UTI In Children - Bowen University · Why important(2) Therefore : investigations : identifying...

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