Urinary Obstruction and Stasis PDF

URINARY OBSTRUCTION AND STASIS UĞUR BOYLU, M.D. Professor of Urology Istinye University, Faculty of Medicine, Department of Urology Liv Hospital Ulus, Istanbul Obstruction of the urinary tract Obstruction of the urin...

URINARY OBSTRUCTION AND STASIS UĞUR BOYLU, M.D. Professor of Urology Istinye University, Faculty of Medicine, Department of Urology Liv Hospital Ulus, Istanbul Obstruction of the urinary tract Obstruction of the urinary tract can occur during fetal development, childhood, or adulthood. The point of obstruction: – Proximal -> calyces – Distal -> urethral meatus. lead to à permanent renal damage à limiting the excretion of metabolic wastes à altering water and electrolyte balance. Definitions Hydronephrosis: - Is the dilation of the renal pelvis or calyces. - Associated with obstruction. - may be present in the absence of obstruction. Obstructive uropathy: - The functional or anatomic obstruction of urinary flow at any level of the urinary tract. - The obstruction causes: functional or anatomic renal damage. GLOBAL RENAL FUNCTIONAL CHANGES Glomerular Filtration, Renal Blood Flow, Collecting System Pressure Functional changes associated with obstructive nephropathy. - Renal hemodynamic variables - Glomerular filtration. influenced by: - The extent and severity of obstruction - Unilateral or bilateral - Persists or has been relieved. Factors influencing GFR Factors influencing GFR are expressed in the following equation: GFR = Kf (PGC −PT −πGC) Kf: glomerular ultrafiltration coefficient PGC: glomerular capillary pressure Influenced by: - Renal plasma flow (RPF) - The resistances of the afferent and efferent arterioles. The hydraulic pressure of fluid in the tubule (PT) oncotic pressure (π) of the proteins Renal plasma flow (RPF) RPF depends upon: - The renal perfusion pressure - Intrarenal resistance to flow is mediated by the resistances in the afferent and efferent arterioles. RPF = aortic pressure − renal venous pressure renal vascular resistance Obstruction can transiently or permanently alter GFR and some or all of the determinants of GFR. Unilateral? Bilateral Unilateral and bilateral ureteral obstructions differ in – the patterns of hemodynamic – ureteral pressure changes – distribution of renal blood flow. Hemodynamic Changes with Unilateral Ureteral Occlusion Animal experiments have demonstrated a triphasic pattern of RBF and ureteral pressure changes in UUO first 1 to 2 hours -RBF increases -high PT and collecting system pressure second phase lasting 3 to 4 hours -pressure parameters remain elevated -RBF begins to decline. third phase beginning about 5 hours after obstruction -a further decline in RBF -decrease in PT and collecting system pressure.  In phase I, renal blood flow and ureteral pressure rise together. In phase II, the left renal blood flow begins to decline and ureteral pressure remains elevated and, in fact, continues to rise. In phase III, the left renal blood flow and ureteral pressure decline together. Hemodynamic Changes with Bilateral Ureteral Occlusion A modest increase in RBF with BUO that lasts approximately 90 minutes followed by a prolonged and profound decrease in RBF that is greater than found with UUO. – The intrarenal distribution of blood flow is quite different with BUO than with models of UUO. – Thus the shift seen with UUO of blood flow from outer to inner cortex is the opposite of that with BUO. Hemodynamic Changes with Bilateral Ureteral Occlusion Ureteral pressure is higher with BUO than with UUO. In both cases ureteral and tubular pressures are increased for the first 4 to 5 hours. – The ureteral pressure remains elevated for at least 24 hours with BUO – The ureteral pressure begins to decline and approaches preocclusion pressures by 24 hours with UUO. Ureteral pressure is higher with BUO than with UUO. In summary, Both UUO and BUO involve increases in renal vascular resistances and increases in ureteral pressures. The timing and regulation of these changes differ With UUO, early renal vasodilation primarily mediated by prostaglandins and NO is followed by prolonged vasoconstriction and normalization of intratubular-ureteral pressure as the contralateral kidney contributes to fluid balance. With BUO, little early vasodilation is seen, and vasoconstriction is more profound. When the obstruction is released, the postobstructive diuresis is much greater with BUO because volume expansion, urea and other osmolytes, and secreted ANP contribute to a profound diuresis and natriuresis. PATHOLOGIC CHANGES OF OBSTRUCTION These may be affected by: -the presence of infection -duration of obstruction -intra versus extrarenal localization of the renal pelvis. Gross Pathologic Findings at 42 hours after obstruction : Dilation of the pelvis and ureter blunting of the papillary tips the weight of this renal unit heavier. at 7 days. Pelviureteric dilation weight further increased parenchyma became edematous at 12 days The cortex remained slightly enlarged increased calyceal dilatation at 21 and 28 days the external renal dimensions of both kidneys were similar. the cortex and medullary tissue diffusely thinned. At 6 weeks The totally obstructed kidneys à enlarged, had a cystic appearance, and weighed less than the contralateral renal unit The partially obstructed kidneys à no gross differences in appearance Microscopic Pathologic Findings Widespread glomerular collapse and tubular atrophy, interstitial fibrosis, and proliferation of connective tissue in the collecting system were reported at 5 to 6 weeks after obstruction This is believed to be a result of interplay of several cellular and molecular mechanisms that collectively lead to the subtle development of tubular atrophy, macrophage infiltration/proliferation in the renal interstitial tissue, interstitial fibrosis and progressive loss of nephrons Electron Microscopic Pathologic Findings Including: -tubular atrophy -glomerular collapse -renal pelvic smooth muscle atrophy at 5 to 6 weeks after obstruction other changes including: -a cell-poor stroma composed of elastic and collagen fibers in the renal interstitium -obstructed portions of the collecting system. Post obstructive Diuresis Mechanisms Following the relief of urinary tract obstruction, post- obstructive diuresis—a period of significant polyuria— may ensue. Urine outputs of 200 mL/hr or greater may be encountered. Postobstructive diuresis occurs primarily with BUO and is usually self-limiting. – mainly after relief of BUO or obstruction of a solitary kidney – rarely occur when there is a normal, contralateral kidney Post obstructive Diuresis Downregulation of sodium transporters The increased ANP induce a saline diuresis other natriuretic peptides, such as the Dendroaspis natriuretic peptide, may play a role. poor responsiveness of the collecting duct to antidiuretic hormone (ADH). due to a downregulation of aquaporin water channels in this segment of the nephron and perhaps in the proximal tubule SELECTED EXTRINSIC CAUSES OF URETERAL OBSTRUCTION Retroperitoneal Fibrosis uncommon a fibrotic and inflammatory mass envelops and potentially obstructs retroperitoneal structures including either or both ureters. Pelvic Lipomatosis Rare benign condition marked by exuberant pelvic overgrowth of nonmalignant but infiltrative adipose tissue, usually in the abdominal and pelvic cavities. Occur in perivesical and perirectal spaces The etiology and incidence are unknown. Obesity play a role radiographic improvement and worsening in response to weight loss and gain, respectively. Obstetric and Gynecologic Pregnancy Hydronephrosis develops commonly during pregnancy occurrence varying between 43% and 100%. Approximately one third of patients may have persistent hydronephrosis during the first postpartum week, but it resolves in the majority within 6 weeks  Two etiologies for hydronephrosis of pregnancy: - hormonal - mechanical. nonmechanical mechanism. Progesterone promote ureteral dilatation and subsequent development of hydronephrosis mechanical etiology after the 20th week of gestation, a time when the uterus is large enough to compress the ureters extrinsically Benign Pelvic Abnormalities Tubo-ovarian Abscess. Tubo-ovarian abscess, occurring in approximately 15% of those afflicted with PID, may cause extrinsic ureteral obstruction, lead to anuria Ureteral obstruction may resolve with: - antibiotic therapy - transvaginal drainage of the abscess. - open surgical or laparoscopic intervention - Placement of an internalized ureteral stent or percutaneous nephrostomy Endometriosis. Defined as the presence of functional endometrial tissue in an ectopic site. potential for malignant transformation 10% to 20% of women of reproductive age peak incidence in the mid-20s Vascular Causes of Ureteral Obstruction Arterial Causes of Obstruction Abdominal Aortic Aneurysm. Clinical signs and symptoms of ureteral obstruction may be the initial manifestation of an abdominal aortic aneurysm (AAA) due to a mass effect or localized inflammation CT scanning Ureteral findings vary. - pushed laterally on both sides - one side may deviate laterally while the opposite side is drawn medially within the perianeurysmal inflammation - both may be medially deviated. lateral deviation of the ureter with AAA - not associated with obstruction The medial deviation of the ureter associated with the desmoplastic reaction of inflammatory aneurysms (IAAA), however, carries a more significant risk of ureteral obstruction. Placement of internalized ureteral stents open surgery or an endovascular approach warrant close monitoring for recurrent or de novo ureteral obstruction