UTI in Pediatrics.pptx

Urinary
Tract Infections
Dr. S Kunal Tejus
Pediatric Resident.

INTRODUCTION U T I
Urinary tract infection (UTI) is a common childhood infection, being second in frequency only
to respiratory infections.
In many children, infections recur, causing significant morbidity and long-term health effects,
like renal scars, hypertension, and chronic kidney disease (CKD).
The increasing prevalence of antimicrobial resistance in bacteria introduces an additional level
of complexity to the management of patients with UTIs.

EPIDEMIOLOGY U T I
Common bacterial infection in children.
Precise data on incidence and prevalence are not available, because of nonspecific signs and
vague symptoms in very young children.
The commonest age for the occurrence of the first symptomatic UTI is the first year of life,
particularly in boys, when it mainly affects the upper urinary tract due to structural
abnormalities.
Above 1 year, prevalence of afebrile symptomatic UTI is 8% and febrile UTI is 7 %.
Beyond 1-2 years, there is a female preponderance, with a male:female ratio of 1 : 10.

E P I D E M I O L O G Y U T I
In females, the first UTI usually occurs by the age of 5 years, with peaks during infancy and toilet
training.
In males, UTIs are much more common in uncircumcised males, especially in the first year of life.
Higher risk in children with malnutrition and chronic diarrhoea.
10 % of UTIs are caused by Obstructive lesions and 30 to 40% patients show vesicoureteric reflux
(VUR).
Delay in starting treatment and presence of VUR or obstruction are the chief risk factors associated
with renal scarring.

DEFNITIONS U T I
Signs and symptoms
• Febrile UTI - UTI associated with temperature 38°C (100.4°F)
• Symptomatic UTI - UTI associated with fever and/or urinary symptoms
• ABU - Significant bacteriuria in a child with no symptoms of UTI
• Sterile pyuria - Increased white cells in urine in the absence of bacteria on urine culture
• BBD - Spectrum of signs and symptoms, including incontinence, constipation and abnormalities of
the bowel, lower urinary tract, and pelvic floor
Renal status
• Reflux nephropathy - Renal cortical abnormalities associated with VUR.
• Renal scarring - Acquired renal damage due to APN.
• Renal dysplasia - Congenital renal cortical abnormalities.

DEFNITIONS U T I
Site of infection
• Upper-tract UTI - UTI involving kidneys and ureters
• Lower-tract UTI - UTI involving bladder and urethra
• Pyelonephritis - Kidney infection (febrile UTI)
• Cystitis - Bladder infection
Severity of infection
• Complicated UTI - UTI in newborns; abdominal and/or bladder mass; kidney and urinary tract
anomalies; urosepsis; organism other than E coli; atypical clinical course, including absence of
clinical response to antibiotic within 72 h; and renal abscess
• Complicated cystitis - Children with comorbid medical conditions, underlying bladder pathology,
indwelling bladder catheter, and atypical clinical course

BACTERIOLOGY U T I
Gram-negative enteric bacteria of the Enterobacteriaceae family cause most UTIs in children
of all ages.
This includes
• Escherichia coli, which is responsible for 80% to 85% of all UTIs in children.
• Klebsiella,
• Proteus,
• Citrobacter,
• Enterobacter species, and
• Morganella morganii.
Pseudomonas aeruginosa, Gram-positive organisms such as Enterococcus, Staphylococcus, and
group B streptococci also can cause UTI in children.

B A C T E R I O L O G Y U T I
Group B streptococcus is almost exclusively seen as a cause of UTI in neonates,
Staphylococcus saprophyticus is seen commonly in adolescent girls.
Staphylococcus aureus is an uncommon cause of UTI but results in hematogenous spread to
the kidney, results in focal renal lesions, such as intrarenal and perinephric abscesses.

B A C T E R I O L O G Y U T I
Bacteria that produce extended-spectrum β-lactamase (ESBL) have increased in prevalence
among nosocomial and community-acquired UTIs.
ESBL bacteria primarily include Gram-negative organisms, particularly Klebsiella & E. coli.
• 11.3% of Klebsiella pneumoniae,
• 3.5% of Citrobacter koseri
• 2.6% of E. coli,
• 1.6% of Serratia marcescens,
• 1.4% of Proteus.

PATHOGENESIS U T I
Infection can reach the urinary tract via the ascending route or by the hematogenous route.
1. ASCENDING INFECTION, mostly post-infancy. Gram negative enteric flora ascends via the
urethra to invade the urinary tract and cause asymptomatic bacteruria, acute cystitis, or
acute pyelonephritis.
2. HEMATOGENOUS SPREAD, mostly during infancy, accounts for fewer than 1% of UTIs and
commonly occurs in association with sepsis, particularly that caused by S. aureus. Resultant
infection leads to focal renal lesions, such as pyelonephritis, intraparenchymal abscess,
and perinephric abscess.
.

BACTERIAL VIRULENCE FACTORS
P A T H O G E N E S I S U T I
Specific microbiologic properties of bacteria, known as virulence factors, strains possessing
these are able to spread to the urinary tract and result in more serious infections.

B A C T E R I A L V I R U L E N C E F A C T O R S
Adhesins, or fimbriae, are microscopic appendages present on the surface of E. coli allow
bacterial adherence to the uroepithelial cell.
the three types of clinically significant fimbriae expressed by uropathogenic E. coli.
1. Type I fimbriae, exhibit mannose-sensitive hemagglutination and attachment to bladder
umbrella epithelial cells, sometimes blocked by D-Mannose.
2. Type II fimbriae (also known as P fimbriae), demonstrate mannose resistant
hemagglutination and are associated with acute pyelonephritis.
3. Dr hemagglutinin, a fimbria-like adhesin, are associated with the development of cystitis
ADHESINS OR FIMBRIAE

SEROTYPES & BACTERIAL VIRULENCE
E. coli contain three major antigens that are identified through antibody serotyping
Associated with invasiveness, virulence, and the ability to evade phagocytosis and
complement-mediated lyses.
These are
• O antigen, in the outer membrane of the cell wall,
• K antigen, the capsular antigen, and
• H antigen, or the flagellar antigen.
O antigen serogroups (1, 2, 4, 6, 7, 8, 16, 18, 25, and 75) are associated with the development of
pyelonephritis.

ADHESINS OR FIMBRIAE

SEROTYPES

HEMOLYSIN & CYTOTOXIC PROTEIN
Hemolysin, a cytotoxic protein that lyses erythrocytes and other cells, contribute to the
inflammation and tissue injury associated with haemolytic E. coli and are associated with the
development of acute pyelonephritis.
Colicin, another cytotoxic protein.

BACTERIAL GENETICS
Many of the genes encoding for the virulence factors in E. coli are located on DNA called
pathogenicity associated islands (PAIs) that are present in the genome of pathogenic
Genes encoding for hemolysin or P fimbriae production are characteristically found in PAIs.
PAIs can be deleted from the chromosome and also can be transferred to other bacteria by
helper phages.
Many pathogenic strains of E. coli may carry more than one PAI.

HOST FACTORS

INFLAMMATORY RESPONSE
Virulence of uropathogenic E coli is largely influenced by P fimbriae and lipopolysaccharide.
Uropathogenic E. coli attach to the glycosphingolipid (receptor) on the uroepithelial cells using P
fimbriae mediated by tip adhesion PapG.
They initiate inflammation by stimulating uroepithelial cells to release cytokines and chemokines, such
as interleukin-6 (IL-6) and IL-8 by using the Toll-like receptor 4 (TLR-4) pathway for signal
transduction and also involved in neutrophil recruitment within the infected urinary tract.
Bacterial endotoxins also facilitate chemotaxis by activating the complement pathway.
The neutrophils recruited by the cytokines kill bacteria and help clear the infection.

I N F L A M M A T O R Y R E S P O N S E
Neutrophils exit the blood vessels, cross the lamina propria and the epithelial barrier, and enter
the urinary lumen, resulting in pyuria.
Urinary IL-6 and IL-8 concentrations are elevated in children with UTI.
H O S T F A C T O R S

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Steps in E coli
Preceding stages: E. coli from colonic flora colonize the perineum, then they rise from urethra into the
urinary tract to reach the urinary bladder.
Step 1: Bacteria attach to mannose receptor on umbrella cells of urinary bladder.
Step 2: Bacteria is internalized, forming Intercellular Bacterial Communities (IBCs).
Step 3: Some bacteria form filamentous forms to evade body’s immune system.
Step 4: Most lining umbrella cells having IBCs are shed off, as body’s defence against UTI.
But some IBCs and filamentous cells escape into urine.

Step 5: Filamentous cells evade killing by WBCs.
Others from IBCs enter into cells of the bladder wall to form Quiescent Intracellular Reservoirs
(QIRs).
Step 6: Filamentous cells cause UTI.
QIRs act as a source of recurrent UTI.

IL-8 has also been found to be elevated in non-infectious renal conditions such as VUR and
non-VUR congenital abnormalities, suggesting that IL-8 is a nonspecific marker of renal
injury.
Recent genomics studies have identified IL-10 upregulation in response to UTI.

PREPUCE & CIRCUMCISION
Enhanced adherence capability of the uropathogenic organisms to the nonkeratinized
mucosa of the prepuce.
This allows enteropathogenic bacteria to harbor and multiply in an uncircumcised male.
Studies suggest 3 to 7 times higher incidence of febrile UTI in uncircumcised males compared
to circumcised infants.

ELIMINATION DYSFUNCTION
Voiding and bowel dysfunction that is an abnormal micturition and stooling pattern
But with normal urinary tract anatomy and intact neurogenic control.
Clinical manifestations include
• Urinary frequency and urgency,
• Prolonged voiding intervals,
• Daytime wetting,
• Perineal and penile pain,
• Holding maneuvers, or posturing to prevent wetting,
• Constipation.
These leads to incomplete bladder emptying, leading to accumulation and proliferation of
uropathogenic bacteria in the bladder.

URINARY OBSTRUCTION
Obstruction at the ureteropelvic junction or along the ureteric length can lead to a
predisposition to UTI.
Urinary obstruction is more commonly in UTI caused by Proteus, Enterococcus, Klebsiella, or
coagulase-negative staphylococcal infections.
Children with posterior urethral valves may first come to medical attention because of febrile
UTI or urosepsis.

VESICOURETERAL REFLUX
Retrograde flow of the urine from the urinary bladder into the ureters is prevented during
micturition by a functional valve mechanism at the level of the ureterovesicular junction (UVJ).
Incompetence of the UVJ valve leads to flow of urine upstream into the ureter and the kidney.

CLINICAL MANISFESTATIONS U T I
From a clinical perspective, infection of the urinary tract may be discussed as a
• Nonfebrile UTI or acute cystitis and
• Febrile UTI or acute pyelonephritis.

C L I N I C A L M A N I S F E S T A T I O N S
U T I
Among pre-schoolers
More commonly in girls than in boys.
In children who can verbalize (usually more than 3 to 4 years of age),
• Dysuria, urgency or frequency
• Suprapubic pain are common manifestations of cystitis.101
• Dysuria may be difficult to ascertain in younger children.
• Enuresis
• Urinary incontinence, especially in girls.
Parental observations may range from reluctance to urinate, to excessive crying and abdominal pain.
CYSTITIS
( N O N F E B R I L E U T I )

ACUTE PYELONEPHRITIS
( F E B R I L E U T I )
U T I
Association of fever (> 39°C )in a patient with a positive urinary culture suggests renal parenchymal
infection or acute pyelonephritis.
It can result in pyelonephritic scarring.
Other symptoms include
• Abdominal pain, Costovertebral angle pain and tenderness,
• Malaise
• Nausea & vomiting
• Diarrhea
• Chills and rigors
• Dysuria, more commonly present in older children and adolescents.
• Excessive crying, irritability, vomiting, feeding problems, and lethargy, In younger children and
infants, in addition to fever.

ACUTE PYELONEPHRITIS
( F E B R I L E U T I )
U T I

NEONATES AND INFANTS
C L I N I C A L M A N I S F E S T A T I O N S U T I
Pyelonephritis is the most common serious bacterial infection in infants younger than 24 months of
age who have fever without an obvious focus
Most common in males.
In infants with known urinary tract abnormalities, such as hydronephrosis, obstructive uropathy, or
VUR, diagnosis of UTI should be considered and ruled out during febrile episodes.
Clinical manifestations in neonates and infants younger than 3 months of age with acute
pyelonephritis
• Hypothermia
• Hypotension

• Shock
• Jaundice
• Failure to thrive
• Diarrhoea & Vomiting
• Feeding problems
• Irritability
• Cyanosis
• Polyuria and
• Metabolic acidosis.
N E O N AT E S A N D I N FA N T S

ACUTE LOBAR NEPHRONIA
U T I
• It is a localized renal parenchymal mass caused by acute focal infection without liquefaction
• More common in older children
• A precursor of a renal abscess
• Manifestations and organisms indentical to those of APN
• CECT is sensitive and specific investigation
• Can cause Renal scarring

RENAL ABSCESS
Renal abscesses can be divided into two anatomic categories: intrarenal and perirenal
abscesses.
1. Intrarenal abscesses include cortical and corticomedullary abscesses.
1a. Cortical abscesses are often a consequence of hematogenous spread from infection
elsewhere in the body.
1b. Corticomedullary abscesses are more likely to be associated with a urinary tract
abnormality and result of an ascending infection.

RENAL ABSCESS

2. Perinephric abscess
• characterized by infection between the renal capsule and Gerota fascia.
• Develop after an intrarenal abscess ruptures and spreads infection into the perinephric
space,
• Or may develop as a complication from a primary infection elsewhere in the body.
• Does not communicate with the collecting system, thus, abnormal findings may not be seen
on urinalysis or culture
• Diffuse throughout the capsule and is not walled off.
R E N A L A B S C E S S

Diagnosis of renal abscess can be made by renal ultrasound or computed tomography (CT) scan
of the abdomen, which may demonstrate a partially filled cystic lesion.
Treatment consists of surgical drainage of the abscess under ultrasound guidance or requires
total or partial nephrectomy and antibiotic therapy for 3 weeks or longer.
R E N A L A B S C E S S

URINALYSIS
U R I N E C O L L E C T I O N
D I A G N O S I S
U T I
Midstream clean-catch
• Widely used in toilet-trained older children.
• The initial urinary stream washes away distal urethral organisms and should be discarded.
• In girls, parents should be instructed to part the labia while passing urine.
• Cleaning of the vulva in prepubescent girls or the meatus in boys is not necessary.
• Early morning urine samples harbour greater bacterial.

D I A G N O S I S U T I
Suprapubic Aspiration
Best technique for obtaining an uncontaminated urine specimen in neonates and infants, the
Performed using a 21 gauge needle, 1-2 cm above the pubic symphysis.
Most important factors in success of the procedure is whether the bladder is palpable at the
time of the aspiration and use of ultrasound guidance.
U R I N A L Y S I S

Transurethral catheterization & a bag specimens.
Bag specimens have unacceptably high contamination rate, even with thorough cleaning of the
prepuce or the perineum. Not recommended. Bacteria multiply in the bags and specimen
obtained from this site is unsuitable.
In children with indwelling catheters, urine can be aspirated from the catheter using a sterile
needle and syringe.
U R I N A L Y S I S

Patients with ureterostomy or vesicostomy, catheterization of the stoma under asepsis is
recommended and the culture result should be interpreted as any catheter specimen.
Transportation
The specimen should be transported to laboratory as early as possible, or stored at 4ºC.
A specimen kept at room temperature should be analyzed within 1 hour, or in 4 hours if
refrigerated.
U R I N A L Y S I S

PYURIA
Light microscopy visualization of
• >10 white blood cells/mm3 in an uncentrifuged or
• >5 white blood cells per high-power field (WBCs/hpf) in centrifuged urinary sediment.
Pyuria (without bacteriuria) alone cannot be used as the sole diagnostic criteria for UTI.
U R I N E M I C R O S C O P Y

URINE COLOUR & SMELL
Turbid urine may be an indication of pyuria and UTI. Clarity of urine has been shown to have a
negative predictive value for absence of UTI.
Parents often report an abnormal smell to be suggestive of onset of UTI in children. Urine smell
is also a poor screening test for UTI.
Neither colour nor odour is taken into consideration for diagnosis in the AAP UTI Practice
Guideline.

URINE MICROSCOPY
Detection of any bacteria in the uncentrifuged urine slide stained by Gram stain has been
used as the gold standard for the presumptive diagnosis of UTI.
The limitations of this test are that it is time-consuming and requires expertise in performing
the Gram stain and identifying the organisms.

LEUKOCYTE ESTERASE
Leukocyte esterase is present in the neutrophils and can be assayed in the urine by dipstick
strips.
For patients with a suspected UTI, the sensitivity of this test is 94%, with an average specificity
of 72%.4
False-negative tests can be caused by the presence of ascorbic acid, high urinary protein,
glycosuria, presence of urobilinogen, gentamicin, nitrofurantoin, cephalexin, and boric acid.
A false-positive test can result from presence of imipenem and clavulanic acid in the urine.

LEUKOCYTE ESTERASE

NITRITE TEST
Bacterial enzyme nitrate reductase can convert urinary nitrate to nitrite, which can be detected using
dipstick test strips.
Specificity 90% to 100% but sensitivity is significantly lower at 16% to 82%.
Not useful in Gram-positive infections because they lack the nitrate reductase enzyme.
Conversion of the urinary nitrate to nitrite requires sufficient time (usually 3 to 4 hours in the bladder)
even in presence of Gram-negative infection, leading to poor conversion of nitrate and infants with
frequent urination, nitrite testing may be particularly insensitive.
High urine specific gravity reduces the sensitivity of this test
High urinary ascorbic acid may produce a negative test in the presence of a small amount of nitrite.

NITRITE TEST

URINE CULTURE
B A C T E R I A L C O U N T S
D I A G N O S I S
U T I
Culturing urine remains the gold standard for confirming the diagnosis of UTI.
Potential contamination of the urine sample is a well-recognized problem that can make interpretation
of the culture results difficult.
1. Any growth of a single organism in a sample obtained by suprapubic aspiration.
2. A growth of more than 5x104 colony-forming units (CFU)/Ml of a single species of bacteria in a
catheterized urine sample.
3. A growth of more than 105 colony-forming units (CFU)/Ml of a single species of bacteria in a
midstream clean catch.

B A C T E R I A L C O U N T
Colony counts lower than those listed in Table may be considered diagnostic of UTI in some
clinical circumstances.
These include patients currently receiving
• antibiotic therapy,
• complete ureteral obstruction preventing the flow of infected urine,
• urinary frequency who may have a reduced dwell time of urine in the bladder,
• infected with organisms that are well known to have lower colony counts in urine culture,
such as S. saprophyticus.
U R I N E C U L T U R E

B A C T E R I A L C O U N T
Certain organisms are not considered clinically relevant in children under 2 years of age.
• Lactobacillus species,
• coagulase-negative staphylococci, and
• Corynebacterium species.

BLOOD TEST
• Increased white blood cells
• Increased CRP levels
• Increased Procalcitonin levels
Procalcitonin is a potential marker for the diagnosis of acute pyelonephritis and
renal scarring in children.
Procalcitonin values 0.8 ng/mL or greater had a sensitivity of 83.3% and
specificity of 93.6% in predicting acute pyelonephritis.

RADIOLOGIC IMAGING
Imaging is not needed to make the clinical diagnosis of UTI or pyelonephritis.
If there is concern about acute lobar nephronia or renal abscess, imaging should be considered.
Ultrasound is the first-line type of imaging for screening - demonstrate an enlarged kidney with
a possible mass in the case of acute lobar nephronia or renal abscess.
CT scan is more sensitive and specific for lobar nephronia - show a wedge-shaped, lower-
density area after contrast administration.

U T I
A diagnosis of UTI based on contaminated urine specimen may lead to unnecessary antibiotic
treatment or delayed treatment in those with true UTIs.
The 2 most common sources of urine contamination are feces and skin.
Presence of
1. >10 per high-power field squamous epithelial cells on urinalysis,
2. insignificant bacterial colony count, or
3. the presence of >2 pathogens on urine culture in midstream urine specimen
Is suggestive of contamination.
C O M M O N E R R O R S
CONTAMINATED URINE SPECIMEN

U T I
Bacteriuria present in children without any clinical manifestations of UTI is known as
asymptomatic bacteriuria (ABU)
Can occur in all age groups and is more common in girls.
Some strains of E. coli associated with ABU are less adherent to epithelial cells & E. coli that do
adhere to epithelial cells, there is a reduced host pro-inflammatory cytokine response
compared to uropathogenic E. coli strains.
ASYMPTOMATIC BACTERIURIA

A S Y M P T O M A T I C B A C T E R I U R I A U T I
Although patients are asymptomatic at the time of initial detection, close evaluation may reveal
a history of nonspecific symptoms, such as urgency, abdominal pain, nocturia, frequency of
urination, or generally poor health.
Patients with ABU need not be treated with antibiotics, unless symptomatic infections are
demonstrated.

P Y U R I A
U T I
Sterile pyuria is urinary WBC excretion without concurrent evidence of bacterial infection or UTI.
Clinical conditions that may be associated with sterile pyuria
1. Partially treated urinary tract infection
2. Interstitial nephritis
3. Renal tubular acidosis
4. Acute post infectious glomerulonephritis
5. Renal cystic diseases
6. Renal stone disease
7. Hydronephrosis
8. Appendicitis
U R I N E M I C R O S C O P Y
STERILE PYURIA

U T I
9. Dehydration
10. Meatal or urethral irritation, especially in males
11. Vaginitis in females
12. Neonates
13. Renal tuberculosis
14. Exercise
15. Kawasaki’s disease

TREATMENT U T I
The aims of antimicrobial treatment for UTI are
1. to clear the acute infection,
2. prevent urosepsis,
3. reduce the likelihood of renal damage.

SIMPLE UNCOMPLICATED UTI IN ≥3MONTHS
T R E A T M E N T U T I
Initial antibiotic therapy is empiric.
Oral antibiotics are preferred for duration of 7-10 days.
1st line include Amoxicillin/clavulanate or Cefixime.
Alternatives like cephalosporins like Cephalexin, Cefadroxil and Ciprofloxacin.
Nelson mentions trimethoprim-sulfamethoxazole (TMP-SMX) and Nitrofurantoin.
Nitrofurantoin avoided in febrile UTI because it doesn’t achieve significant renal tissue levels.
Both Nitrofurantoin and TMP-SMX are contraindicated in G6PD def., as they cause hemolysis.

FEBRILE UTI IN FIRST THREE MONTHS
All infants up to 3 months of age with febrile UTI should be hospitalized and treated with intravenous
therapy at least initially.
Bacteremia and meningitis should be excluded by obtaining blood for culture and examining the CSF.
Inpatient intravenous antibiotic therapy is recommended because of the
• inability of young infants to adequately absorb oral antibiotics,
• the immature immune system, and
• the consequent increased risk for disseminated infection.

Usually a single antimicrobial should be used in community-acquired infections and combinations
should be reserved for sick patients.
Drugs of choice are 3rd gen. Cephalosporins, IV Ceftriaxone or Cefotaxime.
Intravenous therapy with single daily dose of aminoglycoside has also been found to be safe and
effective
Parenteral therapy should continue until the infants improve clinically, then oral antibiotic therapy is
continued to complete a total of 14 days of antibiotic treatment.

FEBRILE UTI IN INFANTS AND CHILDREN
Oral antibiotics, i.e. Oral Cefixime is used to treat older children and adolescents with febrile UTI for
total duration of 7 and 14 days.
Alternatively, a short course of intravenous antibiotic therapy (2 to 4 days), followed by oral antibiotic.
Children with additional risk factors, such as underlying urinary abnormalities, may require a
prolonged course of parenteral therapy.
Note:
Selection of appropriate antimicrobial therapy should be guided by the susceptibility results of the
urine culture.

TREATMENT OF EXTENDED-SPECTRUM β-LACTAMASE URINARY TRACT INFECTION
Empiric coverage of ESBLs with a carbapenems and cephamycins antibiotic is indicated.
ESBL isolates are resistant to all β-lactam antibiotics, including penicillins, monobactams, and
cephalosporins.
Plasmid-mediated gene transfer result in resistance to fluoroquinolones, aminoglycosides, and TMP-
SMX.

Additional therapies
• Plenty of fluids
• Void bladder regularly
• No role of urine alkalinisation
Response to therapy
Fever or systemic toxicity reduce and culture becomes sterile within 24-36h of starting
treatment.
Repeat culture is indicated if
• Symptoms fail to resolve despite 72h of treatment
• Contamination of previous culture is suspected

Follow-up Imaging studies
To identify anatomical abnormalities, VUR or any factors that increase risk of recurrence or scarring.
Done after completing antibiotic therapy.
INFANTS 1-5 YEARS >5 YEARS
Ist visit USG-KUB USG-KUB Only USG-KUB
If MCU indicated, done after 2-
4 weeks after therapy
DMSA Do MCU or DMSA if USG is
abnormal
If DMSA indicated, done after
3-4 months later.
Do MCU only if USG or DMSA
is abnormal

Antibiotics Prophylaxis
Indications
• All infants with UTI, till follow-up imaging is done
• In VUR- longer term prophylaxis needed
• Frequent Febrile UTI i.e. 3 or mlre episodes in a year
Antibiotics
• 1st line Cephalexin 10mg/kg HS
• Alt. Cefodroxil 5mg/kg HS
• Others Cotrimoxazole, Nitrofurantoin. Both are contraindicated in <3 months of age and
G6PD deficiency.

Additional Preventive Therapies
• Circumcision in males reduces VUR, esp. in high grade VUR
• Avoid constipation
• Directed therapies structural anamolies
Preventive therapies with Limited Evidence
• Probiotics, restores both gut and urinary microbiota.
• Cranberry juice, contains Proanthocyanidin PAC, it reduce adherence and biofilm formation
by uropathogens.

U T I
Routine neonatal circumcision: View of the American Academy of Pediatrics, Sep ‘12.
Based on available evidence, the health benefits of newborn male circumcision outweigh the
risks of the procedure.
However, universal circumcision has not been recommended.
If parents choose to, access to the procedure has been advocated.

RECURRENT UTI U T I
Occurs in 30-50% children, usually within first 3 months of the 1st episode, especially
• VUR, most common cause
• Female gender
• Below 6 months of age
• Obstructive uropathy, labial adhesions.
• Constipation.
• Urethral instrumentation or Repeated catheterisation.
• PEM, Immunosuppression
• Uncircumcised males
• External irritation
• Neuropathic bladder
Patients with recurrent UTI should be examined with ultrasound, DMSA and MCU regardless of
age.

FUNGAL UTI U T I
Primarily caused by Candida species.
Most frequently seen in
• Neonates, more commonly seen in preterm and low-birth-weight babies
• older children in the intensive care unit (ICU),
• immunocompromised patients, and
• prolonged indwelling urinary drainage catheters.
Neonates present with nonspecific symptoms of fever, feeding intolerance, respiratory distress,
lethargy, apnea, and abdominal distention.
Oliguria or anuria can be seen as a result of obstruction by a fungus ball (Figure).
Renal involvement also can manifest as rising serum creatinine and nonoliguric renal failure.

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Renal ultrasound showing dilated calyces & pelvis.
An echogenic fungus ball (arrow) is seen.

DIAGNOSIS
F U N G A L U T I U T I
Growth of greater than 104 CFU/mL Candida organism in a single urine culture is diagnostic for
candidal UTI.
Renal ultrasound and CT scan to find renal fungus balls or a fungal abscess, that are reported in
35% to 40% of cases.

TREATMENT
Positive blood culture for fungus or candidemia requires systemic antifungal therapy.
IV Amphotericin B or Fluconazole therapy.
Amphotericin B is preferred to the lipid formulations of amphotericin B in neonates, because
lipid formulations penetrate renal tubules poorly.
Renal function and serum electrolytes should be monitored closely, and the amphotericin B
dose should be decreased if serum creatinine rises.
Surgical intervention is reserved for patients with fungus balls causing severe obstruction of the
urinary tract, or those with renal abscess requiring drainage.

Irrigation of the urinary bladder by an aqueous solution of amphotericin B, has been used for
the treatment of uncomplicated fungal infection.
Such therapy has, however, come into question recently as it has a high relapse rate.
Availability of oral fluconazole as a treatment option, has decreased the use of amphotericin B
bladder irrigation.
It is reserved for refractory infections with resistant organisms ex. fluconazole-resistant Candida
infections.

VIRAL HEMORRHAGIC CYSTITIS U T I
Commonly seen in immunocompromised patients and is especially common in patients with bone
marrow transplantation (BMT).
Either 1 to 2 weeks after transplantation (early onset) or 4 to 6 months later (late onset).
Viruses associated with late-onset hemorrhagic cystitis are adenovirus, polyoma BK virus,
cytomegalovirus, human herpes virus-6, and simian virus 40 (SV40).
A study showed, children who underwent allogenic stem cell transplantation found that 25.5% of
patients developed hemorrhagic cystitis, of which 80.8% were due to BK virus, 15.4% to adenovirus,
and 3.8% to JC virus.207

V I R A L H E M O R R H A G I C C Y S T I T I S U T I
Gross hematuria, severe suprapubic pain, and dysuria are common symptoms.
Diagnosis is made by quantitative polymerase chain reaction (PCR) obtained in the urine.
Serologic methods are less reliable in immunocompromised hosts, who may not be able to
mount a good antibody response.
Ultrasound examination shows a thickened bladder wall.
This finding may resemble the ultrasound features seen in rhabdomyosarcoma of the bladder.

V I R A L H E M O R R H A G I C C Y S T I T I S U T I
Symptomatic therapy is usually sufficient.
Self-limiting and resolves in approximately 2 to 3 weeks.
Cidofovir, a newer antiviral agent, has been used in the treatment of polyoma BK & adenoviral
hemorrhagic cystitis. It causes nephrotoxicity, limits its use to the most severe cases.
Other forms of non-infectious Cystitis are
• Eosinophillic cystitis, present with hematuria.
• Interstitial cystitis, present with irritative voiding symptoms.
• Polypoid cystitis, due to catheterization.

UTI in Pediatrics.pptx

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