uti in children - bowen university · why important(2) therefore : investigations : identifying...
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UTI In Children
DR. Alao MA
Bowen University Teach Hosp Ogbomoso
OUTLINE
• Introduction
• Definition & Classification
• Epidemiology
• Aetiology
• Clinical features
• Diagnosis
• Treatment
• Complication
• VU Reflux DX
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Why UTI
• May indicate structural defects, recurrent symptoms can be troublesome
• UTI + VUR chronic atrophic pyelonephritis scarring
(reflux nephropathy) chronic renal failure Cause of end stage renal failure in children worldwide
• Renal scarring Hypertension(10%)
Why important(2)
Therefore :
investigations : identifying those children with UTI’s that are at risk ofdeveloping chronic renal failure
Treatment aimed at hopefully preventingdamage/further damage
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Definitions/ Classification
• UTI: Conditions in which there is growth of bacteria within the urinary tract
• Sites – Cystitis: bladder involvement
Pyelitis: upper tract involvement without parenchymal involvement
Pyelonephritis: renal parenchymal involvement
Definitions/ Classification
• Bacteriuria: presence of bacteria in bladder urine
Significant bacteriuria: growth of > 105 colony forming units
(CFU)/ml of freshly voided urine
or
any growth from suprapublic specimen except 2-3 x103 CFU/ml of
coagulase negative Staphylococci
• Bacteriuria may be –
(i). symptomatic or
ii. asymptomatic ( covert)
Definitions/ Classification
• Covert bacteriuria: bacteriuria in repeated samples from a child who does not reportsymptoms usually at a health investigationor routine check-up.
• Complicated UTI: those with reduced renal function, obstruction, dilatation, reflux, neurogenic dysfunction of the bladder, indwelling urinary catheter or foreign body in the urinary tract.
Definitions/ Classification
Recurrent Infection Persistence/ RelapseRe-infection
Occurs in 60% of girls“ “ 20% of boys
Relapse: infection with identical organism within 6/52 of Rx but usually within 1/52
Definitions/ Classification
• Re infection: infection by a different organism –there is a propensity for re-invasion of the individual’s urinary tract.
• Most recurrences are re-infections.
Risk factors for Recurrent Infection
• (a) Upper UTI is treated with too short a course of antibiotics
(b) Stones
(c ) Abscess
(d) Gross urological abnormality present
(e) Constipation
(f) Neuropathic bladder
(g) Sexual activity
EPIDEMIOLOGY
• Most UTIs are asymptomatic
• Asymptomatic UTI commoner in preterm than term infants
• In 1st 6/12 UTI commoner in males
• After 6/12 UTI commoner in females
• Overall ½ girls and 1/3 boys
• Prevalence of UTI in child. 4.1 – 7.5% (Pittsburg)
EPIDEMIOLOGY II
• UTIs develop most often in 1st yr of life
• Symptomatic UTI 4.1/1000 newborn
• In infancy, cong structural anomalies of the UT probably account for higher incidence in boys
• UTI 10 times more common in uncircumcised male infants
• SCA patients are at higher risk of UTI
Aetiology
• Escherichia coli ( 75–90%)
• Klebsiella spp
• Proteus spp.
• Staphylococcus saprophyticus
• Enterococcus
• Adenovirus
Aetiology
• Ibadan, Klebsiella spp is the predominant organism.
•• neonates in Nigeria, Klebsiella is the commonest
and E. coli 2nd
•• - Route of infection
• 1st month of life haematogenous
• >1/12: ascending infection from gut via perineum and urethra
Pathogenesis
• Following bacterial introduction into the tract, fimbriae adherence to mucosal receptor & recognition by toll-like receptors/signalling on the urotheliumleads to bacterial colonization, Internalization, apoptosis, hyperinfection,tissue invasion, release of toxins, inflammation & cytokine release.
• There is activation of uroepitheliumand production of pro-inflammatory mediators eg cytokines,chemokines,complementproteins,adhesion molecules which may either clear bacteria or cause tissue damage.
• The structural variability of host cell glycoconjugates characterizes pathogen recognition at mucosal sites. Subsequently, the oncoming inflammation activates the uroepithelial cells, which produce mediators of inflammation, until the pathogens are destroyed and eliminated.
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Pathogenesis
• Recruitment of neutrophils into the urinary tracts and chemokine-chemokine receptor interactions play a major role.
• Intricate molecular interactions govern pathogen recognition on mucosal surfaces as well as bacterial virulence.
• An inhibition of mucosal signaling creates a state of asymptomatic bacterial carriage (asymptomatic bacteriuria).
• The state of the innate host defense mechanisms determine the severity of infection.
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Aetiopathogenesis
• virulence factors in organism
• host factors
VIRULENCE FACTORS
• Fimbriae
• E. coli O, K, H Antigens
Virulence factors contd.
• Some bacteria express some specific O & H antigens on their surfaces. (K – antigen confers resistances to bactericidal effects of serum and enhances bacterial survival in tissues by conferring resistance to phagocytosis).
• O antigen is toxic and induces acute inflammation.
Other Virulence Factors
Adherence factors – (most useful in pathogenicity) is a specific process where by E-coli binds to the glycoconjugate receptors on the surface allowing sufficient contact between bacterial toxins and epithelial surface.
• Some bacteria causing acute pyelonephritisstimulate epithelial and other cells to produce cytokines and other pro-inflammatory factors (Il-6 causes fever) and activation of other acute phase reactants (IL – 8 responsible mainly for chemotaxis)
Host Factors
1. Urine as a culture mediuma. Temp 370c is ideal for incubationb. Urinary glucose is a bacterial nutrientc. Low secretary Ig A
2. Physiological and Functional factorsa. Incomplete bladder emptyingb. Dysfunctional voidingc. Neurogenic bladderd. Sexual intercourse
Host Risk Factors
obstruction
Foreign body
reflux
Genetic predispos
Non circumcision
age
gender
Host Factors
3. Anatomical factorsa. Bladder diverticulumb. Calculic. Shortened urethra in girls
4. Immunological and cellular factorsa. Immature immune system in infantsb. Low levels of secretary Ig A in body
fluidsc. P1 blood groupd. B blood group
Host Factors
5. Iatrogenica. Catheterisationb. Surgery and instrumentation of UTc. Accidental trauma, penetrating injuries
• The elimination of bacteria from the bladder is facilitated by frequent micturition and the capacity of bladder wall epithelium to kill bacteria.
• Therefore incomplete emptying would mean a compromised hydrokinetic mechanism affording bacteria the opportunity to grow.
Host Factors
• Uro-epithelial cells of certain individuals are more receptive to attaching bacteria.
• Secretion of anti-adhesion molecules by the bladder could interfere with the adherence capabilities of certain E-coli (e.g. Tamm Horsfall protein and secretory 1gA.)
Clinical Presentation
• Variable
• High index of suspicion required
• Neonate - non-specific, poor feeding, diarrhoea, vomiting, jaundice,
fever, cyanosis, circulatory collapse
• Older infants: Fever, PUO, weight loss, FTT
Clinical Presentation
Older Children: urinary frequency, abdominal
pains, dysuria, hematuria, 20 onset enuresis
Renal angle tenderness.
Investigations
• Dipstick urinalysis
• Leucocyte esterase
• Nitrite test- bacteriuria
• Proteinuria
• E/U, Cr in the sick child
How to Collect Urine and Diagnose UTI correctly
• Careful attention to detail – NB
• Methods– Clean catch
– Collection pad
– Bag method
– Suprapubic puncture
– In and out catheter
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Urine collection pad
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Bag specimen
• Clean genitalia with sterile water
• Remove immediately after micturition
• good for screening
• If positive (dipstix leucor nitrite) then send another specimen using other collection method (AAP)
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Suprapubic aspiration
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‘In +out catheter’:boy
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Processing urine
• Send to lab within 1 hour – Bact count doubles every 20 min
• In refrigerator <4 degrees for 24 hours
• Summary: do notleaving urine specimens lying around will result in false positive’s
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Side room investigations: Urine dipstix
• Blood/protein: non-specific; many other causes.• Leukocyte esterase test:
• Sensitive for leukocytes but not specific for UTI’s –especially in girls.
• Nitrite test for bacteria:– High specificity (99%)but low sensitivity50%.
• pH: alkaline urine - Proteus infection.
Urine with any positiveparameters should be sent for culture
Negative we accept as negative35
Nice Dipstick guidelines (2007)
Urine Dipstick Diagnosis
Nitrite and LE + UTI – Treat with antibiotics
Nitrite + and LE - Probable UTI – treat with antibiotics
Nitrite – and LE +May or may not be UTI management should be based on clinical judgment
Nitrite and LE - UTI excluded – no antibiotic treatment
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Interpretation contd.• Assessment of granulocyte esterase activity in urine
sediments containing white cells.
• Nitrite test (based on the ability of uropathogens to reduce nitrate to nitrite (reaction is time-dependent, positive test requires long bladder time of not less than 4 hours. Sensitivity would be low in individuals with frequent voiding as in newborns.
• False positive results can be encountered in young children when nitrite-producing bacteria are present in the prepuce.
• HAEMATURIA can also give false positive results.
LABORATORY DIAGNOSIS
MSU > 105 Cfu/ml of a single urinary
Pathogen – Kass criteria
CSU > 50 x 104 CFU/ml
SUA: growth of urinary pathogen in any
Number (except 2 – 3 x 103 CFU/ml of
Coagulase – negative staphylococcus)
(AAP 10*4)
LABORATORY DIAGNOSIS
• A positive bag specimen should alwaysbe confirmed by CSU or SUA
• Pyuriausually found in UTI but not
diagnostic>10/mm3 of unspun urine – more reliable>5-10/HPF of centrifuged urine
Bacteria: • Uncentrifuged: 2-3 moving organisms/h.p.f. • Centrifuged:15-20 organisms/h.p.f
– correlate well with a bacterial count of 100 000 organisms/ml
• Microscopy: wbc +bacteria= 99% specificity
Sterile Pyuria
• Fever
• Acute systemic/virus infections
• Dehydration
• Vulvovaginitis & urine reflux in vagina. Balanitis
• Glomerulonephritis, interstitial nephritis
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Sterile Pyuria
• Half treated UTI’s (Antibiotic)
• Appendicitis
• Tuberculosis (Relatively uncommon in children)
• Kidney stones (Usually infective in children)
• Cystic diseases of the kidneys
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Management Objectives
- To alleviate symptoms
- To prevent/minimize renal damage
- Identify structural abnormalities which require
surgery
Renal imaging
- Detection of anatomic & functional UT Abnormalities
- USS - comparing values to age related ranges
- MCUG
- +/-IVU
- Scintigraphy using 99TC DMSA scanning. (Affected
areas are seen as uptake defects, it may be difficult
to decide if lesions are longstanding).
SPECIFIC INDICATIONS FOR DIAGNOSTIC IMAGING IN PATIENTS AT RISK OF
SCARRING
• Acute pyelonephritis
• Bacteriuria in infancy
• Hypertension
• Presence of abdominal mass
• Posterior midline anomalies
• Decreased renal concentrating ability
• Recurrent cystitis in males.
TREATMENT
Principles:
• Children with symptomatic UTI should be
commenced on treatment immediately
samples have been collected.
• Choice of antibiotics should be based on local
epidemiologic data.
• Oral antibiotics are effective in most cases.
Principles of Treatment contd.
• Parenteral antibiotics indicated where there
is persistent vomiting or when the child has
associated sepsis.
• Treatment duration depends on nature of
organism and presence or absence of
structural anomalies.
• UTI causes significant morbidity in children, inconveniences and anxiety for the family and considerable consumption of medical resources.
• Occurs in 10 – 15% of cases and particularly common with repeated infections and in individuals with congenital malformations.
• Unilateral lesion is commoner. Bilateral involvement can progress ultimately to CRF.
• Other effects include increased incidence of hypertension in later life and increased morbidity during pregnancies.
• -Predisposition to nephrolithiasis and nephrocalcinosis.
• -Reflux nephropathy
• -Failure to thrive
Long-term consequences
SHORT TERM
• -Dissemination of infection
• -Pyonephrosis
DRUGS COMMONLY USED
- Choice of antibiotics depends on sensitivity in each locality
Co-trimoxazole ( high level of resistance)
• Trimethoprim
• Nitrofurantoin
• Nalidixic Acid
• Amoxycillin
• Co Amoxyclav, Gentamicin, cephalosporins
Rx for 5-7/7
Treatment contd.
Repeat urine m/c/s 1/52 after Rx
In acute febrile illness suggestive of
pyelonephritis, treat for 14 days
If child is sick, give iv ceftriaxone and gentamicin
Monitor patient for 1 – 2yrs even if
asymptomatic
PREVENTION
• Careful perineal hygiene
• Prevent constipation/bladder training (complete
bladder emptying)
• Low dose prophylaxis with
- VUR
- Recurrent UTI
- Neurogenic bladder
COMPLICATIONS
Renal Scarring . HT
. CRI
RISK FACTORS FOR DEVT OF
PYELONEPHRITIC RENAL SCARRING
- Obstruction
- Reflux with dilatation
- Age < 3 – 4yrs
- Delay of treatment
- Number of pyelonephritic attacks
VESICO-URETERIC REFLUX
• Backflow of urine from bladder to ureter
through an incompetent ureteric valve
• Found in 30 – 40% of children with UTI
• mechanisms
Mechanisms of VUR
SIGNIFICANCE
-allows organisms and
voiding pressure to be transmitted from
bladder to renal pelvis and on return to
bladder, refluxed urine increases residual
volume encouraging re-infection
- risk of developing renal scars
Management of VUR
Rx Rapid Rx and prevention of recurrent
UTI
low dose prophylaxis
bladder and bowel training
void 2 or 3hrly + double micturition at
bedtime
anticipation of infection
- investigate infants with UT dilatation
detected antenatally and screen siblings of
index patients with VUR
Grades of VUR
• Surgery may be reqd. e.g. Deflux surgery but
some patients have spontaneous
disappearance
• reduce bladder pressure – PUV, Stones,
ureterocoeles
• 3 monthly urine culture and whenever child is
unwell