After the results of urine culture are known, or while pending, acute treatment for the less toxic, older child is usually amoxicillin, 40 mg/kg per day, divided into three doses daily, for 10 days. An alternative is a trimethoprim-sulfamethoxazole preparation: 8 mg/kg per day of the trimethoprim moiety, divided into two daily doses. Hospitalization for intravenous treatment is indicated for the infant and/or toxic-appearing patient. Ceftriaxone, 75 mg/kg parenterally every 24 hours at least until the child is afebrile, is a first-line drug, with other cephalosporins available as acceptable alternatives, depending on antibiotic sensitivities. The urine will usually become sterile within 48 to 72 hours, accompanied by a clinical response, including resumption of a healthy demeanor. The remainder of the 10-day antibiotic course may be completed with amoxicillin or an oral cephalosporin, such as cefixime, 8mg/kg per day, divided into two daily doses.

After acute treatment of the infection, the diagnostic evaluation for risk factors must begin. The purpose of imaging studies is to identify those patients at risk for recurrence of UTI, with its attendant acute morbidity and risk of pyelonephritic scarring (American Academy of Pediatrics [AAP], 1999). While the yield of ultrasonography of the kidneys and bladder is approximately 40% (AAP, 1999), it presents no risk to the patient. Kidney size, number, and position can be determined, as well as dilatation of the pelvis and calyces (hydronephrosis) or ureter (hydroureteronephrosis). The bladder can be evaluated for wall-thickness and for postvoid residual. Ultrasonography is an excellent screen for abnormal urinary tract anatomy, but it provides no functional information.

VCUG should be performed as soon as the urine is sterile. The bladder is catheterized with an 8F feeding tube, and radiographic contrast fills the bladder by gravity. Under fluoroscopic control, the radiologist determines if the contrast enters one or both ureters and goes up into the kidney. Figure 39-1 illustrates the clinical grading of VUR as seen on VCUG. Because the likelihood of detecting VUR declines precipitously after age 5 years; those girls older than 5 with a first episode of cystitis who respond promptly to antibiotic treatment need not undergo VCUG. The yield from ultrasonography is so low as to make this examination also unnecessary. However, below the age of 5, many authorities recommend both sonography and a VCUG with the first UTI in respect of the presence or the absence of fever.

VUR can be unilateral or bilateral, mild, moderate, or severe. When severe, it is frequently associated with kidney scarring from one or more episodes of acute pyelonephritis. Scarring is best seen by the use of a radionuclide renal scan using _99mTc-DMSA.
VUR, when mild or moderate, will often disappear over several years. The patient can be successfully protected against UTI with antibiotic prophylaxis during this period. The preferred agent is trimethoprim-sulfisoxazole, 4 mg/kg per day, administered at bedtime. When VUR is severe, referral to a pediatric urologist is indicated for possible surgical reimplantation of the refluxing ureter(s).

In addition to imaging studies, a more detailed history of the child’s bladder habits may reveal a pattern of dysfunctional voiding. This condition is often observed in preschool- and school-aged children who void infrequently, often have to rush to the toilet when the urge to void overcomes them, and may wet during the day. Often these symptoms are accompanied by chronic constipation. Such children will frequently benefit from a bladder re-education program of timed voiding and anticonstipation therapy. Occasionally, anticholinergic medication, such as oxybutynin (Ditropan), 5 mg two or three times daily, is helpful.

Parents should be counseled that after the diagnosis and treatment of a first UTI, monthly surveillance urine cultures are recommended for 3 months, followed by quarterly urine cultures for at least 2 years.

A positive dipstick reaction for “blood” requires confirmation by urine microscopy, because frequently the dipstick reaction is out of proportion to the quantitation of RBCs per high powered field. Should urine microscopy be negative for RBCs, the patient and family can be reassured that no pathology is present, and thus there is no need for follow up surveillance urinalyses.

In the past, children with confirmed microscopic hematuria were subjected to extensive imaging and serologic evaluations, including renal biopsy (Trachtman, et al., 1984). The yield from these diagnostic investigations is so low that they are no longer recommended, except for patients with a history of gross hematuria, significant proteinuria, or a family history of hematuria (gross or microscopic).

For microscopic hematuria, no more than reassurance is usually indicated. Such patients, however, should be instructed to notify their provider if and when gross hematuria occurs, because this event is much more likely to be associated with significant uropathology. For patients with documented microscopic hematuria, regular (at least annual) surveillance UAs should be continued for the purpose of detecting proteinuria, a much more serious marker of glomerular disease. Figure 39-2 depicts an algorithm for the evaluation and management of hematuria in children.