UTI and Vesicoureteral Reflux Flashcards
How do you diagnose vesicoureteral reflux?
Vesicoureteral reflux (VUR) is the most common disease of the urinary tract in children, occurring in 1 to 2% of the pediatric population and in 30 to 40% of children presenting with a urinary tract infection (UTI).
The familial nature of VUR is well recognized.
Siblings of children with VUR are at a much higher risk for reflux than the general pediatric population with a reported prevalence between 25 and 50%.
The association of VUR, febrile UTI, and renal parenchymal damage is well recognized.
Reflux nephropathy is a cause of childhood hypertension and chronic renal failure.
The diagnosis is made by voiding cystourethrogram (VCUG) which allows grading of the VUR.
The main goals of treatment of children with VUR are to prevent renal parenchymal damage and morbidity associated with recurrent febrile UTIs.
Treatment options for children with VUR include non-surgical and surgical management.
The various treatment options currently available for VUR are:
(1) long term antibody prophylaxis;
(2) minimally invasive endoscopic treatment;
(3) ureteral reimplantation by open, laparascopic or robotic-assisted procedures; and
(4) observation or intermittent therapy with management of bladder/bowel dysfunction (BBD) and treatment of UTI as they occur.
What is the pathophysiology of VUR?
Normally, urine flows down the urinary tract, from the kidneys, through the ureters, to the bladder.
In VUR, there is retrograde flow of urine up through one or both ureters and kidneys.
What is the etiology of VUR?
VUR in children can be divided into primary and secondary. In primary VUR, the valve between the ureter and the bladder does not close well, so urine flows back into the ureters; in secondary VUR, there is an anatomical or functional blockage in the posterior urethra, which stops some of the urine from leaving the bladder, so the urine flows back into the upper urinary tracts. Not infrequently the patient may have neuropathic bladder in which nerves to the bladder may not work well, preventing the bladder from relaxing and contracting normally to release urine.
What is the prevalence of VUR in normal children?
As VUR can resolve spontaneously with age it is difficult to accurately determine
the exact prevalence of VUR. The reported prevalence of VUR is 0.4–1.8%.
What is the incidence of VUR in children with urinary tract infection (UTI)?
The incidence declines with age. Among infants less than 1 year of age presenting with UTI, the incidence of reflux is as high as 70%, those less than 5 years of age have an estimated incidence of 25–40% [1].
Which individual risk factors for UTI (with or without VUR) in children do you know?
Individual risk factors include white race, age <12 months, bladder/bowel dysfunc- tion (BBD), and structural anatomical abnormality of the urinary tract [2].
What is the probability of VUR among febrile infant girls and infant boys?
Girls are more likely than boys to have VUR. However, when a UTI is diagnosed, boys are more likely than girls to have VUR (29% versus 14%). Furthermore, a child is more likely to have VUR if a brother, sister, or parent was diagnosed with VUR. Finally, in children with BBD, VUR is commonly seen.
Do children who present with their first febrile UTI have to be evaluated for VUR?
This is still an ongoing controversy. According to the American Academy of Pediatrics (APP) 2011 clinical practice guidelines, a voiding cystourethrography (VCUG) is not recommended routinely after the first UTI. In contrast, the EAU (European Association of Urology) Guidelines 2012 advocate a VCUG at age 0–2 after the first proven UTI. There is a consensus that VCUG is indicated if renal and bladder ultrasonography reveals hydronephrosis, scarring, or other findings that would suggest either high-grade VUR or obstructive uropathy and in other atypical or complex clinical circumstances. VCUG should also be performed in cases of recurrent febrile UTIs [2].
Does every child with VUR have symptoms?
No, many children with VUR do not have symptoms.
If a child is symptomatic, what are the most common symptoms?
UTI is the most common symptom at presentation with or without fever, dysuria, urgency and frequency of micturition, daytime dribbling and abdominal pain.
What are the most common complications of VUR?
Reflux nephropathy which may lead to childhood hypertension and chronic renal failure.
How do you make the diagnosis of VUR?
Voiding cystourethrogram (VCUG) is the gold standard test to detect the backflow of urine from the bladder to the kidneys (Fig. 48.1).
Abdominal ultrasound is used to rule out structural abnormalities (upper urinary tract obstruction, dilated ure- ters) as well as renal scarring.
Recently a new technique called contrast-enhanced voiding urosonography (ceVUS) has been proposed as an alternative to the VCUG without radiation.
Describe the procedure of a VCUG.
The child lies down on the fluoroscopy table with the legs in butterfly position.
A transurethral catheter is then placed in the bladder.
After emptying, the bladder is filled with contrast media to evaluate for abnormalities of the bladder wall and possible VUR.
When the bladder is filled with contrast the older child may be able to tell the technologist when he/she is not able to hold it any longer.
Infants and young children will not be able to communicate this to the technologist. Then the child micturates under fluoroscopy.
The purpose is to detect a possible VUR and to assess the bladder and urethra during urination.
Finally, complete bladder emptying is confirmed. The catheter is removed as soon as the x-ray is taken.
How is VUR graded?
Reflux is graded according to the International Reflux Classification (Fig. 48.2). In grade I, the urine flows back into one or both nondilated ureters but does not reach the kidney. Grade II demonstrates a urinary flow back into the kidney, but does not cause dilation of the renal pelvis. In grade III there is mild to moderate dilation of the ureter and the renal pelvis. Finally, in grade IV, the ureter is dilated and tortu- ous, the renal pelvis and calyces are dilated with blunting of fornices. In grade V there is severe dilation of the ureters, renal pelvis and calyces with loss of papil- lary impressions.
Can VUR resolve spontaneously?
Yes. When UTIs are prevented by continuous antibiotic prophylaxis (CAP), as many as 87% of grade I, 63% of grade II, 53% of grade III, 33% of grade IV and only approximately 9% of grade V may spontaneously resolve over time [3].
How long does it take for VUR to resolve spontaneously?
The mean time for spontaneous resolution from the initial presentation is about 3 years [3].
Can sterile reflux lead to renal damage?
Sterile reflux usually does not cause kidney damage, but high-grade sterile reflux may contribute.
Which conditions are required to produce renal scarring?
VUR, bacterial infection and intrarenal reflux.
How long does the renal parenchyma take to develop renal scarring?
Scarring can take as long as 5 months to 2 years from the time of the acute urinary tract infection to evolve [4], but the proportion varies in different studies.
What is the most common method to detect renal scarring?
Dimercaptosuccinic acid (DMSA) scintigraphy. Recently contrast-enhanced ultrasound (CEUS) has also been verified as a highly sensitive, rapid and radiation free technique to evaluate renal scars.
What are the treatment options for children with VUR?
Non-surgical and surgical management.
Which non-surgical treatments do you know?
As in some cases VUR resolves spontaneously surveillance and prophylactic antibiotics are the first line treatment.
What is the current concept of continuous antibiotic prophylaxis (CAP)?
Several well-conducted trials have been carried out with the intent to define the role of CAP in the management of VUR, but no definite conclusion could be drawn from the data. Currently CAP is recommended mainly in patients diagnosed with VUR within the first year of life as well as in girls with high-grade (III-V) VUR and recurrent febrile urinary tract infections.
Can antibiotic prophylaxis prevent renal scarring?
Antibiotic prophylaxis does not prevent renal scarring according to a recent meta-analysis.
What are the indications for surgical treatment?
Surgery is indicated in children with a low probability of spontaneous resolution, recurrent pyelonephritis, and breakthrough febrile UTI while on CAP, renal scarring, grade IV–V reflux, VUR into complete duplex systems and parental preference.
What are the surgical options to treat VUR?
Endoscopic injection of bulking agents and ureteral reimplantation by open, lapa-
roscopic or robotic–assisted procedures.
What is the incidence of ureteral obstruction (UO) after endoscopic bulking agent injection for VUR?
Less than 1% of treated cases.
Does the type of injected bulking agent influence the incidence of ureteric
obstruction (UO) after endoscopic injection?
No. The incidence of UO is independent of the injected substance, volume, and technique [5].
Which factors influence the success of the bulking agent injection?
Pre-operative reflux grade, presence of functional or anatomic bladder abnormali- ties such as voiding dysfunction and duplicated collecting systems, surgeon expe- rience, and injection technique.
Which techniques for injecting a bulking agent are used nowadays?
The most commonly used bulking agent for endoscopic injection is Dextranomer/ Hyaluronic Acid. In STING technique, the bulking agent is injected 2 to 3 mm distal to the ureterovesical junction after advancement of the needle in the submucosal plane for 4 to 5 mm.
A correctly placed injection creates the appearance of a nipple, on the top of which is a slit-like orifice.
The Hydrodistention-implantation technique (HIT) describes a method in which the needle is inserted into the floor of the distal ureter.
“Double HIT” means proximal and distal intraluminal injection sites that coapt both the ureteral tunnel and orifice. HIT/STING are also performed in combination.
What are host factors that contribute to the pathophysiology of UTIs?
Host Factors
The establishment of clinical infection and its consequent injury to the urinary tract results from a complex interplay between host resistance and bacterial virulence. Generally, UTI-causing organisms originate from the feces of their host.
Conceptually, four levels of defense are identifiable: periurethral, bladder, ureterovesical junction, and renal papillae. These concepts are illustrated in Figure 55.3.
Bacteria generally possess an ability to adhere to vaginal mucosal cells in order to readily establish infection. The resultant periurethral colonization then allows replication and migration, which ultimately lead to transurethral invasion to the bladder.
Healthy girls have low bacterial colonizations of the periurethral region. Girls prone to UTIs experience greater colonization, especially prior to a new episode of UTI. Moreover, the cultured organism from the introital region belongs to the same strain as that from the urine during the UTI that ensues.
Periurethral bacterial colonization is correspondingly low in UTI patients after resolution of recurrent UTIs.
A similar mechanism may apply to bacterial adherence in the prepuce of males. This may explain why 92% of male infants <6 months old with a UTI are uncircumcised.
A number of bladder defense mechanisms help maintain sterile urine. The most critical is the act of regular and complete voiding. The healthy bladder is capable of eliminating 99% of instilled bacteria, which leaves a small residual urine that minimizes the inoculum at the onset of the following cycle.
High intravesical pressure may also potentiate infection in children. In the absence of an elevated residual urine, uninhibited bladder contractions are associated with an increased risk of recurrent UTI, which may be lessened by anticholinergic therapy.
Dysfunctional elimination syndrome with abnormal voiding habits and constipation can affect the development of UTI as well.
The acidic pH of urine, as well as its osmolality, further discourages bacterial growth.
The uroepithelial cells of healthy individuals suppress bacterial growth and are capable of killing bacteria. The uroepithelial cells secrete a mucopolysaccharide substance that, on coating the surface of the uroepithelium, provides an additional barrier to uroepithelial adherence.
Glycosaminoglycans are continuously shed and thus function to entrap and eliminate bacteria.
Abnormalities at the ureterovesical junction (UVJ) and altered ureteral peristalsis may allow vesicoureteral reflux (VUR), which potentiates but is not always necessary for upper tract invasion.
Distortion of the pyramids allows renal parenchymal invasion, which results in irreversible renal injury.
The anatomy of the renal papillae helps prevent intrarenal reflux (IRR).
Structural abnormalities that potentiate infection include phimosis, obstructive uropathy at any level (e.g., ureteropelvic [UPJ] and UVJ obstructions, posterior urethral valves [PUV]), VUR, bladder diverticula, urinary calculi or foreign bodies, and the renal papillary anatomy.
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What are bacterial factors potentiating UTIs?
Several bacterial factors may potentiate a UTI and are outlined in Box 55.1.
O antigens are lipopolysaccharides that are part of the cell wall. They are thought to be responsible for many of the systemic symptoms associated with infection. Of the more than 150 strains of Escherichia coli identified by O antigens, nine are responsible for the majority of UTIs.
K antigens are also polysaccharides, and their presence on Gram-negative bacterial capsules is an important virulence factor. They are thought to protect against phagocytosis, to inhibit the induction of a specific immune response, and to facilitate bacterial adhesion. Bacterial strains causing UTI exhibit considerably more K antigen than those isolated from the feces. Urease, a virulence factor especially prominent with Proteus species, allows the breakdown of urea to ammonium. This process alkalinizes the urine and facilitates stone formation. Such bacteria are generally incorporated into the stone structure, making eradication extremely difficult.
Mannose-resistant pili are important adherence factors. They promote adherence to uroepithelial cells as well as renal epithelial cells. This factor appears to counter the normal cleansing action of urine flow and allows tissue invasion and bacterial proliferation.
Increasingly invasive urinary infections are associated with bacteria with a high number of virulence factors.
Colonization of the feces with a virulent organism allows periurethral colonization and ultimately bladder entry. Uroepithelial adherence promotes bacterial proliferation and tissue invasion. This series of events is facilitated by the presence of one or more host factors.
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How should UTIs be treated?
Acute Phase
The treatment of an acute UTI is dependent on the clinical presentation. Ill-appearing children with pyelonephritis should be treated immediately and aggressively with broadspectrum antimicrobial therapy and intravenous hydration.
Initial empiric therapy should be initiated with broadspectrum parenteral antibiotics until the cultures results are available.
Prompt, effective treatment is the most important factor in preventing permanent renal injury.
Further therapy is dictated by culture and sensitivity findings. Indications for inpatient parenteral antibiotic therapy include a very young age (<3 months), unusual or multi-resistant pathogens, persistent vomiting/dehydration, concern for compliance with treatment, and/or significant obstructive urinary tract anomalies.
Once clinically stabilized and afebrile for 24–48 hours, patients with pyelonephritis and sensitive organisms may complete the course of culture-specific antibiotics on an outpatient basis, via a peripherally inserted central catheter (PICC) and a home-based nursing service, or oral antibiotics if susceptibilities allow. Some studies have shown that initial parenteral therapy followed by oral antibiotics can be as effective as a prolonged course of intravenous therapy in preventing renal scarring.
Patients with obstruction or renal abscess who do not become afebrile or have persistent severe symptoms require repeat upper tract imaging. A renal abscess or an obstructed kidney may require percutaneous, or rarely, open drainage.
Initial empiric therapy in less toxic appearing children without vomiting can be performed with oral broadspectrum antibiotics (e.g., cephalosporins) after obtaining a reliable urine culture. Short treatment courses appear to be insufficient for treatment of childhood UTI. Therefore, a 7- to 10-day course dictated by culture and sensitivity results is appropriate.
Urinary retention by the toilet trained patient due to fear of voiding or dysuria can be managed with phenazopyridine (Pyridium) and hydration, and by allowing the child to void while sitting in a tub of warm clear bath water.
Prophylactic Antibiotics
Patients who have recurrent UTIs or those who are managed nonoperatively for VUR are often treated with longterm suppressive antibiotics. It is unclear whether the benefit outweighs the risks, particularly in low-grade VUR without nephropathy.
The urothelial injury from an infection takes several months to fully recover. Thus, irritative voiding symptoms, such as dysuria, incontinence, and frequency, may persist for several days despite the finding of sterile urine.
In addition, the fever curve with pyelonephritis may show persistent spiking temperatures (although dampening over time) even with appropriate antimicrobial therapy. A propensity for re-infection also exists.
Bladder and Bowel Dysfunction
Patients without obvious urinary tract structural abnormalities on US and VCUG should be evaluated for bowel and bladder dysfunction. Regular and complete bowel and bladder elimination is helpful to diminish the risk of UTI recurrence.
A post-void residual by US or office bladder scan can be useful for assessing bladder emptying.
A history of constipation should be sought along with a focused physical exam of the left lower quadrant to assess for palpable stool.
A lower back exam should be performed to assess for a sacral dimple, particularly if there are any concomitant neurologic symptoms to suggest a tethered cord.
Along with aggressive treatment of constipation and voiding dysfunction, 3 months of antibiotic suppression therapy may help to break the cycle of recurrent UTIs.
In complex cases associated with urinary incontinence resistant to treatment, filling cystometrography (e.g., urodynamics) and pelvic floor retraining (e.g., biofeedback) can be treatment options.
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What is the pathophysiology of VUR?
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.
As the bladder fills and the intravesical pressure rises, the resulting bladder wall tension is applied to the roof of the ureteral tunnel. This bladder tension results in 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.
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 can 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.
Of critical importance is the concept of IRR (Intrarenal reflux) which has been demonstrated clinically as well as experimentally.
The usual 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.
The critical pressure for IRR is considered to be about 35 mmHg in compound papillae. Experimentally, this same pressure can cause scar formation in the absence of infection.
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.
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How is VUR classified?
Many attempts at VUR classification 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 BOO or a 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 UPJ or UVJ 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 Grading System and is diagrammed in Figure 55.8.
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 is 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. Intrarenal reflux is traditionally considered to be grade V reflux.
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What are the general guidelines for nonoperative management of VUR?
Medical Management
Nonoperative management of VUR (Box 55.2) is successful in most patients and can be categorized into 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 evaluation and treatment of voiding dysfunction and BOO is imperative.
Patients with problematic UDC can be managed with low-dose anticholinergic medication, such as oxybutynin hydrochloride.
Side effects include constipation and facial flushing/dry mouth and are generally manageable.
Voiding dysfunction with retentive characteristics may require timed/double voiding; alpha blockers; biofeedback; and in severe cases, intermittent catheterization (IC).
Secondary reflux from NVD often requires aggressive bladder management with clean intermittent catheterization (CIC) and higher doses of anticholinergic medication.
Good hydration, perineal hygiene, and bowel management are crucial and apply to all patients.
The traditional view is that children will benefit from low-dose continuous antibiotic prophylaxis (CAP). It is important to remember that the prophylactic dose is approximately one-quarter the dose used to treat an acute UTI. However, the use of CAP is currently controversial and concern over adherence and antimicrobial resistance is commonly expressed. Although generally well tolerated and a commonly used practice for decades, the long-term implications of chronic antimicrobial suppression remain incompletely investigated and actively debated.
The previously mentioned RIVUR study has shown the clinical utility of CAP in patients with VUR, but an important outcome of renal scarring was similar between groups.
It is reasonable to observe an asymptomatic toilet-trained child with low-grade reflux and normal kidneys without antibiotic prophylaxis. However, the clinician must use caution in not using antimicrobial suppression in children with risk factors for recurrent UTI and renal scarring, including high-grade VUR with bowel and bladder dysfunction.
Once a nonoperative regimen is selected, the patient is committed to long-term, strict surveillance. Renal imaging is performed every 6–12 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. VCUG or radionuclide cystography 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.
The American Urological Association (AUA) Pediatric Vesicoureteral Reflux Guidelines Panel initially 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), CAP 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 also an option.
There is little solid evidence or consensus about the management of VUR in older school-age patients or the length of time that the clinician should observe a child nonoperatively before recommending operative correction.
Treatment decisions must be carefully individualized after a thorough discussion of all the treatment options with the parents.
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What are indications for the surgical management of VUR?
Surgical Management
While the decision to perform antireflux surgery must be carefully individualized, absolute indications for operative 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 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 ideally exceeds 5:1.
These goals can be attained by a variety of procedures, most commonly via an open Pfannenstiel approach but also laparoscopically and robotically assisted (Fig. 55.11).
There are important differences between these operative procedures. Variables include
(1) presence or absence of a ureteral anastomosis,
(2) need for detrusor closure,
(3) transgression of the 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.
In general, excellent results are nearly uniformly attainable with an open approach. A meta-analysis in 1997 of 86 reports, including 6472 patients (8563 ureters), found overall success for an open ureteral reimplantation to be 96%. 95 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. The robotic-assisted laparoscopic technique for extravesical ureteral reimplantation has become more widespread, and early outcomes have been published. However, there has been concern over the costs and complication rates of the robotic-assisted approach.
At our institution, we prefer the open extravesical detrusorrhaphy approach. Because the lumen of the bladder is not entered, there is no postoperative hematuria, with minimal bladder spasms and typically a short hospitalization of 1–2 days.
The absence of a ureterovesical anastomosis decreases the risk of postoperative obstruction. No ureteral stents, suprapubic catheters, or perivesical drains are utilized.
The urethral catheter can be removed on the first day after unilateral surgery and the second day following bilateral reimplantation. Once the patient voids, he or she is discharged on oral antibiotics for 1 week, and 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 operation, or infiltration of local anesthesia into the incision supplemented by intravenous narcotics as needed. Most children are discharged home on oral acetaminophen alone.
Postoperative imaging includes a renal and bladder US 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, reimplantation of the ureters associated with paraureteral Hutch diverticula, as well as correction of VUR associated with duplicated collecting systems.
Complications of ureteral reimplantation are rare.
The most common complication is de novo contralateral reflux, while the most common technical complications are ureteral obstruction, persistent reflux, and diverticula formation.
Persistent reflux can 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, DSD, and/or urinary retention.
Ureteral obstruction may be due to ureteral kinking (at the neohiatus or obliterated umbilical artery), an excessively high positioned neohiatus, construction of a tight neohiatus, anastomotic stricture, devascularization, and a 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. 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. Risk factors appear to be infants under age 1 and girls with large, thin-walled bladders and preexisting retentive voiding dysfunction.
Complications following open antireflux surgery are quite low but include ureterovesical obstruction and persistent VUR.
Acute management of an obstructed ureter in an ill-appearing child involves urgent drainage of the hydronephrotic kidney.
A percutaneous nephrostomy tube can be placed without concern for finding a ureteral orifice within an edematous bladder to place a ureteral stent and/ or potentially disrupting a fresh ureterovesical anastomosis.
Once the patient has stabilized, the nephrostomy can be used to check the patency of the UVJ with an antegrade contrast study. The nephrostomy can be subsequently exchanged for an internalized ureteral stent.
In 1984, a cystoscopic procedure for the correction of VUR was reported. This subureteral transurethral injection (STING) utilized polytetrafluoroethylene (Teflon™ ) and has been used successfully outside the United States for many years. Many different injectable materials have subsequently been used and reported. This ambulatory procedure performed under a brief general anesthetic has low morbidity, and children often return to full activity as soon as the next day. The initial success rates were promising, but they have not quite matched those of ureteral reimplantation.m
In 2001, the U.S. Food and Drug Administration approved dextranomer/hyaluronic acid copolymer (Deflux® ) as the first injectable substance for grades I–IV VUR. This substance is biodegradable, has no immunogenic properties, and does not seem to have potential for malignant transformation. The injection is typically performed via cystoscopy under a brief general anesthetic. It is typically scheduled as an outpatient procedure. Surgical outcomes vary, but most studies show success rates of around 70–80% for abolishing reflux. Higher success rates with larger injected volumes and multiple injection sites have been reported at some high volume centers. However, in one study, a 54% failure rate was seen on VCUG 1 year after the procedure.
Complications of injection therapy such as ureteral obstruction appear to be very low. The postoperative course is generally well tolerated, and the patients return to normal activities almost immediately. Dysuria, gross hematuria, and urinary frequency occasionally occur, but are selflimiting. Flank pain and fever are rare.
In our institution, a VCUG and renal US are obtained 3 months after the procedure while still under cover of antibiotic prophylaxis. The VCUG is not subsequently repeated if the patient remains asymptomatic off antibiotic prophylaxis.
Patients who develop a febrile UTI after an apparently successful procedure should be re-investigated with a VCUG to assess for recurrent reflux.
Persistent reflux after a dextranomerhyaluronic acid injection can be managed quite nicely with an open extravesical ureteral reimplantation with sharp excision of the often migrated bleb of the implanted material.
It is important to note that the dextranomer implant may become more dense over time and become more apparent on imaging. This appearance on US and computed tomography may be misinterpreted as urolithiasis. The absence of symptoms such as renal colic, hematuria, and hydronephrosis differentiates this benign entity from a ureteral stone.
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