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Adenocarcinoma of the Kidney The most common malignant tumor of the kidney is adenocarcinoma (hypernephroma), arising from the proximal convoluted tubule. It occurs two to three times as frequently in men as in women, with an increased incidence after age 40, and accounts for approximately 2% of adult cancers. Its cause is unknown, but chronic inflammation as from obstruction, cigarette smoking, and other agents is thought to contribute to the development of renal carcinoma. The affected patient often first reports hematuria but may also experience flank pain, a fever, or a palpable mass. Renal carcinoma may also be an incidental finding on an abdominal sonogram or abdominal CT examination.

Confirmation of a mass may be accomplished with an IVU, abdominal sonogram, MRI, or CT. Radiographically, the space-occupying lesion may be evident and can distort, stretch, and displace the kidney’s collecting system, as visualized on an IVU. CT is useful in demonstrating the density of the renal carcinoma and its degree of metastasis, including extension to adjacent areas and lymph nodes, as well as venous involvement. Abnormal vascularity is also readily visualized during angiography, sometimes surrounding an avascular necrotic center. MRI provides information regarding the spread of the renal carcinoma, especially into the renal veins and inferior vena cava.

If the carcinoma is caught early, surgical excision of the kidney provides a good cure rate, but metastatic renal carcinoma has a very poor prognosis. These tumors are relatively insensitive to chemotherapy and radiation therapy. The tendency of adenocarcinoma to metastasize early from the kidneys poses a serious threat. The most common sites of metastasis are the lungs, brain, liver, and bone. Because pulmonary metastases are common, a chest radiograph should be obtained immediately on discovering a renal carcinoma.

Bladder Carcinoma Most commonly originates in the epithelium and is called urothelial carcinoma (previously known as transitional cell carcinoma). Bladder carcinoma is usually seen in men more than 50 years of age and is the fourth most common cancer in men. Many industrial chemicals have been implicated as factors in the development of carcinoma of the bladder. Cigarette smoking has also been associated with bladder tumors, presumably because of carcinogenic metabolites being excreted in the urine.

Carcinoma of the bladder may produce fingerlike projections into the lumen or it may infiltrate the bladder wall. Plain radiographs may demonstrate punctate, coarse, or linear calcifications that are usually encrusted on the surface of the tumor, but occasionally lie within it. On excretory urograms, bladder cancer appears as one or more polypoid defects arising from the bladder wall or as focal bladder wall thickening. However, urography can detect only about 60% of bladder carcinomas because most are small when first symptomatic and are located on the trigone, where they can be difficult to visualize. Therefore all patients with lower urinary tract hematuria should undergo cystoscopy to exclude a bladder neoplasm.

CT with full distention of the bladder demonstrates a neoplasm as a mass projecting into the bladder lumen or as focal thickening of the bladder wall. This modality is excellent when MRI is not available for preoperative staging because it can determine the presence and degree of extravesical extension, involvement of the pelvic sidewalls, and enlargement of pelvic or para-aortic lymph nodes.

MRI can demonstrate the depth of bladder wall invasion. MRI is equal to or better than CT for this purpose.

Many carcinomas of the bladder have a low grade of malignancy, although they tend to recur repeatedly after surgical removal. More invasive tumors require removal of the entire bladder with transplantation of the ureters into a loop of ileum.

Cystitis Inflammation of the urinary bladder is most common in women because the urethra is shorter. The major cause is the inadvertent spread of bacteria present in fecal material, which reaches the urinary opening and travels upward to the bladder. Instrumentation or catheterization of the bladder is another important cause of cystitis, which is the most common nosocomial infection. The radiographer needs to keep the urine bag below the patient to prevent retrograde flow that may cause cystitis. Cystitis can also develop from sexual intercourse, with the spread of infecting organisms from around the vaginal opening. Urinary frequency, urgency, and a burning sensation during urination are typical clinical findings.

Although acute inflammation of the bladder generally does not produce changes detectable on excretory urography, chronic cystitis causes a decrease in bladder size that is often associated with irregularity of the bladder wall.

Using antibiotic and sulfa drug therapy, cystitis generally heals without complication.

Diverticula of the Bladder A bladder diverticula is a sac or pouch that occurs in the bladder walls, usually as a congenital condition. Many people are born with, and have diverticula in the bladder and have no symptoms at all. There may be one of these sac-like pouches or several. These diverticula can create problems over time if they continue to get larger and the exact location may make a difference as to how a person is affected and whether or not treatment will be necessary.

Often, diverticula found in the base of the bladder may create earlier symptoms, while one in the “dome” of the bladder may not produce any symptoms until mid-life or later. Diverticula can become large enough to prevent the bladder from emptying completely and the urine left in the bladder can become infected. With a urine, bladder or urinary tract infection, a person will feel the need to pass urine frequently, there may be blood in the urine as well and a burning or painful sensation upon urination.

Diagnosis cannot be made simply by physical examination. X-rays or a cytoscopy procedure are the screenings used to identify the condition. Often, it will be revealed when a physician is investigating for a cause for reoccurring urine infections.

Treatment will most likely involve a surgical procedure to remove the bladder diverticulum. While removal can sometimes be performed within the bladder, it will often involve dissection of the bladder to remove a large diverticula. The surgery is an in-patient, hospital procedure. Additionally, antibiotics and other medications may be prescribed to clear up and help prevent infections. Recovery is normally good. There may be catheter drainage of the bladder for 1-2 weeks. It is important to note that most diverticula do not cause problems and the chances of needing medical attention for these sacs or pouches increases with age.

Ectopic Kidney Is one that is out of its normal position (found in approximately 1 in 800 urologic examinations). Most are asymptomatic throughout life; however, there is an increased incidence of ureteropelvic junction obstruction or VUR. Ectopic kidneys are usually lower than normal, often in a pelvic or sacral location. In rare cases the ectopic kidney may be intrathoracic. Pelvic kidneys occur much more frequently than intrathoracic kidneys. In severe cases of ectopy, surgical intervention may be necessary. In some lean and athletic persons the kidney is mobile and may drop toward the pelvis in an erect position. This is termed kidney prolapse or nephroptosis. Nephroptosis can be distinguished from a pelvic kidney by the length of the ureter; if the ureter is short, it is a congenital pelvic kidney.

Whenever only one kidney is seen on excretory urography, a full view of the abdomen is essential to search for an ectopic kidney. Although the ectopic kidney usually functions, the nephrogram and the pelvicalyceal system may be obscured by overlying bone and fecal contents. Patient history can distinguish a true pelvic kidney from a kidney transplant, which typically is located in the right pelvis.

Crossed ectopia refers to a situation in which an ectopic kidney lies on the same side as the normal kidney and is very commonly fused with it. This is the second most common fusion anomaly. Both kidneys demonstrate various anomalies of position, shape, fusion, and rotation with crossed ectopy. The crossed kidney generally lies inferior to the uncrossed one, and its ureter crosses the midline to enter the bladder on the proper side. Its drainage may be impaired by malposition of its ureter within the renal pelvis, which may require surgical pyeloplasty repair.

Horseshoe kidney is the most common type of fusion anomaly, with men affected twice as frequently as women. In this condition, both kidneys are malrotated and their lower poles are joined by a band of normal renal parenchyma (isthmus) or connective tissue. The ureters arise from the kidneys anteriorly instead of medially, and the lower pole calyces point medially rather than laterally. The pelves are often large and flabby and may simulate obstruction. Obstruction at the ureteropelvic junction may occur because of the anterior position of the ureters. Kidney function is generally unimpaired with this condition; however, if obstruction is present because of the abnormal location of the ureters, pyeloplastic surgery may be required. The lower bridge frequently lies on a sacral promontory, where it is susceptible to trauma and may be palpated as an abdominal mass. Complete fusion of the kidneys is a rare anomaly that produces a single irregular mass that has no resemblance to a renal structure. The resulting bizarre appearance has been given such varied names as disk, cake, lump, and doughnut kidney.

Hydroureter Also known as megaureter. A megaureter is a wide ureter. It is the distention or abnormal enlargement of the ureter with urine or watery fluid, due to obstruction caused by any blockage that prevents urine from draining into the bladder. Is divided into primary (congenital) and secondary categories. Children present with this condition since it is congenital. Megaureters may be classified as obstructed, refluxing, obstructed and refluxing, and non-obstructed/non-refluxing. Bilateral involvement is present in about 20% of patients with primary obstructed megaureters. Males are affected more than females. The left side is more often affected than the right.

Indications of megaureter are increasing hydroureteronephrosis, decrease in renal function of involved kidney, and development of UTI or recurrent pain.

Primary obstructing megaureter is caused by a structural alteration in the muscular layers of the distal ureter. Partial obstruction in the abnormal distal segment of the ureter leads to progressive dilatation. Progression to hydronephrosis (i.e. dilation of the renal pelvis and calyces) occurs when the ureter no longer accommodates resistance to urinary drainage; pressure is then conveyed more proximally. Complete obstructions are rare and are invariably associated with a nonfunctioning renal unit at diagnosis.

Primary obstructed megaureters enter the bladder in a normal location on the trigone, with the ureteral orifice appearing unaffected.

Children with an obstructed megaureter may present with vague abdominal pain, hematuria, UTI, fever of unknown origin, or an abdominal mass. Associated abnormalities may include contralateral renal agenesis (9%-15%), contralateral ureteroceles, renal dysplasia and ureteral duplication. Increasing ureteral dilation warrants consideration of renal and ureteral drainage. Megaureters detected in neonates and infants may require drainage for infections that do not respond to antibiotics alone.

The diagnosis of obstructed megaureter is established radiographically based on definition of a dilated distal ureteral segment that inserts into a normal ureteral meatus. Diagnostic tests include renal or bladder ultrasonography and voiding cystourethrography (VCUG): This is performed to assess for the presence of vesicoureteral reflux and to further delineate the anatomy of the bladder and outlet. In boys with bilateral megaureter, posterior urethral valves must be excluded.

In mild cases of obstructed megaureter, physicians may monitor symptoms, perform periodic radiological imaging, and administer antibiotic prophylaxis. With improving or stable renal or ureteral dilatation and continued renal growth, prognosis (over 8 years of follow-up) is excellent.

Neurogenic Bladder Also called neuropathic bladder. A bladder dysfunction caused by interference with the nerve impulses concerned with urination. Neurogenic bladder causes periodic but unpredictable voiding; related to paralysis or abnormal function of the bladder.

The muscles and nerves of the urinary system work together to hold urine in the bladder and then release it at the appropriate time. Nerves carry messages from the bladder to the brain and from the brain to the muscles of the bladder telling them either to tighten or release. In a neurogenic bladder, the nerves that are supposed to carry these messages do not work properly.

With loss of motor function of the bladder, reduced filling pressures and detrusor pressures are observed. Increased residual volume of urine is also noted. Sensation of fullness and temperature is often diminished or absent. There are several different classifications of neurogenic bladder. Kinds of neurogenic bladder are flaccid bladder, spastic bladder. Spina bifida, cord injury, cord compression, acute infections, accidents that cause trauma to the brain or spinal cord, genetic nerve problems, heavy metal poisoning, demyelinating diseases or a lesion of the nervous system can cause a neurogenic bladder. Diabetic neuropathy, anticholinergics (inhibit parasympathetic nerve impulses), and alpha-adrenergic antagonists also diminish bladder muscle tone. Extensive pelvic surgery can interrupt the peripheral nerve fibers to the bladder, thereby creating a neurogenic bladder.

The following problems are often associated with a neurogenic bladder:

  • Urine leakage often occurs when the muscles holding urine in do not get the right message.
  • Urine retention often happens if the muscles holding urine in do not get the message that it is time to let go.
  • Damage to the tiny blood vessels in the kidney often happens if the bladder becomes too full and urine backs up into the kidneys, causing extra pressure.
  • Infection of the bladder or ureters often results from urine that is held too long before being eliminated.

The following are the most common symptoms of neurogenic bladder:

  • urinary tract infection
    • kidney stones
  • urinary incontinence
  • small urine volume during voiding
  • urinary frequency and urgency
  • dribbling urine
  • loss of sensation of bladder fullness

When neurogenic bladder is suspected, both the nervous system (including the brain) and the bladder itself are examined. Diagnostic procedures for neurogenic bladder may include the following: x-rays of the skull and spine, electroencephalogram (EEG), IVU, and cystogram.

Treatment is aimed at preventing infection, controlling incontinence, and preserving kidney function by enabling the bladder to empty completely and regularly. Specific treatment for neurogenic bladder will be determined on an individual basis by the physician. Treatment may include:

  • insertion of a catheter
  • prophylactic (preventive) antibiotic therapy
  • placement of an artificial sphincter – a procedure that involves placing an artificial cuff around the neck of the bladder that can be inflated to prevent urinary incontinence and deflated when it is time to empty the bladder.
  • surgery

Posterior Urethral Valve Are mucosal folds that protrude into the posterior (prostatic) urethra as a congenital condition. This valve is the most common cause of bladder outlet obstruction in male children. These can cause significant obstruction to urine flow. Such “valves” occur in men, are usually discovered during infancy or early childhood, and are commonly diagnosed by voiding cystourethrography. The valve is believed to result from abnormal embryologic development of the fetal posterior urethra. The classic categorization of posterior urethral valves is types I, II, and III.

All valves essentially obstruct normal bladder emptying. This mechanical obstruction increases voiding pressures and may alter normal development of the fetal bladder and kidneys. Typically, children with higher degrees of obstruction present earlier with the most severe symptoms. Permanent defects in the function of the kidneys, ureters, and bladder may result from prenatal maldevelopment — despite adequate decompression of the urinary tract after birth.

The clinical presentation of posterior urethral valve is extremely variable. Complications include impaired renal function, hydronephrosis, vesicoureteral reflux, and bladder dysfunction.

It is common for newborns to not void for the first 24 hours of life; thus, a history of anuria may be misleading. A presentation in the neonatal period of abdominal distention due to a dilated bladder, ureters, and kidneys or due to urinary ascites has also been recognized.

If the diagnosis of posterior urethral valve is not recognized at birth, within weeks of birth, severely affected boys often present with urosepsis, dehydration, electrolyte abnormalities, or failure to thrive. A poor, dribbling urine stream may be noted. Toddlers often present with voiding dysfunction or UTI, and school-aged boys usually come to the clinician’s attention because of urinary incontinence.

VCUG is necessary to confirm the diagnosis and to assess the bladder for associated findings of trabeculation, diverticula, and vesicoureteral reflux. The proximal urethra is dilated and the thin, lucent transverse membrane of the valve can be identified. The bladder neck is typically hypertrophic, leading to a lucent ring or collar. On voiding, the posterior urethra is dilated (i.e. shield shaped), and valve leaflets may be seen as lucencies, giving the appearance of a spinning top. If leaflets are not visible, a commonly associated finding of posterior urethral bulging distally over the bulbar urethra may be noted. The anterior urethra is typically underfilled, and voiding is incomplete.

The condition is corrected by endoscopic surgery at an early age to prevent renal damage.

Pyelonephritis Is a suppurative inflammation of the kidney and renal pelvis caused by pyogenic (pus-forming) bacteria. Unlike glomerulonephritis, which primarily involves the parenchyma (glomeruli and tubules) of the kidney, the inflammatory process of pyelonephritis affects the interstitial tissue between the tubules. The infection is patchy in distribution, often involves only one kidney, and is asymmetric if both kidneys are involved. Although the infection may spread from the bloodstream or lymphatics, the infection usually originates in the bladder and ascends by means of the ureter to involve the kidneys. Pyelonephritis often occurs in women and children. The disease frequently develops in patients with obstruction of the urinary tract (enlarged prostate gland, kidney stone, congenital defect), which causes stagnation of the urine and provides a breeding ground for infection. Instrumentation or catheterization of the ureter is also an important contributing factor to the development of pyelonephritis.

Patients with pyelonephritis have high fever, chills, and sudden back pain that spreads over the abdomen. Painful urination (dysuria) usually occurs. Large amounts of pus may be detected in the urine (pyuria), and bacteria can be cultured from the urine or observed in the urinary sediment.

In most patients with acute pyelonephritis, the excretory urogram is normal. Occasional abnormalities include generalized enlargement of the kidney on the symptomatic side, delayed calyceal opacification, and decreased density of the contrast material. A characteristic finding is linear striation in the renal pelvis, which probably represents mucosal edema.

The urographic hallmark of chronic pyelonephritis is patchy calyceal clubbing with overlying parenchymal scarring. Initially, there is blunting of the calyces, which then become rounded or clubbed. Fibrotic scarring causes a cortical depression overlying the dilated calyx. Progressive cortical atrophy and thinning may be so extensive that the tip of the blunted calyx appears to lie directly beneath the renal capsule. The urographic findings may be unilateral or bilateral and are often most pronounced at the poles. Chronic pyelonephritis may progress to end-stage renal disease with small, usually irregular, poorly functioning kidneys.

CT has become the modality of choice. Contrast-enhanced CT demonstrates the cortical changes and may show an associated abscess.

With the availability of antibiotic therapy, pyelonephritis generally heals without complication. However, fibrous scarring can cause irregular contraction of the kidney. Severe infection can destroy large amounts of renal tissue, leading to uremia or septicemia as a result of diffuse spread of infection throughout the body. In cases of chronic pyelonephritis, a long-term regimen of antibiotics is appropriate. If this is ineffective, more aggressive therapy may be required. Percutaneous drain placement is an alternative to surgery in such cases.

Renal Failure Acute renal failure refers to a rapid deterioration in kidney function that is sufficient to result in the accumulation of nitrogen-containing wastes in the blood and a characteristic odor of ammonia on the breath. In prerenal failure, there is decreased blood flow to the kidneys caused by low blood volume (e.g., because of hemorrhage, dehydration, or surgical shock), cardiac failure, or obstruction of both renal arteries. Postrenal failure is caused by obstruction of the urine outflow from both kidneys, most commonly a result of prostatic disease or functional obstruction of the bladder neck. Acute renal failure may also be the result of specific kidney diseases, such as glomerulonephritis, bilateral acute pyelonephritis, and malignant (severe) hypertension. Other causes of acute renal failure include nephrotoxic agents (antibiotics, radiographic contrast material, anesthetic agents, heavy metals, organic solvents), intravascular hemolysis, and large amounts of myoglobin (muscle protein) in the circulation resulting from muscle trauma or ischemia. Urine output may decrease to less than 400 ml per 24-hour period (oliguria).

Excretory urography in the patient with acute renal failure demonstrates bilateral renal enlargement with a delayed and prolonged nephrogram; vicarious excretion of contrast material by the liver occasionally results in opacification of the gallbladder. However, in most instances excretory urography is unnecessary in the patient with acute renal failure, especially as it is possible that intravenous contrast material can cause further damage to the kidneys in this condition.

Ultrasound is especially useful in the evaluation of patients with acute renal failure. In addition to demonstrating dilatation of the ureters and pelves caused by postobstructive hypernephrosis, ultrasound can assess renal size and the presence of focal kidney lesions or diffuse renal cystic disease. Renal parenchymal disease appears as a diffuse increase in echogenicity, with loss of corticomedullary differentiation. If a vascular cause is suggested clinically, color Doppler studies allow visualization of patency or occlusion. If this is unsuccessful, a radionuclide scan or an MRI study may show these vessels without the use of an intravenous contrast agent.

Treatment of predisposing conditions reduces the risk of acute renal failure becoming chronic or continued. Some physicians use diuretics to increase urine flow, and vasodilators to increase renal blood flow to help prevent the likelihood of more severe renal failure. Dietary modifications, including decreasing potassium and protein intake and increasing carbohydrates, can decrease the load on the kidneys. Antibiotics may be used to prevent or treat infections because of the high associated risk of sepsis with renal failure. In some cases, renal dialysis provides time for the kidneys to recover.

Like acute renal failure, chronic kidney failure may reflect prerenal, postrenal, or intrinsic kidney disease. Therefore, underlying causes of chronic renal failure include bilateral renal artery stenosis, bilateral ureteral obstruction, and intrinsic renal disorders, such as chronic glomerulonephritis, pyelonephritis, and familial cystic diseases.

A failure to clear nitrogen-containing wastes adequately from the circulation leads to the accumulation of excessive blood levels of urea and creatinine (waste products of protein metabolism) in the blood. This condition, called uremia, produces toxic effects on many body systems. Irritation of the gastrointestinal tract produces nausea, vomiting, and diarrhea. In the nervous system, uremia causes drowsiness, dim vision, decreased mental ability, convulsions, and eventually coma. A decreased ability of the kidney to synthesize erythropoietin, which helps regulate the production of red blood cells, leads to the development of anemia. In the skin, uremia causes intense itching (pruritus) and a sallow (yellowish) coloring resulting from the combined effects of anemia and retention of a variety of pigmented metabolites.

Because of the kidney’s role in maintaining water balance and regulating acid-base balance and electrolyte levels, chronic renal failure causes abnormalities involving all these vital functions. Retention of sodium leads to increased water retention and the development of generalized edema and congestive heart failure. An elevated serum potassium level is potentially life threatening because of its direct effect on cardiac muscle contractility and the possibility of causing an arrhythmia or cardiac arrest. A reduction of serum calcium can produce the muscle twitching commonly seen in uremic patients. Low calcium levels also lead to increased activity of the parathyroid glands, which results in the removal of calcium from bones and a high incidence of renal stones.

Ultrasound is most often the initial procedure in the evaluation of patients with chronic renal failure and demonstrates a small echogenic kidney. This modality can also allow assessment of renal size and the presence of focal kidney lesions or diffuse renal cystic disease, and it can be used to localize the kidneys for percutaneous renal biopsy.

The initial goal of treatment is to slow the nephron loss and minimize complications. Antihypertensive drugs assist in preventing the continuation of this process. It is essential to properly balance intake and output of fluids and electrolyte levels. The inevitable occurrence of kidney failure requires dialysis to maintain the balance of body fluids. At this point, kidney transplant may be suggested.

Ureterocele A simple ureterocele is a cystlike dilatation of a ureter near its opening into the bladder. In the simple (adult) type, the opening in the ureter is situated at or near the normal position in the bladder, usually with stenosis of the ureteral orifice and with varying degrees of dilatation of the proximal ureter. The stenosis leads to prolapse of the distal ureter into the bladder and dilatation of the lumen of the prolapsed segment. Ureteroceles usually result from congenital stenosis of the ureteral orifice. Ectopic ureteroceles are found almost exclusively in infants and children; most are associated with ureteral duplication. Children with ureteral duplication have an 80% incidence of an associated ureterocele. Ectopic ureteroceles often cause substantial obstruction, primarily of the upper pole, and kidney infection, and potentially can lead to renal failure. Treatment in this situation involves endoscopic or open surgical repair to allow for increased flow of urine into the bladder.

The appearance on excretory urography depends on whether opaque medium fills the ureterocele. If it is filled, the lesion appears as a round or oval density surrounded by a thin radiolucent halo representing the wall of the prolapsed ureter and the mucosa of the bladder (cobra head sign). When the ureterocele is not filled with contrast material, it appears as a radiolucent mass within the opacified bladder in the region of the ureteral orifice. Ultrasound is the modality of choice to evaluate infants and children. On ultrasound images, a ureterocele appears as a round cystlike structure within the bladder.

On excretory urography, an ectopic ureterocele typically appears as a large, eccentric filling defect impressing the floor of the bladder. The ureterocele arises from the ureter draining the upper segment of the duplicated collecting system. A mass effect, representing hydronephrosis, often involves the upper pole of the kidney and causes downward and lateral displacement of the lower portion of the collecting system.

Ureteroceles may need to be treated to preserve kidney function and to reduce the risk of infection. An endoscopic incision of the ureterocele (at the vesicoureteral junction) allows normal urine drainage into the bladder. More aggressive treatment includes surgical resection of the ureterocele with bladder reconstruction.

Vesicovaginal Fistula Is an abnormal connection between the urinary tract and the vagina that allows the continuous involuntary discharge of urine in the vaginal vault. It is the most common type of urinary tract fistula.

A vesicovaginal fistula can be caused by injury to the urinary tract, which can occur accidentally during surgery to the pelvic area, such as a hysterectomy. It can also be caused by a tumor in the vesicovaginal area or by reduced blood supply due to tissue death (necrosis) caused by radiation therapy, cesarean delivery or prolonged labor during childbirth, (the head of the fetus compresses the trigone or the bladder neck against the anterior arch of the pubic symphysis. This may result in tissue ischemia, necrosis and eventual fistula formation. Today, this cause is rare.).

The most common symptom is constant urine leakage from the vagina. Patients with vesicovaginal fistula often report painless unremitting urinary incontinence. This is also called total, or continuous, incontinence. Urinary incontinence may be exacerbated during physical activities, leading some women to confuse this with stress incontinence. Patients with vesicovaginal fistulas do not present with abdominal or flank symptoms. The patient may also experience irritation in the area of the vulva, and frequent urinary tract infections. Acute onset of vesicovaginal fistula immediately after pelvic surgery does not cause constitutional symptoms. If the Foley catheter is still in place, the first sign of impending fistula formation is the presence of hematuria.

Approximately 10-15% of fistulas do not appear for 10-30 days. Some fistulas may not manifest for months. Radiation-induced fistulas may not become apparent for many years after radiation treatment. The development of a typical radiation-induced fistula is heralded by radiation cystitis, hematuria, and bladder contracture. These symptoms are improved dramatically by the sudden presence of vesicovaginal fistula.

Diagnostic tests include intravenous pyelography to rule out coexisting ureterovaginal fistula or ureteral obstruction. When a ureter is involved in the margin of the vesicovaginal fistula, IVP may demonstrate a standing column of contrast within the ureter, extravasation of contrast around the distal ureter, or hydronephrosis. Cystography often demonstrates contrast leaking from the fistula tract and confirms the presence of vesicovaginal fistula. Most fistulas discovered after hysterectomy are located immediately behind the interureteric ridge and on the anterior vaginal vault.

If a vesicovaginal fistula is suspected, as an immediate therapy, the insertion of a urethral catheter to minimize urine leakage should be performed. In most cases, vesicovaginal fistulas must be closed surgically (either transabdominal or transvaginal).


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