Diagnosis

Localized clinical signs and symptoms are important clues in the diagnosis, but they are age dependent. Combinations of findings can be more useful than individual ones in identifying affected children.⁶ For example, neonates rarely present with symptoms specific to the urinary tract. Nonspecific symptoms of lethargy, irritability, temperature instability, anorexia, emesis, or jaundice predominate. Bacteremia is common with neonatal UTI, and a urine culture is an important aspect in the evaluation of neonatal sepsis.⁷ Confirmation of a UTI by microscopic examination and quantitative culture of a properly collected specimen is important. Older infants may present with nonspecific abdominal discomfort, emesis, diarrhea, poor weight gain including failure to thrive, and fever. Malodorous or cloudy urine may be reported by the parents.

Older children frequently present with dysuria and urinary frequency, urgency, and enuresis. Table 55-1 outlines the incidence of UTI symptoms as a function of age.^8,9 As the symptoms can sometimes be obscure, it is important that care providers have a high index of suspicion in ill-appearing children. An unexplained high fever in an infant or toddler should prompt the clinician to obtain a urine sample.

Analysis of a properly collected urine sample is the cornerstone in the diagnosis of UTI.¹⁰ Errors in diagnosis most commonly result from failure to confirm a clinically suspected UTI by culture, or by reliance on a specimen that has been inadequately collected or mishandled. Specimens may be obtained by bag collection, clean catch, urethral catheterization, and suprapubic aspiration. Although invasive, urethral catheterization (or suprapubic aspiration) clearly offers the lowest risk of false-positive results.¹¹ The results of a bag specimen or clean-catch specimen in a non-toilet-trained child are helpful only if negative.¹² Bag specimens can be useful in an infant with a history of UTIs or structural abnormalities in whom a fever is present, but the suspicion for a UTI is otherwise low. Positive findings should be confirmed using a catheter or aspiration specimen unless the clinical presentation and laboratory findings are unequivocal. The accuracy of positive findings from a bag specimen in an infant has been estimated at 7.5%,¹³ whereas those of the midstream clean catch specimen varies with age: 42% under 18 months of age and 71% from 3 to 12 years of age.¹⁴ Specimens should be either analyzed and plated immediately, or placed on ice to minimize bacterial multiplication prior to testing.

The accepted gold standard for diagnosis remains the quantitative urine culture. The historically accepted criterion for diagnosis is greater than 10⁵ colony-forming units per milliliter of a single bacterial species. The accuracy of such a positive finding on culture is estimated at 80% (single specimen) and 96% (confirmed by second culture).¹⁵ Table 55-2 outlines the probability of infection as a function of colony count and methods of collection that are used in children.¹⁶ One must avoid applying these criteria too strictly. The colony count varies as a function of hydration (dilution) and urinary frequency (bacterial multiplication time). One study of six untreated children with proven bacteriuria found colony counts to vary from 10³ to 10⁸ over a 24-hour period.¹⁷

Although clearly the most accurate laboratory test, urine culture results cannot provide an immediate diagnosis. As a result, initial treatment is generally guided by the urinalysis. Microscopic evaluation of a urine specimen should be done immediately on collection. This practice minimizes misleading ex vivo bacterial multiplication and deterioration of cellular elements. The identification of bacteria in an unspun urine specimen is very suggestive of significant bacteriuria.¹⁷ Pyuria (more than 10 leukocytes/mm³) is suggestive,¹⁸ but may also be seen in vaginitis, dehydration, calculi, trauma, chemical irritation, gastroenteritis, and viral immunization. Urinary Gram stain has been found to be reliable in detecting UTIs in young infants.¹⁹

A popular and indirect measurement of bacteriuria employs nitrite and leukocyte esterase analysis. Nitrate, normally present in urine, is converted to nitrite in the presence of bacteria. A positive nitrite reaction is indicative of bacteria with specificity and a positive predictive value approaching 100%.²⁰ The nitrate-to-nitrite reaction requires a relatively long incubation period. Thus, urinary frequency and hydration may produce a false-negative result. Inadequate dietary nitrate and infection caused by nitrite-negative organisms may also cause false-negative reactions.²¹ The combination of nitrite and leukocyte esterase is more sensitive and specific than either alone.²² Overall, the combination of dipstick analysis and microscopic examination for bacteria have a sensitivity and negative predictive value approaching 100%.²⁰

Classification

Classification of UTIs helps to determine the need for hospital admission and parenteral antibiotic therapy as opposed to outpatient oral antibiotic therapy. An attempt is made to distinguish between upper tract (pyelonephritis) and lower tract infections (cystitis). Fever, flank pain, and/or tenderness, and leukocytosis suggest pyelonephritis, and require antibiotics to minimize the risk of renal injury.

Laboratory studies designed to distinguish a lower tract from an upper tract UTI include antibody-coated bacteria assay, β₂-microglobulin excretion, antibodies to Tamm–Horsfall protein, and urinary lactic dehydrogenase assay and procalcitonin.23,24 These tests are not sufficiently reliable for routine clinical use and thus are not typically employed. Direct culture by ureteral catheterization or percutaneous puncture is reliable, although cumbersome, and represents an option in complicated clinical situations. A quite useful study for localizing infection to the kidney is a radioisotope renal cortical scan (e.g., technetium-99m dimercaptosuccinic acid) during the initial presentation of the patient with a documented infection (Fig. 55-1).

Another important consideration regarding classification is the distinction between re-infection and persistent infection. Re-infection with a new organism is very common. Persistent UTI with the same organism, although less common, is important as it implies either an ineffective antimicrobial therapy or a structural abnormality, such as a urinary tract calculus or ureteral obstruction.

Epidemiology

Figure 55-2 outlines the age- and gender-related incidence of UTIs. At all ages, with the exception of the neonatal period, the incidence of UTI is greater in females than in males. In both males and females, the incidence increases with advanced age. Although the male has one early peak in the newborn period, the female has two peaks, one at 3 to 6 years, and the other at the onset of sexual activity. The actual incidence of infection as a function of age and gender is difficult to determine from the literature. Table 55-3 summarizes the available data.¹⁶

Pathophysiology

Investigation

Treatment

Pathophysiology

Figure 55-7 depicts the various anatomic components of the competent UVJ as well as the abnormalities most often implicated in the genesis of VUR. The normal UVJ is characterized by an oblique entry of the ureter into the bladder and a length of submucosal ureter providing a high ratio of tunnel length to ureteral diameter. This anatomic configuration provides a predominantly passive valve mechanism.^58,59 As the bladder fills and the intravesical pressure rises, the resulting bladder wall tension is applied to the roof of the ureteral tunnel. This results in a compression of the ureter which prevents retrograde passage of urine. Intermittent increases in bladder pressure, such as the act of voiding, upright posture, activity, and coughing, are met with an equal and immediate increase in resistance to retrograde urine flow. This effect is supplemented by the active effects of ureterotrigonal muscle contraction and ureteral peristalsis. ^59,60

Ureters with marginal tunnels can be made to reflux during infection due to UVJ distortion, loss of compliance of the valve roof, and intravesical hypertension. Excessively high intravesical pressure in neurovesical dysfunction (NVD) or bladder outlet obstruction (BOO) may also potentiate reflux as may a structurally weak detrusor floor (e.g., diverticulum or ureterocele). As the submucosal ureter tends to lengthen with age, the ratio of tunnel length to ureteral diameter increases, and the propensity for reflux may disappear.58,59

Of critical importance is the concept of intrarenal reflux (IRR), which has been demonstrated clinically⁶¹ as well as experimentally.⁶² The usually oblique entry of the papillary ducts onto the surface of simple papillae inhibits IRR. In contrast, the papillary duct entrance onto compound papillae facilitates IRR (see Fig. 55-4). The critical pressure for IRR is considered to be about 35 mmHg in compound papillae.^62,63 Experimentally, this same pressure may cause scar formation in the absence of infection.^62,64 When occurring intravesically, this pressure has been associated with an increased risk of renal deterioration. Higher pressure is thought to be necessary to induce IRR in simple papillae. The combination of infection and IRR is particularly devastating. Focal scarring appears to result from the difference in susceptibility of the renal papillae to IRR. The polar distribution of compound papillae corresponds closely to the predominant occurrence of renal scarring in the upper and lower poles of the kidney.

Classification

Many attempts at classification of VUR have been advanced. Reflux has been described as low pressure (occurring during the filling phase of the VCUG) or high pressure (occurring only during voiding). Reflux due to a congenitally deficient UVJ is referred to as primary reflux, whereas that due to a BOO or neurogenic bladder is referred to as secondary reflux. Further classification includes simple reflux and complex reflux. Complex reflux includes the refluxing megaureter, the refluxing duplicated ureter, the refluxing ureter associated with a diverticulum or ureterocele, and the occasional refluxing ureter associated with ipsilateral ureteropelvic or ureterovesical obstruction.

The most clinically pertinent classification systems, however, have attempted to quantitate the degree of reflux. At the present time, VUR is graded from I to V according to the international classification system diagrammed in Figure 55-8.⁶⁵ This classification system is based not only on the proximal extent of retrograde urine flow and ureteral and pelvic dilatation, but also on the resultant anatomy of the calyceal fornices. This system is currently universally accepted and used extensively in the literature.

Grade I VUR refers to the visualization of a nondilated ureter only, whereas grade II VUR refers to visualization of a nondilated renal pelvis and calyceal system in addition to the ureter. Grade III reflux involves mild to moderate dilatation or ureteral tortuosity with mild to moderate dilatation of the renal pelvis and calyces. The fornices, however, remain sharp or only minimally blunted. Once the forniceal angle is completely blunted, grade IV reflux has developed. Papillary impressions in the majority of calyces can still be appreciated. Loss of the papillary impressions along with increased dilatation and tortuosity is referred to as grade V reflux.

Epidemiology

The incidence of VUR in otherwise normal children is thought to be quite low.⁶⁶ A much higher incidence of VUR, between 30–40%, is reported in patients undergoing evaluation for UTI.^67–70 It is important to note that the incidence rises as age decreases.⁷¹ Thus, the infant who is most vulnerable to the combination of UTI and VUR is precisely the pediatric patient in whom this combination is most likely to occur.

Although females account for the majority of reflux patients, a few important characteristics of males with VUR require comment. Although males account for approximately 14% of patients with VUR,⁷² an increased incidence of VUR (30%) is found in those males presenting with UTI.⁶⁹ Boys with VUR tend to present at a relatively young age (25% under 3 months) and younger children tend to have the more severe degrees of reflux.⁷²

Multiple studies have documented a significant risk of VUR in family members of patients with reflux. The reported risk of sibling reflux ranges from 27–34%,73–75 while as much as 66% of offspring of women with reflux also have VUR.⁷⁶ As a result of these studies, it has been suggested that siblings, especially those under 2 years of age, should have a screening investigation.^56,73,76 Another option is to perform a renal and bladder ultrasound in younger siblings and defer the VCUG if the ultrasound is normal, unless they have a documented UTI.

A particularly important subset of patients with reflux includes those who have secondary reflux. Most have NVD or BOO as the primary disease. Many patients, however, have reflux not because of increased bladder pressure alone, but rather because UVJ deficiency is associated with other congenital anomalies, such as imperforate anus,⁷⁷ ureterocele,⁷⁸ and bladder exstrophy. Although many patients with PUV have reflux due to or exacerbated by high intravesical pressure, as demonstrated by VUR resolution after valve ablation or vesicostomy, the incidence of VUR in PUV patients is only approximately 50%. Many have congenitally abnormal ureteral insertions.⁷⁹

Although a significant incidence of NVD exists in patients with imperforate anus, this is not a prerequisite for VUR.⁸⁰ The diagnosis of VUR in imperforate anus thus assumes a critical importance to the pediatric surgeon. Not only may the association of NVD potentiate increased severity of reflux and the development of infection, the presence of a rectourethral or rectovesical fistula provides the opportunity for severe urinary contamination. Consequently, we believe that the patient with a rectovesical or rectourethral fistula should be managed with a completely diverting colostomy rather than a loop.

In addition to these structural associations, important functional associations are found as well, including florid NVD, as seen in myelodysplasia,⁸¹ and a variety of more subtle voiding disturbances.^82–84 A particularly important subset of VUR patients are those who have uninhibited detrusor contractions (UDCs). Three important components of maturation are found with successful toilet training: (1) growth in bladder volume; (2) development of volitional control over the striated muscle sphincter; and (3) control over bladder smooth muscle. Delay in this maturation leads to UDCs. Many children with reflux and recurrent UTI have UDCs. Such involuntary or uninhibited bladder contractions are not caused by neurologic disease. Intense voluntary constriction of the striated sphincter occurs in an attempt to ensure continence and results in excessively high intravesical pressures. Pressures often exceeding 150 cmH₂O have been observed resulting in intravesical distortions, such as diverticula, saccules, trabeculations, and abnormal ureteral orifices.⁸⁵ Reflux occurred in almost half of the children studied with UDC and UTI.

Thus, all patients with VUR should be screened for frequency, urgency, and incontinence, which suggest UDC’s and voiding dysfunction. Vincent’s curtsy, a squatting maneuver spontaneously employed to prevent incontinence, is particularly suggestive.⁸⁴ That these UDCs may cause reflux is suggested by an enhanced resolution of reflux with anticholinergic drug therapy. Equally important is the potential for UDCs to cause a false-negative cystogram.

Diagnostic Evaluation

VUR is diagnosed with a cyclic voiding cystourethrogram (VCUG), with either radiopaque contrast medium or radioisotope.86,87 Body temperature contrast material, which is not excessively concentrated, is instilled into the bladder through a small catheter by gravity with modest pressure in a non-anesthetized child.

Imaging of the upper urinary tract (kidneys and ureters) is extremely important and may be accomplished by ultrasound and/or isotope renography. Both may detect scarring, but isotope renography is particularly sensitive and also defines the split differential function in the case of a small kidney. Ultrasound is helpful in quantitating renal growth and dilatation of the renal pelvis and/or ureters. Bladder views are important to obtain to check for bladder wall thickening, diverticula, distal ureteral dilatation, ureteroceles, and bladder emptying.

Patients with frequency, urgency, incontinence, and Vincent’s curtsy should also be considered for non-invasive urodynamic studies including a uroflow and perineal electromyogram with a postvoid residual. A filling cystometrogram is indicated to follow neurovesical dysfunction or in those who have failed therapy. The presence of UDCs or detrusor-sphincter dyssynergia should be resolved before consideration is given to an antireflux operation. Although not formally described in the literature, our impression is that intervention in an unstable bladder is likely to result in a failed repair.

Natural History

The natural history of VUR is extremely variable, and ranges from spontaneous resolution without nephropathy to clinically silent scar formation to recurrent pyelonephritis with hypertension and end-stage renal disease (ESRD). Numerous factors may contribute to the potential for resolution, including the patient’s age, the grade of reflux, the appearance of the ureteral orifice, the length of the ureteral submucosal tunnel, and the intravesical dynamics. The American Urological Association Pediatric Vesicoureteral Reflux Guidelines Panel in 1997 analyzed 26 reports comprising 1,987 patients with conservative follow-up, to estimate the probability of reflux resolution (Fig. 55-9).⁸⁸ In general, a lower reflux grade correlated with a better chance of spontaneous resolution.

Younger children are thought to have better prognoses for resolution of VUR, particularly infant males in the first year of life. This may be due to a heightened degree of trigonal growth, but the diminishing prominence of UDCs with age is also likely. Spontaneous resolution is relatively independent of grade in secondary reflux, implicating management of primary bladder dysfunction as the primary prognostic variable (Fig. 55-10).⁸⁹

Renal injury due to VUR may take the form of focal scarring, generalized scarring with atrophy, and failure of renal growth.⁹⁰ As a result, kidneys drained by refluxing ureters should be observed not only for scarring but also for renal growth with serial upper tract imaging by ultrasound.⁹¹ Reflux-induced renal injury is usually a result of the association of VUR with UTI.⁹² It has been generally considered that such injury is most likely in children under the age of 2 years.⁷¹ It is now clear, however, that the risk of renal injury from VUR extends well beyond this age.^70,92–94 Reflux can also cause renal injury in the absence of UTI because of the pressure effects from NVD and BOO. The ability of high intravesical pressure, when associated with VUR, to cause renal injury has been confirmed experimentally.⁹⁵

Significant renal injury in the absence of BOO, NVD, and UTI can be found in infants.96,97 The ureteral bud theory postulates that VUR associated with displacement of the ureteral orifice is associated with anomalies of renal differentiation.⁹⁸ Such ureters probably do not arise from the appropriate segment of the Wolffian duct and consequently make ectopic contact with the nephrogenic cord, resulting in abnormal renal development. Although this mechanism may be present in some patients, it is now clear that congenital VUR-associated renal injury in the absence of BOO, NVD, and UTI may occur in the presence of a normally positioned ureteral orifice.⁹⁹ This finding implies that pressure from in utero VUR may injure the developing kidney.

In a longitudinal study of 923 children, high-pressure bladder dynamics, severity of reflux, and frequency of UTIs were the chief contributing factors in the development of new scars or the worsening of old scars.⁹⁴ Children with low-grade VUR were relatively unlikely to develop progressive renal injury when compared with those children with grades IV and V reflux. A similar relationship is seen in infants and children with secondary reflux. When monitoring these patients for progression of renal injury as an indicator of success of a therapeutic regimen, one must be cognizant of the fact that sonographic evidence of new renal injury may take several months to become apparent.

There is little consensus regarding the long-term sequelae of minor renal scars detected by high-resolution renal cortical scans. However, in a small number of patients, a spectrum of symptomatic nephropathy exists, most notably renal parenchymal hypertension and ESRD. The significance and predominance of reflux nephropathy (RN) as a cause of renal parenchymal hypertension has been reviewed.¹⁰⁰ Approximately 30–65% of childhood hypertension is associated with RN. RN is an important cause of end-stage renal failure in children and adults.101–103 The 2008 report of the North American Pediatric Renal Trials and Collaborative Studies (NAPRTCS) lists reflux nephropathy as being the primary diagnosis in 5% of 9854 children who received transplants over the previous 20 years.²

Some patients so affected may not have had an evident prior infection or will have the first recognized infection at or near the time of diagnosis of ESRD.¹⁰¹ As histologic evidence of chronic pyelonephritis is found, preceding infection is likely, underscoring the silent progressive nature of RN and the need for meticulous long-term follow-up of children with VUR. Glomerular lesions play an important role in the progression of RN. There is a clear association between RN, ‘heavy’ proteinuria, and glomerular lesions that resemble focal segmental glomerulosclerosis.¹⁰⁴ Although the mechanisms of this disease remain uncertain, immunologic injury, macromolecular trapping with mesangial injury, vascular alterations with hypertension, and glomerular hyperfiltration have been implicated. The latter theory of glomerular hyperfiltration is presently favored.

Treatment

Nonoperative management of VUR (Box 55-2) is successful in most patients. Such management may be considered in four stages: (1) diagnostic evaluation; (2) avoidance of infection; (3) voiding dysfunction treatment; and (4) active surveillance. Diagnostic evaluation has been previously reviewed. However, it is important to stress that the exclusion and treatment of voiding dysfunction and BOO is imperative. Patients with problematic uninhibited detrusor contraction can be managed with low-dose anticholinergic medication, such as oxybutynin hydrochloride. Side effects are manageable and include constipation and facial flushing/dry mouth. Voiding dysfunction with retentive characteristics may require timed/double voiding, alpha blockers, biofeedback, and in severe cases, intermittent catheterization (IC). Secondary reflux from neurovesical dysfunction often requires aggressive bladder management with IC and anti-cholinergics.

Good hydration, perineal hygiene, and bowel management are crucial and apply to all patients. With the exception of the asymptomatic toilet-trained child with low-grade reflux and normal kidneys, most children will benefit from low-dose continuous suppressive antibiotics (Table 55-4). It is important to remember that the prophylactic dose is approximately one-quarter the dose to treat an acute infection. Although generally well tolerated and having been a common practice for decades, the long-term implications of chronic antimicrobial suppression remain incompletely investigated and are actively debated.^4,45,105 Currently a prospective, multicenter, double-blind, placebo-controlled clinical trial of 600 patients funded by the National Institutes of Health is underway called the Randomized Intervention for Children with Vesicoureteral Reflux (RIVUR study).¹⁰⁶ This may help further define the role of antibiotic prophylaxis in the management of VUR. Until more evidence-based guidelines are published, the clinician must use caution in treating children with risk factors for recurrent UTI and renal scarring, including VUR.

Once a nonoperative regimen is selected, the patient is committed to long-term, strict surveillance. Renal imaging is performed every six to 12 months, depending on the age at diagnosis and the stability of the disease. Attention is directed at both renal growth as well as the detection of focal scarring. Voiding cystourethrography is generally performed no more often than once a year. The child’s growth, renal function, and blood pressure are monitored. The role of urodynamics has been previously outlined. Cystoscopy is rarely necessary except at the time of antireflux surgery when it is performed to exclude urothelial inflammation and to confirm the position and number of ureteral orifices.

While the decision to perform antireflux surgery must be carefully individualized, absolute indications for surgical correction of VUR include (1) progressive renal injury; (2) documented failure of renal growth; (3) breakthrough pyelonephritis; and (4) intolerance or noncompliance with antibiotic suppression. Other relative indications for correction of VUR are high grade (IV–V) reflux in young children after a year of conservative follow-up, pubertal age with nephropathy at diagnosis, parental preference, and failure to spontaneously resolve with watchful waiting.

The American Urological Association (AUA) Pediatric Vesicoureteral Reflux Guidelines Panel published their recommendations for management of VUR in children in 1997 and updated their guidelines in 2010. For VUR in an infant diagnosed after a febrile UTI or found to be high grade (III–V), then continuous antibiotic prophylaxis is still recommended. It is also recommended for an older child (>1 year of age) with recurrent febrile UTI, bowel/bladder dysfunction, and/or renal cortical anomalies. For asymptomatic older children with normal kidneys, suppression is an option. Breakthrough UTI management guidelines are summarized in Table 55-5.^4,88 There is little solid evidence or consensus about the management of VUR in older school-age patients or about the length of time that the clinician should observe nonoperatively before recommending surgery. The actual decision must be carefully individualized after a thorough discussion of all the treatment options with the parents.

The established principles of successful ureteral reimplantation include: (1) adequate ureteral exposure and mobilization; 2) meticulous preservation of the blood supply; and (3) creation of a valvular mechanism whose submucosal tunnel length to ureteral diameter ratio exceeds 4 : 1. These goals can be attained by a variety of procedures, most commonly via an open Pfannensteil approach but also laparoscopically and robotic-assisted (Fig. 55-11).

Important differences exist between these operative procedures. Variables include (1) presence or absence of a ureteral anastomosis; (2) need for detrusor closure; (3) transgression of urothelium; and (4) whether the neohiatus is fashioned by an appropriately sized detrusor incision or by the closure of the detrusor around the ureter. Performance of a ureteral anastomosis increases the risk of postoperative obstruction, whereas the need for detrusor closure increases the risk of diverticula. Table 55-6 outlines the specific advantages and disadvantages of some representative procedures. Three of the most commonly employed operations for the treatment of primary VUR are diagramed in Figures 55-12 to 55-14.

In general, excellent results are nearly uniformly attainable with an open approach and early reports of robotic-assisted laparoscopic outcomes are encouraging.¹⁰⁷ A meta-analsysis in 1997 of 86 reports, including 6472 patients (8563 ureters), found overall success for an open ureteral reimplantation to be 96%.⁸⁸ Success was achieved in 99% with grade I, 99.1% with grade II, 98.3% with grade III, 98.5% with grade IV and 80.7% in grade V.

At our institution, we prefer the extravesical detrusorrhaphy approach (see Fig. 55-12).^108–110 Because the lumen of the bladder is not entered, there is no postoperative hematuria, with minimal bladder spasms and a short hospitalization. The absence of a uretero-vesical anastomosis decreases the risk of postoperative obstruction. No ureteral stents, suprapubic catheters, or perivesical drains are needed. The urethral catheter is removed on the first day after unilateral surgery and the second day following bilateral reimplantation. Once the patient voids, he/she is discharged on oral antibiotics for 1 week, then is placed back on suppression for 3 months.

Postoperative analgesia can be maintained with either an indwelling or single-shot epidural placed at the time of surgery, or infiltration of local anesthesia in the incision supplemented by intravenous narcotics as needed. The majority of children are discharged home simply on oral acetaminophen alone. Postoperative imaging includes a renal and bladder ultrasound at 2 weeks, 3 months, 12 months, and 24 months after the procedure. A VCUG is not typically obtained in an asymptomatic patient due to the high success rate of the procedure.

The four major principles of a successful extravesical detrusorrhaphy are: (1) complete mobilization of the ureter from the peritoneal reflection to the UVJ, leaving a wide sheath of its peri-adventitial blood supply; (2) distal fixation of the ureter with long-acting absorbable sutures; (3) wide mobilization of the detrusor muscle flaps to enable firm approximation of the detrusor over the ureter; and (4) development of a sufficient tunnel length. The use of the extravesical detrusorrhaphy has been successfully expanded to include a tapered excisional megaureter repair,¹⁰⁹ reimplantation of the ureters associated with paraureteral Hutch diverticula,¹¹¹ as well as correction of VUR associated with duplicated collecting systems.¹¹²

Complications of ureteral reimplantation are rare.88,113 The most common complication is de novo contralateral reflux,¹¹⁴ while the most common technical complications are ureteral obstruction, persistent reflux, and diverticula formation. Persistent reflux may be caused by an insufficient tunnel length to ureteral diameter ratio. However, the greatest risk for postoperative reflux is related to the high-pressure voiding dynamics due to uninhibited bladder contraction, detrusor sphincter dyssnergia, and/or urinary retention. Ureteral obstruction may be due to ureteral kinking (at the neohiatus or obliterated umbilical artery), an excessively high placed neohiatus, construction of a tight neohiatus, twisting, anastomotic stricture, devascularization, and tight tunnel.

With attention directed toward the avoidance of technical complications and the selection of a procedure associated with the lowest complication rate, ureteral reimplantation remains a safe and highly successful operation. The extravesical approach for bilateral ureteral reimplantation has been questioned because of a reportedly high incidence of postoperative urinary retention.¹¹⁵ In our experience with a large group of patients, we have found acceptable rates of temporary incomplete bladder emptying (4%) which is transient and has minimal morbidity.¹¹⁶ Risk factors appear to be infants under age one and girls with large, thin-walled bladders and preexisting retentive voiding dysfunction.

In 1984, a minimally invasive endoscopic procedure for the correction of VUR was reported (Fig. 55-15). This subureteral transurethral injection (STING) utilized polytetrafluoroethylene (Teflon) and has been used successfully outside the USA for many years.¹¹⁷ Many different injectable materials have subsequently been investigated and reported.118–120 This ambulatory procedure performed under a brief general anesthetic has low morbidity and children may return to full activity as soon as the next day. The initial success rates were promising; however, they did not quite match those of ureteral reimplantation.¹²¹

In 2001, the Food and Drug Administration approved dextranomer/hyaluronic acid copolymer (Deflux) as the first injectable substance indicated in the USA for grades I-IV vesicoureteral reflux.¹²² This substance is biodegradable, has no immunogenic properties, and does not seem to have potential for malignant transformation. Results vary, but most studies show success rates of around 70–80% for abolishing reflux.^122–125 Higher success rates with larger injected volumes and multiple injection sites have been reported.¹²⁶ Long-term reflux resolution rates appear to be stable, but recurrence has been found a year after the procedure.¹²⁷

Other complications such as ureteral obstruction appear to be very low. Dysuria, gross hematuria, and urinary frequency occasionally occur, but are self-limiting. Flank pain and fever are rare. In our institution, a VCUG and renal ultrasound are obtained 3 months after the procedure, but the cystogram is not subsequently repeated if the patient remains asymptomatic off antibiotic prophylaxis. Patients having a febrile UTI after an apparently successful procedure should be re-investigated with a VCUG to assess for recurrent reflux.¹²⁸

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