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Obstructive Uropathy
Chapter 40
Obstructive Uropathy Christopher J. Cutie and W. Scott McDougal CHAPTER CONTENTS OVERVIEW
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CALCULI 469 Treatment Options 470 Prevention 470 Surgical Intervention 470
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BLADDER DYSFUNCTION
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EXTRINSIC COMPRESSION
URETEROPELVIC JUNCTION OBSTRUCTION BENIGN PROSTATIC HYPERPLASIA Treatment Options 472 Medications 472 Surgery 472
GENITOURINARY MALIGNANCY
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Obstructive uropathy is defined as any functional impedance to the anterograde flow of urine. This obstruction may occur in the upper tract (renal pelvis, ureters), lower tract (bladder, urethra), or both, and may be the result of an intrinsic defect or extrinsic process. A common cause of renal function compromise, urinary obstruction may be diagnosed and treated with multiple modalities, depending on the nature and location of the obstruction. Timely diagnosis and treatment of acute obstruction, as well as the appropriate management of chronic obstruction, is a multidisciplinary effort requiring contributions by primary care providers, internists, nephrologists, urologists, and radiologists.
OVERVIEW The degree of urinary obstruction typically correlates with the patient’s clinical presentation. Complete bilateral obstruction results in anuria, whereas partial or unilateral obstruction may present with intermittent episodes of oliguria and polyuria. Clinical symptoms of urinary obstruction may include flank, suprapubic, or groin discomfort; recurrent urinary tract infections; dysuria; hematuria; stranguria; and acute or chronic renal failure. Acute bilateral obstruction results in postrenal failure. The serum blood urea nitrogen-to-creatinine ratio approximates 10:1 and the urine-to-plasma urea and urine-toplasma creatinine ratios are indistinguishable from intrarenal failure. Complete anuria requires a prompt evaluation for an obstructing process. Management of obstruction relies on adequate drainage of the urinary system. Bladder decompression may be achieved by placement of either a urethral catheter or suprapubic cystotomy tube. Drainage of the renal collecting system is possible both endoscopically in a retrograde fashion with a ureteral stent or percutaneously with a nephrostomy tube. Endoscopic procedures typically require administration of spinal or general anesthesia. In the setting of a critically ill patient with
POSTOBSTRUCTIVE DIURESIS
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other significant comorbidities, nephrostomy tube placement is often the preferred technique because this can be performed under ultrasound guidance with either minimal intravenous sedation or local anesthesia. In either scenario, definitive intervention is necessary for the ultimate preservation of renal function. Although acute urinary obstruction must be managed expeditiously, chronic urinary tract obstruction also requires timely diagnosis and management. Chronic obstruction may predispose the afflicted patient to a variety of conditions that are wide-ranging in severity. Urine stasis often leads to bacterial colonization, with sequelae ranging from urinary tract infections and pyelonephritis to fulminant urosepsis and concomitant cardiovascular collapse. Long-standing partial obstruction may also compromise the functional integrity of various structures, particularly the bladder and upper tracts of the renal collecting system, both of which are fairly sensitive to intraluminal pressure changes. This chapter discusses the multiple causes of urinary obstruction as well as the diagnostic considerations and available treatment modalities of each.
CALCULI Urolithiasis is the most common cause of urinary obstruction, accounting for approximately $2.1 billion in health care expenditures annually.1 In the United States, 13% of men and 7% of women will be diagnosed with kidney stones at some point throughout their lifetime.2 Peak age at diagnosis in men is 30 years, whereas women exhibit a bimodal distribution, with peaks at 35 and 55 years. Although many of these stones are found incidentally and are not associated with symptoms of pain, obstruction, or infection, the risk of hospitalization and surgical intervention is ever present and increasing as the general population grows. Furthermore, 50% of patients with a history of urolithiasis will re-form stones within 5 years.2
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The majority of calculi are composed of uric acid, calcium oxalate monohydrate, calcium oxalate dihydrate, cystine, or ammonium magnesium phosphate (struvite) or some combination thereof. Stones typically form within the collecting system of the kidney and subsequently travel to distal portions of the urinary tract. However, they may also form at the site of a foreign body (i.e., stent, catheter, suture material, human hair). Depending on their size, composition, and conformation, stones may either pass spontaneously in the urine or impact anywhere along the course of the urinary tract. The three most common sites for stone impaction are the ureteropelvic junction (UPJ), the mid-ureter at the level of the iliac vessels, and the ureterovesicle junction. The ureteric caliber at the UPJ and ureterovesicle junction is generally smaller than that along the course of the ureter. Extrinsic compression by the iliac vessels where the mid-ureter crosses causes a narrowing of the ureteral lumen at this level. The likelihood of spontaneous passage of calculi is dependent on several criteria. These include stone size and shape, as well as patient anatomy and history of stone passage.3 However, due to the intrinsic variability of an individual’s ureteral caliber, as well as the conformation of calculi, these criteria serve merely as a guide and must be appropriately incorporated into each clinical setting. Reported percentages of spontaneous stone passage vary widely in the literature, ranging from 29% to 98% for stones 0.5 cm or smaller located in the proximal ureter compared with rates of 71% to 98% for those of comparable size located in the distal ureter.3 Stones ranging from 0.5 to 1.0 cm have a lower likelihood of spontaneous passage, with rates ranging from 10% to 53% for those in the proximal ureter; rates are somewhat better for the distal ureter, ranging from 23% to 53%.3 Moreover, recent studies have demonstrated the utility of -adrenergic blockers, calcium channel blockers, and nonsteroidal anti-inflammatory medications in facilitating spontaneous stone passage via ureteral smooth muscle relaxation.4,5
Treatment Options Dissolution therapy is an appropriate first-line treatment modality for uric acid and cystine stones. Uric acid stones, comprising 5% to 10% of all urinary stones, typically form in an acidic urine (pH 5.5).6 They are relatively soft compared with calcium oxalate and cystine stones and are associated with hyperuricosuria, low urinary volume, and persistently acidic urine. These stones are often radiolucent on radiographic imaging and measure a density of 500 Hounsfield units or less on computed tomography. Dissolution therapy with oral urine alkalinizing medications (potassium citrate) has been shown to be efficacious in as many as 80% of patients.6 Those patients failing dissolution therapy may then be further treated with a surgical intervention. Cystine stones, which account for approximately 1% of all urinary calculi, also form in acidic urine. Cystinuria results from a defect in the renal tubular absorption of the amino acids cystine, ornithine, lysine, and arginine. Patients with the inherited autosomal recessive disorder excrete in excess of 600 mg of cystine daily in their urine (normal 100 mg/day). In addition to increasing urine volume, first-line therapy remains urine alkalization with a goal urine pH of more than 7.0. Should dissolution therapy be ineffective, patients may also be treated with oral chelating agents, such as d-penicillamine (250 mg
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every 6 hours) or -mercaptopropionylglycine (250 mg every 6 hours) to increase urine cystine solubility.7 Cystine stone formers will often present with staghorn calculi. These stones are extremely dense ( 1200 Hounsfield units) and are therefore not amenable to certain treatment modalities, such as extracorporeal shock wave therapy (ESWL). Struvite stones, in comparison, form in alkaline urine. Commonly associated with chronic urinary tract infections secondary to urea-splitting pathogens (Proteus mirabilis, Klebsiella pneumoniae, Pseudomonas aeruginosa), these stones exist in a urine pH of more than 7.5. Urease splits urea into component ammonia groups, resulting in alkaline urine. Because these stones are closely associated with infection, definitive treatment relies on clearance of all stone burden and maintenance of a sterile urine, typically through antibiotic prophylaxis.
Prevention Prevention of recurrent urolithiasis is based on maintaining high urine volume, increasing the concentration of stoneinhibiting substances in the urine, and decreasing the concentration of lithogenic substances. Patients are encouraged to consume more than 2.5 L of fluid daily and to supplement their fluid intake with citrate-rich fluids, such as lemonade.8 Citrate binds calcium in the urine and inhibits calcium oxalate crystal formation. Foods rich in oxalate, such as tea, coffee, leafy green vegetables (spinach), rhubarb, nuts, and beer should be avoided. Meats and other protein-rich foods should also be consumed in moderation, as degradation of these purine-heavy foods results in elevated serum uric acid concentrations. Allopurinol may also be prescribed for those patients with hyperuricemia. Cystine stone formers should be counseled to reduce their intake of methionine-containing foods, such as meats and dairy products.
Surgical Intervention Recent advances in the endoscopic treatment of calculi and the significant improvement of lithotripsy devices have allowed the majority of surgical treatments to be performed in an outpatient setting. Holmium pulsed-dye lasers have become ever more powerful and are relatively easy to use. Furthermore, ureteroscopes and imaging equipment have dramatically improved, allowing excellent visualization of ureteral and renal pelvic anatomy and calculi. Renal stones measuring as large as 2 cm may now be treated with staged ureteroscopic procedures or ESWL, depending on the location and hardness of the stone. Selection criteria for surgical stone management include stone location, size, composition, collecting system/ ureteral anatomy, patient health/performance status, and patient preference. ESWL involves delivery of shock waves generated by electromagnetic energy sources. These shock waves are propagated through water and delivered to the stone burden under direct, real-time fluoroscopic imaging. To reliably use ESWL, patient selection is vitally important. The stone must be radiopaque and visualized on standard radiographs because fluoroscopy or ultrasonography is used intraoperatively to identify and target the stone. Shock waves are then delivered to the stone until evidence of fragmentation is identified. ESWL may often be performed under conscious sedation, although some
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patients may require administration of general anesthesia for improved tolerability. Although ESWL is noninvasive, it has been associated with specific risks, including cardiac arrhythmias, renal contusions, hemorrhage, and bruising. Recent studies also suggest that ESWL may be associated with the delayed development of diabetes due to pancreatic fibrosis secondary to shock wave injury.9 ESWL is appropriate for stones measuring as much as 1.5 cm located above the bony pelvis. The ischial body may impede shock wave propagation and mute the fragmentation effects on stones located in the distal ureter. Moreover, patients undergoing ESWL treatment must be warned of the risks of steinstrasse, literally translated as “a road of stone.” This occurs when a stone is broken into multiple smaller fragments and the lead fragment is unable to spontaneously pass, which causes ureteral obstruction proximal to the stone burden. Classic symptoms of flank pain, dysuria, and hematuria may result, and a secondary procedure (e.g., stent or nephrostomy tube placement, salvage ureteroscopy) is often necessary because the lead fragment will not pass. Ureteroscopy is defined as any endoscopic manipulation of the ureter and its contents. Since its development in the early 1980s, ureteroscopy has revolutionized the treatment of ureteral and renal stones.10 Whereas open ureterolithotomy for stone extraction was commonly performed through the 1970s and required an inpatient hospitalization, ureteroscopy allows outpatient treatment of most urinary stones today. Rigid and flexible ureteroscopes are currently available and are used either independently or in tandem depending on stone size and location. Standard ureteroscopes measure approximately 8 French in size and are introduced via the urethra to the level of the stone. Various tools, including holmium lasers and nitinol extraction baskets, are then used to fragment, retrieve, and remove the stone. A ureteral stent is typically placed for temporary renal decompression and to allow residual stone fragments to pass. This stent also mitigates the risk of ureteral obstruction from posttreatment ureteral inflammation and edema. If dissolution therapy fails or is not feasible, staghorn calculi and large renal stones are best treated with percutaneous nephrolithotomy, which requires nephrostomy access to the kidney via the flank. This procedure allows for high stone-free rates with fewer secondary procedures necessary.11 Open surgery, including pyelolithotomy and anatrophic nephrolithotomy, is rarely performed and reserved for those patients with highly complicated anatomy (e.g., crossed-fused ectopia, horseshoe kidney) or grossly enlarged stone burden (5 cm). With the increased popularity of laparoscopic procedures, minimally invasive pyelolithotomy is also frequently offered for large renal pelvic or ureteropelvic junction stones.
URETEROPELVIC JUNCTION OBSTRUCTION UPJ obstruction accounts for approximately 50% of prenatally diagnosed hydronephrosis. Classically, UPJ obstruction presents as a unilateral process; however, bilateral obstruction may occur. Causes of UPJ obstruction may be both intrinsic and extrinsic in nature. In some instances, there is a crossing anatomic vessel (an accessory renal artery or vein), which kinks the ureter at the level of the UPJ. Surgical correction of
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the anomaly with pyeloplasty and vessel transposition is the definitive treatment. Intrinsic defects within the ureter, including an aperistaltic segment secondary to malformation of the ureteral musculature as well as ureteral valves (Ostling’s valves) are a cause of UPJ obstruction in children.12 Diagnosis typically is made based on a 99mTc-mercaptoacetylglycine study or intravenous pyelography. Again, treatment involves a pyeloplasty and excision of this aperistaltic segment. Impacted ureteral stones and previous endoscopic ureteral manipulation, with concomitant ureteral inflammation and fibrosis, may also result in ureteral strictures, leading to UPJ obstruction. Excision of this stenotic segment and primary reanastomosis is the recommended treatment. Endopyelotomy or ureteroscopic incision of ureteral strictures and balloon dilatation have been reported as other initial management options with varying degrees of success.13 Before a major surgical repair, the degree of function in the affected kidney should be calculated. This is commonly performed using a dimercaptosuccinic acid scan, a radionuclide study that measures the uptake of tracer material within the renal tubules and is a reliable means of assessing renal function. Because the goal of therapy is to maintain existing renal function, which is not apt to improve after pyeloplasty, a simple nephrectomy as definitive treatment should be considered.
BENIGN PROSTATIC HYPERPLASIA Benign prostatic hyperplasia (BPH) is a commonly diagnosed condition that is responsible for a significant proportion of lower urinary tract complaints in middle-aged and elderly men. In the United States in 2000, this condition accounted for 117,000 emergency department visits and 105,000 hospitalizations, accounting for $1.1 billion in expenditures.1 A consequence of persistent testosterone stimulation, BPH occurs as a result of growth of adenomatous prostatic tissue. This is a benign condition and may be managed expectantly, pharmacologically, or surgically. Chronic obstruction, left untreated, results in recurrent bladder overdistention, which may lead to bladder trabeculation and formation of diverticula and cellules. These outpouchings of bladder epithelium can further predispose the patient to urinary tract infections, stone formation, and, most importantly, deterioration of the upper tracts leading to compromised renal function and ultimately renal failure. Patients with significant lower urinary tract symptoms should be evaluated by a urologist. Although symptoms of urinary frequency, hesitancy, and urgency may be attributed to BPH, evaluation of the lower urinary tract is required. Thorough physical examination should include suprapubic palpation and inspection of the penis for evidence of meatal stenosis or phimosis. A digital rectal examination is required, and patients are encouraged to complete a symptom score questionnaire. This questionnaire rates symptoms of nocturia, urgency, frequency, stranguria, force of urine stream, intermittency, and the need for second voiding and serves as a baseline for subsequent comparison after initiation of medical therapy or surgery. Cystoscopy is recommended for specific indications, such as hematuria, suspected bladder stones, or early bladder cancer. Transition cell carcinoma in situ is often associated with irritative urinary symptoms.14 A postvoid residual and uroflow are
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also important studies in the diagnosis of BPH. A postvoid residual greater than 200 mL is significant, as is a uroflow rate of less than 15 mL/sec.15 Ultimately, because this is a benign condition, informed treatment decisions should be based on patient satisfaction and perceived quality of life.
Treatment Options Medications There are two main classes of medications prescribed for treatment of symptoms of BPH: 1-adrenergic receptor blockers and 5-reductase inhibitors. -Blockers (terazosin, doxazosin, tamsulosin, alfuzosin) result in blockade of sympathetic peripheral 1 receptors, resulting in relaxation of both prostatic and bladder neck smooth muscle. These medications are generally well tolerated but, given their mechanism of action, may cause hypotension, dizziness, or syncope. -Blockers have been definitively shown to exhibit efficacy in the treatment of men with urinary symptoms attributable to BPH, but do not decrease the incidence of acute urinary retention episodes.16 5-Reductase inhibitors (finasteride, dutasteride) inhibit the enzyme 5-reductase, thus preventing conversion of testosterone to dihydrotestosterone, which is chemically active within the prostate and stimulates prostatic tissue growth. Such deprivation of dihydrotestosterone results in prostatic epithelial atrophy. Dutasteride (Avodart) inhibits both the type I and II forms of 5-reductase and may provide an increased benefit to patients.17 These medications are often used in tandem with -blockers and have been shown to demonstrate great efficacy in multiple studies.16,18 5-Reductase inhibitors do affect serum prostate-specific antigen (PSA) levels, typically decreasing them by 50%. Therefore, this decrease must be noted before initiation of 5-reductase therapy because treatment may influence the subsequent care of patients managed with routine PSA screening and monitoring tests. Furthermore, patients applying topical 5-reductase for hair growth (Propecia) must be informed that their serum PSA level will be reduced, typically by 50% as well.19 Combination therapy with both -blockers and 5-reductase inhibitors appears to have a synergistic effect, as studies have shown an approximately 50% decrease in disease progression compared with monotherapy.16 Of note, medications are not effective in patients with enlarged prostatic median lobes. The median lobe may serve as a ball valve, intermittently obstructing the bladder neck, resulting in outflow obstruction. These patients are best served by transurethral resection of this tissue. BPH may result in an elevated PSA, although not typically to the levels seen in aggressive prostate cancer. However, an elevated PSA may not simply be attributed to prostatic hyperplasia, and an appropriate evaluation and work-up is warranted.
Surgery Several technologic advances have vastly improved the urologist’s armamentarium of surgical options for treatment of BPH. In addition to the standard transurethral resection of prostate tissue using the electrosurgical resectoscope, new devices incorporating laser and microwave energy have resulted in safer, faster, and more cost-effective treatment strategies. Various laser vaporization technologies, including holmium
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and KTP (potassium titanyl phosphate), allow for significantly smaller intraoperative blood loss as well as fewer risks of postprocedure absorptive hyponatremia.20 Many patients are catheter free after these procedures and do not require an inpatient hospitalization. These devices use a wavelength of light (523 nm) that is absorbed by both blood and tissue, allowing for more exact tissue destruction and simultaneous hemostasis. Microwave therapy has also exhibited efficacy as an officebased treatment modality, using a special urethral catheter with a thermal coil that delivers highly focused energy to the prostatic bed with resultant tissue necrosis. After administration of mild sedatives and topical urethral lidocaine, this catheter is inserted in the standard fashion by a urologist and left in place for approximately 30 to 60 minutes. Expanding titanium urethral stents (UroLume) have also been developed for treatment of bladder outlet obstruction. These devices are endoscopically placed within the prostatic urethra and serve to stent open the urethral lumen by inhibiting coaptation of the prostatic lobes. Although success rates vary considerably for this procedure, these stents are associated with significant morbidity and are difficult to remove once urothelium has grown into them.21 These devices are often reserved for poor surgical candidates who are unable to endure general anesthesia for more invasive procedures, such as transurethral resection.
GENITOURINARY MALIGNANCY Occasionally, bladder, prostate, and urethral tumors may cause urinary obstruction. Muscle invasive bladder cancer arising from the trigone or base of the bladder can obstruct the ureteral orifices, resulting in hydroureteronephrosis. Transurethral resection of the tumor may alleviate this obstruction, but the cancer may recur if the resection is incomplete. Highly advanced prostate cancer may present with bladder outlet obstruction. Transurethral resection of the obstructing lesion is again the preferred treatment of choice. Both bladder and prostate cancers may often present in this situation with gross hematuria or clot retention. Urethral tumors, albeit rare, may also result in an intrinsic obstruction of urinary flow. Often, a catheter may be placed around the obstructing lesion as a temporary measure, followed by further workup and definitive treatment.
URETHRAL STRICTURE/STENOSIS A urethral stricture is a narrowing of the urethral lumen, resulting in a slowing or cessation of urine flow.22 Urethral strictures are significantly more common in males, given the far longer course of the male urethra compared with that of the female. Risk factors for urethral stricture disease include recurrent urinary tract infections or urethritis (i.e., gonococcal), trauma, previous urethral instrumentation or surgery, pelvic irradiation, and advanced age. Diagnosis is typically based on direct vision with cystoscopy as well as retrograde urethrography to delineate the anatomic location and length of the stricture. Treatment modalities include manual dilatation (metal sounds, balloon dilators), transurethral incision/ resection, and open primary repair. Because these strictures are typically composed of dense scar tissue, they tend to recur
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in the absence of definitive open surgery. A biopsy of the tissue at the stricture site should always be performed to rule out a coincident urethral tumor as the obstructing lesion. Presenting symptoms of urethral strictures often include urinary urgency and hesitancy, decreased force or caliber of the urine stream, persistent suprapubic fullness, recurrent urinary infections, the need for frequent second voids, and urinary retention. In some patients, the stricture is such that urethral catheter placement in the standard blind fashion is not possible, requiring placement of a catheter over a wire under cystoscopic guidance or placement of a suprapubic cystostomy tube for acute bladder decompression.
BLADDER DYSFUNCTION In the normal state, voiding is a reflex function under voluntary control. Coordinated voiding, characterized by external sphincter relaxation and subsequent detrusor contraction, is controlled by the pontine micturition complex’s effect on the sacral cord (S2-S4).23 The pontine micturition complex, in turn, is under cortical control. Detrusor hyperreflexia with coordinated external sphincter activity results from suprapontine lesions (e.g., stroke, Parkinson’s disease). This is in contrast to detrusor hyperreflexia without coordinated external sphincter activity, which is caused by a suprasacral spinal lesion (e.g., myelodysplasia, multiple sclerosis). Detrusor areflexia is caused by damage to the sacral reflex arc (e.g., neuropathy, disk herniation), and also occurs during the acute spinal shock phase after a spinal cord injury. Urodynamics, a real-time study that measures bladder pressure, abdominal pressure, sphincter activity, bladder compliance, and flow rate, is commonly used to delineate these disorders. Optimal bladder function relies on adequate maintenance of filling and emptying pressures in both the storage and expulsion of urine. During the filling stage, bladder pressures must be low enough to allow for transit of urine from the ureter to the bladder. Should the bladder pressure exceed the ureteral and renal pelvic pressures, urine will reflux in a retrograde fashion, resulting in ureteral dilatation. The ureter can withstand continuous intravesicle pressures as high as approximately 40 cm H2O. Higher resting pressures lead to ureteral damage and resultant renal compromise. The voiding stage is dependent on an important interplay between the bladder detrusor smooth muscle and the external skeletal muscle sphincter. At the initiation of a void, the external sphincter is relaxed under voluntary control, followed by contraction of the detrusor muscle. This allows for the coordinated flow of urine in an anterograde fashion. A defect in the detrusor muscle, external sphincter, or signaling neuron pathways therein results in bladder dysfunction. The result is a high-pressure bladder with inadequate voiding. Treatment modalities include anticholinergic medications (e.g., tolterodine, oxybutynin) to inhibit detrusor contraction. Clean intermittent catheterization is the ideal modality for bladder decompression in the patient with urinary obstruction secondary to neurogenic bladder dysfunction.24 Long-term indwelling catheters are not recommended because these can result in a host of complications, including recurrent urinary tract infections, urethral meatal erosion,
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orchitis, epididymitis, prostatitis, bladder calculi, and squamous metaplasia of the bladder epithelium, a premalignant condition.25 Clean intermittent catheterization requires diligent attention to patient hygiene, catheter care, and catheterization technique. Those patients with detrusor-sphincter dyssynergia, characterized by bladder hyperreflexia with coordinated external sphincter relaxation, are plagued by poor bladder compliance and outlet obstruction. Bladder augmentation with subsequent clean intermittent catheterization may be recommended for these patients to ensure adequate urine storage and drainage. However, in those not suitable for augmentation or the necessary maintenance techniques required, urinary diversion is also a viable option. A sphincterotomy may also be performed, but this ultimately results in incontinence.
EXTRINSIC COMPRESSION A variety of other oncologic and inflammatory conditions may result in obstructive uropathy as a result of extrinsic compression of one or both ureters, the bladder, or the urethra. Gynecologic malignancies arising from pelvic organs, such as the cervix, ovary, and uterus, may result in a mass effect on the ureters or trigone of the bladder, resulting in urinary obstruction. This may also result from masses of the colon and inflammatory processes, such as sigmoid diverticulitis, Crohn’s disease, and ulcerative colitis. Such inflammatory reaction may result in a reactive fibrosis around one or both ureters, leading to proximal obstruction of urine. With regards to tumor compression, this typically occurs as a chronic process, with the gradual onset of flank pain. Ultrasonography or computed tomography will often demonstrate unilateral or bilateral hydronephrosis in the setting of an enlarging pelvic mass, potentially in the absence of symptoms (silent hydronephrosis). Decompression of the renal collecting system with either a percutaneous nephrostomy tube or ureteral stent is indicated, as this obstruction may predispose the patient to renal failure in the setting of chemotherapy for the primary tumor. Moreover, as many of these patients are immunosuppressed due to immunotherapy or as a consequence of the disease, an obstructed collecting system may be a setup for urinary tract infections and subsequent urosepsis, which may prove fatal in the debilitated patient.
POSTOBSTRUCTIVE DIURESIS Urinary obstruction, either unilateral or bilateral, may result in fluid overload, renal insufficiency, and electrolyte abnormalities. However, relief of this obstruction may also result in profound effects on the patient’s volume status and electrolyte homeostasis. Acute decompression of the bladder will often result in polyuria and, in some cases, hematuria. This hematuria is due to decompression of previously dilated mucosal cystic vessels, which rupture in the setting of intravesicle pressure changes. It may be fairly significant and require clot evacuation and continuous bladder irrigation. Postobstructive diuresis may be physiologic, pathologic, or a combination of the two. Physiologic diuresis occurs as a result of fluid overload and elevated urea levels, which are
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excreted when the obstruction is relieved. Pathologic diuresis occurs as a result of increased tubule permeability and lack of an osmotic gradient in the renal medulla. Postobstructive polyuria is characterized by increased salt and water excretion and may vary widely with respect to volume. As many as 10% of patients will exhibit excessive diuresis, requiring intravenous fluid replacement. To accurately assess clinical improvement and normalization of volume status, daily weight, urine output, and orthostatic blood pressures are recorded. Plasma electrolytes should be monitored carefully (every 6–12 hours in the acute setting), particularly potassium, sodium, and magnesium, because these values demonstrate the degree of nephron recovery post-obstruction. Urine output is replaced with half normal saline, as the sodium content of the diuresis is typically approximately 70 mEq/L. Careful attention must be paid to avoid overhydration of the patient, thereby perpetuating the disease. Many patients with modest diuresis may eat and drink their way back to a normal volume state. Intermittent bladder drainage, once believed to mitigate hematuria, is not recommended as this typically serves only to confuse the accurate recording of urine output.
FETAL AND PEDIATRIC UROPATHIES Advances in diagnostic and treatment modalities for fetuses, infants, and children have had a tremendous impact on the management of urinary obstruction in this patient population. Congenital malformations, such as posterior urethral valves, a persistent prostatic utricle, or the sequelae of such neurological disorders as spina bifida may all result in obstruction. Posterior urethral valves, present in males, are remnant flaps of mucosal tissue within the urethra, typically at the level of the veru montanum in the prostatic urethra. These patients often present with prenatal oligohydramnios, bladder distention, and bilateral hydronephrosis. Diagnosis is confirmed with a voiding cystourethrogram, and treatment includes endoscopic valve ablation. Temporary decompression of the obstructed bladder in the setting of posterior urethral valves may be accomplished with a cutaneous vesicostomy, which is an incontinent urinary diversion. Longterm sequelae of renal obstruction may include an inability of the kidney to maximally concentrate urine. This predisposes affected children to polydipsia and intolerance to fluid deprivation.
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6. Shekarriz B, Stoller ML: Uric acid nephrolithiasis: Current concepts and controversies. J Urol 2002;168:1307–1314. 7. Barbey F, Joly D, Rieu P, et al: Medical treatment of cystinuria: Critical reappraisal of long-term results. J Urol 2000;163: 1419–1423. 8. Seltzer MA, Low RK, McDonald M, et al: Dietary manipulation with lemonade to treat hypocitrauric calcium nephrolithiasis. J Urol 1996;156:907–909. 9. Krambeck AE, Gettman MT, Rohlinger AL, et al: Diabetes mellitus and hypertension associated with shock wave lithotripsy of renal and proximal ureteral stones at 19 years of follow-up. J Urol 2006; 175:1742–1747. 10. Harmon WJ, Sherson PD, Blute ML, et al: Ureteroscopy: Current practice and long-term complications. J Urol 1997;157: 42–43. 11. Preminger GM, Assimos DG, Lingeman JE, et al: Chapter 1: AUA guideline on management of staghorn calculi: Diagnosis and treatment recommendations. J Urol 2005;173: 1991–2000. 12. Park JM, Bloom DA: The pathophysiology of UPJ obstruction. Current concepts. Urol Clin North Am 1998;25: 161–169. 13. Gerber GS, Kim JC: Ureteroscopic endopyelotomy in the treatment of patients with ureteropelvic junction obstruction. Urology 2000;55:198–202. 14. Utz DC, Zincke H: The masquerade of bladder cancer in situ as interstitial cystitis. J Urol 1974. 111:160–161. 15. Kaplan SA, Roehrborn CG, McConnell JD, et al: Baseline symptoms, uroflow and post-void residual urine as predictors of BPH clinical progression in the medically treated arms of the MTOPS trial. J Urol 2003;169(4 Suppl):332–333. 16. McConnell JD, Roehrborn CG, Bautista OM, et al: The long-term effect of doxazosin, finasteride and combination therapy on the clinical progression of benign prostatic hyperplasia. N Engl J Med 2003;349:2387–2398. 17. Hagerty J, Ginsberg P, Harkaway R: A prospective, comparative study of the onset of symptomatic benefit of dutasteride versus finasteride in men with benign prostatic hyperplasia in everyday clinical practice (Abstract 1353). Presented at the Annual Meeting of American Urological Association, San Francisco, CA, 2004. 18. Roehrborn CG, Boyle P, Bergner D, et al: Serum prostate-specific antigen and prostate volume predict long-term changes in symptoms and flow rate: Results of a four-year randomized trial comparing finasteride to placebo. PLESS Study Group. Urology 1999;54:662–669. 19. DiAmico A, Roehrborn C: Effect of 1 mg/day finasteride on concentrations of serum prostate-specific antigen in men with androgenic alopecia: A randomized controlled trial. Lancet Oncol 2007;8:21–25. 20. Malek RS, Kuntzman RS, Barrett DM: High power potassiumtitinyl-phosphate laser vaporization prostatectomy. J Urol 2000; 163:1730–1733. 21. Masood S, Djaladat H, Kouriefs C, et al: The 12-year outcome analysis of an endourethral wallstent for treating benign prostatic hyperplasia. BJU Int 2004;94:1271–1274. 22. Santucci RA, Joyce GF, Wise M: Male urethral stricture disease. In Litwin MS, Saigal CS (eds): Urologic Diseases in America. U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases. Washington, DC: U.S. Government Printing Office, NIH Publication No. 07-5512, pp 533–551. 23. Weiss RM, George NJR, O’Reilly PH: Comprehensive Urology. New York: Mosby International, 2001. 24. Lapides J, Diokno AC, Silber SJ, Lowe BS: Clean, intermittent self-catheterization in the treatment of urinary tract disease. Trans Am Assoc Genitourin Surg 1971;63:92–96.
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25. Kaufman JM, Fam B, Jacobs SC, et al: Bladder cancer and squamous metaplasia in spinal cord injury patients. J Urol 1977;118:967–971.
Further Reading Jones DA, George NJR, O’Reilly PH, Barnard RJ: The biphasic nature of renal functional recovery following relief of chronic obstructive uropathy. Br J Urol 1988;61:192–197.
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Klahr S: Obstructive uropathy. In Giebisch GH, Seldin DW (eds): The Kidney: Physiology and Pathophysiology, 3rd ed. Philadelphia: Lippincott–Raven, 2000, pp 2473–2512. Preminger GM, Harvey JA, Pak CY: Comparative efficacy of ‘specific’ potassium citrate therapy versus conservative management in nephrolithiasis of mild to moderate severity. J Urol 1985; 135:658–661.
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Obstructive Uropathy Christopher J. Cutie and W. Scott McDougal CHAPTER CONTENTS OVERVIEW
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CALCULI 469 Treatment Options 470 Prevention 470 Surgical Intervention 470
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BLADDER DYSFUNCTION
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URETEROPELVIC JUNCTION OBSTRUCTION BENIGN PROSTATIC HYPERPLASIA Treatment Options 472 Medications 472 Surgery 472
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Obstructive uropathy is defined as any functional impedance to the anterograde flow of urine. This obstruction may occur in the upper tract (renal pelvis, ureters), lower tract (bladder, urethra), or both, and may be the result of an intrinsic defect or extrinsic process. A common cause of renal function compromise, urinary obstruction may be diagnosed and treated with multiple modalities, depending on the nature and location of the obstruction. Timely diagnosis and treatment of acute obstruction, as well as the appropriate management of chronic obstruction, is a multidisciplinary effort requiring contributions by primary care providers, internists, nephrologists, urologists, and radiologists.
OVERVIEW The degree of urinary obstruction typically correlates with the patient’s clinical presentation. Complete bilateral obstruction results in anuria, whereas partial or unilateral obstruction may present with intermittent episodes of oliguria and polyuria. Clinical symptoms of urinary obstruction may include flank, suprapubic, or groin discomfort; recurrent urinary tract infections; dysuria; hematuria; stranguria; and acute or chronic renal failure. Acute bilateral obstruction results in postrenal failure. The serum blood urea nitrogen-to-creatinine ratio approximates 10:1 and the urine-to-plasma urea and urine-toplasma creatinine ratios are indistinguishable from intrarenal failure. Complete anuria requires a prompt evaluation for an obstructing process. Management of obstruction relies on adequate drainage of the urinary system. Bladder decompression may be achieved by placement of either a urethral catheter or suprapubic cystotomy tube. Drainage of the renal collecting system is possible both endoscopically in a retrograde fashion with a ureteral stent or percutaneously with a nephrostomy tube. Endoscopic procedures typically require administration of spinal or general anesthesia. In the setting of a critically ill patient with
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other significant comorbidities, nephrostomy tube placement is often the preferred technique because this can be performed under ultrasound guidance with either minimal intravenous sedation or local anesthesia. In either scenario, definitive intervention is necessary for the ultimate preservation of renal function. Although acute urinary obstruction must be managed expeditiously, chronic urinary tract obstruction also requires timely diagnosis and management. Chronic obstruction may predispose the afflicted patient to a variety of conditions that are wide-ranging in severity. Urine stasis often leads to bacterial colonization, with sequelae ranging from urinary tract infections and pyelonephritis to fulminant urosepsis and concomitant cardiovascular collapse. Long-standing partial obstruction may also compromise the functional integrity of various structures, particularly the bladder and upper tracts of the renal collecting system, both of which are fairly sensitive to intraluminal pressure changes. This chapter discusses the multiple causes of urinary obstruction as well as the diagnostic considerations and available treatment modalities of each.
CALCULI Urolithiasis is the most common cause of urinary obstruction, accounting for approximately $2.1 billion in health care expenditures annually.1 In the United States, 13% of men and 7% of women will be diagnosed with kidney stones at some point throughout their lifetime.2 Peak age at diagnosis in men is 30 years, whereas women exhibit a bimodal distribution, with peaks at 35 and 55 years. Although many of these stones are found incidentally and are not associated with symptoms of pain, obstruction, or infection, the risk of hospitalization and surgical intervention is ever present and increasing as the general population grows. Furthermore, 50% of patients with a history of urolithiasis will re-form stones within 5 years.2
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The majority of calculi are composed of uric acid, calcium oxalate monohydrate, calcium oxalate dihydrate, cystine, or ammonium magnesium phosphate (struvite) or some combination thereof. Stones typically form within the collecting system of the kidney and subsequently travel to distal portions of the urinary tract. However, they may also form at the site of a foreign body (i.e., stent, catheter, suture material, human hair). Depending on their size, composition, and conformation, stones may either pass spontaneously in the urine or impact anywhere along the course of the urinary tract. The three most common sites for stone impaction are the ureteropelvic junction (UPJ), the mid-ureter at the level of the iliac vessels, and the ureterovesicle junction. The ureteric caliber at the UPJ and ureterovesicle junction is generally smaller than that along the course of the ureter. Extrinsic compression by the iliac vessels where the mid-ureter crosses causes a narrowing of the ureteral lumen at this level. The likelihood of spontaneous passage of calculi is dependent on several criteria. These include stone size and shape, as well as patient anatomy and history of stone passage.3 However, due to the intrinsic variability of an individual’s ureteral caliber, as well as the conformation of calculi, these criteria serve merely as a guide and must be appropriately incorporated into each clinical setting. Reported percentages of spontaneous stone passage vary widely in the literature, ranging from 29% to 98% for stones 0.5 cm or smaller located in the proximal ureter compared with rates of 71% to 98% for those of comparable size located in the distal ureter.3 Stones ranging from 0.5 to 1.0 cm have a lower likelihood of spontaneous passage, with rates ranging from 10% to 53% for those in the proximal ureter; rates are somewhat better for the distal ureter, ranging from 23% to 53%.3 Moreover, recent studies have demonstrated the utility of -adrenergic blockers, calcium channel blockers, and nonsteroidal anti-inflammatory medications in facilitating spontaneous stone passage via ureteral smooth muscle relaxation.4,5
Treatment Options Dissolution therapy is an appropriate first-line treatment modality for uric acid and cystine stones. Uric acid stones, comprising 5% to 10% of all urinary stones, typically form in an acidic urine (pH 5.5).6 They are relatively soft compared with calcium oxalate and cystine stones and are associated with hyperuricosuria, low urinary volume, and persistently acidic urine. These stones are often radiolucent on radiographic imaging and measure a density of 500 Hounsfield units or less on computed tomography. Dissolution therapy with oral urine alkalinizing medications (potassium citrate) has been shown to be efficacious in as many as 80% of patients.6 Those patients failing dissolution therapy may then be further treated with a surgical intervention. Cystine stones, which account for approximately 1% of all urinary calculi, also form in acidic urine. Cystinuria results from a defect in the renal tubular absorption of the amino acids cystine, ornithine, lysine, and arginine. Patients with the inherited autosomal recessive disorder excrete in excess of 600 mg of cystine daily in their urine (normal 100 mg/day). In addition to increasing urine volume, first-line therapy remains urine alkalization with a goal urine pH of more than 7.0. Should dissolution therapy be ineffective, patients may also be treated with oral chelating agents, such as d-penicillamine (250 mg
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every 6 hours) or -mercaptopropionylglycine (250 mg every 6 hours) to increase urine cystine solubility.7 Cystine stone formers will often present with staghorn calculi. These stones are extremely dense ( 1200 Hounsfield units) and are therefore not amenable to certain treatment modalities, such as extracorporeal shock wave therapy (ESWL). Struvite stones, in comparison, form in alkaline urine. Commonly associated with chronic urinary tract infections secondary to urea-splitting pathogens (Proteus mirabilis, Klebsiella pneumoniae, Pseudomonas aeruginosa), these stones exist in a urine pH of more than 7.5. Urease splits urea into component ammonia groups, resulting in alkaline urine. Because these stones are closely associated with infection, definitive treatment relies on clearance of all stone burden and maintenance of a sterile urine, typically through antibiotic prophylaxis.
Prevention Prevention of recurrent urolithiasis is based on maintaining high urine volume, increasing the concentration of stoneinhibiting substances in the urine, and decreasing the concentration of lithogenic substances. Patients are encouraged to consume more than 2.5 L of fluid daily and to supplement their fluid intake with citrate-rich fluids, such as lemonade.8 Citrate binds calcium in the urine and inhibits calcium oxalate crystal formation. Foods rich in oxalate, such as tea, coffee, leafy green vegetables (spinach), rhubarb, nuts, and beer should be avoided. Meats and other protein-rich foods should also be consumed in moderation, as degradation of these purine-heavy foods results in elevated serum uric acid concentrations. Allopurinol may also be prescribed for those patients with hyperuricemia. Cystine stone formers should be counseled to reduce their intake of methionine-containing foods, such as meats and dairy products.
Surgical Intervention Recent advances in the endoscopic treatment of calculi and the significant improvement of lithotripsy devices have allowed the majority of surgical treatments to be performed in an outpatient setting. Holmium pulsed-dye lasers have become ever more powerful and are relatively easy to use. Furthermore, ureteroscopes and imaging equipment have dramatically improved, allowing excellent visualization of ureteral and renal pelvic anatomy and calculi. Renal stones measuring as large as 2 cm may now be treated with staged ureteroscopic procedures or ESWL, depending on the location and hardness of the stone. Selection criteria for surgical stone management include stone location, size, composition, collecting system/ ureteral anatomy, patient health/performance status, and patient preference. ESWL involves delivery of shock waves generated by electromagnetic energy sources. These shock waves are propagated through water and delivered to the stone burden under direct, real-time fluoroscopic imaging. To reliably use ESWL, patient selection is vitally important. The stone must be radiopaque and visualized on standard radiographs because fluoroscopy or ultrasonography is used intraoperatively to identify and target the stone. Shock waves are then delivered to the stone until evidence of fragmentation is identified. ESWL may often be performed under conscious sedation, although some
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patients may require administration of general anesthesia for improved tolerability. Although ESWL is noninvasive, it has been associated with specific risks, including cardiac arrhythmias, renal contusions, hemorrhage, and bruising. Recent studies also suggest that ESWL may be associated with the delayed development of diabetes due to pancreatic fibrosis secondary to shock wave injury.9 ESWL is appropriate for stones measuring as much as 1.5 cm located above the bony pelvis. The ischial body may impede shock wave propagation and mute the fragmentation effects on stones located in the distal ureter. Moreover, patients undergoing ESWL treatment must be warned of the risks of steinstrasse, literally translated as “a road of stone.” This occurs when a stone is broken into multiple smaller fragments and the lead fragment is unable to spontaneously pass, which causes ureteral obstruction proximal to the stone burden. Classic symptoms of flank pain, dysuria, and hematuria may result, and a secondary procedure (e.g., stent or nephrostomy tube placement, salvage ureteroscopy) is often necessary because the lead fragment will not pass. Ureteroscopy is defined as any endoscopic manipulation of the ureter and its contents. Since its development in the early 1980s, ureteroscopy has revolutionized the treatment of ureteral and renal stones.10 Whereas open ureterolithotomy for stone extraction was commonly performed through the 1970s and required an inpatient hospitalization, ureteroscopy allows outpatient treatment of most urinary stones today. Rigid and flexible ureteroscopes are currently available and are used either independently or in tandem depending on stone size and location. Standard ureteroscopes measure approximately 8 French in size and are introduced via the urethra to the level of the stone. Various tools, including holmium lasers and nitinol extraction baskets, are then used to fragment, retrieve, and remove the stone. A ureteral stent is typically placed for temporary renal decompression and to allow residual stone fragments to pass. This stent also mitigates the risk of ureteral obstruction from posttreatment ureteral inflammation and edema. If dissolution therapy fails or is not feasible, staghorn calculi and large renal stones are best treated with percutaneous nephrolithotomy, which requires nephrostomy access to the kidney via the flank. This procedure allows for high stone-free rates with fewer secondary procedures necessary.11 Open surgery, including pyelolithotomy and anatrophic nephrolithotomy, is rarely performed and reserved for those patients with highly complicated anatomy (e.g., crossed-fused ectopia, horseshoe kidney) or grossly enlarged stone burden (5 cm). With the increased popularity of laparoscopic procedures, minimally invasive pyelolithotomy is also frequently offered for large renal pelvic or ureteropelvic junction stones.
URETEROPELVIC JUNCTION OBSTRUCTION UPJ obstruction accounts for approximately 50% of prenatally diagnosed hydronephrosis. Classically, UPJ obstruction presents as a unilateral process; however, bilateral obstruction may occur. Causes of UPJ obstruction may be both intrinsic and extrinsic in nature. In some instances, there is a crossing anatomic vessel (an accessory renal artery or vein), which kinks the ureter at the level of the UPJ. Surgical correction of
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the anomaly with pyeloplasty and vessel transposition is the definitive treatment. Intrinsic defects within the ureter, including an aperistaltic segment secondary to malformation of the ureteral musculature as well as ureteral valves (Ostling’s valves) are a cause of UPJ obstruction in children.12 Diagnosis typically is made based on a 99mTc-mercaptoacetylglycine study or intravenous pyelography. Again, treatment involves a pyeloplasty and excision of this aperistaltic segment. Impacted ureteral stones and previous endoscopic ureteral manipulation, with concomitant ureteral inflammation and fibrosis, may also result in ureteral strictures, leading to UPJ obstruction. Excision of this stenotic segment and primary reanastomosis is the recommended treatment. Endopyelotomy or ureteroscopic incision of ureteral strictures and balloon dilatation have been reported as other initial management options with varying degrees of success.13 Before a major surgical repair, the degree of function in the affected kidney should be calculated. This is commonly performed using a dimercaptosuccinic acid scan, a radionuclide study that measures the uptake of tracer material within the renal tubules and is a reliable means of assessing renal function. Because the goal of therapy is to maintain existing renal function, which is not apt to improve after pyeloplasty, a simple nephrectomy as definitive treatment should be considered.
BENIGN PROSTATIC HYPERPLASIA Benign prostatic hyperplasia (BPH) is a commonly diagnosed condition that is responsible for a significant proportion of lower urinary tract complaints in middle-aged and elderly men. In the United States in 2000, this condition accounted for 117,000 emergency department visits and 105,000 hospitalizations, accounting for $1.1 billion in expenditures.1 A consequence of persistent testosterone stimulation, BPH occurs as a result of growth of adenomatous prostatic tissue. This is a benign condition and may be managed expectantly, pharmacologically, or surgically. Chronic obstruction, left untreated, results in recurrent bladder overdistention, which may lead to bladder trabeculation and formation of diverticula and cellules. These outpouchings of bladder epithelium can further predispose the patient to urinary tract infections, stone formation, and, most importantly, deterioration of the upper tracts leading to compromised renal function and ultimately renal failure. Patients with significant lower urinary tract symptoms should be evaluated by a urologist. Although symptoms of urinary frequency, hesitancy, and urgency may be attributed to BPH, evaluation of the lower urinary tract is required. Thorough physical examination should include suprapubic palpation and inspection of the penis for evidence of meatal stenosis or phimosis. A digital rectal examination is required, and patients are encouraged to complete a symptom score questionnaire. This questionnaire rates symptoms of nocturia, urgency, frequency, stranguria, force of urine stream, intermittency, and the need for second voiding and serves as a baseline for subsequent comparison after initiation of medical therapy or surgery. Cystoscopy is recommended for specific indications, such as hematuria, suspected bladder stones, or early bladder cancer. Transition cell carcinoma in situ is often associated with irritative urinary symptoms.14 A postvoid residual and uroflow are
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also important studies in the diagnosis of BPH. A postvoid residual greater than 200 mL is significant, as is a uroflow rate of less than 15 mL/sec.15 Ultimately, because this is a benign condition, informed treatment decisions should be based on patient satisfaction and perceived quality of life.
Treatment Options Medications There are two main classes of medications prescribed for treatment of symptoms of BPH: 1-adrenergic receptor blockers and 5-reductase inhibitors. -Blockers (terazosin, doxazosin, tamsulosin, alfuzosin) result in blockade of sympathetic peripheral 1 receptors, resulting in relaxation of both prostatic and bladder neck smooth muscle. These medications are generally well tolerated but, given their mechanism of action, may cause hypotension, dizziness, or syncope. -Blockers have been definitively shown to exhibit efficacy in the treatment of men with urinary symptoms attributable to BPH, but do not decrease the incidence of acute urinary retention episodes.16 5-Reductase inhibitors (finasteride, dutasteride) inhibit the enzyme 5-reductase, thus preventing conversion of testosterone to dihydrotestosterone, which is chemically active within the prostate and stimulates prostatic tissue growth. Such deprivation of dihydrotestosterone results in prostatic epithelial atrophy. Dutasteride (Avodart) inhibits both the type I and II forms of 5-reductase and may provide an increased benefit to patients.17 These medications are often used in tandem with -blockers and have been shown to demonstrate great efficacy in multiple studies.16,18 5-Reductase inhibitors do affect serum prostate-specific antigen (PSA) levels, typically decreasing them by 50%. Therefore, this decrease must be noted before initiation of 5-reductase therapy because treatment may influence the subsequent care of patients managed with routine PSA screening and monitoring tests. Furthermore, patients applying topical 5-reductase for hair growth (Propecia) must be informed that their serum PSA level will be reduced, typically by 50% as well.19 Combination therapy with both -blockers and 5-reductase inhibitors appears to have a synergistic effect, as studies have shown an approximately 50% decrease in disease progression compared with monotherapy.16 Of note, medications are not effective in patients with enlarged prostatic median lobes. The median lobe may serve as a ball valve, intermittently obstructing the bladder neck, resulting in outflow obstruction. These patients are best served by transurethral resection of this tissue. BPH may result in an elevated PSA, although not typically to the levels seen in aggressive prostate cancer. However, an elevated PSA may not simply be attributed to prostatic hyperplasia, and an appropriate evaluation and work-up is warranted.
Surgery Several technologic advances have vastly improved the urologist’s armamentarium of surgical options for treatment of BPH. In addition to the standard transurethral resection of prostate tissue using the electrosurgical resectoscope, new devices incorporating laser and microwave energy have resulted in safer, faster, and more cost-effective treatment strategies. Various laser vaporization technologies, including holmium
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and KTP (potassium titanyl phosphate), allow for significantly smaller intraoperative blood loss as well as fewer risks of postprocedure absorptive hyponatremia.20 Many patients are catheter free after these procedures and do not require an inpatient hospitalization. These devices use a wavelength of light (523 nm) that is absorbed by both blood and tissue, allowing for more exact tissue destruction and simultaneous hemostasis. Microwave therapy has also exhibited efficacy as an officebased treatment modality, using a special urethral catheter with a thermal coil that delivers highly focused energy to the prostatic bed with resultant tissue necrosis. After administration of mild sedatives and topical urethral lidocaine, this catheter is inserted in the standard fashion by a urologist and left in place for approximately 30 to 60 minutes. Expanding titanium urethral stents (UroLume) have also been developed for treatment of bladder outlet obstruction. These devices are endoscopically placed within the prostatic urethra and serve to stent open the urethral lumen by inhibiting coaptation of the prostatic lobes. Although success rates vary considerably for this procedure, these stents are associated with significant morbidity and are difficult to remove once urothelium has grown into them.21 These devices are often reserved for poor surgical candidates who are unable to endure general anesthesia for more invasive procedures, such as transurethral resection.
GENITOURINARY MALIGNANCY Occasionally, bladder, prostate, and urethral tumors may cause urinary obstruction. Muscle invasive bladder cancer arising from the trigone or base of the bladder can obstruct the ureteral orifices, resulting in hydroureteronephrosis. Transurethral resection of the tumor may alleviate this obstruction, but the cancer may recur if the resection is incomplete. Highly advanced prostate cancer may present with bladder outlet obstruction. Transurethral resection of the obstructing lesion is again the preferred treatment of choice. Both bladder and prostate cancers may often present in this situation with gross hematuria or clot retention. Urethral tumors, albeit rare, may also result in an intrinsic obstruction of urinary flow. Often, a catheter may be placed around the obstructing lesion as a temporary measure, followed by further workup and definitive treatment.
URETHRAL STRICTURE/STENOSIS A urethral stricture is a narrowing of the urethral lumen, resulting in a slowing or cessation of urine flow.22 Urethral strictures are significantly more common in males, given the far longer course of the male urethra compared with that of the female. Risk factors for urethral stricture disease include recurrent urinary tract infections or urethritis (i.e., gonococcal), trauma, previous urethral instrumentation or surgery, pelvic irradiation, and advanced age. Diagnosis is typically based on direct vision with cystoscopy as well as retrograde urethrography to delineate the anatomic location and length of the stricture. Treatment modalities include manual dilatation (metal sounds, balloon dilators), transurethral incision/ resection, and open primary repair. Because these strictures are typically composed of dense scar tissue, they tend to recur
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in the absence of definitive open surgery. A biopsy of the tissue at the stricture site should always be performed to rule out a coincident urethral tumor as the obstructing lesion. Presenting symptoms of urethral strictures often include urinary urgency and hesitancy, decreased force or caliber of the urine stream, persistent suprapubic fullness, recurrent urinary infections, the need for frequent second voids, and urinary retention. In some patients, the stricture is such that urethral catheter placement in the standard blind fashion is not possible, requiring placement of a catheter over a wire under cystoscopic guidance or placement of a suprapubic cystostomy tube for acute bladder decompression.
BLADDER DYSFUNCTION In the normal state, voiding is a reflex function under voluntary control. Coordinated voiding, characterized by external sphincter relaxation and subsequent detrusor contraction, is controlled by the pontine micturition complex’s effect on the sacral cord (S2-S4).23 The pontine micturition complex, in turn, is under cortical control. Detrusor hyperreflexia with coordinated external sphincter activity results from suprapontine lesions (e.g., stroke, Parkinson’s disease). This is in contrast to detrusor hyperreflexia without coordinated external sphincter activity, which is caused by a suprasacral spinal lesion (e.g., myelodysplasia, multiple sclerosis). Detrusor areflexia is caused by damage to the sacral reflex arc (e.g., neuropathy, disk herniation), and also occurs during the acute spinal shock phase after a spinal cord injury. Urodynamics, a real-time study that measures bladder pressure, abdominal pressure, sphincter activity, bladder compliance, and flow rate, is commonly used to delineate these disorders. Optimal bladder function relies on adequate maintenance of filling and emptying pressures in both the storage and expulsion of urine. During the filling stage, bladder pressures must be low enough to allow for transit of urine from the ureter to the bladder. Should the bladder pressure exceed the ureteral and renal pelvic pressures, urine will reflux in a retrograde fashion, resulting in ureteral dilatation. The ureter can withstand continuous intravesicle pressures as high as approximately 40 cm H2O. Higher resting pressures lead to ureteral damage and resultant renal compromise. The voiding stage is dependent on an important interplay between the bladder detrusor smooth muscle and the external skeletal muscle sphincter. At the initiation of a void, the external sphincter is relaxed under voluntary control, followed by contraction of the detrusor muscle. This allows for the coordinated flow of urine in an anterograde fashion. A defect in the detrusor muscle, external sphincter, or signaling neuron pathways therein results in bladder dysfunction. The result is a high-pressure bladder with inadequate voiding. Treatment modalities include anticholinergic medications (e.g., tolterodine, oxybutynin) to inhibit detrusor contraction. Clean intermittent catheterization is the ideal modality for bladder decompression in the patient with urinary obstruction secondary to neurogenic bladder dysfunction.24 Long-term indwelling catheters are not recommended because these can result in a host of complications, including recurrent urinary tract infections, urethral meatal erosion,
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orchitis, epididymitis, prostatitis, bladder calculi, and squamous metaplasia of the bladder epithelium, a premalignant condition.25 Clean intermittent catheterization requires diligent attention to patient hygiene, catheter care, and catheterization technique. Those patients with detrusor-sphincter dyssynergia, characterized by bladder hyperreflexia with coordinated external sphincter relaxation, are plagued by poor bladder compliance and outlet obstruction. Bladder augmentation with subsequent clean intermittent catheterization may be recommended for these patients to ensure adequate urine storage and drainage. However, in those not suitable for augmentation or the necessary maintenance techniques required, urinary diversion is also a viable option. A sphincterotomy may also be performed, but this ultimately results in incontinence.
EXTRINSIC COMPRESSION A variety of other oncologic and inflammatory conditions may result in obstructive uropathy as a result of extrinsic compression of one or both ureters, the bladder, or the urethra. Gynecologic malignancies arising from pelvic organs, such as the cervix, ovary, and uterus, may result in a mass effect on the ureters or trigone of the bladder, resulting in urinary obstruction. This may also result from masses of the colon and inflammatory processes, such as sigmoid diverticulitis, Crohn’s disease, and ulcerative colitis. Such inflammatory reaction may result in a reactive fibrosis around one or both ureters, leading to proximal obstruction of urine. With regards to tumor compression, this typically occurs as a chronic process, with the gradual onset of flank pain. Ultrasonography or computed tomography will often demonstrate unilateral or bilateral hydronephrosis in the setting of an enlarging pelvic mass, potentially in the absence of symptoms (silent hydronephrosis). Decompression of the renal collecting system with either a percutaneous nephrostomy tube or ureteral stent is indicated, as this obstruction may predispose the patient to renal failure in the setting of chemotherapy for the primary tumor. Moreover, as many of these patients are immunosuppressed due to immunotherapy or as a consequence of the disease, an obstructed collecting system may be a setup for urinary tract infections and subsequent urosepsis, which may prove fatal in the debilitated patient.
POSTOBSTRUCTIVE DIURESIS Urinary obstruction, either unilateral or bilateral, may result in fluid overload, renal insufficiency, and electrolyte abnormalities. However, relief of this obstruction may also result in profound effects on the patient’s volume status and electrolyte homeostasis. Acute decompression of the bladder will often result in polyuria and, in some cases, hematuria. This hematuria is due to decompression of previously dilated mucosal cystic vessels, which rupture in the setting of intravesicle pressure changes. It may be fairly significant and require clot evacuation and continuous bladder irrigation. Postobstructive diuresis may be physiologic, pathologic, or a combination of the two. Physiologic diuresis occurs as a result of fluid overload and elevated urea levels, which are
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excreted when the obstruction is relieved. Pathologic diuresis occurs as a result of increased tubule permeability and lack of an osmotic gradient in the renal medulla. Postobstructive polyuria is characterized by increased salt and water excretion and may vary widely with respect to volume. As many as 10% of patients will exhibit excessive diuresis, requiring intravenous fluid replacement. To accurately assess clinical improvement and normalization of volume status, daily weight, urine output, and orthostatic blood pressures are recorded. Plasma electrolytes should be monitored carefully (every 6–12 hours in the acute setting), particularly potassium, sodium, and magnesium, because these values demonstrate the degree of nephron recovery post-obstruction. Urine output is replaced with half normal saline, as the sodium content of the diuresis is typically approximately 70 mEq/L. Careful attention must be paid to avoid overhydration of the patient, thereby perpetuating the disease. Many patients with modest diuresis may eat and drink their way back to a normal volume state. Intermittent bladder drainage, once believed to mitigate hematuria, is not recommended as this typically serves only to confuse the accurate recording of urine output.
FETAL AND PEDIATRIC UROPATHIES Advances in diagnostic and treatment modalities for fetuses, infants, and children have had a tremendous impact on the management of urinary obstruction in this patient population. Congenital malformations, such as posterior urethral valves, a persistent prostatic utricle, or the sequelae of such neurological disorders as spina bifida may all result in obstruction. Posterior urethral valves, present in males, are remnant flaps of mucosal tissue within the urethra, typically at the level of the veru montanum in the prostatic urethra. These patients often present with prenatal oligohydramnios, bladder distention, and bilateral hydronephrosis. Diagnosis is confirmed with a voiding cystourethrogram, and treatment includes endoscopic valve ablation. Temporary decompression of the obstructed bladder in the setting of posterior urethral valves may be accomplished with a cutaneous vesicostomy, which is an incontinent urinary diversion. Longterm sequelae of renal obstruction may include an inability of the kidney to maximally concentrate urine. This predisposes affected children to polydipsia and intolerance to fluid deprivation.
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Further Reading Jones DA, George NJR, O’Reilly PH, Barnard RJ: The biphasic nature of renal functional recovery following relief of chronic obstructive uropathy. Br J Urol 1988;61:192–197.
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Klahr S: Obstructive uropathy. In Giebisch GH, Seldin DW (eds): The Kidney: Physiology and Pathophysiology, 3rd ed. Philadelphia: Lippincott–Raven, 2000, pp 2473–2512. Preminger GM, Harvey JA, Pak CY: Comparative efficacy of ‘specific’ potassium citrate therapy versus conservative management in nephrolithiasis of mild to moderate severity. J Urol 1985; 135:658–661.
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