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Children under 5 years of age with fever constitute a substantial proportion of out-patient and emergency department visits1,2,3. Unlike occult bacteremia or severe bacterial illness (in infants and children) little attention is paid to the identification of UTI in febrile children in the emergency department. Recent information suggests a high prevalence of urinary tract infections and significant associated morbidity in these patients4. Quite often, children with urinary tract infections receive antibiotics empirically, without adequate diagnosis.
Fever with significant bacteriuria and pyuria in children with undocumented sources of infections must be presumed to be symptoms of pyelonephritis requiring prompt treatment.
Recent studies with nuclear scans to determine the presence of pyelonephritis have revealed that more than 75% of children under 5 years of age with febrile urinary tract infection had evidence of pyelonephritis.4,5,6
Pyelonephritis leads to renal scarring in 27% to 64% of children with urinary tract infection in each year of life5,8 especially in those with gross reflux or obstruction and in those who had a delay in initiation of therapy for urinary tract infection. Also children under 3 years of age with recurrent urinary infections, are under higher risk for renal scarring and one third of these children may be asymptomatic9. Hence it is essential to identify urinary tract infections in febrile children and institute prompt treatment to reduce the potential for life-long morbidity. Progressive renal damage from unrecognized pyelonephritis in childhood may lead to hypertension and chronic renal failure in later life. A study from Sweden showed that focal renal scarring caused by pyelonephritis in children carried a 23% risk for hypertension a 10% risk for end stage renal disease, and a 15% risk for toxemia during pregnancy as an adult.10
Approximately 13% to 15% of end stage renal disease is thought to be related to urinary tract infection in childhood which was often unrecognized and therefore, under treated.11
The present study is undertaken to estimate the prevalence of urinary tract infection in febrile children aged one month to five years without any focus and to assess the validity of routine microscopic urine analysis, enhanced urine analysis, urine dipstick and urine culture in the diagnosis of urinary tract infection.
Aims and Objectives
To determine the prevalence of Urinary tract infection (UTI) in febrile children from 1 month to 5 years of age who do not have any obvious focus of infection.
1. To determine sensitivity, specificity, positive predicitve value and negative predictive value of urine pus cells, enhanced urine analysis and urine dipstick method in the diagnosis of UTI in febrile children aged 1 months to 5 years.
2. To correlate the results of urine pus cells, enhanced urine analysis and urine dipstick method with urine culture result.
Review of Literature
Roberts K. et al12 (1983) studied 193 febrile children less than 2 years and reported the prevalence of urinary tract infection to be 4.1%.
Bauchner et al13 (1987) evaluated 664 febrile children younger than 5 years of age and reported prevalence of only 1.7%.
In a study by Hoberman et al14 (1993) the prevalence of urinary tract infection in febrile infants was 5.3% and the prevalence in infants less than 2 months it was 4.6%. And also coexistence of UTI in infants with other illness was found to be 5.1% in the same study.
Dharnidharka et. al15 (1993) reported an overall prevalence of UTI to be 5.4% among febrile infants.
P.R. Srivaths et. al16 (1996)showed a prevalence of 2.48% in children less than 2 years of age which is the lowest reported from a developing country and is similar to the prevalence rates reported from developed countries.
Shaw KN and Gorelick MH 4in 1999 reported 3-5% prevalence of uti with higher rates for white girls, uncircumcised boys, and those without another potential source of fever.
A study done by M.H. Fallahzadeh et al17(1999) among preschool children estimated the prevalence of urinary tract infections to be 4.4%.
Lin DS18 in 2000 reported a prevalence of 13.6% in febrile infants younger than 8 weeks age.
William19 (2001) found that UTI was more common in girls less than 6 years of age probably because of short urethra and translocation of fecal bacteria. Close to 0.2% of circumcised and 0.7% of uncircumcised infant boys are found to be at risk of UTI, which reaches to 0.1-0.2 during 1-5 years and 0.04-0.2 in school age [i] . UTI may lead to transient renal damage in 40% and permanent renal scarring in 5% of patients2.
Andrew Dziewit J20 in 2002 studied febrile infants less than 8 weeks and reported a prevalence of urinary tract infection to be 4.2%.
According to Steven L et al,21 during the first year of life, boys have a higher incidence of UTI; in all other age groups, girls are more prone to develop UTI. The incidence of UTI in girls was 0.7% compared to 2.7% in boys during the first year of life. In the first 6 months, uncircumcised boys22 had a 10- to 12-fold increased risk for developing UTI. In children aged 1 to 5 years, the annual incidence of UTI is reported to be 0.9% to 1.4% for girls and 0.1% to 0.2% for boys.23
Sastre et al24 (2007) also reported a higher prevalence of UTI in males during neonatal period and early infancy [ii] .And they were found to be associated with anatomical abnormalities and outlet obstruction.
According to Nader Shaikh et al25 (2008) prevalence rates of febrile UTIs in females aged 0-3 months, 3-6 months, 6-12 months, and >12 months were 7.5%, 5.7%, 8.3%, and 2.1% respectively. Among febrile male infants less than 3 months of age, 2.4% of circumcised males and 20.1% of uncircumcised males had a UTI. .
Ismaili et al (2011)26 provided the clinical characteristics, uropathogen frequencies, and antimicrobial resistance rates of first UTI diagnosed in febrile Belgian children. The ability of noninvasive Ultrasound to detect renal abnormalities and Vesicourethral reflex in these patients was also assessed. Among these children, 63% were females and 37% were males, and 75% of them had their first episode of UTI before the age of 2 years. The most common causative agent was Escherichia coli 91% with high rate resistance to ampicillin (58%) and trimethoprim/sulfamethoxazole (38%).
Msaki et al (2012) 27,28conducted a study to determine the relative prevalence of UTI among children under five years of age presenting with fever. A total of 231 febrile under-fives were enrolled in the study. Of all the children, 20.3% (47/231, 95% CI,15.10-25.48), 9.5% (22/231, 95%CI, 5.72-13.28) and 7.4% (17/231, 95%CI, 4.00-10.8) had urinary tract infections, P. falciparum malaria and bacteremia respectively.
According to Sobel et al29,30 (1991) urinary tract infections may occasionally be caused by viruses and fungi, however overwhelming majority of urinary tract infections are caused by bacteria.Most infections are caused by facultative anaerobes that usually originate from the flora of the bowel. Other pathogens such as group B streptococcus, staphylococcus epidermidis and candida albicans, originate in the flora of the vagina or perineal skin in women
Escherichia coli was the most common urinary pathogen accounting for 85% of community acquired urinary tract infection in a study done by Byran CS et al31 1984.This is similar to study done by
Arvind Bagga et al31 (2000) in their study reported that 90% of first symptomatic urinary tract infection and 70% of recurrent infection's are due to Escherichia coli.Instrumentations and infections with Proteus and Pseudomonas were also associated with recurrent UTI.
According to Steven L et al (2006)21 UTI may be caused by any pathogen that colonizes the urinary tract (eg, fungi, parasites, and viruses), most causative agents are bacteria of enteric Origin. The causative agent varies based on age and associated comorbidities. E coli was the most frequent documented uropathogen. Among neonates, UTI secondary to group B streptococci was more common than in older populations32. In immunocompromised children and children with indwelling catheters, Candida may be isolated from the urine33. Nosocomial infections were found to be caused by E. coli, Candida, Enterococcus, Enterobacter, and Pseudomonas34
The main causative organisms for UTI are
Streptococcus group B
Streptococcus group D
[Data from Chon C, Lai F, Shortliffe LM. Pediatric urinary tract infections.
Pediatr Clin N Am 2001;48(6):1443]
UTIs have been classified by the site of infection (ie, pyelonephritis (kidney), cystitis (bladder), urethra (urethritis) and by severity (ie, complicated versus uncomplicated). A complicated UTI describes infections in urinary tracts with structural or functional abnormalities or the presence of foreign objects, such as an indwelling urethral catheter. UTI is categorized as first infection depending on occurrence once or several times. Recurrent infections is further divided into (1) unresolved bacteriuria, (2) bacterial persistence and (3) reinfection.
The initial UTI documented by a proper urine culture is the first infection. In neonates and infants, however, they are presumed to be complicated because of the high association between urinary tract malformation and concurrent bacteremia, which predispose children to acute morbidity and long-term renal insufficiency35,36 The recurrence of a UTI may be caused by several reasons. Unresolved bacteriuria is most commonly caused by inadequate antimicrobial therapy. In these cases, infection typically resolves after altering the therapy according to antimicrobial sensitivities determined by a proper urine culture.
Bacterial persistence and reinfection occur after sterilization of the urine has been documented. In the case of bacterial persistence, the nidus of infection in the urinary tract is not eradicated. Characteristically, the same pathogen is documented on urine cultures during subsequent episodes of UTI despite negative cultures after treatment. The uropathogen frequently resides in a location that is shielded from antimicrobial therapy. These protected sites are often anatomic abnormalities, including infected urinary calculi37, necrotic papillus38, or foreign objects, such as an indwelling ureteral stent39,40 or urethral catheters41, which once infected may not be sterilized. Identification of the anatomic abnormality is essential because surgical intervention (extirpation) may be necessary to eradicate the source of infection.
In bacterial reinfection it is characterized by different pathogens confirmed on proper urine cultures with each new episode of Urinary tract infection. UTI most commonly occurs by periurethral colonization22 and by the fecal-perinealurethral route42. Rarely, a fistula between the urinary tract and gastrointestinal tract serves as the source of reinfection. It is important to note thatEscherichia coli occurs in many different serotypes, and documentation of what seems to be recurrent E coli UTI may, in fact, represent reinfection rather than bacterial persistence. Serotyping (or careful examination of antimicrobialsensitivity profile) ultimately can establish a diagnosis of reinfection in equivocal situations
Bacterial clonal studies strongly support entry into the urinary tract by the fecal-perineal-urethral route with subsequent retrograde ascent into the bladder42. Girls are at a higher risk of UTI in first year of life because of anatomical differences also the moist periurethral and vaginal areas promote the growth of uropathogens. The shorter urethral length increases the chance for ascending infection into the urinary tract. Once the uropathogen reaches the bladder, it may ascend to the ureters and then to the kidneys by some as-yet undefined mechanism. Additional pathways of infection include nosocomial infection through instrumentation, hematogenous seeding in the setting of systemic infection or a compromised immune system, and direct extension caused by the presence of fistulae from the bowel or vagina.
The urinary tract (ie, kidney, ureter, bladder, and urethra) is a closed, normally sterile space lined with mucosa composed of epithelium known as transitional cells. The main defense mechanism against UTI is constant antegrade flow of urine from the kidneys to the bladder with intermittent complete emptying of the bladder via the urethra. This washout effect of the urinary flow usually clears theurinary tract of pathogens. The urine itself also has specific antimicrobial characteristics, including low urine pH, polymorphonuclear cells, and Tamm-Horsfall glycoprotein, which inhabits bacterial adherence to the bladder mucosal wall43. UTI occurs when the introduction of pathogens is associated with adherence to the mucosa of the urinary tract. If uropathogens are cleared inadequately by the washout effect of voiding, then microbial colonization potentially develops. Colonization may be followed by microbial multiplication and an associated inflammatory response. Bacteria that cause UTI in otherwise healthy hosts often have virulence factors - to overcome the normal defenses of the urinary system44,45,46. In serotypes of E coli frequently isolated in UTI, bacterial adherence to the uroepithelium is enhanced by adhesions, often fimbriae (pili), which bind to specific receptors of the uroepithelium.45,46,47 The interaction of fimbriae with the mucosal receptor triggers internalization of the bacterium into the epithelial cell, which leads to apoptosis, hyperinfection, and invasion into surrounding epithelial cells or established of a bacterial focus for recurrent UTI. Uropathogenic strains of E coli have been recognized torelease toxins, including cytolethal distending toxin, alpha hemolysin, cytotoxic necrotizing factor-1, secreted autotransporter toxin that causes cellular lysis, cause cell cycle arrest, and promote changes in cellular morphology and function48,49,50 To promote survival, various uropathogens possess siderophore systems capable of acquiring iron, an essential bacterial micronutrient, from heme Uropathogenic strains of E coli have a defensive mechanism that consists of a glycosylated polysaccharide capsule that interferes with phagocytosis and complement-mediated destruction.51study by Thulesius O. et al53 (1987) it was inferred that lipopolysaccharide also acts to reduce ureteric peristalsis, hence facilitating ascent of Escherichia coli via the relatively dilated, hypotonic ureters to the kidneys. Hemolysins are thought to contribute to spread of Escherichia coli within renal parenchyma as was found in a study by Hughes C. el. At54
Varian S. et. Al52(1980) observed relationship between in vitro adherence of E.Coli and severity of urinary tract infection in vivo.
Two mechanisms of iron uptake in Escherichia coli were identified by. 1983Stuart SJ et al55(1980) the hydroxymate type of siderophore, aerobactin and the catechol type of siderophore, enterochelin.
Although all individuals are susceptible to UTI, most remain infection free during childhood because of the innate ability to resist uropathogen attachment. There are specific subpopulations with an increased susceptibility to UTI,
RISK FACTORS FOR PEDIATRIC URINARY TRACT INFECTION
Fecal and perineal colonization
Urinary tract anomalies
126.96.36.199NEONATES AND INFANTS
Neonates and infants in their first few months of life are at a higher risk for UTI. This susceptibility has been attributed to an incompletely developed immune system. Breastfeeding has been proposed as a means of supplementing the immature neonatal immune system via the passage of maternal IgA to the child, providing the presence of lactoferrin, and providing the effect of anti-adhesive oligosaccharides. Several recent studies have demonstrated the protective effect of breastfeeding against UTI in the first 7 months of life.56
188.8.131.52UNCIRCUMCISED INFANT BOYS
Since the 1980s, studies have shown an increased frequency of UTI in uncircumcised boys during the first year of life22. Boys with foreskin tend to harbor significantly higher concentrations of uropathogenic microbes that potentially may ascend into the urinary tract and lead to UTI .Bacteuria is much more common during the first 6 months of life for uncircumcised boys
184.108.40.206 FECAL AND PERINEAL COLONIZATION
Because most UTIs result from fecal-perineal-urethral retrograde ascent of uropathogens, fecal and perineal flora are important factors in the development of a UTI42. The flora of the colon and urogenital region is a result of native host immunity, existing microbial ecology, and the presence of microbe-altering drugs and foods. A recent investigation by Schlager and colleagues 41supported the theory that a subset of the colonic microflora expressing particular virulence factors is most likely to infect the urinary tract. The selection for microbes resistant to antimicrobial agents is well recognized. As a result, the inappropriate use of antibiotics in the treatment of active nonurinary infections and in the prophylactic setting may place children at a higher risk for developing uropathogenic strains of microbe that may develop into symptomatic UTI.
Anatomic abnormalities of the urinary tract predispose child to UTI because of inadequate clearance of uropathogens. Infections associated with urinary tract malformation generally appear in children younger than 5 years of age. It is essential to identify these abnormalities early because if uncorrected they may serve as a reservoir for bacterial persistence and result in recurrent UTI. Surgical intervention may be required to correct the anatomic abnormality.
However, congenital anatomic anomalies, such as posterior urethral valves and subsequent vesicoureteral reflux (VUR), do not predispose children to colonization but perhaps increase the likelihood of inadequate washout in the routine ways. These urinary tract malformations increase the likelihood that infections of the lower urinary tract (ie, bladder and urethra) will ascend to the upper tracts with possible pyelonephritis and potential renal deterioration. Children with known urinary malformation may be on chronic antimicrobial prophylaxis. Consequently, this patient population is associated with a higher incidence of multidrug-resistant uropathogens and non-E coli uropathogens, particularly Pseudomonas and Enterococcus.
Children with a functional abnormality of the urinary tract are also at a higher risk of developing a UTI. Inability to empty the bladder, as in the case of neurogenic bladders, frequently results in urinary retention, urinary stasis, and suboptimal clearance of bacteria from the urinary tract. Clean intermittent catheterization is helpful for emptying the neurogenic bladder, but catheterization itself may introduce bacteria to this normally sterile space. Chronically elevated bladder pressure secondary to poor emptying also may cause secondary VUR, in which the elevated pressure increase the potential renal damage of pyelonephritis.
Children with UTI do not present with the characteristic signs and symptoms compared to adult population. There are various clinical presentations for children with UTI based on age. Infants younger than 60 to 90 days may have vague and nonspecific symptoms o illness like failure to thrive, diarrhea, irritability, lethargy, malodorous urine, fever asymptomatic jaundice, and oliguria or polyuria57,58,59 In fact, it has been recommended that testing for UTI be part of the evaluation of asymptomatic jaundice in infants younger than 8 weeks.59
In children less than 2 years of age, common symptoms include fever, vomiting, anorexia, and failure to thrive58. In children between 2 and 5 years of age abdominal pain and fever were the most common symptoms 60. Children at 5 years of age symptoms include dysuria, urgency, urinary frequency, and costovertebral angle tenderness, are more common60. As a result, UTI must be considered in all children with serious illness even if there is strong evidence of infection outside the urinary system. .
DIAGNOSIS OF URINARY TRACT INFECTION
The diagnosis of urinary tract infection is based on culture of a properly collected specimen of urine. Urine analysis is helpful in providing immediate information to suspect urinary tract infection and enable initiation of treatment.
The detection of significant numbers of pathogenic bacteria from culture of the urine has remained the gold standard for the diagnosis of urinary tract infection since Kass defined > 105 CFU/ml of a single pathogenic bacterium isolated from urine culture as being significant in women with pyelonephritis or asymptomatic bacteriuria.61
The specimen for urine culture should be obtained carefully to prevent contamination of periuethral flora. Washing the genitalia with soap and water minimizes contamination. The urine specimen for culture can be obtained in following ways.
Clean catch midstream urine
Suprapubic aspiration has been consider the "gold standard" for obtaining urine as it is least likely to be contaminated. Urine obtained by transurethral bladder catheterization is next best. A clean-catch midstream urine specimen is most widely used.
Prompt plating of urine specimen within 1 hour of collection is important. The specimen is inoculated into blood agar and MacConkey media and incubated for 24 hours to obtain an accurate colony count
INTERPRETATION OF URINE CULTURE
Method of Colony count Probability of
Collection Infection (%)
Suprapubic Any number of 99%
Urethral >50 x 104 CFU/ml 95%
Midstream clean >105CFU/ml 90-95%
3.7.2 URINE ANALYSIS
A careful urinalysis, on a fresh urine sample, can identify children with a high likleihood of a urinary tract infection. Several rapid screening tests are commonly used. Urinalysis may show
2) bacteria on gram stain
3) mild proteinuria
4) Positive leukocyte esterase and nitrite test by dipstick
The most accurate method of measuring pyuria is to measure urinary leucocyte excretion. An excretion rate of 4,00,000 leukocytes / hours or greater correlates with symptomatic urinary tract infection.62 The presence of >5 leukocytes / high power field in a centrifuged sample or >10 leukocytes / mm3 in an uncentrifuged sample is suggestive of urinary tract infection
Direct microscopy for the detection of baceteriuria is a readily available but highly variable method of determining bacteria. Jenkins et al63 determined that uncentrifuged gram-stained urine that revealed atleast one organism per oil immersion field correlated with >105CFU / ml urine with sensitivity and specificity of almost 90%. Additionally, finding five or more organisms per oil immersion field increased the specificity to 99%. It was also found that, the use of unstained, centrifuged urine is a convenient and reliable method of determining significant bacteriuria, but the method was most reliable only when 106CFU / ml or greater were isolated by culture.
A rapid diagnostic test for the detection of bacteriuria, the nitrite test, is both widely available and easily performed. The test is performed by the dispstick method, which utilizes an amine - impregnated pad to detect the presence of urinary nitrate. Nitrite in the urine is produced by the action of bacteria on dietary nitrate through nitrate reductase, a bacterial enzyme, The presence of urinary nitrite is indicated by the development of a pink colour on the pad within 60 seconds.
False negative assays may be the result of
1. The lack of dietary nitrate
2. Insufficient urinary nitrate levels due to diuretics.
3. Infection due to an organism that is unable to produce nitrate in the urine through a lack of nitrate reductase.
Eg. : Staphylococcus sp.
220.127.116.11 SENSTIVITY AND SPECIFICITY OF TESTS USED TO DIAGNOSE URINARY TRACT INFECTION64,65
Chemical Sensitivity Specificity
1. Nitrite 30-90% 90 - 95%
2. Leukocyte esterase 50-75% 80%
1. Urinalysis (Pyuria) 30-80% 30-80%
2. Gram stain (Bacteriuria) 90% 90%
1. Clean catch 80-98% 80%
2. Catheterization 90-95% 80-90%
3. Suprapubic aspiration >95% >98%
The goal of imaging studies in children with a urinary tract infection is to identify abnormalities that predispose to infection.
A renal ultrasonogram should be obtained to rule out hydronephrosis and renal or perirenal abscesses; ultrasonography may also show acute pyelonephritis by demonstrating an enlarged kidney. Ultrasonography demonstrates 30% of reanl scars, Renal ultrasonography is also sensitive for detecting pyonephrosis, a condition that may require prompt drainage of the collecting system by percutaneous nephrostomy. Sonography is insensitive in detecting reflux. A voiding cystourethrogram (VCUG) is indicated in all children younger than 5 years with a urinary tract infection, any child with a febrile urinary tract infection, school aged girls who have had two / more urinary tract infections, and any male with a urinary tract infection. The most common finding is vesicoureteral reflux, which is identified in approximately 40% of patients When the diagnosis of acute pyelonephritis is uncertain, renal scanning with technetium labelled Dimercaplosuccinic acid scan (DMSA) or glucoheptonate is useful. The presence of parenchymal filling defect on the renal scan supports the diagnosis of pyelonephritis but may not differentiate an acute from a chronic process. DMSA scan shows a filling defect in approximately 50% of children with a febrile urinary tract infection, irrespective of age. In children with grade III, IV or V reflux, 80-90% of patients with a febrile urinary tact infection have a focal defect. The DMSA scan is considered the most sensitive and accurate study for demonstrating scarring. Computed tomography is another diagnostic tool that can diagnose acute pyelonephritis.
Treatment should be started after obtaining a urine culture ,childs age,activity ,state of hydration and ability to take oral intake and the likelihood of compliance with medication help in deciding between outpatient therapy and hospitalization.
In infants less than 3 years of age complicated urinary tract infection are treated with parenteral antibiotics. A combination of Ampicillin and Gentamicin or a third generation cephalosporin is preferred. Antibiotics may be administered orally once the condition of the child improves .Infants and children with a positive blood culture should receive parenteral anibiotics for the entire duration of treatment.
Oral medications are used in children above 3 months of age with a simple urinary tract infection. The duration of treatment is 10-14 days for infants and children with complicated urinary tract infection and 7-10 days for uncomplicated urinary tract infection . Imaging of urinary tract is recommended for all children with urinary tract infection.
MANAGEMENT OF FUNGAL URINARY TRACT INFECTION
Although fungus in the urinary tract is rare among healthy children, the incidence of fungal UTI is increased in hospitalized patients. In large tertiary care neonatal intensive care units, Bryant and colleagues66 found the overall incidence of candiduria to be 0.5%, whereas Phillips and Karlowicz33 reported Candida sp in 42% of patients with UTI. Risk factors for the development of funguria include long-term antibiotic treatment, use of urinary drainage catheters, parenteral nutrition, and immunosuppression. The overwhelming majority of fungal UTIs are caused by Candida sp followed by Aspergillos spp, Cryptococcus spp, and Coccidioides spp. The clinical presentation of patients with funguria ranges from an absence of symptoms to fulminant sepsis. Urine cultures with more than 104 colonies/mL have been used as the criterion for therapy67. The presence of a positive urine culture result mandates an evaluation of the upper urinary tract with renal ultrasonography for additional foci of funguria. Renal fungal balls have been identified in 35% of patients with candidal UTI in the pediatric population33,66. Symptomatic patients can be treated with bladder irrigations of amphotericin B or oral fluconazole. Although there is no consensus on optimal treatment dose or duration, amphotericin bladder irrigations consist of daily irrigations of 50 mg/L for 7 days or continuous irrigations (42 mL/h) for 72 hours. Fungal bezoars in the collecting system may cause obstruction in children. Patients with these upper tract foci of funguria should be treated with systemic therapy that consists of amphotericin B or fluconazole. In cases of obstruction, percutaneous nephrostomy is then used for drainage and potential local irrigation. Surgical removal may be necessary should the fungal balls persist.
LONG TERM CONSEQUENCES OF PEDIATRIC URINARY TRACT IN FECTION
Children with upper UTI (ie, pyelonephritis) are at risk for irreversible renal parenchymal damage as evidenced by renal scarring. Renal scarring is noted in 10% to 30% of children after UTI 68,69. The most widely used method of detecting renal scarring is 99Tc-labeled dimercaptosuccinic acid scintigraphy scan. Although the exact mechanisms responsible for renal scarring secondary to UTI are currently unclear, risk factors include underlying VUR or obstructive urinary tract abnormalities and recurrent UTI and a delay in treatment of UTI. A recent study by Orellana and colleagues 70 found a significantly higher incidence of renal damage in children with non-E coli UTI. Smellie and colleagues35 found renal scarring more commonly in infants and young children and less frequently in older children and young adults, which suggests that younger kidneys are more susceptible to damage.
First Urinary Tract Infection
Age < 1 yr Ultrasound MCU
DMSA renal scan
Age 1-5 yr Ultrasound DMSA scan
Age> 5 yr Ultrasound
MCU if ultrasound or DMSA scan is Abnormal
If ultrasound abnormal: MCU and DMSA scan