This document discusses urinary tract infections (UTIs) in children. It notes that UTIs are most common in children under 1 year of age and are more common in females than males. The most common causative bacteria is E. coli. Symptoms can include fever, back/flank pain, nausea, vomiting, and diarrhea for pyelonephritis or dysuria, urgency, frequency for cystitis. Diagnosis involves urinalysis, urine culture, and imaging tests as needed. Treatment involves antibiotics for 7-14 days with hospitalization sometimes needed for severe cases.
2. PREVALENCE AND ETIOLOGY
UTIs commonly occur in children of all ages.
Most common in chidren under 1years of age.
MALE :FEMALE RATIO 2.4:5.4 in first year of life.
Beyond 1-2 years there is female preponderance 1:10 male
female ratio.
UTIs mutch more common in uncircumsed male.
4. PREVALENCE AND ETIOLOGY
UTIs caused primarly by colonic bacteria .
Escerichia coli caused 54-67 % of all UTIs.followed by
klebsiella spp.and proteus spp, Enterococus,and
pseudomonase.
Other Bacteria include staphlococus saprophyticus
,Group B streptococus.
Less common staphylococus aureus,candida spp and
salmonela spp
UTIs have been considred a risk factor for the
development of renal insufficiensy or end- stage of
renal disease.
5. CLINICAL MANIFESTATION AND
CLASSIFICATION
Two form of UTI pyelonephritis and cystitis.
PYELONEPHRITIS characterized by any or all the
following;
BACK OR FLANK PAIN
FEVER
MALAISE
NAUSEA
VOMITING
DIARRHEA
6. CLINICAL MANIFESTATION AND
CLASSIFICATION
Neobrns can show nonspecific symptoms such as;
POOR FEEDING
IRRITABILITY
JAUNDICE
WEIGHT LOSS
Pyelonephritis is the most common seriuse pacterial
infectin in an infant younger than 24 month of age
have fever whithout obvius focus.
7. CLINICAL MANIFESTATION AND
CLASSIFICATION
Involvement of renal parenchyma is term acute
pyelonephritis.
Pylitis no parenchymal involvment.
Aute lobar nephrona is alocalized renal parenchymal
mass caused by acute focal infection without
lequefacton. Fever and flank pain and other
manifestations of pyelonephritis.
Renal abcess typically occurs followed hematogenous
spreed of s.aureus or pyelonephritic infection.
PERINEPHRIC ABSCESS
XANTHOGRANOLOMATOUS PYELONEPHRITIS
9. CYSTITIS
THERE IS ONLY BLADDER INVOLVMENT
DYSURIA
URGENSY
FREQUENSY
SUPRAPUBIC PAIN
INCONTINENCE
MALODORS URINE
ACUTE HEMORRHAGIC CYSTITIS
EOSINOPHILIC CYSTITIS
10. PATHOGENISIS AND PATHOLOGY
Nearly all UTIs are ascending infection .
Bacteria arise from the fecal flora clonized the
perneum,and enter the bladder via the urethra.
Rarely renal infection occur by hematogenuse spread
as in endocarditis or in some bacterimic neonate .
CHILDREN OF ANY AGE WITH FEBRILE UTI CAN
HAVE ACUTE PYELONEPHRITIS AND
SUBSEQUENT RENAL SCARING
11. RISK FACTOR FOR UTI
VUR
FEMAL GENDER
UNCIRCUMCISE MALE
SOURSE OF EXTERNAL IRRITATION
BOWEL- BLODDER DYSFUNCTION
OBSTRUCTIVE UROPATHY
UROGENIC BLODDER DYSFUNCTION
CONSTIPATION
ANATOMIC ABNORMALITIS
SEXUAL ACTIVITY
12. DIAGNOSISE
SYMPTOMS
FINDIG OF URINALYSISE
URINE CULTURE
Urine culture remains the gold standard for
diagnosing
13. IMAGING FINDING
IS NOT NEEDED TO MAKE THE CLINICAL
DIAGNOSISE OF UTI OR PYELONEPHRITIS
ULTRASOUND THE FIRST LINE TYPE OF IMAGING
CT SCAN MORE SENSITIVE AND SPECIFIC FOR
LOPAR NEPHRONIA
14. LABORATORY INVESTIGATIONS
The presence of 5 white blood cells per high power field
in centrifuged urine or 10 white blood cells as detected by
hemocytometer in uncentrifuged urine, respectively, is the
gold standard for pyuria .
However, pyuria is not diagnostic of UTI . Pyuria has a
specificity of approximately 81% and sensitivity of 73% .
Sterile pyuria can be associated with infection due to
anaerobic bacteria, tuberculosis, viral pathogens, chemical
or allergic inflammation, cervical or vaginal secretion,
Kawasaki disease, crystalluria,appendicitis, regional
enteritis, glomerulonephritis, and interstitial nephritis .
15. LABORATORY INVESTIGATIONS
Conversely, the absence of pyuria on a single specimen does
not rule out UTI.
Serial urinalysis in patients with UTI eventually shows
pyuria.
Dipstick tests are inexpensive, convenient, readily
available, and useful for diagnosis of UTI.
The leukocyte esterase dipstick test demonstrates the
presence of pyuria by histochemical methods that detect
this enzyme in neutrophils .
Leukocyte esterase is also present even if leukocytes are
lysed.
16. LABORATORY INVESTIGATIONS
Neutrophilia, elevated erythrocyte sedimentation rate, elevated
serum C-reactive protein, and white blood cell casts in the
urinary sediment are suggestive of acute pyelonephritis.
Children with very high serum procalcitonin levels during UTI
are more likely to have acute pyelonephritis
A meta-analysis of 18 studies involving 831 children with acute
pyelonephritis and 651 children with lower UTI were analyzed .
The authors found that a serum procalcitonin cutoff value of
1.0ng/ml provides a good diagnostic value for discriminating
acute pyelonephritis from lower UTI. Because of the marked
heterogeneity between studies, more intensive studies are
necessary before this test can be routinely recommended in the
evaluation and management of a child with UTI.
17. LABORATORY INVESTIGATIONS
According to the American Academy of Pediatrics (AAP)
clinical practice guidelines, the diagnosis of UTI in
children 2 to 24 months requires positive dipstick test
(leukocyte esterase and/or nitrite test), microscopy positive
for pyuria or bacteriuria, and the presence of
50,000cfu/ml of a uropathogen in a catheterized or
suprapubic aspiration specimen
According to the Canadian Paediatric Society (CPS)
guidelines, a positive dipstick test (leukocyte esterase
and/or nitrite) and a positive urine culture of a single
uropathogen ( 100,000cfu/ml in a midstream urine
specimen, 50,000cfu/ml in a catheterized specimen, and
any organism in a suprapubic aspiration specimen) are
required for the diagnosis of UTI .
18. LABORATORY INVESTIGATIONS
The European Association of Urology (EAU) /
European Society for Paediatric Urology (ESPU)
guidelines state that growth of 10,000 or even
1,000cfu/ml of a uropathogen from a catheterized
specimen or any counts from a suprapubic aspiration
specimen is sufficient to diagnose a UTI .
In toilet-trained children, a clean-catch
midstream urine specimen rather than a
catheterized or a suprapubic aspiration specimen
should be submitted for urinalysis and urine
culture
19. LABORATORY INVESTIGATIONS
In the work-up of children with UTI, physicians must
judiciously utilize imaging studies to minimize exposure of
children to radiation.
Renal and bladder ultrasonography is the method of
choice to image the urinary tract .
Ultrasonography is noninvasive, safe, easy to perform, and
radiation-free .
A renal and bladder ultrasound can define the kidney size,
shape and position, echotexture of the renal parenchyma,
the presence of duplication and dilatation of the ureters,
obstructive uropathy, and structural abnormality of the
bladder
20. LABORATORY INVESTIGATIONS
Renal imaging with 99mTc-Dimercaptosuccinic Acid
(DMSA) can be used to detect acute pyelonephritis
and renal scarring .
Decreased renal uptake of the isotope suggests acute
pyelonephritis or renal scarring .
In addition, a DMSA renal scan can detect majority (>
70%) of children with moderate to severe
vesicoureteric reflux
The NICE guidelines recommend DMSA renal scan 4
to 6 months after atypical UTI in children under 3
years of age and recurrent UTI in children of any age .
21. LABORATORY INVESTIGATIONS
A voiding cystourethrogram is the preferred screening
test for vesicoureteric reflux.
This study accurately grades vesicoureteric reflux;
identifies posterior urethral valves, ureteroceles,
obstructive uropathies, and other abnormalities of the
urethra, ureter, and bladder (e.g., bladder diverticuli or
trabeculations); and provides clues to the presence of
urge syndrome and dysfunctional voiding 25 to 30% of
children with UTI have vesicoureteric reflux .
24. Cystoscopy is indicated in children with severe
vesicoureteric reflux, moderate vesicoureteric reflux
unresponsive to conservative treatment, suspected
duplicated collecting system, ureterocele, urethral
obstruction, or neurogenic bladder
25. TREATMENT
Acute cystitis shoud be treated promptly to prevent
possible progression to pyelonephritis
If the symptoms are severe ,presumptive treatment is
started pending results of the culture
If the symptoms are mild or the diagnosise is doubtful
treatment can be delay until the results of culture are
known.
26. TREATMENT
In acute febrile UTIs the clinical symptoms of UTI and
peylonephritis are difficult to differentiate
A COURSE OF ANTIBIOTIC for 7 to 14 days oral or
parental
Children who are dehydrated ,are vomiting,are unable
to drink fluids,have complicated infection,or in who
urosepsise is possibility shoud be admittted to hospital
for IV rehydration and iv antibiotic therapy.
Local antimicrobial sensitivity pattern shoud be
considered when selecting emprical antibiotic
treatment
27. TREATMENT
For cystitis trimethoprim sulfamethoxazole
Or nitrofurantoin or amoxiciline
In acute febrile UTI ceftriaxone 50 mg kg辿24h or
cefipime 100 mg辿kg辿24 h or cefotaxime 100-150 mg kg
24h
Clinical treatment with fluoroquinolones in children
shoud be used with caution becouse of potiential
cartilage damage
28. TREATMENT
The optimal duration of treatment of UTI is controversial .
A 2003 Cochrane systematic review of 10 randomized and
quasi-randomized controlled studies involving 652
children with lower UTI found no significant difference
between 2 to 4 days and 7 to 14 days of oral antibiotic
therapy in terms of frequency of positive urine cultures,
development of resistant organisms, or recurrence of UTI.
A 2012 Cochrane systematic review of 16 randomized and
controlled studies involving 1,116 children with lower UTI
found that 10 days of antibiotic treatment is more likely to
eliminate bacteria from the urine than single-dose therapy.
29. TREATMENT
unless further studies and more updated systematic review
show it otherwise.
A 2007 Cochrane review of 23 randomized and quasi
randomized controlled studies involving 3,295 children
with acute pyelonephritis found no significant difference
between oral antibiotic therapy (10 to 14 days) and
intravenous antibiotic therapy (3 days) followed by oral
antibiotic therapy (10 days) in terms of duration of fever
and subsequent persistent renal damage .
Similarly, there was a significant difference between
intravenous antibiotic therapy (3 to 4 days) followed by oral
antibiotic therapy and intravenous antibiotic therapy (7 to
14 days) in terms of persistent renal damage
30. CONCLUSION
Management of UTI in children can be challenging
because symptoms can be vague and nonspecific in
young children.
A high index of suspicion is essential.
UTI should be considered in any child < 2 years
presenting with fever.
On the one hand, over-diagnosis may lead to
unnecessary and potentially invasive testing,
unnecessary treatment, and the emergence of bacterial
resistance to antibiotics.
31. CONCLUSION
On the other hand, under-diagnosis and delayed
treatment may lead to recurrence and risk for renal
scarring which may lead to hypertension and chronic
renal failure.
Timely and accurate diagnosis and appropriate
treatment are therefore essential.