Updated: Dec 15, 2009
In the pediatric patient, urinary tract infections (UTIs) are among the most common serious bacterial infections (SBI) encountered.[1 ]They are a frequent cause of fever and can cause significant morbidity if not properly identified and treated.
Presentation varies based on the age of the patient. Neonates and infants often present with vague, nonspecific symptoms, necessitating a high index of suspicion for UTIs in this age group. Older pediatric patients are more likely to present with more typical and localized complaints.
Treatment should be tailored to treat the most commonly encountered causative organisms, keeping in mind increasing antibiotic resistance among urinary pathogens. If not properly identified or treated, UTIs can progress to pyelonephritis or urosepsis. Long-term complications from UTIs may include renal scarring, hypertension, and even renal failure.
The urinary tract is normally a sterile environment and has several mechanisms that work to maintain urine sterility (urethral sphincter, length of urethra, constant anterograde flow). In most cases, failure of one of these mechanisms leads to or exacerbates infection.
The most common causative organisms are bowel flora, typically gram-negative rods. Escherichia coli is the most commonly isolated organism from pediatric patients with UTIs. However, any organism that gains access to the urinary tract system may cause infection, including fungi (Candida species) and viruses.
Pathogens can infect the urinary tract through direct spread via the fecal-perineal-urethral route or from hematogenous seeding. Hematogenous spread is much more likely in neonates than in older children. Most infections begin in the bladder, and, from there, pathogens can spread up the urinary tract to the kidneys (pyelonephritis) and possibly the bloodstream (bacteremia). Pyelonephritis may lead to renal scarring and long-term complications such as hypertension and chronic renal failure.
Prevalence and incidence of UTIs varies based on age, sex, and gender. Overall, UTIs are estimated to affect 2.4-2.8% of all children every year. As many as 5% of all children younger than 2 years who present to the emergency department with fever have a UTI. An approach using low-risk criteria for febrile infants younger than 3 months who have temperature of more than 38 º C is shown in the image below.
International prevalence and incidence is difficult to accurately assess, especially in developing countries, but is assumed to be similar to that in the United States.
Bacteremia or urosepsis may develop from UTI. This risk is highest in neonates and very young infants. Simple cystitis may progress to pyelonephritis. Predicting which patients will develop pyelonephritis is difficult, although evidence suggests that genetics may play a role. Approximately 10-30% of children with UTIs develop renal scarring. Severe and/or recurrent cases of pyelonephritis may lead to kidney damage. This may cause hypertension, renal insufficiency, or renal failure.
Studies indicate that nonblacks have a higher incidence of UTI than blacks.
Uncircumcised males have a significantly higher incidence of UTIs than circumcised males. Uncircumcised male infants have a higher incidence of UTI than female infants during the first year of life. After the first year of life, females have a much higher incidence of UTIs than males. Incidence is highest in sexually active adolescent females.
Prevalence of UTIs in the first 3 months of life is estimated to be as high as 7.5%. During the first year of life, males have an incidence of UTIs of 2.7% compared with 0.7% for girls. For children older than 1 year, females have a 1-2% incidence of UTIs and males have a 0.1-0.2% incidence of UTIs. In sexually active teenaged females, the incidence of UTIs approaches 10%.
History varies with the age of the patient with urinary tract infection (UTI) and is often nonspecific for younger children.
| Pediatrics, Appendicitis | Urinary Obstruction |
| Pediatrics, Bacteremia and Sepsis | Vaginitis |
| Pediatrics, Fever | Vulvovaginitis |
| Pediatrics, Gastroenteritis | Wilms Tumor |
| Pinworms | |
| Renal Calculi | |
| Urethritis, Male |
Cystitis
Pregnancy
Urolithiasis
Vesicoureteral reflux
The primary goal should be to identify UTIs and begin appropriate treatment.
Start antibiotics after urinalysis and culture are obtained in patients with urinary tract infections (UTIs). A 10-day course of antibiotics is recommended, even for uncomplicated infection. Typical short course treatments should be reserved for non-toxic-appearing adolescent females with UTIs. Be aware of increasing rates of antibiotic resistance and to choose antibiotic therapy accordingly.
Empiric antibiotics should be chosen for coverage of the most common uropathogens, namely E coli and Enterococcus, Proteus, and Klebsiella species. For suspected pyelonephritis, parenteral antibiotics are recommended. Recent evidence indicates that oral antibiotics are adequate therapy for febrile UTIs in young infants and children; short-term (fever) and long-term (renal scarring) outcomes are comparable to that with parenteral therapy. For uncomplicated cystitis, oral antibiotic therapy is generally adequate. The possibility of antibiotic resistance must be considered when choosing empiric therapy, especially ampicillin. Knowledge of the local antibiotic resistance helps in guiding antibiotic choice.
Provides bactericidal activity against susceptible organisms. Administered parenterally and used in combination with gentamicin or cefotaxime.
1-2 g/d IV/IM divided q6h
100-200 mg/kg/d IV/IM divided q6h
Probenecid and disulfiram elevate levels; allopurinol decreases effects and has additive effects on ampicillin rash; may decrease effects of PO contraceptives
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in renal failure; evaluate rash and differentiate from hypersensitivity reaction; caution in cephalosporin allergy.
Resistance rates are high.
Aminoglycoside antibiotic for gram-negative coverage. Provides synergistic activity with ampicillin against gram-positive bacteria including enterococcal species. Inhibits protein synthesis by irreversibly binding to bacterial 30S and 50S ribosomes. Dosing regimens are numerous; adjust dose based on CrCl and changes in volume of distribution. May be administered IV/IM.
3-5 mg/kg IV qd; alternatively, 1 mg/kg IV q8h
<5 years: 2.5 mg/kg/dose IV/IM q8h
>5 years: 1.5-2.5 mg/kg/dose IV/IM q8h
Coadministration with other aminoglycosides, cephalosporins, penicillins, and amphotericin B may increase nephrotoxicity; aminoglycosides enhance effects of neuromuscular blocking agents thus prolonged respiratory depression may occur; coadministration with loop diuretics may increase auditory toxicity of aminoglycosides; possible irreversible hearing loss of varying degrees may occur (monitor regularly)
Documented hypersensitivity; non–dialysis-dependent renal insufficiency
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Narrow therapeutic index (not intended for long-term therapy); caution in renal failure (not on dialysis), myasthenia gravis, hypocalcemia, and conditions that depress neuromuscular transmission; adjust dose in renal impairment
Third-generation cephalosporin with gram-negative spectrum. Lower efficacy against gram-positive organisms. Used as initial parenteral therapy for pediatric patients with acute complicated pyelonephritis. May be used for neonates or jaundiced patients. Requires dosing at q6-8h intervals.
1-2 g IV/IM q6-8h
100-200 mg/kg/d IV/IM divided q6-8h
Probenecid may increase levels; coadministration with furosemide and aminoglycosides may increase nephrotoxicity
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in severe renal impairment; has been associated with severe colitis; caution in penicillin allergy
Interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria. Activity against gram-positive and some gram-negative bacteria.
250-500 mg PO q8h
30-50 mg/kg/d PO divided q8h
Reduces the efficacy of PO contraceptives
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in renal impairment; caution in cephalosporin allergy
Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid. Antibacterial activity of TMP-SMZ includes common urinary tract pathogens, except Pseudomonas aeruginosa.
160 mg TMP/800 mg SMZ PO bid (ie, 1 double-strength tab bid)
<2 months: Not recommended
>2 months: 5-10 mg/kg/d PO divided q12h, based on TMP component
May increase PT when used with warfarin (perform coagulation tests and adjust dose accordingly); coadministration with dapsone may increase blood levels of both drugs; coadministration of diuretics increases incidence of thrombocytopenia purpura in elderly persons; phenytoin levels may increase with coadministration; may potentiate effects of methotrexate in bone marrow depression; hypoglycemic response to sulfonylureas may increase with coadministration; may increase levels of zidovudine
Documented hypersensitivity; megaloblastic anemia due to folate deficiency; age <2 mo
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Do not use during last trimester of pregnancy due to potential toxicity to newborn (eg, jaundice, hemolytic anemia, kernicterus); discontinue at first appearance of skin rash or sign of adverse reaction; obtain CBC counts frequently; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; prolonged IV infusions or high doses may cause bone marrow depression (if signs occur, administer 5-15 mg/d leucovorin); caution in folate deficiency (eg, persons with chronic alcoholism, elderly persons, those receiving anticonvulsant therapy, those with malabsorption syndrome); hemolysis may occur in individuals with G-6-PD deficiency; patients with AIDS may not tolerate or respond to TMP-SMZ; caution in renal or hepatic impairment (perform urinalyses and renal function tests during therapy); give fluids to prevent crystalluria and stone formation
First-generation cephalosporin that inhibits bacterial replication by inhibiting bacterial cell wall synthesis. Bactericidal and effective against rapidly growing organisms forming cell walls.
Resistance occurs by alteration of penicillin-binding proteins. Effective for treatment of infections caused by streptococcal or staphylococci, including penicillinase-producing staphylococci. Used PO when outpatient management is indicated.
250-1000 mg PO q6h for 10-14 d; not to exceed 4 g/d
25-50 mg/kg/d PO divided q6h; not to exceed 3 g/d
Probenecid increases serum concentrations; coadministration with aminoglycosides increases nephrotoxic potential
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Documented hypersensitivity with penicillin; colitis; dosage modification required with renal impairment
Third-generation PO cephalosporin with broad activity against gram-negative bacteria. By binding to one or more of the penicillin-binding proteins, arrests bacterial cell wall synthesis and inhibits bacterial growth. Has shown poor activity against staphylococcal and enterococcal species. Cefixime compared favorably to a quinolone in one study.
400 mg PO qd
8 mg/kg PO qd; not to exceed 400 mg/d
Probenecid increased serum concentration; coadministration of aminoglycosides increase nephrotoxicity; possible increase in serum carbamazepine concentration
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Documented hypersensitivity to penicillin; impaired renal function; colitis; dosage modification needed with impaired renal function
Fluoroquinolone that inhibits bacterial DNA synthesis and, consequently, growth, by inhibiting DNA gyrase and topoisomerases, which are required for replication, transcription, and translation of genetic material. Quinolones have broad activity against gram-positive and gram-negative aerobic organisms. Has no activity against anaerobes. Continue treatment for at least 2 d (7-14 d typical) after signs and symptoms have disappeared.
250-500 mg PO bid for 7-14 d
<1 year: Not established
1-17 years: Consult with specialist, evidence suggest use appears safe, although not first choice in children
PO: 10-20 mg/kg/dose PO bid for 10-21 d; not to exceed 750 mg/dose
IV: 6-10 mg/kg/dose IV q8h for 10-21 d; not to exceed 400 mg/dose
>18 years: Administer as in adults
Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; ciprofloxacin reduces therapeutic effects of phenytoin; probenecid may increase ciprofloxacin serum concentrations
May increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Not drug of first choice in pediatrics due to increased incidence of adverse events compared to controls, including arthropathy; no data exist for dose for pediatric patients with renal impairment (ie, CrCl <50 mL/min)
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urinary tract infection, UTI, urinary tract infection in kids, urinary tract infection in infants, UTI in children, cystitis, UTI in infants, urosepsis, pyelonephritis, treatment, diagnosis, symptoms
Stephen L Thornton, MD, Attending Physician, Department of Emergency Medicine, St John's Hospital
Stephen L Thornton, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
David S Howes, MD, Residency Program Director, Professor of Medicine, Section of Emergency Medicine, University of Chicago/Pritzker School of Medicine
David S Howes, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Physicians-American Society of Internal Medicine, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Grace M Young, MD, Associate Professor, Department of Pediatrics, University of Maryland Medical Center
Grace M Young, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Emergency Physicians
Disclosure: Nothing to disclose.
John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Richard G Bachur, MD, Associate Professor of Pediatrics, Harvard Medical School; Associate Chief and Fellowship Director, Attending Physician, Division of Emergency Medicine, Children's Hospital of Boston
Richard G Bachur, MD is a member of the following medical societies: American Academy of Pediatrics, Society for Academic Emergency Medicine, and Society for Pediatric Research
Disclosure: Nothing to disclose.
The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors, Terrance K Egland, MD, and Ann G Egland, MD, to the development and writing of this article.
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