VESICOURETERAL REFLUX
Vesicoureteral reflux (VUR) is defined as the retrograde flow of urine from
the bladder into the ureter and, in many cases, the renal pelvicalyceal system.
This condition is considered problematic because it facilitates propulsion of
bacteria toward the kidneys, which can cause recurrent pyelonephritis, renal
scarring, and eventual renal dysfunction.
VUR is generally diagnosed during
childhood. The overall incidence has been difficult to estimate because the condition
is often undetected and frequently resolves with age. It has been reported,
however, that 70% of infants who have urinary tract infections (UTIs) also have
reflux. Although VUR is more common in male infants, it is more common in
females after the first year of life.
Pathogenesis
Normal ureteral continence relies on a
valve mechanism formed as the ureter courses between the bladder mucosa and
detrusor muscle before terminating at the ureteric orifice. When the bladder
contracts, compression of the intramural segment of each ureter prevents the
retrograde flow of urine.
Primary reflux occurs when the
ureterovesical junction (UVJ) is abnormal. In nonrefluxing UVJs, the length of
the ureter’s intramural segment is at least five times the ureteral diameter. In
refluxing UVJs, in contrast, the intramural segment is too short or, less often,
the ureteral diameter is too wide. As a result, the valve mechanism is
inadequate to prevent the reflux of urine during bladder contraction. Although
there is a clear genetic basis for VUR, as evidenced by high rates of
concordance among monozygotic twins, the genes that modulate UVJ structure have
not been identified.
Secondary reflux occurs when there are
very high filling pressures in the bladder, which overwhelm otherwise normal
ureterovesical junctions. In male infants, a common cause is posterior urethral
valves (see Plate 2-34), which cause congenital bladder outlet obstruction.
Other causes include neurogenic bladder, dysfunctional voiding, and ureterocele
(see Plate 2-26).
Although VUR is not itself a risk
factor for lower urinary tract infection, it does permit the passage of bacteria
from the bladder to the kidneys. Over time, repeated episodes of pyelonephritis
can result in renal scarring and dysfunction, especially if infections occur in
the first year of life. In contrast, the reflux of sterile urine does not appear
to cause renal scarring at any age. Of note, VUR also appears to be associated
with a variable degree of renal dysplasia that is unrelated to infection.
Indeed, both VUR and renal dysplasia could be expected to result from an abnormally
caudal posi- tion of the ureteric bud on the mesonephric duct (see Plate 2-1)
because this arrangement would cause both (1) suboptimal interaction between
the ureteric bud and metanephric mesenchyme, as well as (2) a short intramural
course for the ureter.
Presentation And Diagnosis
VUR is generally first suspected when
prenatal ultrasound reveals hydronephrosis or when a child develops a UTI. Among infants, further
workup is indicated if a repeat postnatal ultrasound reveals persistent
hydronephrosis. Among children, further workup is indicated if a male child has
a UTI, a female child less than 5 years of age has a UTI, or a female child of
any age has a febrile UTI.
The gold standard diagnostic test is a
voiding cystourethrogram (VCUG). In a VCUG, the bladder is instilled with
contrast and examined under fluoroscopy while the patient voids. The diagnosis
of VUR is established if contrast is seen entering one or both ureters. The
severity of the reflux can be classified into one of five grades based on the
International Reflux Grading system, as shown in the illustration on the
opposite page.
Treatment
Patients with bilateral high grade
VUR, particularly those with renal scarring, should undergo regular eval-
uation with measurement of height, weight, blood pressure, and serum creatinine
concentration. Correction of any bladder or bowel dysfunction is critical, as
it lowers the rate of UTIs and improves the probability that VUR will
spontaneously resolve. Urinalysis should be performed on a regular basis, along
with follow-up urine culture if there is evidence of bacteriuria or pyuria.
Finally, ultrasound or renal scan may be performed to assess for the presence
and degree of renal scarring.
The available treatment options for
VUR depend on grade and laterality. They include observation with or without
antibiotic prophylaxis, endoscopic bulking of the ureteric orifice, and ureteral
reimplantation (see Plate 10-35). The relative risks and benefits of these
different options remain uncertain, and as a result there is a wide variation
in management strategies.
A majority of the children with
low-grade primary reflux (grades I-III) experience spontaneous resolution,
presumably because growth of the bladder leads to lengthening of the intramural
ureteral segment. Thus most authorities recommend careful observation of such
children and continuous antibiotic prophylaxis until the reflux resolves. Common
agents include low dose trimethoprim-sulfamethoxazole or nitrofurantoin.
Patients who have persistent reflux at 6 years of age that is either bilateral
or associated with renal scarring may be candidates for surgical intervention.
The first-line therapy should be endoscopic injection of bulking agents adjacent
to the refluxing ureteric orifice, a minimally invasive procedure with high
success rates in this group. A majority of the children with high-grade primary
reflux (grades IV and V) will not experience spontaneous resolution, and thus
surgical treatment may be offered to lower the risk of renal scarring.
Endoscopic techniques often fail to correct high-grade reflux, and thus open or
laparoscopic reconstruction of the ureterovesical junction is typically
performed. The cross trigonal ureteral implant is a popular technique (see
Plate 10-35). Until the reflux is corrected, antibiotic prophylaxis should be
provided to maintain sterile urine.
