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VUR.pptx
1. Urinary Tract infection &
Vesicoureteral Reflux
PRESENTER;
YESHIGETA HAILEMARIAM
(PEDIATRIC SURGERY RESIDENT)
MODERATOR;
PROF. MILIARD DERBEW
(CONSULTANT GENERAL &
PEDIATRIC SUREON)
2. Outlines
1. Introduction
2. Pathophysiology of
UTI
3. Diagnosis of UTI
4. Further evaluation of
UTI
5. Definition &
epidemiology of VUR
6. Pathophysiology of
VUR
7. Classification of VUR
8. Management of VUR
9. Outcome
10.References
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3. 1. Introduction
• UTI; 2nd site of infection
• By 7 years; >1 episodes (8% of girls & 2% of boys)
• Once UTI, risks for another attacks
• UTI; marker of anatomic abnormalities
• UTI has several long term sequelae
• Risk factors;
• Renal & bladder structural abnormalities
• Functional bladder & bowel dysfunctions
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9. 3. Diagnosis of UTI
Most; not have
serious illness
Clinical signs &
symptoms;
Vary with age
Mostly are
non-specific
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10. 3. Diagnosis…cont’d
Presentation can be;
1.Asymptomatic bacteriuria
2.Symptomatic UTI
• Lower UTI (cystitis)
• Upper UTI (pyelonephritis)
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Persistent vs re-
infection
Simple vs
complicated
11. 3. Diagnosis…cont’d
• U/A (dipstick
+ microscopy)
sensitivity is
~100%
• Urine culture
accuracy
depends on
method of urine
collection
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13. 4. Further evaluation of UTI
Proponent of imaging after
1st UTI
Opponent of imaging after
every UTI
Is 1st episode really 1st UTI?
Early detection of anomalies
may prevent permanent renal
damage
UTI in presence of VUR has
increased risk of renal damage
Find all VUR
No evidence that decrease risk
of renal injury in low grade VUR
Antibiotic Px only decrease
recurrence not scarring
Painful, expensive, irradiation
for every patient with UTI is
unnecessary
Find clinically significant VUR
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14. 4. Further evaluation…cont’d
• In addition to history and physical examination,
imagings are required to further evaluate UTI patients;
• Emphasis is to see the presence of renal damage or risk of
renal damage (VUR)
• Two approaches
• Top-Down; 1st do renal scan with USG & see renal scarring, if
scarring go to VCUG. Aim to plan prevention of recurrent APN
• Bottom-Up; first do lower tract imaging ( VCUG). Aim to abolish VUR
• Timing;
• For VCUG, when urine is sterile
• For renal scan, (when stabilized to confirm APN, after 6 months to
see renal scarring)
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15. 5. Definition & epidemiology of VUR
• Retrograde passage of urine
• Incidence;
• 1% in general population
• In UTI high 30-40%
• Sibling 27-34%
• Offspring of VUR mother up to 66%
• In PUV patients 50%
• In UDC + UTI patients 50%
• F>M
• As age increase incidence decrase
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16. 6. Pathophysiology of VUR
• Normal UVJ;
• Passive (ureteric muscle tone, flap valve)
• Active (Bell’s muscle & waldayer’s sheath)
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23. 8. Management…cont’d
Surgical Correction;
• Absolute indications;
• Progressive renal injury
• Documented failure of renal growth
• Breakthrough pyelonephritis
• Intolerance or noncompliance with antibiotic suppression
• Relative indications;
• High grade (IV–V) reflux in young children after a year of
conservative follow-up
• Pubertal age with nephropathy at diagnosis
• Parental preference
• Failure to spontaneously resolve with watchful waiting
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34. 9. Outcomes
• In experts hand the success rate reaches to 100%
especially in low grades
• USG is required every 6-12 months
• Complications;
• Early ( persistence, contralateral reflux, obstruction)
• Long term (obstruction , recurrent reflux
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Once treated, infants with symptomatic urinary infections are at risk for recurrent infection (26%-50%), usually in the first 3 months of follow-up
Urinary abnormality found in 50% of patients upto age 12 (VUR in 35%, obstructive (8%) & non-obstructive non reflexive (7%))
The long-term sequelae include renal scarring, hypertension, chronic renal insufficiency, and pregnancy-related complications
Predisposing risk factors for UTIs include renal and bladder structural abnormalities as well as functional bladder and bowel dysfunction
Bacteria are the most common causes of UTI, but viruses and fungi can be the causes.
There are four major pathways by which bacteria gain access to the urinary tract: ascending(commonest) , hematogenous (immunocompromised & neonate), lymphatic, and direct extension (if fistula with vagina or GI).
Most UTI beyond the newborn period are the result of ascending infection, that is why only 4-9% are bacteremic
The uroepithelial cells of healthy individuals suppress bacterial growth and are capable of killing bacteria. They produce mucopolysaccharide which coat surface and prevent adherence, and GAG continuously hade and eliminate bacteria.
The sensitivity of positive urine culture is 95%, and the specificity is 99%.
it is clear that infection, not reflux alone, is a prerequisite for acquired renal scarring.
Congenital reflux nephropathy(dysplasia and nephropathy) is a pattern of impaired renal function and development that is particularly associated with high-grade VUR, especially males.
Most pediatric urologists would agree that children under 5 years of age and boys of any age with febrile UTI or documented APN should be evaluated when infection is first recognized, to determine if further testing is needed.
VUR is diagnosed during evaluation for UTI (most commonly) Hypertension Proteinuria Voiding dysfunction Chronic renal insufficiency Asymptomatic and sibling screening
If sibling of VUR patient< 2year require screening USG and if having UTI screening must include VCUG
The VUR in PUV and ARM associated NVD is not due to high intravesical pressure rather due to associated abnormal congenital ureteric insertion. But high intravesical pressure worsen the condition
Passage of the distal ureter through the ureteral hiatus in the bladder wall. Ureteral inner longitudinal muscle fibers extend into the trigone to form Bell’s muscle. The Waldeyer sheath anchors the distal ureter at the hiatus.
Abnormal ureteric insertion from abnormal bud (laterally displaced)
Short intravesical ureteral lenth
Lower intravesical length to diameter ratio
Denervation (sympathectomy L3-L5)
Distal ureteral muscle atrophy
Inadequate trigonal tone and contractility that fail to close ureteral orfice
Abnormal ureteric orifices
low pressure (occurring during the filling phase of the VCUG) or high pressure (occurring only during voiding)
Reflux due to a congenitally deficient UVJ is referred to as primary reflux, whereas that due to a BOO or neurogenic bladder is referred to as secondary reflux
Simple reflux and complex reflux. Complex reflux includes the refluxing megaureter, the refluxing duplicated ureter, the refluxing ureter associated with a diverticulum or ureterocele, and the occasional refluxing ureter associated with ipsilateral ureteropelvic or ureterovesical obstruction.
At the present time, VUR is graded from I to V according to the international classification system which is based on proximal extent of retrograde urine flow, ureteral and pelvic dilatation, on the resultant anatomy of the calyceal fornices.
1. Spontaneous resolution of reflux is very common. (80% of low grade & 50% of grade III)
2. High-grade reflux is less likely to resolve spontaneously.
3. Sterile reflux is benign.
4. Extended use of prophylactic antibiotics is benign.
5. Success of (open) surgical correction is very high.
Principles of surgical correction of VUR
rule out secondary VUR
Adequate mobilization of distal ureter
preserve the blood supply of ureter
submucosal tunnel (5:1)
avoid angulation and twisting
juntle handling of bladder
