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Urinary Tract Infection (UTI)

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Urinary tract infection (UTI) is defined by > 5 × 104 colonies/mL in a catheterized urine specimen, or in older adolescents by repeated voided specimens with > 105 colonies/mL. In younger children, UTIs are frequently caused by anatomic abnormalities. UTI may cause fever, failure to thrive, flank pain, and signs of sepsis, especially in young children. Treatment is with antibiotics. Follow-up imaging studies of the urinary tract are obtained.

Mechanisms that maintain the normal sterility of the urinary tract include urine acidity and free flow, a normal emptying mechanism, intact ureterovesical and urethral sphincters, and immunologic and mucosal barriers. Abnormality of any of these mechanisms predisposes to UTI.

Etiology and Pathophysiology

One to 2% of neonates develop UTI, and the female:male ratio is 1:5. Predisposing factors include malformations and obstructions of the urinary tract, prematurity, indwelling catheters, and lack of circumcision.

UTIs occur in 3 to 6% of children 2 mo to 2 yr of age. The female:male ratio rises with age, being about 2:1 between 2 mo to 1 yr, 4:1 during the 2nd year, and > 5:1 after 4 yr. In girls, infections usually are ascending and less often cause bacteremia. The marked female preponderance is attributed to the shorter female urethra; male circumcision may decrease boys' risks. Other predisposing factors for UTI in children include indwelling catheters, constipation, Hirschsprung's disease, and anatomic abnormalities of the urinary tract. Risk factors in older children include diabetes, trauma, and, in adolescents, sexual intercourse.

UTIs in children are a marker of possible urinary tract abnormalities (eg, obstruction, neurogenic bladder, ureteral duplication); these are particularly likely to result in infection if vesicoureteral reflux (VUR—see also Congenital Renal and Genitourinary Anomalies: Vesicoureteral reflux) is present. The likelihood of VUR varies inversely with age at the 1st UTI. About 30 to 40% of infants and toddlers with UTI have VUR. Severity of reflux may determine the probability of subsequent hypertension and renal failure (caused by repeated infection), but proof is lacking. VUR is classified by grade (see Table 4: Infections in Infants and Children: Grades of Vesicoureteral Reflux*Tables). Reflux of infected urine into the renal pelvis or presence of infected urine behind an obstruction can lead to chronic pyelonephritis, renal scarring, poor kidney growth, and renal failure.

Table 4

Grades of Vesicoureteral Reflux*

Grade

Characteristics

I

Only the ureters are involved, but not the renal pelvis

II

Reflux reaches the renal pelvis; no dilation of calyces

III

The ureter and renal pelvis are dilated; minimal or no blunting of calyces

IV

Dilation increases, and the sharp angle of the calyceal fornices is obliterated

V

The ureter, pelvis, and calices are grossly dilated; papillary impressions frequently are absent

*As defined by the International Reflux Study Committee.

Many organisms cause infection in anatomically abnormal urinary tracts. In relatively normal urinary tracts, the most common pathogens are strains of Escherichia coli with specific attachment factors for transitional epithelium of the bladder and ureters. E. coli causes > 75% of UTIs in all pediatric age groups. The remaining causes are other gram-negative enterobacteria, especially Klebsiella , Proteus mirabilis, and Pseudomonas aeruginosa. Enterococci (group D streptococci) and coagulase-negative staphylococci (eg, Staphylococcus saprophyticus) are the most frequently implicated gram-positive organisms. Fungi and mycobacteria are rare causes, mainly in immunocompromised hosts. Adenoviruses rarely cause UTIs, predominantly hemorrhagic cystitis.

Symptoms and Signs

In neonates, symptoms and signs are nonspecific and include poor feeding, diarrhea, failure to thrive, vomiting, mild jaundice, lethargy, fever, and hypothermia. Neonatal sepsis (see Infections in Neonates: Neonatal Sepsis) may develop.

Infants and toddlers may also present with poorly localizing signs, such as fever, GI symptoms (eg, vomiting, diarrhea, abdominal pain), or foul-smelling urine.

In children > 2 yr, the more classic picture of cystitis or pyelonephritis can occur. Symptoms of cystitis include dysuria, frequency, hematuria, urinary retention, suprapubic pain, urgency, pruritus, incontinence, foul-smelling urine, and enuresis. Symptoms of pyelonephritis include high fever, chills, and costovertebral pain and tenderness.

Findings suggesting associated urinary tract abnormalities include abdominal masses, enlarged kidneys, urethral abnormalities, and signs of lower spinal malformations. Diminished force of the urinary stream may be the only clue to obstruction or neurogenic bladder.

Diagnosis

Urine tests: Diagnosis requires demonstration by culture of significant bacteriuria in properly collected urine. Most clinicians obtain urine by transurethral catheterization in infants and young children, reserving suprapubic aspiration of the bladder for boys with moderate to severe phimosis. Both procedures require technical expertise, but catheterization is less invasive, slightly safer, and has sensitivity of 95% and specificity of 99% compared with suprapubic aspiration. Bagged specimens are unreliable and should not be used for diagnosis.

If urine is obtained by suprapubic aspiration, the presence of any bacteria is significant. In a catheterized specimen, > 5 × 104 colonies/mL commonly defines UTI. Clean-catch, midstream-voided specimens are significant when colony counts of a single pathogen (ie, not the total count of “mixed flora”) are > 105/mL. Urine should be examined and cultured as soon as possible or stored at 4° C if a delay of > 10 min is expected. Occasionally, UTI may be present despite colony counts lower than the above guidelines, possibly because of prior antibiotic therapy, very dilute urine (specific gravity < 1.003), or obstruction to the flow of grossly infected urine. Sterile cultures generally rule out UTI unless the child is receiving antibiotics or the urine is contaminated with antibacterial skin cleansing agents.

Microscopic examination of urine is useful but not definitive. Pyuria (> 5 to 10 WBCs/high-power field in spun urine sediment) is about 70% sensitive for UTI. A WBC count (using a hemocytometer) > 10/μL in unspun urine has sensitivity of 90% but is not used by many laboratories. Presence of bacteria on Gram stain of spun or unspun urine is about 80% sensitive. Specificity of microscopy also is about 80%.

Dipstick tests on urine to detect bacteria (nitrite test) or leukocytes (leukocyte esterase test) are typically performed; if either is positive, the diagnostic sensitivity for UTI is about 93%. The specificity of the nitrite test is quite high; a positive result on a freshly voided specimen is highly predictive of UTI. Specificity of leukocyte esterase is much lower.

Differentiating an upper from a lower UTI can be difficult. High fever, costovertebral angle tenderness, and gross pyuria with casts indicate pyelonephritis. However, many children without these symptoms and signs have an upper UTI. Tests to distinguish upper from lower infection are not indicated in most clinical settings, because treatment is not altered.

Blood tests: A CBC and tests for inflammation (ESR, C-reactive protein) may help diagnose infection in those with borderline urine findings. Some authorities measure serum BUN and creatinine during a 1st UTI. Blood cultures are appropriate for infants with UTIs and for children > 1 to 2 yr who appear toxic.

Urinary tract imaging: Many major renal or urologic anomalies now are diagnosed in utero by routine prenatal ultrasonography. However, the high incidence of anatomic anomalies still warrants imaging the urinary tracts of all children 2 mo to 2 yr of age after a 1st UTI. If a 1st UTI occurs at 2 yr, most authorities recommend imaging; however, some physicians postpone imaging until after a 2nd UTI in girls > 2 yr of age. Options include voiding cystourethrogram (VCUG), radionuclide cystogram (RNC) with technetium 99m pertechnetate, and ultrasound.

VCUG and RNC are better than ultrasound for detecting VUR and anatomic abnormalities. RNC delivers about 1% of the gonadal radiation of VCUG; it is sensitive in detecting VUR, and some recommend it as the initial test. However, most authorities prefer the better anatomic definition of contrast VCUG as the initial test, using RNC in follow up to determine when VUR has resolved. Low-dose radiographic equipment has narrowed the gap in radiation between the contrast VCUG and RNC. These tests are recommended at the earliest convenient time after clinical response, typically toward the end of therapy, when bladder reactivity has resolved and urine sterility has been regained. If imaging is not scheduled until after therapy is due to be completed, the child should continue antibiotics at prophylactic doses until VUR is excluded.

Ultrasound helps exclude obstruction and hydronephrosis and is typically done within a week of diagnosing UTI in infants, especially if they do not respond quickly to antimicrobials. Otherwise, ultrasonography can be delayed until VCUG is done.

Prognosis

Properly managed children rarely progress to renal failure unless they have uncorrectable urinary tract abnormalities. However, repeated infection, particularly in the presence of VUR, may cause renal scarring, which may lead to hypertension and end-stage renal disease. High-grade VUR has a 4- to 6-fold greater rate of long-term renal scarring than low-grade VUR and an 8- to 10-fold greater rate than in children without VUR. Extreme scarring after VUR leads to end-stage renal disease in 3 to 10% of patients, although these data are likely biased because affected children may also have other renal abnormalities.

Treatment

Treatment aims to eliminate the acute infection, prevent urosepsis, and preserve renal parenchymal function. Antibiotics are begun presumptively in all toxic-appearing children and in nontoxic children with likely UTI (positive leukocyte esterase or nitrite, or microscopy showing pyuria or bacteriuria). Others can await culture results.

In infants 2 mo to 2 yr with toxicity, dehydration, or inability to retain oral intake, parenteral antibiotics are used, typically a 3rd-generation cephalosporin (eg, ceftriaxone Some Trade Names
ROCEPHIN
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75 mg/kg IV/IM q 24 h or cefotaxime Some Trade Names
CLAFORAN
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50 mg/kg IV q 6 h). A 1st-generation cephalosporin (eg, cefazolin Some Trade Names
ANCEF
KEFZOL
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) may be used if typical local pathogens are known to be sensitive. Aminoglycosides (eg, gentamicin Some Trade Names
GARAMYCIN
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), although potentially nephrotoxic, are useful to treat potentially resistant gram-negative bacilli such as Pseudomonas in complex UTIs (eg, urinary tract abnormalities, presence of indwelling catheters, recurrent UTIs). If blood cultures are negative and clinical response is good, an appropriate oral antibiotic (eg, a cephalosporin, trimethoprim-sulfamethoxazole Some Trade Names

[TMP-SMX], or amoxicillin Some Trade Names
AMOXIL
TRIMOX
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) selected on the basis of antimicrobial sensitivities can be used to complete a 10- to 14-day course. A poor clinical response suggests a resistant organism or an obstructive lesion and warrants urgent evaluation with ultrasonography and repeat urine culture.

In nontoxic, nondehydrated infants and children who are able to retain oral intake, oral antibiotics may be given initially. The drug of choice is TMP-SMX, 3 to 6 mg/kg (of TMP component) bid. Alternatives include cephalosporins such as cefdinir Some Trade Names
OMNICEF
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7 mg/kg bid, cefprozil Some Trade Names
CEFZIL
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15 mg/kg bid, cefixime Some Trade Names
SUPRAX
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4 mg/kg bid, and cephalexin Some Trade Names
KEFLEX
KEFTAB
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12.5 to 25 mg/kg qid. Therapy is changed based on the results of cultures and antimicrobial sensitivities. Treatment is generally for > 10 days, although many older children with uncomplicated UTI can be treated for 7 days. Urine culture is repeated 2 to 3 days after therapy starts if efficacy is not clinically apparent.

Vesicoureteral reflux: Children with grades I to III VUR can be followed clinically and given antibiotic prophylaxis; about 13%/yr resolve. Although it is generally thought that antibiotic prophylaxis reduces recurrences and prevents kidney damage, few long-term data are available. Drugs include nitrofurantoin Some Trade Names
FURADANTIN
MACROBID
MACRODANTIN
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2 mg/kg po once/day or TMP-SMX 2 mg/kg po (of TMP component) once/day, usually given at bedtime. If grade IV or grade V VUR or a major renal abnormality is detected, prophylactic antibiotics are used; surgery is often needed because 5%/yr resolve.

Last full review/revision November 2005

Content last modified November 2005

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