and gradually emptied obstructed dog bladders.[3] They found that hematuria was correlated strongly with the degree of bladder wall damage prior to relief of obstruction and was not correlated with the rate of emptying. Urine should be drained completely and rapidly from an obstructed bladder. Prolonged urine stasis only predisposes the patient to UTI, urosepsis, and renal failure.
- Calculi are the most common causes of unilateral ureteral obstruction. More than 90% of renal calculi less than 5.0-7.0 mm in size pass spontaneously. Obstruction in these cases can be treated conservatively with intravenous fluids and analgesia. Surgical drainage is necessary only for patients with unrelenting pain, UTI, or persistent obstruction. Position of the stone in the ureter determines the preferred method of removal. Calculi in the renal pelvis and proximal ureter are amenable to nephroscopy and removal under direct visualization. Percutaneous nephrostomy drainage is used for midureteral stones. Distal ureter stones can be removed cystoscopically by the use of a loop or basket. Extracorporeal shock wave lithotripsy is another viable option for stones in any position in the ureter.
- Bilateral obstruction of the ureters is almost always an asymmetric process. Generally, whatever the etiology of ureteral obstruction, one ureter is obstructed slowly and asymptomatically over a long period of time. Not until the second ureter is obstructed are symptoms of renal failure, hyperkalemia, or acidosis observed. For distal obstruction, cystoscopic placement of a ureteral stent can be attempted. Cases of renal recovery have been detected by radionucleotide scan in kidneys without renal blood flow.In case of suspected urosepsis from bilateral ureteral obstruction, bilateral percutaneous nephrostomy tubes must be placed to ensure that both potentially infected systems are drained. Intrarenal obstruction secondary to crystals or protein casts is not amenable to surgical drainage. Maintenance of adequate hydration to promote high rates of urine output to dilute crystals and casts is the main treatment.
- Occurs in BUO or obstruction in a solitary kidney The natriuresis is due to the excretion of retained urea(osmotic diuresis) and dpressed salt and water reabsorption (or diuresis results in the appropriate excretion of the excess of retained salt and water.
- Complete obstruction with infection can lead to total destruction of the kidney within days. Partial return of glomerular filtration rate may follow relief of complete obstruction of 1 and 2 weeks' duration, but after 8 weeks of obstruction, recovery is unlikely. ( the longer the duration, the greater the severity of obstruction. In the absence of definitive evidence of irreversibility, every effort should be made to decompress the obstruction in the hope of restoring renal function at least partially. The presence of a concomittant infection can lead to worse prognosis.The prognosis is favorable if the renal function is normal, the infection is cleared and the obstruction is relieved in a timely manner.