Summary on Paediatric Urology

1. Pediatrics urologyPediatrics urology
Edmond

2. Outline
• Embryology of renal tract
• Renal physiology of neonatal (refer to notes)
• Foreskin: circumcision
• Hypospadias
• Scrotum: acute scrotum, undescended testis
• Paed UTI
• Paed Incontinence & neurogenic bladder
• Neonatal hydronephrosis : approach
• PUJO
• VUR, megaureter
• Duplex kidney
• Posterior urethral valve
• Intersex problem
• Bladder extrophy, cloacal extrophy & epispadias
• Sacral agenesis
• Renal Mass: Wilms tumor
• Imaging and workup for RFT

3. Embryology

4. Embryology of urinary tractEmbryology of urinary tract
• Following fertilization, a blastocyte (sphere of
cells) is created, which implants into the uterine
endometrium on day 6
• It develops into yolk sac and amniotic cavity,
from which are derived ectoderm, endoderm
and mesoderm
• Organ formation occurs between 3-10 weeks
gestation
• Most of the genitourinary tract is derived from
intermediate mesoderm

6. • The pronephros, derived from mesoderm, is present between
weeks 1-4. It then regresses
• The mesonephros functions from weeks 4-8, and is also
associated with 2 duct systems, the mesonephric duct and
paramesonephric duct
• The mesonephric (Wolffian) ducts develop laterally, and
advance downwards to fuse with the primitive cloaca (hindgut),
above it eventually develop into the gonads
• By week 4, a ureteric bud grows from the distal part of the
mesonephric ducts and induces formation of the metanephros
by “reciprocal induction”
• Branching of the ureteric bud forms the renal pelvis, calyces,
and collecting ducts

7. • Glomeruli and nephrons are created from
metanephric mesenchyme
• During weeks 6-10, fetal kidney effectively moves up
the posterior abdominal wall to the lumbar region.
Urine production starts at week 10
• The paramesonephric (Mullerian) essentially forms
the female genital system (fallopian tubes, uterus,
upper vagina) In males, it regresses.
• The mesonephric duct forms the male genital duct
system (epididymis, vas deferens, seminal vesicles,
ejaculatory duct, central zone of prostate); in the
female, it regresses

8. • The mesonephric ducts and ureters drain into the cloaca,
• Cloaca later subdivided into the urogenital sinus
(anteriorly) and the anorectal canal (posteriorly) during
weeks 4-6
• The bladder is formed by the upper part of the
urogenital sinus. Detrusor developed from dome to
bladder neck
• The lower part forms the urethra in females
• In males, the mesonephric ducts form the trigone,
posterior urethra and closure of the urogenital groove
creates the anterior urethra
• Urachus > median umbilical ligament
• Urine production by fetal kidney accounts for 90% of
amniotic fluid by week 36
• Adequate amniotic fluid is essential for fetal pulmonary
development

10. Clinical consideration
• Renal agenesis:
– One or both kidney congenitally absent
– Intrinsic defect of embryonic metanephric mesenchyme
(unilateral agenesis)
– Failed induction of nephrogenesis
– Involution of a multicystic dysplastic kidney
• Renal dysplasia:
– Faulty interaction btw ureteric bud and metanephric
tissue
– Major insult to fetal kidney (obstructive uropathy)
– Kidney is present , but small and dysplastic internal
architecture
• Retrocaval ureter:
– More on right ureter
– Result of abnormal development of posterior cardinal
veins (precursor of IVC) [see below]

12. Embryology of Gonads
• 5 week: primordial germ cell migrate from yolk sac to
posterior body wall
• Paramesonephric duct (Mullerian) develop lateral to
mesonephric duct (Wolffian) in both male and
female
• From then it diverge
• In male:
– Differentiation of Sertoli cell in response to SRY gene (sex-
determining region of the Y chromosome)  secret MIS
(Mullerian inhibiting substance)  regression of Mullerian
duct  remnant: appendix testis, prostatic utricle
– 8-12 week: mesonephric duct (induced by testosterone) 
epieididymis, vas, rete testis, ED, SV
– Androgenic stimulation of the genital tubercels results in
development of the male phallus

13. • In female:
– Absence of SRY
  absence of Sertoli cell  NO MIS
mesonephros regress  remnant : Gartner’s cyst
– Mullerian duct develop into : fallopian tubes, uterus
(fused portion of the Mullerian duct), vagina (upper
2/3)
– Distal 1/3 of vaginal originate from urogenital sinus
– Introitus and external genitalia derived from ectoderm

17. Renal physiology

18. In utero
• 8 week: 1st functional nephrons appear
• 10 weeks: glomerular filtration starts
• 34 week: the full number of glomeruli is reached
• renal blood flow and glomerular filtration rate
(GFR) gradually increase owing to the
development of new nephrons
• renovascular resistance is high, renal blood flow
is limited in utero despite the gradual increase in
the proportion of cardiac output distributed to the
kidneys during gestation

19. Post-Partum
• Day 1, the neonate is oliguric
• Over the next 1 to 2 days, dramatic shifts in fluid from the
intracellular to extracellular compartment result in diuresis
– contributes to weight loss during the 1st week of life
• 5-10% in term neonates
• 10-20% in premature infants
– this diuresis occurs regardless of fluid intake or insensible losses
– may be related to a postnatal surge in atrial natriuretic peptide
• By Day 5: urinary excretion begins to reflect the fluid
status of the infant
• Eventually, renovascular resistance decreases
– resulting in a rapid rise in GFR over the first 3 months of life
– followed by a slower rise to adult levels by 12-24 months of age

20. • Difficulties in the laboratory measurement
of plasma creatinine concentration (Pcr) at
the low concentrations of infants
• In term infants
– At birth: Pcr ~70-90 micromol/l (1mg/dl)
– 1 week to 1 month: half (0.3-0.5mg/dl)

21. PhimosisPhimosis

22. What are the types ofWhat are the types of
phimosis?phimosis?
• Definition : inability to retract the prepuce
• Primary (physiological) with no sign of scarring
– Adhesions between prepuce and the glans (preputial adhesions):
epithelial desquamation, penile growth and erection  eventual
separation of two layers
– Preputial opening is too narrow
– P/E: on drawing back over the glans penis , inner mucosa of the foreskin
pouts out like  “flowering” of prepuce,
– Conservative treatment with parental reassurance, hygiene
• Secondary (pathological) to a scarring such as balanitis xerotica obliterans
– Autoimmune aetiology
– Affecting glans, urethral meatus or urethra
– Thickened scar fissure prepuce with white patches (no flowering)
– Rare in child, more common in adult, associated with later development
of Ca penis (at least 17 years later)

23. What is the natural history ofWhat is the natural history of
phimosis?phimosis?
• Incidence of phimosis and among Danish
school boys 9545 serial observation [Oster]
– <10% in 6-7 year old
– Only 1% in 16-18 year
• Conclusion: non-retractile foreskin is common
is boys and usually correct itself (99%) not
every boy needs a circumcision !!!!

24. What is the differential diagnosis of
Foreskin balloons when voiding?
• Buried penis megaprepuce:
– Outer prepuce joined abdominal wall directly
dorsally and scrotum ventrally
– Copious fold of inner preputial skin
– Standard circumcision should be avoided
– Surgical correction involving excising inner
preputial skin and reapply outer preputial skin
to the shaft

25. What are the indications ofWhat are the indications of
circumcision?circumcision?
1. Secondary phimosis (BXO)
2. Recurrent balanoposthitis
– Balanoposthitis (redness and painful swelling of foreskin with
purulent discharge, E.coli  antibiotics + analgesics)
3. Recurrent urinary tract infections
4. Associated VUR
• 11 in recurrent UTI & 4 in high grade VUR need to be circumcised
to prevent one UTI
• In normal boy, > 100 circumcision needed to prevent 1 UTI
• Thus routine circumcision for prevention of UTI is not justified
• Simple ballooning of the foreskin during micturition is not a
strict indication for circumcision
• Routine neonatal circumcision to prevent penile carcinoma
is not indicated – due to possible operative morbidities
• Circumcised adult are relatively protected from HIV

26. What is the contra-indication of
circumcision?
1. Coagulopathy
2. Acute local infection
3. Hypospadias
4. Buried penis
• because the foreskin may be required for
a reconstructive procedure

27. How to perform circumcision
• Plastic or radical circumcision after 1 yo
• GA , supine
• Retract the foreskin : may require dorsal slit
• Inspect urethral meatus to rule out hyposapdias
• Separate preputial adhesions
• Excised prepuce
• Hemostasis: biopolar diathermy or ties
• Close skin and wound dressing

28. Complication and alternatives?
• Complications <10%
1. Infection (2%)
2. Post-operative bleeding (2%)
3. Not happy about cosmesis (4%)
4. Meatal stenosis , abnormal cordee or partial amputation
(rare)
• Alternative : Betamethasone cream (0.05-0.1%) : BD x few
weeks
– No side effects or systemic toxicity
– Accelerate the release of physiological phimosis in 80%
patients
– Topical steroid cr must be combined with regular attempts
at retraction of the prepuce to achieve success

29. What is the plastic
circumcision?
• Achieving a wide foreskin circumference
with full retractability, while the foreskin is
preserved
• Potential for recurrence of the phimosis

30. HypospadiasHypospadias

31. • Diagnosis? (1)
• Which 3 components is this entity comprised of? (3)
• What is the incidence of this condition? (1)
Q34

32. • Hypospadias
– Defined as developmental failure of the ventral aspect of the penis
3 components:
• Ventral ectopic urethral opening:
– Urethral development from 8-20 weeks Under influence of testosterone
– Posterior and middle urethra: urethral folds coalesce in midline from base to tip
– Anterior urethra: develop in proximal direction
– Join at the level of corona (commonest site)
– Failed canalized result in hypospadias
– Urethra, glans and corpora may be hypoplastic to varying degree
• Ventral curvature of penis (Chordee)
– Growth disparity btw dorsal corporal bodies and ventral urethra
– Spongiosal tissue distal to urethral meatus form tethering fibrous band
• Dorsal Hooded prepuce and deficient ventrally:
• Failure of ventral fusion of urethral folds impede grow of prepuce ventrally
– If glandular cleft with intact prepuce  megameatus intact prepuce (MIP)
variant
• Incidence : 1 in 300 live male births
– Race: White (Jewish /Italian) >> blacks
– Runs in family: Father and sibling

34. What is the classification?
• Classification :
[Duckett]
– Distal-anterior (50%) :
glanular / subcoronal
– Intermediate –middle
(20%): distal penile ,
midshaft, proximal penile
– Proximal- posterior
(30%): penoscrotal ,
scrotal , perineal

35. What are the risk factors?
1. 5x in IVF boy: higher maternal exposure to progesterone (competitive
inhibitor for 5-alpha reductase) [Silver 1999]
2. 8x in monozogotic twins: inadequate HCG for 2 fetus urethral development
3. Genetics: Father : 8% , Siblings : 14%
4. Babies of young or old mothers
5. Babies with a low birth weight
6. Abnormal androgen production: mutation in 5-alpha reductase enzyme
[Aaronson 1997]
7. Significant estrogenic activity
– Pesticides on fruits and vegetables
– Milk
– Plastic lining in metal cans and pharmaceuticals
• Limited androgen sensitivity
• Premature cessation of androgenic stimulation
• Use of oral contraceptive prior to pregnancy (NO!!!!!)

36. What need to be consider?
• DSD: Severe hypospadias with unilaterally or
bilaterally impalpable testis (9%), or with
ambiguous genitalia, require a complete genetic
and endocrine work-up immediately after birth to
exclude intersexuality, especially congenital
adrenal hyperplasia
• Look for inguinal hernias
• Urine trickling and ballooning of the urethra
requires exclusion of meatal stenosis
• No increase in incidence of upper tract
anomalies

37. Why need to correct?
1. Downward deflecting urinary stream
(require sitting)
2. Chordee cause painful erection & failed
vaginal insertion
3. Potential psychological insult

38. What are the aims of the
surgery?
1. Correct penile curvature (Orthoplasty)
2. Neo-urethra of an adequate size
(Urethroplasty)
3. Bring neomeatus to the tip of the glands
(Glanuloplasty)
• Achieve overall acceptable cosmetic
appearance

39. What is the time of the surgery?
• The age at surgery for primary hypospadias
repair is 1 year of age
• Prehormonal treatment:
– Decrease hypospadias severity and chordee
– Increase vascularity and thickness of proximal
corpus spongiosum
– Increase transverse length of inner prepuce
– Helpful with small penis and for repeat surgery

40. Correction of penile curvatureCorrection of penile curvature
• By degloving the penis and by excision of the connective
tissue of the genuine chordee on the ventral aspect of
the penis under Artificial erection
• If urethral plate tissue adequate:
– TIP / Snodgrass repair by longitudinal incision on urethral plate 
Tubularization of urethral plate  Dartos pedicle flap to provide
an additional cover over the suture line
• If inadequate :
– two-stage repair with free graft of inner preputial skin applied to
ventral surface of penis and then tubularised with Dartos layer
covering it
• The residual chordee (curvature) is caused by corporeal
disproportion and requires straightening of the penis,
mostly using dorsal orthoplasty (modification of Nesbit
dorsal corporeal plication)

41. Preservation of urethral plate
Distal hypospadias
• MAGPI (Meatal Advancement and Glanuloplasty) Duckett
• TIP (Tubularized incised plate urethraplasty) Snodgrass
• Mathieu
Middle Hypospadias:
• Onlay island flap
Proximal hypospadias:
– Onlay island flap
– Buccal mucosa graft Two-stage procedure

42. MAGPI
• a. circumferential
degloving of penis
• b vertical incision at
glanular groove
• c transverse closure: open
meatus, flatten groove ,
advance meatus
• d elevate ventral meatal
edge forward
• e redundent skin at midline
excised , approximate in
normal conical anatomy
• f sleeve re-approximation
of skin cover
•95% success, 2% reop

43. Tubularized incised plate
urethroplasty (Snodgrass)
• (A) Circumscribing incision along dashed lines to deglove penis.
• (B)Glans wings mobilized laterally off the corpora cavernosa and
separated from the urethral plate.
• (C) Longitudinal incision in the midline of the urethral plate. The
incision widens the urethral plate.
• (D) Tubularization of urethral plate with a two-layer subepithelial
approximation.
• (E) Dartos pedicle flap dissected off the inner preputial skin and
transposed ventrally to provide an additional cover over the suture
line.
• (F) Glans wings are approximated in the midline with subepithelial
sutures.
• (G) Meatus sewn to glans at two positions and urethral stent
secured in place.

47. Mathieu
(parameatal base flap)
For meatus 1cm from corona
but wide and fix so MAGPI
not suitable
Must not have any Chordee
Ventral skin must be thick
a. Incision line
b. Byar’s ventral rotation
c. Glan wings approximated to
create conical configuration

48. Onlay Island Flap
Good distal urethral plate
a. Strip of urethral plate 8mm outline
b. Proximal urethral cut back to good
spongiosal tissue
c. Raise of preputial island flap
d. Rotation of island flap
e. Parallel running suture from
meatus to tip of glans both side.
Interrupted suture at proximal
meatus to ensure 12-14Fr
f. Glanoplasty and skin covering

50. Complications
1. Urethral-cutaneous fistula (<10%)
2. Meatal stenosis + spraying of urine
3. Urethral stricture
4. Urethral diverticulum
5. Hair in urethra: UTI and stone formation,
6. Dissatisfaction with penile size

51. Congenital penile curvatureCongenital penile curvature

52. What is the background of penile
curvature?
• Incidence : 0.6%
• Cause by asymmetry of the cavernous bodies
• Ventral : hypospadias (chordee or ventral
dysplasia of cavernous bodies)
• Dorsal: epispadias
• Clinically significant: >30 degree,
• >60 degree: affect sexual intercourse

53. Dx and Mx
• Artificial erection during hypo/epispadias
repair
• Mx: Surgical
– Artificial erection : degree of curvature and
check symmetry after repair
– Hypospadias: release of chordee, plication of
corpora cavernosa (orthoplasty)
– Epispadias: release of urethral body from
corpora , corporoplasty +/- corporotomy

54. CryptorchidismCryptorchidism

55. What is embryology of testis
development?
• Weeks 6
• Under influence of SRY gene of gonad
differentiation, testes differentiate and
influence phenotype

56. Descend depends on
• SRY (F)
• MIS (T)
• Testosterone (T)
• Genitofemoral nerve (T)
– Neural tube defects are associated with UDT
• Gubernaculum (T)
• Two phases
– 1st
– MIS induces testes from urogenital ridge to internal
inguinal canal in week 12
– 2nd
– testosterone induces testes from canal to scrotum in
week 25 - 30

57. What is the background?What is the background?
• The commonest urogenital abnormality at birth Incidence:
5% at birth (normal birth weight)
• Premature boy: 30%
• R >> L
• Bilateral : 20%
• After birth: Testicular descend is possible due to the
infantile LHRH surge that peaks at 3 months
• By 3 months: Only 1% of boys
• After 3 months, do not descend anymore  so no need to
wait if pt present after 3m

58. What are the aetiologies?What are the aetiologies?
1. Abnormal testis or gubernaculum (tissue
which guides the testis into the scrotum
during development)
2. Endocrine abnormalities (low androgens,
HCG, LH)
3. Decreased intra-abdominal pressure (prune-
belly syndrome, gastroschisis)
4. Denys Drasch syndrome : renal mesangial
sclerosis + bilateral undescended testes

59. History
• Has the missing testis ever been presence?
• Risk factors:
1. Positive family history (14%)
2. Preterm
3. Low birth weight
4. Twins ~30% incidence

60. What are the types of UDT?What are the types of UDT?
• Undescended testis
– Palpable 80%: commonest at superficial inguinal pouch
– Non-palpable 20% - DSD?, asso with hypospadias
• urgent endocrinological and genetic evaluation need
• Intra-abdominal, at internal ring or at inguinal canal but impalpable
• Ectopic testes: perineal , femoral or trasverse ectopia
• Retractile testes
– Can be brought into scrotum by milking and remain in place
– Cremateric reflex (touching inner thigh) will retract it again into
groin
– No need for surgical treatment but require close follow-up until
puberty
– Watch out for “ascending testis”  need treatment
• Gliding testis – come down to scrotum by force & pain  require
surgery

61. Physical examination
• Testis palpable:
– In position along the line of descend
• Not able to bring down  undescended testis
• Able to bring down to scrotum without pain and stay there 
rectractile testis
• Able to bring down but causing pain  gliding testis
– In position outside line of descend  ectopic testis
• Look for at femoral, penile and perineal region
• Testis not palpable:
– Is the contralateral testis palpable?
• No  suspected DSD
• Yes  unilateral non palpable testis
– Is the scrotum hypoplastic?
– No additional benefit for imaging  offer EUA + laparoscopy
• USG  high false –ve
• MRI  need a GA anyway

62. Investigation
• Endocrine testis:
  FSH & LH , no T  anorchia
  FHS & LH & T  bilateral UDT
   FSH & LH &T  hypopit
• HCG stimulation test if bil UDT at 3m:
– Baseline T, then 4 days of HCG (2000unit)
then repeat T
– 10X increase T  functioning testis
– No increase T  anorchia

63. Why should be treated?
• Ideally should be treat at 1 year of age
• However: immediate txn if concomitant hernia
1. To preserve fertility:
– Degeneration of Sertoli cells; loss of Leydig cells; atrophy and
abnormal spermatogenesis start at age 2
– If orchidopexy before 2 yo:
• Unilateral undescended testis have a lower fertility rate but the
same paternity rate as normal boys (90%)
• Bilateral undescended testes have both a lower fertility and
paternity rate – 50%
2. Increase risk of malignancy (10x)
– Orchidopexy facilitate self examination, +/- reduce risk of malignancy
– recent Swedish study revealed treatment before puberty decreases risk of
testicular cancer
3. Increased risk of testicular torsion and inguinal hernias
– Patent processus vaginalis
4. Cosmesis

64. What is the medical treatment?
• RCT: hormone therapy is ineffective in treating congenitally
undescended testes
• although success rate up to 50% in retrospective study
• Use of hormonal manipulation
– Preoperatively to facilitate a potentially difficult orchidopexy
– Distinguish between true maldescent and ‘high retractile testis’
• hormonal treatment consists of
– human chorionic gonadotrophin (100IU/kg) given by intramuscular
injection once or twice weekly for 3 weeks
– 3-week course of intranasal luteinising hormone-releasing hormone
(100mg in each nostril) administered 4-6 times daily
• Hormonal therapy rarely used, nearly all children with
congenital or acquired cryptorchidism are offered
orchidopexy

65. Surgical treatment of palpable testis (80%)?
• EUA to confirm position of testis
• Inguinal exploration
• Divide gubernaculum , look out for vas
• Mobilization of spermatic cord
• Ligation of processus vaginalis
• Mobolized vas and vessels to gain length
• Securing the testis into a dartos pouch in
the scrotal wall (orchidopexy)

66. What if inguinal approach could not
identify testis?
• if there is a patent processus vaginalis, this should
be opened
• usually the ‘emergent’ testis will be easily delivered
into the inguinal canal and a standard single-stage
orchidopexy should be achieved
• if testis if not found by this approach, a preperitoneal
(Jones) approach should be used (achieved through
the same skin incision)
– oblique abdominal muscles are split to gain access to the
peritoneum above the inguinal canal
– testis is mobilised transperitoneally
– testis passes to the scrotum
• through the inguinal canal, or
• more directly through the posterior wall of the canal medial to the
inferior epigastric vessels if necessary

67. What is the surgical treatment of
palpable testis?
• Success rate: Domico MA JU 1995
– 70-90%
• Complications:
– Later ascent of testis
– Injury to testicular vessels or vas (5%)  testicular
atrophy
• Lymph drainage of a testis that has undergone
surgery for orchidopexy has been changed from
iliac drainage to iliac and inguinal drainage

68. Surgical treatment of non-palpable testis
(20%)?
• If clinically not palpable  proceed to EAU + laparoscopy
• Procedure depend on intra-op finding after GA
• Testis palpable in inguinal region (10%)  inguinal orchidopexy
• Testis not palpable after GA  proceed to Laparoscopy:
– Intra-abdominal testis (40%)  Fowler-Stephens procedure
• First stage: divide testicular artery (testis will depend on vasal artery)
• Second stage (6m later) : mobilize testis into scrotum
• Risk of testicular loss (20%)
• 2 stage has higher success rate : 80% vs 60% (1 stage)
• 1 stage can be consider if testis lying adj to internal inguinal ring
– Vas & vessels end blindly into nubbin of tissue at internal ring (30%)
• Vanishing testis due to previous torsion
• Remove the nubbin of tissue +/- orchidopexy on the other side
– Vas and vessels end in the inguinal canal (20%)
• Re-examine the inguinal region  missing a an inguinal testis?
• Do nothing because risk of GCT is low
• Microvascular autotransplantation can also be performed with 90% testicular
survival rate
• UDT diagnosed after the age of 10-12 is better treated by orchidectomy

70. What is the prognosis?
• Testicular volume: related to initial position of testis
• Fertility
– Related to timing of surgery : Before 2: 90% vs At 3:
60%
– Uni UDT 90% paternity rate
– Bil UDT 50% paternity rate
– Testis arrest at higher position  poorer fertility
• Risk of Ca testis: <5% of boys
• The risk of Ca testis is related to the degree of
descent and is significantly higher for
intraabdominal testis than for intracanalicular testis

71. Any proof that orchidopexy reduce
risk of malignancy?
• Swedish study of 17,000 men treated surgically for
undescended testis
– Txn before 13 yo: decreases the risk of testicular cancer
– RR of Ca testis with orchidopexy
• Before reaching 13 years of age : 2.23
• Treated at 13 years of age or older: 5.40
• meta-analysis from American group also
concluded similarly that prepubertal orchiopexy
may indeed decrease the risk of testicular
cancer

72. HydroceleHydrocele

73. What are the types ofWhat are the types of
hydrocele?hydrocele?
• Communicating hydrocele:
– incomplete obliteration of processus vaginalis
• Hydrocele of cord:
– complete obliteration with patency of mid-portion
– Can get above it
• Non-communicating hydrocele:
– secondary to minor trauma, torsion, epididymitis,
varicocele operation, tumor
• DDX: Indirect inguinal hernia

75. What is the diagnosis?
• Scrotal ultrasound should be performed
• 100% sensitivity in detecting intrascrotal
lesions
• Doppler ultrasound studies help to
distinguish hydroceles from varicocele

76. What is the treatment?
• Indications for surgery
– Concomitant inguinal hernia or underlying testicular pathology
– Persistence of simple scrotal hydrocele > 2yo because of the
tendency for spontaneous resolution after the first year of age
(90%)
• Ligation of patent processus vaginalis via inguinal incision and the
distal stump is left open
• hydrocele of the cord the cystic mass is excised or unroofed
• Sclerosing agents should not be used because of the risk of
chemical peritonitis in communicating processus vaginalis
• Scrotal approach (Lord or Jaboulay technique) is used in the
treatment of a secondary non-communicating hydrocele

77. Acute scrotumAcute scrotum

78. Case scenarioCase scenario
• M/12
• Good past health
• Sudden onset left sided scrotal pain X 2
hours
• No trauma
• No UTI symptoms

79. Scrotal pain and swelling
• Age of the patient ?
• 1st
time? Recurrence?
• Onset? Sudden, gradual
• Progressive? Resolving?
• UTI symptom, AROU , LUTS, urethral
discharge
• Trauma
• PMH: STD, orchidopexy before

80. Cause
• Testicular torsion
• Torsion of the appendix testes (Torted hydatid of Morgagni)
 blue dot sign
• Acute epididymitis / orchitis  for renal USG to RO ectopic
ureter
– Mumps orchitis
– Idiopathic scrotal edema (under 10 years of age)
– Varicocele
– Scrotal haematoma
– Incarcerated hernia
– Appendicitis
– Systemic disease (Henoch-Schönlein purpura)
• Hemorrhage of a testicular tumor

81. What are the types of testicularWhat are the types of testicular
torsion?torsion?
• Intravaginal torsion – most common in
adolescents, high investment of tunica
vaginalis on the cord, resulting in
horizontally lying of testis (bell-clapper)
deformity, often bilateral
• Extravaginal torsion – attachment
between tunica vaginalis and the scrotum
was loose, i.e. incomplete fixation of
gubernaculum to the scrotal wall

83. Physical examination
• General: pain , vitals?
• Abdomen : full bladder , mass ?
• External genitalia:
– Scar for previous operation
– Torsion: Tender testis, horizontal lie, high-
riding testis, mild erythema of scrotal skin
• Absent cremasteric reflex (Rabinowitz’s sign)
– Epididymal-orchitis: swollen epididymis and
testis
• Elevation of testis relief pain (Prehn’s sign)

85. Mx: Scrotal pain and swelling
• DAT/ NPO/IVF
• BP/P, vitals
• Bld: CBP, LRFT, INR (C/ST)
• MSU/CSU: may not be +ve
• Urethral swab for gonorrhoea
• USG Doppler: Sn 70%, Sp 97-100%, PPV
100%, NPV 97% [Baker 2000]
• Radionuclide scanning (not during
emergency)

86. USG
• May also show a misleading arterial flow in the early
phases of torsion and in partial or intermittent torsion
• Persistent arterial flow does not exclude testicular torsion
• In a multicentre study of 208 boys with torsion of the testis,
24% patients had normal or increased testicular
vascularization
– Kalfa N, et al. Multicenter assessment of ultrasound of the spermatic cord in children with acute
scrotum. J Urol 2007;177(1):297-301.
• Better results were reported using high-resolution
ultrasonography (HRUS) for direct visualization of the
spermatic cord twist with a sensitivity of 97.3% and a
specificity of 99%
• No value in acute scrotum less than 48 hours

88. Mx: Testicular Torsion
• If in doubt  Explore !!!!!!
• Manual detorsion ? Probably not  still need
orchidopexy
• Early exploration: within 6 hr from symptom
• Cag A: Scrotal exploration +/- bilateral
orchidopexy +/- orchidectomy
• Why bilateral orchidopexy: 40% chance of torsion
in contralateral side
• Not affect fertility if contralateral testis normal
• Orchidectomy for non-viable testis to avoid
abscess , sinus and anti-sperm antibody
• Small risk of retorsion despite fixation (5%)

89. Scrotal exploration
• Midline scrotal incision
• Skin, dartos, ESF, CF, ISF, TV
• Testis deliver: inspect color, appendix
• If in doubt:
– Wrap it in warm saline gauze and wait 10min
– Open TA : observe bleeding  salvage
• Non-viable: orchidectomy and transfix at cord
• Bilateral orchidopexy (3 pt fixation or dartos
pouch)
• Remove testicular appendage

90. Scrotal explorationScrotal exploration
• Layers of scrotum including skin, dartos, external
spermatic fascia, cremasteric fascia, internal spermatic
fascia and tunica vaginalis were divided
• Bilateral orchidopexy in cases of torsion, 40% chance of
torsion in contralateral side
• No fixation if no torsion to avoid complications including
bleach of the blood-testis barrier
• If orchidopexy, 3-point fixation with non-absorbable
suture at medial, lateral and inferoanterior scrotal wall
• If questionable viability, tunica albuginea stab incision for
signs of bleeding
• If non-viable > orchidectomy to avoid abscess, sinus and
anti-sperm antibody
• Small risk of torsion, despite fixation (4.5%)

91. How about torsion of appendixHow about torsion of appendix
testis?testis?
• Torsion of the appendix testis can be
managed conservatively
• During the six-week-follow-up, clinically
and with ultrasound, no testicular atrophy
was revealed
• Surgical exploration is done in equivocal
cases and in patients with persistent pain

92. Gangrenous testis
Torsion of testicular
appendages

93. Mumps orchitisMumps orchitis

94. What is mumps orchitis?
• Rare in prepubertal
• Affecting ~30% epididymoorchitis in
aldolescent and adult
• 50% will result in reduced testicular size
• 25% will result in abnormalities of semen
analysis
• Sterility is rare

95. Varicocele

96. What is the background?
• Varicocele is defined as an abnormal dilatation
of testicular veins in the pampiniformis plexus
caused by venous reflux
• 15-20% of adolescents
• In adolescents, a testis that is smaller by more
than 2 mL compared to the other testis is
considered to be hypoplastic

97. What is indication criteria for
varicocelectomy?
• Varicocele associated with a small testis
• Additional testicular condition affecting fertility
• Pathological sperm quality (in older adolescents)
• Varicocele associated with a supranormal
response to LHRH stimulation test
• Symptomatic varicocele
– No evidence that treatment of varicocele at
pediatric age will offer a better andrological
outcome than an operation performed later

98. What is the surgical approach?
• Inguinal (or subinguinal) microsurgical
ligation
– Lymphatic-sparing varicocelectomy is preferred to
prevent hydrocele formation
• Suprainguinal ligation, using open or
laparoscopic techniques
• The advantage of the former is the lower
invasiveness of the procedure, while the
advantage of the latter is a considerably lower
number of veins to be ligated and safety of the
incidental division of the internal spermatic artery
at the suprainguinal level

99. How about embolisation?
• Angiographic occlusion of the internal
spermatic veins - less invasive, it appears
to have a higher failure rate

100. UTI in childrenUTI in children

101. What are the risk factors ofWhat are the risk factors of
UTI?UTI?
1. Age: <6 yr, 7% girls, 2% boys
2. Girls : 5%, Boys : 1%
– Male more common UTI in first year
3. Urinary stasis
• Vesicoureteric reflux, PUJO or VUJO; ureterocele;
posterior urethral valves
4. Voiding dysfunction (abnormal bladder activity,
compliance, or emptying)
5. Foreskin. Uncircumcised boys have a 10-fold
higher risk of UTI in the first year due to bacterial
colonization of the glans and foreskin
6. Constipation
7. Periurethral bacterial colonisation

102. What are the methods of urine
collection?
1. Suprapubic bladder aspiration :most
sensitive
2. Bladder catheterization :risk of
introduction of nosocomial pathogens
3. Plastic bag attached to the genitalia
4. Clean catch
– Older child prefer clean-catch - Urine collection after
cleaning genitalia
5. MSU

103. What is the criteria of UTI?
• Dipstick: +ve urine leukocyte esterase
• Dipstick: +ve urine nitrite
• Microscopy: > 5 WBC / HPF
• Any bacteria on HPF
• Epithelial cells strongly suggestive on contamination
• WBC casts pathognomonic of pyelonephritis

104. Urine culture
• Any growth on a SP aspiration
• > 10^5 CUF/ml  UTI
• Not necessary if both LE & nitrate +ve, but
c/st will guide further treatment

105. Clinical features

107. Treatment
• <3m of age or pyelonephritis:
– IV antibiotics (cefotaxime or ceftriazone)
– IV antibiotics for 2-4 days  oral antibiotics for total of
10 days
– Or oral antibiotics for 7-10 days (cephalosporin)
• Afebrile, LU infection, >3m
– Oral antibiotic (trimethoprime, cephalosporin ,
nitrofurantoin or amoxicillin)
– At least 3-7 days
• USG for ALL
• Antbiotic prophylaxis should not be routinely
given after 1st
time UTI, it may be consider in
recurrent UTI

108. What is the antibiotic of
choice for severe UTI?
• Chloramphenicol, sulphonamides, tetracyclines
(because of teeth staining), rifampicin,
amphotericin B and quinolones should be
avoided
• The use of ceftriaxone (Rocephin) must also be
avoided due to its undesired side effect of
jaundice
• Aminoglycosides if necessary, serum levels
should be monitored for dose adjustment

109. What are the types of UTI?What are the types of UTI?
• Simple
– No temp, responds well within 48 hours, E coli
• Atypical – any of the following (NICE guideline)
1. Seriously ill
2. Septicemia
3. Failure to respond to antibiotics in 48 hours
4. Non- E coli
5. Poor urine flow
6. Abdominal or bladder mass
7. Raised creatinine

110. How to define recurrent UTI in
children?
• NICE GL: over a period of 1 year
– ≥ 3 cystitis
– ≥2 acute pyelonephritis
– 1 acute pyelonephritis + ≥ 1 cystitis

112. When do we need investigation?
• If the UTI was "simple" what investigations would you
perform?
– NICE states no investigation required except baby < 6
months
– < 6m has increase risk of renal scarring
• Why? USS in acute infection / 6 weeks, MCUG and DMSA
in 6 months
1. 30% having significant renal tract anomaly
2. 20% having UTI recurrence within 1 year
3. Young kidneys were susceptible to scarring after
UTI/intrarenal reflux  HT in long run
• But risk of over-investigation

114. What to look at in USG
• USG is an effective , radiation free tool for screening of underlying
abnormality
• Should be perform within 6 weeks
1. Hydronephrosis: PJUO, VUR, VUJO, PUV
2. Renal scarring: VUR
3. Dysplasia
4. Calculi
5. Duplex kidney
6. Bladder wall thickness + RU: voiding dysfunction
• USG is not a sensitive test for renal scarring and will miss 30% of
the case
• What to do after USG?

115. 0-6m

116. 6m – 3yr

117. > 3 yr

118. UTI Age USG acute USG 6w DMSA4-6m MCUG
Typical UTI <6m YES
6m-3yr
>3yr
Atypical
UTI
<6m Yes Yes Yes
6m-3yr Yes Yes Consider
>3yr Yes
Recurrent
UTI
<6m Yes Yes Yes
6m-3yr Yes Yes Consider
>3yr Yes Yes

119. What is the clinical use of
DMSA?
• Bound to the basement membrane of proximal
renal tubular cells
• A star-shaped defect in the renal parenchyma
may indicate an acute episode of pyelonephritis
• A focal defect in the renal cortex usually
indicates a chronic lesion or a ‘renal scar’
defects
• Defeat at 6 months is considered to be renal
scarring

120. What is the clinical use of
MCU?
• Voiding cystourethrography is mandatory in the
assessment of febrile childhood UTI, even in the
presence of normal ultrasonography
• Up to 25% of these patients may reveal VUR
• Procedure:
– Cath urethrally
– Contrast medium injected into bladder
– X-ray taken : during filling and when child void
• Risk: pain during cath, introduce UTI (cover with
short course of antibiotics)

121. What is Radionuclide
cystography (indirect)?
• DTPA/MAG-3
• FU patients with reflux
• Lower dose of radiation
• Disadvantages are a poor image
resolution and difficulty in detecting lower
urinary tract abnormalities

122. What is the schedule of investigation of
a UTI in a child?

124. After acute episode
• Underlying factor identified  treat accordingly
• No recurrent with normal Ix  no FU
• Recurrent UTI in girls:
– Increase fluid intake
– Treatment of constipation
– Treatment of voiding dysfunction
– Improve frequency & effectiveness of bladder
emptying
– Cranberry juice or bioactive yoghurt
– Period of prophylatic antibiotics

125. Urinary incontinenceUrinary incontinence

126. • What is the expected bladder capacity (EBC)?
– 1-12 yr : (Age+1) x 30 (ml)
– < 1 yr: Weight in kg X 7 (ml)
– Post void RU > 20  significant
– FVC show maximum void volume : = 60-150% of EBC
• What is the normal bladder control?
– Neonates: sacral spinal cord reflex voiding.
– Infants: primitive reflexes are suppressed, bladder capacity
increases, and voiding frequency is reduced
– 2-4 years: development of conscious bladder sensation and
voluntary control
• What is the aetiology of urinary incontinence?
– 95% functional cause
• Urge incontinence, voiding postponement, dysfunctional voiding, stress
incontinence, giggle incontinence and associated with constipation
– 5% organic cause
• Ectopic ureter or neurogenic bladder.

128. What is the classification of voiding dysfunction?
• Mild:
– Daytime urinary frequency syndrome
– giggle incontinence
– post-void dribbling (urine refluxes into the vagina, then dribbles into
underwear on standing)
– nocturnal enuresis
• Moderate
– Lazy bladder syndrome (large capacity, poor contractility, infrequent voids)
– overactive bladder (detrusor overactivity associated with urgency and
frequency)
– Children may demonstrate holding manoeuvres (leg crossing, squatting,
Vincent's curtsey)
– There is increased risk of UTI, vesicoureteric reflux, and upper tract dilatation
• Major
– Hinman's syndrome (non-neurogenic neurogenic bladder) involves
dyscoordination between the bladder muscle and external urethral sphincter
activity resulting in a small, trabeculated bladder, VUR, UTI, hydronephrosis,
and renal damage.
– Caused by abnormal learned voiding training causing staccarto voiding
pattern

129. What is voiding postponement?
• Children habitually postpone micturition
• Until its too late  urinary incontinence
• More in girls
• Detrussor  hyporeflexic & decrease
sensation
• Advance case:
– Overflow + stress incontinence
– Recurrent UTI

130. What is dysfunctional voiding ?
• Tendency for intermittent or continuous
sphincter contraction to occur during
bladder emptying
• Result in RU & UTI

131. What to ask in urinary incontinence?What to ask in urinary incontinence?
• Primary (organic) vs secondary?
– Nocturnal enuresis in children is often hereditary
– Whereas when one parent suffered enuresis then 50% of the
children will also have it , if both parents  80%
– Primary: child has never been dry
– Secondary: previously been dry for at least 6m
• Continuous or intermittent?
– Continuous?  ectopic ureter
– Shortly after voiding ?  vaginal reflux
– Asso with urgency?  urgency incontinence
– Asso with giggle and laughing?  giggle incontinence
• If intermittent is it during the day or at night?
• Severity?
– Need of pads
– Need to change cloths?

134. History regarding risk factors
1. Assess fluid intake (artificial colouring / blackcurrant
drink / soft drink)
2. Voiding frequency & behavior:
– FVC
– To hold the urine until last minute
– Curtseying or sitting with hell of foot pushed into perinuem 
OAB
3. Assess associated LUTS
4. Urinary tract infection (cause of incontinence)
5. Assess bowels
6. Age of potty training , antenatal history
7. Past medical/surgical history
8. Family/social social history

136. 1. Abdomen - constipation, palpable kidneys or
bladder
2. External genitalia :
• rule out epispadias (def external sphincter)
• BXO
• Meatal stenosis
• Ectopic ureteric orifice (female)
3. Stigmata of neurological disease - hairy
patch, lipoma, dimple on lower back may
indicate lumbosacral spine abnormalities
4. Lower limb reflexes
Physical exam

137. What are the Investigations?
1. Urinalysis – infection, protein for UTI/renal disease,
glucose for DM
2. Voiding diary
3. Flow rate: normal if FR2
> VV
4. In selected cases: USS renal tract (hydronephrosis,
thicken bladder wall, RU );
5. micturating cystourethrogram (VUR, post-void
residual);
6. videourodynamics (neurogenic bladder, sphincter
dyssynergia);
7. X-ray or MRI spine (if clinical suspicion of
neurological cause)

138. • What is the management?
– Behavioural (bladder retraining, timed voiding, change of
voiding posture, psychological support)
– Medication (antibiotics for infection, anticholinergics for
bladder overactivity and urgency, laxatives or enemas for
constipation)
– Intermittent catheterization to drain post-void residuals
• What is the prognosis?
– 15% spontaneously resolve per year.

139. What is the nocturnal enuresis?
• Wetting during sleep above the age of 5 years is
enuresis
• Enuresis - involuntary voiding in the absence of
demonstrable abnormality of urinary tract
• Nocturnal enuresis - involuntary loss of urine during
sleep
• Monosymptomatic nocturnal enuresis - involuntary
loss of urine during sleep only, not associated with
other urinary symptom
• Prevalence – 15% of 5-year-old, 10% of 7-year-old
• If untreated – 15% will get better every year
• The prevalence in adults is ~0.5%

140. What is the pathophysiology of
nocturnal enuresis?
1. Decreased level of ADH - High night-
time urine output
2. Reduce functional bladder capacity +/-
increased detrussor activity
3. Arousal disorder

141. What is treatment of nocturnalWhat is treatment of nocturnal
enuresis?enuresis?
1. Reassurance and counseling (motivational technique
to improve self-esteem)
2. Treat constipation
3. Bladder training – e.g. decrease fluid intake before
sleep, avoid bladder stimulants (blackcurrent drinks /
caffeine)
4. Alarm treatment is the best form of treatment for
arousal disorder – triggered with first few drops of
urine
5. Waking the child to void
6. Star chart – positive feedback
• Success rates of - 70%

142. Medical treatment of nocturnalMedical treatment of nocturnal
enuresis?enuresis?
• Desmopressin (DDAVP)
– success rates of 70%, better in nocturnal polyuria
– Nasal spray is no longer recommended due to an increased risk
of overdosing
– Relapse rates are high after DDAVP discontinuation
• Imipramine-TCA + anticholinergic
– moderate response rate of 50%
– high relapse rate
– Better in functionally reduced bladder capacity
– Cardiotoxicity and death with overdose are described. Its use should
therefore be discouraged
– Never combine TCA and DDAVP

143. Neurogenic bladder in childrenNeurogenic bladder in children

145. What is myelodysplasia?
• Myelodysplasia (incidence 1/1000) includes a group of
developmental anomalies that result from defects in
neural tube closure
– Myelomeningocele is by far the most common defect seen
and the most detrimental - cord and meninges (the tissues
covering the spinal cord) to stick out of the child's back
– Meningoceles - tissue covering the spinal cord sticks out of
the spinal defect but the contain no neural tissue
– Spina bifida occulta - bones of the spine do not close but
the spinal cord and meninges remain in place
• Asso cutaneous abnormality: dimple, skin tag, tuft of hair, dermal
vascular malformation or subdermal lipoma
• 40% SBO as asso lower urinary tract dysfunction

146. What is the background of
neurogenic bladder?
• Not only has it made conservative management
a very successful treatment option, but it has
also made surgical creation of continent
reservoirs a very effective treatment alternative,
with a good outcome for quality of life and
kidney protection
• Introduction of clean intermittent catheterisation
(IC) has revolutionised the management of
children with neurogenic bladder

147. How can it affect the urinary tract?
It can cause:
• Voiding dysfunction
• Recurrent UTI
– (asso with VUR) need antibiotic prophylaxis
• VUR (3%)
– Asso with detrussor hyperreflexia or dyssynergia
• Renal scarring
• Renal failure requiring RRT

148. What are the important points of
urodynamic study?
• Slow fill cystometry (filling rate < 10
mL/min) is recommended by the
International Children’s Continence
Society (ICCS) for use in children
• But some suggested Infusion rate
should be set according to the child’s
predicted capacity, based on age and
divided by 10

149. UD finding
• Detrussor areflexia: void with straining / IC
• DSD: IC , anticholinergic , sphincterotomy
• Detrussor hyperreflexia: IC/ anti-cho
• Outflow obstruction: IC/ sphincterotomy/
diversion

151. What is the medical therapy?
• Oxybutynin, tolterodine, trospium and
propiverine are the most frequently used drugs,
with oxybutynin being the most studied
• The extended release formulation of tolterodine
has been found to be as efficient as the instant
release form, with the advantages of being
single dosage and less expensive
• Although the clinical outcome is encouraging,
the level of evidence is low for anticholinergic
medication because there are no controlled
studies

152. What is the botulinum toxin
therapy?
• Neurogenic bladders that are refractory to
anticholinergics and remain in a small-capacity,
high-pressure state, a novel treatment
alternative is the injection of botulinum toxin into
the detrusor
• More effective in bladders with evidenced
detrusor overactivity
• While noncompliant bladders without obvious
detrusor contractions are unlikely to respond to
this treatment

153. What is the botulinum toxin
therapy?
• A single study, urethral sphincter
botulinum-A toxin injection has been
shown to be effective in decreasing
urethral resistance and improve voiding.
The evidence is still too low to recommend
its routine use in decreasing outlet
resistance

154. What is the treatment of UTI?
• Strong evidence for not prescribing
antibiotics to patients who have bacteriuria
but no clinical symptoms

155. What are the important points of
bladder augmentation?
• Autoaugmentation and seromuscular cystoplasty (e.g. avoiding
mucus, decreased malignancy rate and fewer complications), have
not proven to be as successful as standard augmentation with
intestine
• Anastomosing a detubularized segment of bowel to bladder
• To increase capacity & lower pressure  minimized UT deterioration
• When ileum is used a 25 cm segment is chosen starting from 25 cm
proximal to the IC valve in an attempt to avoid the segment of ileum
involved inB12 absorption and the enterohepatic circulation.
• Overall 90% of patients undergoing augmentation cystoplasty for
incontinence will report to be dry postoperatively. About 40% will
require to self cath. for urine retention
• Daily production of mucous in patients having ileocystoplasty is
estimated to be 40 g
• Biochemical metabolic acidosis is common but typically is subclinical.
clinically apparent and needs treatment in 10-20% of cases

157. Antenatal HydronephrosisAntenatal Hydronephrosis

158. At what gestational age can hydronephrosis
be detected?
• 16-20 weeks
– When almost all amniotic fluid consists of urine
• Incidence: 0.5% (~50% bilateral)
• Most common cause of neonatal mass –
hydronephrosis
• 2nd
most common – multicystic kidney
• (most common cause of abdominal mass > 1 year –
tumor)
• Renal pelvis length > 12mm consider significant
obstruction

159. Persistent fetal abn ass with
APD
• > 6 mm < 20 weeks
• > 8 mm 20 – 30 weeks
• > 10 mm > 30 weeks

160. Any role of fetal intervention?
• Not proven benefit/ experimental (complication,
renal dysplasia already exist)
• Counseling is important
• Potential situation for intervention
– Oligohydraminos with presumed BOO that life of
neonate is at risk (pulmonary hypoplasia)
• Needs normal karyotype, no systemic anomaly, singleton, non
cystic kidneys, favorable urinary indices (Na<100, Cl<90,
Osmo< 200) x3, informed consent
• In form of vesico-amniotic shunt
• High complication rate but no different in outcome or long term
result

161. What is the role in the antenatal USG?What is the role in the antenatal USG?
• Unilateral or bilateral
• Degree of HN
• Any change in degree of HN (may be reflux)
• Any dilated ureter (not PUJO, may be others)
• Bladder status:
– distended bladder (not upper tract obstruction, may be VUR/
PUV)
– thickened bladder wall (not VUR, may be PUV, neurogenic)
– intravesicle cystic lesion (ureterocele)
– dilated post. urethra – keyhole sign (PUV)
– failed identify bladder on several occasion (bladder exstrophy)
• Oligohydramino (usu PUV) may not be presence early
(<20wk)
• Any hypoplasic or dysplasic changes
• Other associated anomaly in other system

162. What is DDx of hydronephrosis?What is DDx of hydronephrosis?
1. Transient HN: immature PUJ / VUJ, increase fetal
urine output, ureteric fold
2. Unilateral
1. PUJO (MAG3)
2. VUR (MCUG, DMSA)
3. VUJO (MAG3 – Homsy’s sign)
4. Megaureter (>7mm, normal <5mm)
5. Ureterocele (MCUG)
3. Posterior urethral valves (MCUG)  bilateral
4. MCDK / PKD
5. Prune Belly syndrome
6. Neurogenic bladder (MCUG)

163. Grading scale for fetus >20 weeks
• I: APD 1cm , normal calyces, 50% resolve
• II: APD 1-1.5 cm, normal calyces, 36%
• III: > 1.5 cm, slight caliectasis, 16%
• IV: > 1.5 cm moderate calyces, 3%
• V: >1.5 cm severe caliectasis, thinning
renal cortex (< 2 mm thick)

164. What is the grading system for congenital
hydronephrosis? (post-natal)
Grade Central renal complex Renal parenchyma
0 intact Normal
1 Sl splitting of pelvis normal
2 Evident splitting of pelvis & calices normal
3 wide splitting of pelvis & calices normal
4 further splitting of pelvis & calices reduced

166. Grade 0

167. Grade 1

168. Grade 2

169. Grade 3

170. Grade 4

171. Choosing patient for VCUG in
congenital hydronephrosis
1. Bilateral
2. Dilatation of collecting sys increase with
voiding during gestation
3. Visualization of ureter
4. Fam Hx of reflux

172. Post-natal management
• Spontaneous voiding within 24 hours exclude obstructive course
• P/E
– For abd mass (gross HN), distended bladder, any poor stream (PUV),
evidence of Prune Bellly, bladder exstrophy, other associated anomaly
• (RFT on the first day reflect mother’s RFT)
• USG
– Timing : at least 48hr , better 7-10 days
– Usually 1 week later (avoid newborn dehydration and oliguria in first
48hr)
– 2nd
scan ~6 week later if 1st
scan normal
– Exception – If severe bil HN, solitary kidney, oligohydraminos, then
immediate USG
– Look for: Degree of hydronephrosis, cortical thinning, Bladder wall
thickness &
– If 1st
2 USG after birth is normal  low likelyhood of VUR
– If USG abnormal  proceed to the following test (VCUG & DMSA)

173. • VCUG :
– Dx VUR (up to 25% of cases) and PUV, ureterocele,
neuropathic bladder
– Then Mx accordingly
• If neg VCUG, then MAG 3 scan ~6 wk later (let the kidney
mature)
– Diuretic response is proportional to renal function, avoid
if GFR<15ml/min
– Dx PUJO with info of differential fx
• Some advocate no VCUG for mild uni HN (for RPD 5 to
9mm), as most are low grade VUR (resolved later), mild
PUJO (no need surgery), and VCUG have risks discomfort,
cost
• Tx: Prophylactic antibiotics

178. Radionuclide scintigraphy
• DMSA for renal scarring/ static scan
• MAG3/ DTPA scan for differential function
and assessment of obstruction/ dynamic
scan MAG3 DTPA
Glomerular filration < 5% > 95%
Tubular secretion 95% Minimum
Clearance Predominantly by
tubular secretion;
small proportion by
glomerular filtration
Min. tubular
secretion
or absorption
Almost completely
by
glomerular filtration
Cost Higher Lower

179. Radionucline scintigraphy
• Patient prep:
– Adequate hydration
– Empty bladder before procedure
• Factors affecting the scan:
– Renal function
– Hydration status
– Collecting system capacity
– Bladder effect

180. What are the advantages of
Renal scan?
• No intravenous contrast
• No need to worry about nephropathy
• Does not induce allergic reaction
• No reported toxic reaction

181. Radiopharmaceuticals in renal
scintigraphy
• 1. Glomercular: Technetium-99m(99m
Tc) diethylenetriamine
pentaacetic acid (DTPA): 2-6% protein binding; extraction efficiency
20%, peak renal activity 3-4 min after injection; 90% glomerular
filtration in first 2 hr; Used to access renal blood flow, function and
drainage; Measure GFR as only glomerular filtration with no tubular
reabsorption / excretion
• 2. Tubular: 99m
Tc-mercaptylacetyltriglycine: 70-90% protein binding;
89% tubular excretion and 11% glomerular filtration in animal study;
extraction efficiency: 50-60%; Measure renal plasma flow, renal
function and function; Especially for patients with decreased renal
function and of infants
• 3. Cortical:99m
Tc-dimercaptosuccinic acid: uptake in proximal
convoluted tubules; 75% protein binding at first 6hr but only 5-20%
urine excretion in the first 2 hrs=> pelvicalyceal system not
visualized; 40%-50% renal cortical localization and maximum
activity 3rd
-6th
hr

182. MAG-3
• Mercaptoacetyltriglycine bound to radio-isotope technetium-99
• ½ life of 99mTC : 6hour
• Dynamic scan, radiation dosage: 0.4mSv (millisieverts)  less than
plain x-ray
• 90% tubular secretion , 10% glomerular filtration
• Well hydrated pt , tracer inject
• Gamma camera placed posterior to the patient , Sit up / supine
• Gamma radiation given off by tracer measured by gamma camera 
serial photo
• Provide information such as differential fxn and washout curves
• Use when there is suspected UT obstruction (PUJO or VUJO)
• Lasix can be given 20min after injection (F+20) or 15 min before (F-15)
• Max effect 18min after injection
• F-15 result in maximal stress on PUJ  reduce equivocal rate 
investigation of choice

183. • Image:
– Q2s for 1min
– Q10-60s for 30min (uptake and excretion)
– Post-void image
• At the end of study: 30s image of injection site (to make
sure that the radioisotope is intravenous not interstitial)
• Can be use as MAG-3 cystography to see VUR (replace
MCUG)
• Best defer until 6 week of age  renal tubule to mature
• Quantification of renal function:
– Computer Analysis of Renal Scans with reference of regions of
interest (ROIs) over the kidney, and a background area for
comparison
– Differential renal function measurements
• Renogram (time activity curves)

184. • 99m
Tc-MAG3
– Excreted by tubular
secretion independent
of GFR
– T1/2 6 hours
– Renal uptake 55%
– Excellent imaging
characteristics
– Favored agent for
diuretic renography

185. MAG-3
Three phase:
• Vascular phase: 0-10 s
– Reflect renal blood flow (blush)
• Extraction/ uptake phase : 10s – 5m
– Reflect renal uptake or parenchymal fxn
• Excretory phase : > 5m
– Radio-isotope excreted into renal pelvis

186. Diuresis renogram (O’Reilly’s curves)
• Type 1: normal renal uptake and drainage
• Type 2: obstructed pattern with no response to
diuretic
• Type 3a: curve rise initially but falls rapidly on lasix
(normal drainage from hypotonic renal pelvis)
• Type 3b: curve risk initially but neither fall or
continue to rise on lasix (Equivocal)
• Type 4: Diuretic result in transient response ,
represent obstruction or intermittent hydronephrosis
(VUR)  Homsy’ sign
– F-15 will eliminate Homsy’s sign and confirm obstruction

188. What is the Procedure of DiureticWhat is the Procedure of Diuretic
RenographyRenography
• Adequate hydration (excretion of tracer &
response to frusemide impaired when patient is
dehydrated)
• Method of hydration
– Adult: orally 5-10 ml/kg
– Infant: IV 15ml/kg over 30 min
• Bladder emptied before the procedure
(remember to catheterize the patient with Mitrofanoff)
• Frusemide
– 0.5 – 1 mg/ kg IV if abnormal result encountered
– Max 20mg in child,40 mg in adults

189. What is diuretic T1/2 (renal washout)?
< 20 min non-obstructed
> 20 min obstructed

190. What are the factors affecting T
1/2 ?
1. Hydration state
2. Renal function
3. Vol & contractility of renal pelvis
4. Patient position
5. Bladder filling
6. Timing & dose of diuretic administration

191. • 99m
Tc-DTPA
– 1970
– Equilibrium in blood stream
2 hours after IVI
– Only excreted by
glomerular filtration
– Renal uptake 20%
– Ideal agent for assessment
of glomerular filtration rate
(GFR)
– Need a reasonable GFR
for good imaging

192. DMSA
• Dimercaptosuccinic Acid + 99mTC
• Radiation dosage: 1mSv
• Extracted from peritubular extracellular fluid
• Deposited in tubular cells
• Static scan produce still image (3-4hr after injection)
• View: planar posterior , L &R posterior oblique, coronal
tomographic view
• Much better detail and resolution than MAG-3
• Advantage:
– Good measure of differential function
– Cortical defect in acute pyelonephritis
– Cortical scarring (Sn 90%, Sp 100%)
– Good moiety fxn of duplex kidney
• Best use where detailed information is require but no
concern about obstruction (VUR)

193. • 99m
Tc-DMSA
– Localizes in renal
cortex
– identify renal cortical
abnormalities
– Locate aberrant kidney

194. MRI
• + contrast (gadopentetate dimeglumine)
• Cleared by glomerular filtration
• Ana imaging + functional renography

195. PUJOPUJO

196. Recurrent loin pain, selective arteriogram

197. What is shown?What is shown?
• How does this affect management?
• Other method to demonstrate such
finding?

198. Crossing vessel
• Pyeloplasty with dismembering is
treatment of choice. Endopyelotomy
dangerous
• MRU allow non invasive demonstration of
crossing vessel (endoluminal US more
invasive)

199. PUJO
• Incidence 1:1000
• M : F ~ 2:1
• L >>> R : 2:1
• Bilateral up to 40%
• Presentation:
1. Antenatal hydronephrosis (most common cause of neonatal abdominal mass)
2. Loin pain after larger amt of fluid (Dietel’s crisis)
3. incidental findings / UTI
4. Haematuria as hydronephrotic kidney more prone to have trauma
• Causes: Primary
1. Hypoplastic and aperistaltic PUJ
2. Compression by lower pole segmental vessels (40%)
3. Valvular mucosal fold (Oestling folds)
4. Upper ureteric polyp
5. High insertion of PUJ: horseshoe kidney
– Secondary: severe VUR
– Others: horseshoe kidney /retrocaval ureter

200. Asso anormalies
1. Contralateral PJUO: up to 40%
2. Renal dysplasia / multicystic dysplastic
kidney
3. Renal agenesis (5%)
4. Ipsilateral VUR (10%) : mild , don’t
simultaneous repair
5. VATER syndrome (20%)

201. What is Ix of PUJO?
• USG (antenatal & 1 week post-partum)
– Normal neonate AP <6mm
– Unlikely significant obstruction if <15mm
– >50mm associated with diminished function
• MAG-3: Confirm obstruction and differential function
• IVU – provides anatomical information
• VCUG : to rule out VUR
• Whitaker’s test if equivocal:
– Pt prone
– 10ml/minute to PCN to stress the renal pelvis
– Measure pressure difference btw renal pelvis and bladder
– <15cmH2O – normal
– 15-22cmH2O – equivocal
– >22cmH2O – obstructed
• Anatomical detail: MRU (modality of choice)
• MCUG if Bilateral, visualization of ureter, fhx of reflux

202. Assessment
• Confirm obstruction: MAG3
• Monitor differential function: MAG3/DMSA
• Monitor extent of hydronephrosis: US
• Anatomical detail: US / MRU / IVU / RP

203. What is the natural history of
PUJO?
• Great Ormond Street Hospital experience
(Dhillon)
• 15% obstructed requiring pyeloplasty
• 25% with resolving obstruction
• 60% stable with persistent obstruction but
no deterioration of function

204. What are the indications for
surgery?
1. Symptomatic obstruction
2. Impaired split renal function (<40%)
3. Failed conservative management:
• A decrease of renal function > 10%
• Increase in AP > 30mm
4. AP > 50mm : RFT would deteriorate if not treated
(Natural history of PUJO by Dhillon)
5. Grade III (minor calyx dilated) and IV (thinning of
parenchyma) as defined by the society of fetal
urology
• Angiogram , CT or doppler USG to identify LP
vessels before operation

205. Open repair
• Flap type
– Foley operation (Y-V plasy) – high ureteric insertion
• Incision – intubated type
– Davis intubated ureterotomy
– Depended on secondary healing with epithelialization
– Particular suitable when multiple or extensive strictures of
proximal ureter are present but cannot be bridged by a pelvic
flap
• Dismembered type
– Anderson – Hynes dismembered pyeloplasty [operation
of choice]
• Preservation of anomalous vessels
• Excision of pathologic PUJ
• Reduction pyeloplasty
• Ureterocalicostomy : when uretro length not enough

206. Advantage of Dismembered
pyeloplasty
1. Excision of stricture and accurate anastomosis
2. Allow transposition of urinary axis anterior to
aberrant vessel
3. Allow reduction pyeloplasty
4. Easy to perform and can be done with various
approach
5. In case of long stricture  renal decensus can
be performed to gain extra length

207. Anderson – Hynes dismembered
pyeloplasty
• Approach:
– Ant subcostal
– Post lumbotomy
– Supra-12 loin
• Ureter divided & incised
just distal to PJUO
• Portions of redundant
dilated renal pelvis
excised
• Interrupted suture
• Water tighted , tension
free
• Over stent

208. Lap vs open
• Better cosmetic result
• Shorter hospital stay and reduced post-op
analgesic requirement
• Longer operative time
• Success rate ~95% (Inagaki, Kavoussi,
BUJI 2005); similar to open series (e.g.
O’Reilly, BJUI 2001 ~96%)

209. Result
• Overall success with dismembered
repair >90%
• Re-operation rate: 2%
• FU: USG, renal scan
• Complications:
1. Urinary extravasation
2. Stricture
3. Peri-op morbidity

210. Endoscopic
Endopyelotomy
• Success rate 70-80%; avoid lower pole vessel
• Retrograde
– Lower complication, higher successful rate and shorter hospital stay when
compared with antegrade
– If there are any lower pole vessels they run anteromedical to the PUJ and therefore
the endopyelotomy incision should be made longitudinal in a posteriorlateral
orientation to avoid these vessels
• Antegrade (can deal with renal stone at the same time)
• Acucise - may be more useful in children older than 4 years with a failed
pyeloplasty, where only a small dilation of the anastomosis may be required to
produce good renal decompression
– Fr 13 device; 75W cutting; directed posterolaterally in C-arm
– Balloon inflated from 1to 2ml during cut; till extravasation
– PUJ bridge with endopyelotomy stent , removed in 6 weeks
– Success rate ~50-70%; worse if aberrant vessel/gross hydronephrosis
Balloon dilation
• Less risk of bleeding / recurrent case
• 2 year success rate 70%; failure with aberrant renal vessels

211. Pyeloplasty vs endopyelotomy
• Schenkman (JU 1998)
– Success rate: endopyelotomy 88%; open pyeloplasty
93%
– Similar hospital stay
– Higher operative time and hospital cost for
endopyelotomy
– Conclusion: Endopyelotomy may be performed
effectively for primary ureteropelvic junction
obstruction in children but with increased costs.
• Concomittent reduction pyeloplasty
• Preserve aberrant vessel

212. VUJO & megaureter

213. Megaureter
Definition:
• Grossly dilated and tortuous ureter (>7mm)
Primary obstructed megaureters:
– 20% bilateral
– M:F = 4:1
– Left side is more often affected than the right
Classification
1. Refluxing megaureter
2. Obstructed megaureter  VUJO
3. Non-reflexing, non-obstructed megaureter 
Resolved VUJO

214. VUJO
• 1: 2000
• M> F
• L> R
• Sporadic
• Stenotic ureteric segment above VUJ with
proximal dilated tortuous ureter
• Result from adynamic , aperistaltic distal
segment of ureter

215. Presentation & Ix
• UTI (most common)
• Intermittent loin & abd pain
Investigation:
• USG: HN + dilated ureter along the course
• Ureter >1cm
• MCUG: diff obstruction vs VUR
• MAG: difficult to observe drainage, mainly for
differential function

216. • Intravenous
urogram
demonstrating left
primary megaureter
in comparison to
normal right
collecting syste

217. Natural course
• 10% require surgery
• 40% stable
• 50% complete resolution

218. Indication for surgery
1. Pain
2. Differential function < 35%
3. Deteriorating renal function
4. Recurrent or severe UTI (not responding to
antibiotic prophylaxis)
• Don’t do surgery before 1 yr of life
– High failure rate
– More morbidity: neurological impairment 
incontinence

219. Ureteral tailoring
• Appropriate length-diameter ratio for reimplantation
• Allow wall to coapt more properly  effective peristalsis
Types:
1. Hendren’s excisional tapering:
• Redundant ureter is excised with medial blood supple
preserved
2. Starr plication:
• Redundant ureter invaginated and plicated with Lembert
suture
3. Kalicinsky plication:
• Running suture through ureter to create 2 lumen
• Redundant portion is fold and tacked anteriorly

220. Surgery
• Unilateral
– Ureter < 1cm
• Excision of stenotic segement , Cohen cross-trigonal tunnel
ureteric reimplantation
– Ureter > 1cm:
• Leadbettter- Politano reimplnatation +/- ureter plication
(Starr)
• Psoas hitch to minimized risk of kinking during bladder filling
• Bilateral:
– TUU
– One ureter is implant with LP procedure
– Contralateral ureter is anastomosed to the
reimplanted ureter

221. FU
• USG + renogram : 6-12 m
• If VUR: prophylatic antiobitics

222. VURVUR

223. What is reflux
• Definition: Abnormal retrograde flow of urine from bladder to the upper
urinary tract
• Primary reflux:
– Deficiency of longitudinal muscle of the intramural ureter & inadequate
submucosal length  inefficient flap valve mechanism
• Secondary reflux: reflux due to clearly defined pathology
– BOO (PUV, Urethral stenosis, ureterocele)
– UTI
– Neurogenic bladder (DI , hyperreflexic bladder , non-N neurogenic bladder)
• Pathology:
– Failure of VUJ as one-way valve  reflux of LU tract bacteria to usually sterile
upper tract
– Resulting in recurrent UTI / pyelonephritis
– Renal scarring and eventual renal failure (20%) + HT
– HT: Arterial damage in area of scarring → segmental ischaemia → renin-driven
HT
– Also asso with small kidney
– Direct relationship btw grade of reflux and incidence of nephropathy

224. Embryology of UVJ

225. How common is reflux?
• 2% of pediatric population
• Risk factor:
1. Sex: female 85%
2. Age with UTI is present (younger the age of 1st
UTI
, higher risk of VUR)
3. UTI: 40% in children with UTI
4. Race: White girl
5. Familial case AD inheritance
– Offspring of affected parent: 35%
– Sibling of affected child: 30%

226. What is the mechanism of
VUR?• Length of submucosal tunnel increase with age 
spontaneous resolution of VUR
• Normal Anti-reflux mechansim
1. oblique course
2. adequate submucosal length ( Paquin’s 5 : 1 in normal children )
3. proper muscular attachment to provide fixation and posterior support
4. Active contraction of longitudinal muscle to close ureteric orifice during
voiding
5. Passive flap-valve mechanism
• Appearance of UOs changes with severity – stadium,
horseshoe, golf-hole, or patulous
• In duplex kidney: Weigert-Meyer rule – lower pole
moiety ureter enters bladder proximally and laterally,
shorter intramural tunnel, prone to reflux

227. How do they present?
1. Pre-natal dx of hydronephrosis
• 40% of pre-natal HN has VUR
• Male predominance
2. Clinical UTI
3. Advance reflux nephropathy :
• headache, HT, CHF, uremic symptom
4. Loin pain
5. Double voiding
• PE:
– Loin , Bladder & abd mass
– Spinal problem & LL spaticity

228. Do we need to screen VUR?
• FOR
– Screening of sibilings and offspring of pt with reflux is advocated
by some
– Because:
• 10% of them will have renal damage on IVU [Noe]
• 40% of them will have scarring on DMSA [Buonomo]
– < 5 yo: VCUG
– > 5 yo: USG  VCUG if abnormal
• Against:
– screening asymptomatic individuals is likely to result in
significant over-treatment of clinically insignificant VUR
• EAU 2011:
– The lack of RCT for screened patients to assess clinical health
outcomes makes evidence-based guideline recommendations
difficult

229. EUA 2011

230. Approach: Children with UTI
• VCUG is indicated when: in 0-2yo
– Rirst proven UTI in males
– After recurrent UTIs in girls
– Both sexes after the first febrile UTI
• If VCUG abnormal  DMSA
• Alternatively , an upside-down approach
– DMSA first  if abn  VCUG
– This will miss 5-27% of minor VUR
– But avoid 50% of unecessary VCUG

231. Approach: Children with LUTs and
VUR
• Detection of LUTS is essential because:
– Reflux due to LUTS will resolved faster after
LUTS corrected
– Pt with LUTS are at higher risk of UTI and
renal scarring
– High risk of co-prevalence
• LUTS with VUR has a poorer prognosis
[Swedish Reflux study]

232. What is the background of
VUR?• Big bang theory: [Ransley 1978]
• Most severe degree of parenchymal injury occur with the 1st
infection
because all susceptible segments are simultaneously affected
– 2 observations:
• Most scarring occurs after initial bout of pyelonephritis
• Further scarring in the absence of repeated pyelonephritis is unlikely to occur
– Emphasize the susceptibility of young children with reflux to UTI
• With VUR of significant grade and intrarenal reflux
• the initial urinary tract infection/bacteruria results in a local
inflammatory response in those segments where intrarenal reflux occurs
• causing renal parenchymal damage and ultimately scar formation
• Most commonly on concave papilla on the polar region
• Preventing recurrent infection and permanent renal parenchymal damage
and its late complications by antibiotic prophylaxis and/or surgical correction
of reflux

233. Spontaneous resolution of
VUR?
Favor resolution:
• age < 1 year at
presentation
• lower grade of reflux
(grade 1-3)
• Asymptomatic
presentation with
prenatal
hydronephrosis or
sibling reflux
-ve factor for resolution:
• diffuse scarring
• major renal abnormality
• bladder dysfunction
• breakthrough febrile
UTIs

234. Aim of assessment
• Evaluate the overall health
• Development of the child
• Presence of UTIs
• Renal status
• Presence & grade of VUR
• Lower urinary tract function

235. What is the assessment of
VUR?• Bld: Cr , CBP
• Urine: c/st
• USG:
– Kidney (hydronephrosis + scar)
– bladder (thickening of bladder wall signified 2nd
VUR)
• DMSA :
– Perform at least 4-6m after pyelonephritis
– for renal scarring (cold spot)+ differential function
• SPECT (single-photon emission CT)
– More accurate detection of scarring than DMSA
• MCUG:
– Performed after fully recover from UTI
– Confirm VUR & grading
– Rule out PVU in boys
– Can be done: fluroscopic, Indirect MCU (MAG-3)
• Urodynamic study
– Rule out neurogenic cause
– Inconclusive Ix findings refractory to treatment

236. What are the association
1. PUJO: 15%
– XR signs to suggest existence of PUJO in reflux:
• Pelvis shows little or no filling whereas the ureter is dilated
by contrast
• Pelvis will exhibit markedly reduced radiodensity in
comparison to the ureter or bladder
• Large pelvis that fails to exhibit prompt drainage
2. Duplex kidney: lower pole
3. Bladder diverticulum
4. Renal: MCDK, Renal agenesis
5. Megacystitis-megaureter association

237. What is grading of reflux? 1981
IRSC
Grading according to international Reflux Study grading (1985) by appearance
by VCUG but is not accurate enough with radionuclide cystogram

238. International Reflux Study Committee grading of VUR
Grade of
VUR
Characteristics % with scarring: Rate of
spontaneous
resolution (%)
I up to ureter 5 90
II up to renal pelvis, no
dilatation of calyces
6 80
III mild to moderate calyceal
dilatation with minimal
blunting
15 50
IV moderately dilated calcyes
with loss of angles of
fornices, impressions of
papillae preserved
25 20
V grossly dilated calyces and
tortuous, loss of papillary
impressions;
intraparenchymal reflux
50 <10

239. 5 yr old girl with bilateral VUR.
• What is this investigation? (1)
• What is the isotope used (full name please)? (1)
• What is the finding? (1)
Q49

240. • DMSA scan (1)
• Technetium-99m labelled
dimercaptosuccinic acid (1)
• Scarring in LEFT kidney (1, no mark for
wrong side)

241. What is the treatment of primary
VUR?

242. Why need to treat girls > 5 but not
boys?
Pregnancy and VUR:
• Women with VUR have increase risk of
complication during pregnancy
– More pyelonephritis
– More HT, preeclampsia & miscarriage
• Thus surgical repair in girls with VUR that
persist as puberty approaches

243. Principles of management of reflux
• Individualized VUR diagnosed
Daily low-dose prophylatic antibiotic suppression of infection
Offer the time to resolve spontaneously, despite grade
Children Adult
Asymptomatic boys Symptomatic boys or girls
Cessation of prophylactic antibiotics Surgical correction

244. Goal of treatment
• The objectives are 2-fold:
• 1. prevention of episodes of acute pyelonephritis
with its associated morbidity and mortality
• 2. to prevent the scarring of the kidney
associated with VUR (reflux nephropathy), which
increases the risk of hypertension and renal
failure in children and adults with VUR

245. Management
1. Medical management
– Antibiotic prophylaxis
– Conservative management: observation
– Patient and parent education
2. Interventional management
– Endoscopic subureteral injection of tissue-augmenting substances
(bulking agents)
– Laparoscopic reflux correction (considered, but not recommended
as a routine procedure)
– Open surgical correction of reflux: Lich-Gregoir; Politano-Leadbetter,
Cohen and Psoas-Hitch ureteroneocystostomy; intravesical
antireflux procedures for bilateral reflux
3. Treatment of underlying condition in cases of secondary
vesicoureteral reflux
4. Follow-up: voiding cystourethrogram, sonography, blood
pressure, urinalysis (routine radionuclide studies considered, but not
recommended)

246. Medical/ Conservative Mx
• Circumcision
• Prompt treatment of any UTI - reduce
likelihood of long-term scarring
• Maintain a good fluid intake
• Maintain a regular bowel habit and avoid
constipation
• Older child - regular voiding 3-hourly
• Prophylactic antibiotics - continued until
VUR resolved/ is corrected

247. Treament of UTI
• Initial management of the child with UTI
– involves supportive care and prompt
administration of appropriate antibiotics
– animal studies: permanent renal damage
occurs if antibiotics are not started within 72
hours; other studies indicate an even shorter
window of opportunity
– high index of suspicion for UTI needed

248. Antibiotic prophyalxis
• Rationale for Continuous antibiotic prophylaxis :
(CAP)
– observation that VUR can resolve spontaneously
with time, mostly in young patients with low-grade
reflux – 80%, Grade III –V : 39%
– Resolution rate of 20% per year, regardless of age is
observed (Connolly)
– Severe sterile reflux does not result in reflux
nephropathy
– Long-term antibiotic prophylaxis in children is safe

249. Antibiotic prophylaxis
• When to start prophylactic antibiotics ?
Once a child has been treated for UTI or has had
an VUR identified on imaging
• Who should be given ?
Virtually all children with a new diagnosis of grade I-
IV reflux, and some with grade V, are given a trial of
medical management
Since a substantial number of children experience
spontaneous resolution of VUR (50-85% of cases
with grade I-III VUR), medical management spares
this group the morbidity of surgery while protecting
the kidneys from further damage

250. Antibiotic prophylaxis
• What antibiotic should be given ?
Amoxicillin or ampicillin (5 mg/kg/day) is
recommend for children up to 6 weeks of age
After 6 weeks, the biliary system is mature
enough for Septrin (Trimethoprim-
sulfamethoxazole) to be used (2 mg/kg/day)
• S/E : GI upset, Steven-Johnson, leukopenia
Nitrofurantoin is another choice (1-2 mg/kg/day)
• S/E : pulmonary fibrosis, interstitial pneumonia

251. Antibiotic prophylaxis
• What dosage should be given ?
one fourth of the therapeutic dosage
usually administered as suspensions and single night-
time dose to maximize overnight intravesical drug
levels
• Monitoring ?
MSU x 3 Q3mth for any breakthrough UTI
Renal ultrasound and VCUG or nuclear cystogram
Q12-18 mth
Regular DMSA is not necessary unless recurrent UTI
with scarring is suspected

252. Antibiotic prophylaxis
• When to stop ?
 When surgery is indicated
 When VUR resolved on subsequent FU
 Boys after puberty when the chance of UTI decreased
(However, due to concerns about future pregnancies, surgery
usually is recommended in girls approaching puberty with
persistent VUR)
• Randomized controlled trials : medicine vs surgery
– No difference between conservative treatment and surgery
in terms of UTI, renal function and growth or new scars
– Only difference between the 2 approaches was the higher
risk of febrile UTI in the conservatively treated group
of patients

253. Surgical treatment
• Indication:
1. Breakthrough infection
2. Deterioration of renal function with new scar
3. Poor compliance to drugs
4. Girls > 5 years
5. Grade 4-5 reflux
6. Parental choice
• Options include
1. Circumcision
2. endoscopic injection of DEFLUX
3. ureteric re-implantation

254. • What procedure is this? (1)
• What is the indication? (1)
• Name the material that is commonly used now
and what is it made of (2)
Q41

255. • Endoscopic injection for correction of VUR
(1)
• VUR (1)
• Deflux (1) from G3 or below
• Dextranomer microspheres in hyaluronic
acid
(1)

256. Endoscopic Treatment
• Use as initial reflux txn for Grade III and below
• Not proven to be as effective as surgery
• Historical: STING (sub-trigonal injection) of PTFE/ teflon
(teflon can migrate to distant organs)
• Conventional: Deflux injection (dextranomer/ hyaluronic
acid copolymer)
• Semifilled bladder, injected beneath the intramural part
of the ureter in a submucosal location (1-2ml per ureter)
• Elevate UO & distal ureter  cooptation increase
• success rate > 80%, repeated injections may be needed

257. Result of endoscopic method?
• Meta-analysis including >5000pt : the reflux
resolution rate following one treatment
– grades I and II reflux was 80%
– grade III 70%
– grade IV 60%
– grade V 50%
– 2nd
treatment had a success rate of 70%
– 3rd
treatment 30%.
– Overall success rate : 85%

258. What is Deflux?
• Dextranomer microspheres + hyaluronic acid that serves
to stabilize the microspheres
• Biocompatible
• Not to migrate
• Non immunogenic
• Foreign body type inflammatory response
• No fibrosis – not affect future surgery
• Hyaluronic acid replaced by collagen that stabilize
microspheres
• Implant vol (up to 1ml) decreases over time by 20%

259. How about surgical repair of VUR?
• Open reimplantation method:
– All need mobolize ureter & create submucosal tunnel 5x the diameter of
ureter (Paguin’s rule)
– Psoas-hitch ureteroneocystostomy
– Extravesical : Lich-Gregoir
• burying the ureter in a tunnel of detrusor, bladder not opened
– Transvesical:
• Politano-Leadbetter (reinsertion in higher and medial position)
– Intravesical
– Bring the ureter in through a new hiatus superior to the original insertion
• Cohen (cross-trigonal reimplantation)
– Intravesical
– Direct the submucosal tunnel across the trigone toward the contralateral bladder wall
– Success rate of 99%
• Adv: less post-op bladder dysfunction (no touch on nerve plexus)
• Dis: hematuria, need catheter
• Lap: similar success rate , but longer operation , no obvious advantage
cannot be recommended as a routine procedure
• Surgical re-implantation - success rate > 95%

260. • Complications:
• Early
– Persistent reflux
– Contralateral reflux
– Obstruction
• Longterm
– Obstruction (suprahiatal, hiatus, tunnel, orifice)
– Recurrent or persistent reflux
• Obstruction : may require temp drainage or revision
• Persistent reflux: observe with antibiotic, VUD to RO
bladder dysfunction

262. How about FU after definitive
treatment?
• MAG-3 to rule out obstruction at 6 week
• VCUG at 6m
• Continue prophylaxis until VCUG show no
reflux
• Obstruction of the upper urinary tract is ruled
out by sonography at discharge and 3
months post-operatively
• The follow-up protocol should include blood
pressure measurement and urinalysis.

263. Some important study
• International Reflux Study in Children (IRSC, 1981)
– Medical vs surgical in grade III & IV reflux
– Surgery better in preventing pyelonephritis
– Similar overall rate of UTI
– Equally effective in preventing new scar formation
• Birmingham Reflux study 1987
– Medical vs Surgical in high grade VUR
– Equally effective in preventing new scar formation
– Resolution of VUR occurred in approx. 20% to 50% of patients treated medically
during 5 year FU
– 98% success rate in ureteric re-implantation
• Southwest Pediatric Nephrology Group study
– Efficacy of medical txn in Grade I to III VUR
– Grade related scarring in 15%
– Breakthru infection in 30%
– Resolution in 70%

264. Cochrane review 2011
• Prophylactic antibiotic vs no txn:
– No reduction in symptomatic or febrile UTI
– Reduce risk of new scaring of DMSA
– Increase likelihood of bacterial resistance (3x)
• Prophylactic antibiotic vs surgery (open or
endoscopic)
– No difference in risk of symptomatic UTI
– No difference in new scarring formation
– Decrease number of febrile UTI

265. EAU 2011
• Regardless of the grade of reflux or presence of renal scars, all patients
diagnosed at infancy should be treated initially with CAP
• Immediate, parenteral, antibiotic treatment should be initiated in case of
febrile reakthrough infections.
• A definitive surgical correction is the preferred treatment in patients with
breakthrough infections
• Surgery:
– Surgical correction should be considered in patients with a persistent high-
grade reflux (grades IV-V reflux) after a period of antibiotic therapy
– no evidence for correction of persistent low-grade reflux (grades I-III)
without symptoms
• endoscopic injection may be an option for lower grades of reflux or
those who wish not to continue antibiotics
• meticulous investigation for the presence of LUTS and LUTD should be
performed in all children after toilet training. If LUTD is found, the initial
treatment should always be for LUTD.
• Refer to separate sheet

266. Urinary tract stoneUrinary tract stone

267. What is the imaging of urinary stone?
• Ultrasonography
– 1st
line
– If no stone is found but symptoms persist  NCCT
• Non-contrast helical CT scanning
– The most sensitive test for identifying stones
– It is safe and rapid
– 97% sensitivity and 96% specificity
• IVU:
– Rarely used in children
– Needed to delineate the caliceal anatomy prior to
percutaneous or open surgery

269. What are the treatment options?

270. Duplex systemDuplex system
Ureterocele
Ectopic ureter

271. Child
• Name the 4
abnormalities
seen on this
IVU
• (1 mark each)
A
B
C
Q62
D

272. • A. Right side duplex kidney with functional, non-
dilated upper moiety (1)
• B. Nonfunctional “invisible” left upper moiety
causing the lower functioning moiety to “droop”
(1)
• C. “Scalloped” or laterally displaced lower moiety
ureter suggestive of an adjacent very dilated
upper moiety ureter (1)
• D : Duplex system ectopic left ureterocele
connecting to the NF left upper moiety (1)
• (Note the lower moiety is dilated likely from L
VUR)

273. What is duplex kidney?
• A duplex kidney has an upper pole and a
lower pole, each with its own separate
pelvicalyceal system and ureter
• 2 ureters may join to form a single ureter
– At PUJ (bifid system)
– More distally before entering the bladder
through one ureteric orifice (bifid ureter)
– Pass down individually to the bladder (complete
duplication)

274. Weigert-Meyer rule
• Upper-pole ureter
– always opens onto the bladder medially and inferiorly
to the ureter of the lower pole
– Predisposing to ectopic placement of the ureteric
orifice and obstruction [ureterocele] (due to the
longer intramural course of the ureter through the
bladder wall)
• Lower-pole ureter
– opens onto the bladder laterally and superiorly
– reducing the intramural ureteric length  VUR (85%)

276. What is the embrology of duplex kidney?
• 4 week : Ureteric bud arises from the lower mesonephric duct joins the
metanephros and results in renal development by reciprocal induction
• Renal ascend occurs between 6-10 weeks
• Urine production starts at 10 weeks gestation and by term 90% of the
amniotic fluid is urine
• Renal pelvis, ureter, major and minor calyces, collecting ducts were derived
from ureteric bud
• Early branching or extra ureteric bud also meets metanephros
• Nephrogenesis ceases at 36 weeks and from there on the number of
nephron will remain constant
• Although renal maturation continues postnatally, nephrogenesis is
completed by birth
• Extra ureteric bud is generated and head to metanephros and develop into
second ureter and duplex kidney will form
• The more caudal ureteric bud will me the more crainal metanephros (upper
pole)

277. Duplex kidney
• 1 in 125 , 2%
• F: M = 2:1
• R = L
• Unilateral >> bilateral (25%)
• Presentation:
– UTI
– Loin pain + pyelonephritis
– Incidental

278. Complication of Duplex
• Upper pole: Ureterocele may be associate with
– upper renal-pole hydronephrosis (secondary to
obstruction)
– hypoplasia or dysplasia (renal maldevelopment
related to ectopic displacement of ureteric orifice)
• Ectopic ureter may insert into urethra or vagina
 incontinence
• Lower pole are prone to reflux 
hydronephrosis and hydroureter
• Lower pole also associate with PUJO
• Bifid ureter cause urine passing from one
system to another  stasis and infection

279. Investigation
• USG: duplex, hydronephrosis +/- hydroureter
• DMSA: assess pole function
• IVU:
– decreased contrast excretion from renal upper pole ±
hydronephrosis (which may displace the lower pole
downward and outward, producing a “drooping lily”
appearance)
• MCUG: reflux
• CT and MRI: anatomical detail

280. Ureterocele
• Definition: Cystic dilatation of the lower
end of the ureter where it joins the lower
urinary tract
• F > M (4-7:1)
• 1 in 4000 births
• 80% ectopic (40% bilater), 15% orthotopic,
5% caecoureterocele

281. Pathophysiology
• Incomplete dissolution of the Chwalle’s
membrane ( which transiently divided the
early ureteric bud from the urogenital
sinus
• Abnormal muscular development : without
the appropriate muscular backing, the
distal ureter assume a balloon morphology

282. Classifications
• American Association of Paediatrics
– Intravesical (entirely within bladder) vs
ectopic (some portion permanently situated in
bladder neck or urethra)
• EAU:
– Orthotopic
– Ectopic
– Caecaureterocele (blind ending ureterocele in
urethra below bladder neck, associated with
ectopic ureter

283. What is the classification of
ureterocele?
• Intravesical or orthotopic 20%
– Exclusively in female
– stenotic
– Non-obstructive
• Ectopic 80%
– Sphincteric, found proximal to bladder neck, within
internal sphincter, wide orifice
– Sphincterostenotic, stenotic orifice, found proximal to
the bladder neck
– Ceco-ureterocele – orifice within bladder but extends
into the urethra

284. Presentation
• Hx
– Antenatal USG
– UTI
– AROU
– Haematuria, abd/flank
pain, incontinence,
dysuria, urgency
– Failure to thrive
– Nonspecific GI
symptoms
• PE
– Prolapsed ureterocele
– Abd or flank mass

285. Diagnosis
• Antenatal USG
– Hydronephrosis
– Duplex renal units
– Urethral dilatation ending
at upper pole moiety
– Intravesical cystic
dilatation with dilated
ureter posterior to
bladder
– Increased echogenicity
and renal cysts are
sonographic signs of
renal dysplasia

286. Diagnosis
• IVU
1. Cobra head/spring onion deformity of distal ureter
2. Drooping lily sign
3. Lateral displacement of lower pole tortuous ureter
4. Filling defect in bladder
5. Radiolucent halo
6. Single system intravesical/orthotopic ureterocele:
adequate renal function for excretory phase

287. IVU• Excretory urogram
demonstrates the
classic cobra-head
appearance of a
ureterocele and
radiolucent rim

288. IVU
• Voiding
cystourethrogram
(VCUG) demonstrates a
large, smooth, central
filling defect
peripherally outlined by
contrast material. The
catheter is deviated to
the patient's right. This
finding is consistent
with a large ureterocele

289. IVU
• Bilateral single-system
ureteroceles. The
collecting systems and
their associated
ureteroceles are
opacified on
intravenous
pyelography (IVP).
Multiple stones in the
ureteroceles may be
discerned within the
ureteroceles (white
arrows) as filling
defects

290. IVU
• Reflux into lower pole:
A voiding
cystourethrography
(VCUG) that
demonstrates reflux
into the lower pole
ureter with classic
"drooping lily"
configuration.

291. VCUG
• Mandatory
• Aim
– To assess ispilateral and contralateral reflux
– To assess the extent of intraurethral prolapse
of ureterocele
• In duplex ureterocele, 50% Ipsilateral
reflux,, 25% contralateral reflux

292. MAG3
• Determine segmental renal function, eps
upper pole
• Determination of salvageability
• Selection of operative technique.
• Quantitate the degree of obstruction in
those moieties with preserved function.

293. • Left duplicated kidney
with upper pole
ureterocele. This renal
scan shows the typical
findings of an upper
pole duplicated system
subtended by a
ureterocele. The left
upper pole (black
arrow) shows minimal
uptake when compared
with the left lower pole
or right kidney.

294. Cystoscopy
• Optional
• To differentiate ectopic megaureter from
ureterocele

295. Treatment
• Endoscopic decompression vs partial
nephroureterectomy vs primary
reconstruction
• Depend on:
– Clinical status, age, function of upper pole
moiety, reflux, obstruction of ipsilateral ureter,
pathology of contralateral kidney, pt and
surgeon’s preference

296. Treatment
• EAU GL 2010:
– Early Dx:
• If asymptomatic + non/hypofunctioning upper pole + no
significant obstruction of lower pole + no BOO 
prophylactic Abx
• If severe obstruction or infection  immediate
endoscopic decompression (incision or puncture)
– FU
• If effective decompression without reflux (25% cases)
 conservative
• If ineffective decompression/significant
reflux/ipsi/contralaterla obstruction/BOO  OT

297. Treatment
• Intravesical ureterocele
– Used for single and duplex kidney
– Endoscopic decompression
• A transverse incision at the base of the
ureterocele as distally on the ureterocele and as
close to the bladder as possible.
– Successful in 90%
– 30% reflux

298. Treatment
• Ectopic ureterocele
– Endoscopic decompression ineffective: 50-80%  secondary surgery
– Nonfunctioning upper pole + no VUR to lower pole:
• Upper pole partial nephrectomy + ureterocele decompression +/- later
staged bladder level surgery
• Ureter excised at iliac vessel (common sheath with lower pole ureter, affect
blood supply, risk of contralateral UO damage, affect voiding function) and
left open to facilitate ureterocele decompression (avoid retention of urine in
ureteric stump
– Nonfunctioning upper pole + lower pole high grade VUR
• Traditional procedure
– excision of the ureterocele,
– reconstruction of the detrusor,
– reimplantation of the ipsilateral lower pole ureter and the contralateral
ureter, if required.
– a separate flank incision for upper pole partial nephrectomy.
– Salvageable upper pole
• Excision of ureterocele and common sheath reimplanted
• Tailoring of very dilated ureter
• Renal level ureteroureterostomy or ureteropyelostomy