This document discusses bladder outlet obstruction (BOO). It begins by defining BOO and describing that it can be partial or complete. It then discusses the various causes of BOO including congenital and acquired factors. The pathophysiology of BOO is explained, noting how it can lead to renal damage over time if not treated. The document outlines the evaluation and management of BOO, including various imaging modalities and the importance of early surgical treatment to prevent long term renal issues. Posterior urethral valves are highlighted as a common cause of BOO in boys.

1. Bladder Outlet Obstruction
Presenter : Dr PASHI
Moderator : Prof Munkonge

2. Introduction
• BOO describes blockage of urine outflow from the bladder and
through the urethra
• Obstruction may be partial or complete
• Childhood Urethral obstruction are mostly congenital
• Only posterior urethral valves commonly give rise to secondary
changes in the upper renal tracts
• Compared with the adult kidney, the developing kidney is highly
susceptible to injury from obstruction to urine flow
• The earlier the obstruction develops the worse the impact on the
upper tracts

3. Incidence
• Various causes of BOO and vary in incidence
• In Africa, reports on the incidence are scanty, probably
• Voiding dysfunction describe abnormalities in either the filling and/or
emptying of the bladder
• Constitutes 40% of paediatric urology clinic visits.

4. The Urinary system
• The urinary tract includes two kidneys, two
ureters, a bladder, and a urethra.
• Urine flows from the kidneys through the
ureters to the bladder which stores urine until
releasing it through the urethra by urination
• Lower urinary tract – bladder and urethra
• Obstruction may occur anywhere
• More common in males

5. Embryology
• Lower urinary tract development is closely interrelated with genital
tract and the hindgut.
• 3rd week of gestation, the cloaca meets the ectoderm of body wall at
cloacal membrane
• 5th week, cloaca divided by urorectal septum to form the primitive
rectum posteriorly and urogenital sinus anteriorly
• Allantois, bladder, pelvic, and phallic portions of the urogenital system
are recognisable in the 6th week.

6. Embryology

7. Embryology
• 7th week gestation, the mesonephric ducts (vas deferens) shift
further caudal in the sinus and come to lie close to each other
• Metanephric buds (ureters) arise from mesonephric ducts
• root of the mesonephric duct exstrophies into the posterior wall of
the developing bladder
• This process brings the openings of the ureteric buds into the bladder
wall
• mesonephric duct is carried inferiorly to the level of the pelvic urethra
• The triangular region of exstrophied mesonephric duct incorporated
into the posterior bladder wall forms the trigone of the bladder

8. Embryology

9. Embryology
• 9th week of gestation, the bladder cavity expands, urachus elongates
and continues with the allantoic stalk at the umbilicus.
• 12th week gestation, extra embryonic allantois degenerates, urachus
closes forming the median umbilical ligament.
• BOO manifest in some foetuses with closure of urachus, but delayed
closure may protect others.

10. Embryology
• The early bladder epithelium initially consists of a single cell layer, but
later become transitional
• Bladder epithelium or Chwalla’s membrane temporarily covers and
occludes the ureteral orifice
• Bladder muscle arises from mesenchyme as a longitudinal layer on
the dorsal surface and spreads cephalad to the intrarenal collecting
system
• 16th week of gestation, the bladder is completely muscularized and
the urachus is closed

11. Developmental Anomalies
• Bladder Agenesis : rare, is due to failure of allantoic stalk to develop
• Urachal anomalies (e.g., patent urachus) result from delayed closure
of the urachus, that arise from lower urinary tract obstruction at less
than 12 weeks gestation
• Some anomalies result from a general mesodermal failure (the
urachal diverticulum of the Prune belly syndrome).
• Intravesical (simple) ureterocoeles are thought to be due to the
persistence of Chwalla’s membrane beyond the time when urine flow
begins

12. • Bladder outlet obstruction caused by the urethral obstruction of
posterior urethral valves or urethral hypoplasia may be detected from
4 weeks gestation concurrent with the absorption of the mesonephric
duct and the resorption of the urogenital membrane.
• Abnormal dilatation of Cowper’s glands may give rise to an
obstructive urethral syringocele

13. Bladder Innervation
• Autonomic nervous system
Parasympathetic (S2–S4)
Sympathetic (T11–L2)
• Inhibit parasympathetic to allow detrusor relaxation and expansion
• Constrict internal sphincter
• Somatic nervous system (pudendal nerve(S1–S4)
• Control external sphincter

14. Physiology of voiding
• Normal voiding cycle is a two-phased process, consisting of
• low-pressure and adequate volume bladder filling
• complete evacuation of the bladder.
• Bladder filling is passive determined by
• Vesicoelastic properties of the bladder wall
• Inhibition of bladder contraction
• Increased urinary sphincter
• Urinary continence
• maintained by contraction of sphincter complex which keeps
urethral pressure above normal bladder pressure

15. Physiology of voiding
• Normal voiding is a spinal reflex modulated by the CNS (brain, pontine
micturition centre, and spinal cord), which coordinates the functions
of the bladder and urinary sphincter
• As the bladder fills, the pudendal nerve becomes excited, resulting in
contraction of the external urethral sphincter
• As the bladder approaches fullness, tension receptors in the bladder
wall trigger afferent nerves that send signals of the need to void.
• Voluntary voiding involves inhibition of sphincter contractions and
coordinated contraction of the bladder smooth muscle.

16. Physiology of voiding
• Bladder filling in neonates is followed by reflexive emptying
• This micturition cycle occurs hourly under sacral spinal cord control
• After 6 months of age, the urinary volumes increase, the frequency of
voiding decreases as the control of voiding shifts from the sacral cord
to the pontine voiding center
• Brain maturation and development, leads to bladder and urinary
sphincter control to inhibit involuntary voiding
• At 2 years the child develops conscious sensation of bladder fullness
and has urge incontinence

17. Physiology of voiding
• Between 2 and 4 years of age acquires voluntary control of bowel and
bladder function according to the following sequence:
• 1. nocturnal bowel control
• 2. daytime bowel control
• 3. daytime bladder control
• 4. nocturnal bladder control.
• By 4 years of age, most children demonstrate adult voiding pattern.
• The timing of this sequence is influenced by ethnic, cultural,
economic, and individual family differences.

18. Pathophysiology of BOO
• BOO results in an elevation of intravesical storage pressure
• Detrusor muscles generate excessive force against outlet resistance
• Massive hypertrophy of the detrusor muscles results
• Formation of sacculation, trabeculation, and ultimately diverticula
• The antireflux mechanism of the ureterovesical junction becomes
incompetent
• Ureteral peristalsis is overcome
• increased hydrostatic pressures are transmitted directly to the nephron
• Results in impairment of renal development and function

19. Pathophysiology of BOO

20. Pathophysiology of BOO
• GFR falls as pressure in the proximal tubule and bowman space increase
• After 12–24 hours of complete obstruction, intratubular pressure
decreases to preobstruction levels
• If not relieved, a depressed GFR is maintained by decreases in renal blood
flow mediated by thromboxane A2 and angiotensin II
• With continued obstruction, there is a progressive fall in renal blood flow,
ischaemia, and nephron damage.
• GFR falls, but tubular function is particularly severely affected, with a high
water and sodium loss resulting in the high output renal failure of
obstructive nephropathy.

21. Pathophysiology of BOO
• In the foetus, the placenta functions as the primary excretory organ in
place of the kidney throughout gestation.
• Hence, in the new-born with BOO, the renal function is usually similar
to the normal maternal levels initially because of the placental
function.
• The kidneys commence gradual glomerular filtration by the 11th to
12th weeks of gestation.
• About 90% of amniotic fluid is produced in the kidneys, and only 10%
comes from the GIT, lungs, and skin.

22. Pathophysiology of BOO
• Inadequate foetal urine production leads to oligohydramnios
• lung movement is therefore restricted
• Poor acinar growth and decreased surfactant production due to
decreased fluid in the bronchial tree
• The newborn may have compressed limbs, Potter’s facies, and
pulmonary hypoplasia presenting with respiratory distress and
pneumothorax

23. Pathophysiology of BOO
• The pathophysiology of this process is complex and incompletely
understood.
• Long-term bladder dysfunction may plague these patients in their
daily lives despite relieving the obstruction.
• Obstruction impacts renal concentrating ability, glomerular filtration
rate, and renal morphology.

24. Classification
• Primary causes :
• Anatomical ( congenital or acquired)
• functional (congenital or acquired)
• Anatomical causes
• Intraluminal
• Intramural
• extrinsic.
• Functional causes
• Neurogenic
• Nonneurogenic

25. Aetiolgy
Congenital urinary anomalies
Male Female
Posterior urethral valves Vaginal obstruction
Anterior urethral valves Urogenital sinus
Posterior urethral polyps Cloacal abnormalities
Urethral diverticulum, atresia, duplication, stricture
Ureterocele
Prune belly syndrome
Acquired urogenital anomalies
Bladder neck fibrosis
Trauma
Urethral strictures
Tumors

26. Clinical Presentation
• History Elicit prenatal health, birth and development, perinatal
complication, and bowel and bladder habits.
• Many are asymptomatic for a long time or present with constitutional
features that often are misleading to an unsuspecting practitioner
• Acute or chronic urinary retention, overflow incontinence, UTI, or
renal failure.

27. Neonate
• Presentation is characterised by
• abdominal distention
• palpable suprapubic or flank masses (bladder and the kidneys);
• And/or urachal cyst, fistula, or abscess.
• Neonatal sepsis and respiratory distress may also be present.
• Parents may give a history of urine dribble, poor stream, and failure
to thrive in the young infant

28. Infants and children
• Enuresis, weight loss, vomiting, and diarrhoea.
• Constipation may be present in cases of dysfunctional voiding, faecal
impaction, Hirschsprung’s disease, or compression from pelvic
masses.
• Other features include urine dribbling, incontinence, straining,
frequency, and intermittency or “staccato” stream.

29. Physical Examination
• In the African setting, many children present with complications , due
to late presentation and lack of prenatal diagnosis
• small stature for age,
• anaemia,
• gross pitting pedal oedema,
• ascites, and
• abdominal masses

30. Physical examination
• Other features depend on primary or secondary causes.
• SPINE examine for defects, and the lower extremities for reflexes,
muscle mass and strength, sensation, and gait.
• PERINEUM check for gluteal fold symmetry, natal cleft depth, absent
coccyx, perineal sensation, tone and reflexes.
• Digital Rectal Examination check anal sphincteric tone, faecal
impaction, distended rectum, and presacral and pelvic masses.

31. Investigations
• Depend on availability and condition
• A variety of tests may be required to confirm the diagnosis and
determine the extent of damage
• Imaging may be sufficient to define:
• site and extent of an obstructing pathology;
• extent of urinary tract reaction to the BOO
• split and total renal function and scarring;
• presence and degree of reflux; and
• associated anomalies, where present.

32. Investigations
• Haemogram to quantify anaemia. The platelet count may also drop.
• Serum biochemistry to assess the electrolytes, urea, creatinine, and
acid-base balance

33. Investigations
• Plain radiography
• can identify radio-opaque stones.
• May suggest an enlarged or poorly emptying bladder,
• displacement of the bowel shadow from the hypochondrium by a
large fluid-filled kidney, and/or outline associated vertebral and
other bony anomalies.

34. Investigations
• Ultrasonography
• Demonstrate filling, dilated, or narrow posterior urethra or the
presence of intraluminal lesions.
• Size and shape of the kidneys
• bladder as well as dilated pelvicaliceal system and ureter.
• US should be performed with a moderately filled urinary bladder,
and if an anomaly is found, US should be repeated with the
bladder empty.
• It can be used to estimate the post void residual volume of urine,
and a spinal ultrasound in children younger than 3 months of age
is useful for spinal lesions (tethering, defects, or masses)

35. Investigations
• CT scan/MRI
• Done with or without contrast enhancement
• Provide precise anatomical details of the lesion
• Extent of damage
• Good-quality ultrasound with Doppler is a good substitute.

36. Investigations
• Micturating cystourethrography
• Essential for demonstration of bladder shape and capacity,
including diverticulum and vesicoureteric reflux and grading,
posterior urethral dilatation, and possible filling defects and
urinary incontinence.
• A filling phase is important to identify ureterocoele

37. Investigations
• Scintigraphy
• Dimercaptosuccinic acid (DMSA) scintigraphy is a radionuclide
technique that provides a functional cortical map of the kidney,
quantifying renal tubular cell mass.
• Useful for identifying scars of reflux nephropathy and estimating
differential function, provided there is no obstruction.
• Diethylenetriamine penta-acetic acid (DTPA) scintigram, the DTPA is
filtered by the glomerulus and gives a dynamic study similar to an IVU.
• It identifies dilatation and obstruction, and in the latter stages of the
study it can give information concerning reflux.
• Differential renal function can also be quantified.

38. Investigations
• Intravenous urogram
• An IVU study shows morphology of the urinary tract, provided the
kidney is working well enough.
• Is disappointing and sometimes dangerous in infants
• In the neonate, due to the low GFR, the urinary tract does not
opacify well.
• The x-ray exposure for IVU is relatively high, and US scans are
performed where possible

39. Investigations
• Urodynamic studies
• Urodynamic studies of the physiologic function of the bladder
mechanics during filling and voiding
• used to ascertain the aetiology and epidemiology of
nonneurogenic bladder sphincter dysfunction (NNBSD) with the
aid of x-ray screening
• Egs of such studies include uroflowmetry and cystometrogram.

40. Investigations
• Cystourethroscopy
• Approach of choice for identification and treatment of structural
abnormalities.
• Posterior urethral valves, ureterocoeles may be treated, and
Polyps May Be biopsied or resected.
• In the African setting, however, appropriate scopes may not be
readily available or accessible for either adults or paediatric
surgical services

41. Management
• BOO is a potentially curable form of lower urinary tract and renal
disease
• Determinants of bladder dysfunction - Degree and duration of
obstruction
• Early recognition and treatment are key to preventrenal function loss
• Definitive treatment of mechanical causes of BOO is mostly surgical

42. Posterior Urethral Valves (PUV)
• History
• First reported by Langenbeck in 1802 (Dewan et al, 1999)
• Hugh Humpton Young developed Classification (Young et al, 1919)
• Most common anatomic cause of BOO in pediatric population in
boys
• PUVs are not valves, have no function, are not part of normal
development

43. PUV

44. PUV classification
• Classification(Young)
• Type I – 95%
2 folds extend anteroinferiorly from caudal aspect of
verumontanum often fusing anteriorly at a lower level
• Type II - now discounted as non-obstructive folds of superficial
muscle and mucosa, between the verumontanum and the bladder
neck
• Type III – 5%
Circular diaphragm with a central or eccentric narrow aperture in
membranous urethra

45. PUV classification

46. • Dewan and Ransley’s challenged Youngs
classification; the types are secondary to urethral
instrumentation
• Characteristics of the urethral valve vary but include:
• attachment posteriorly to the distal part of the
verumontanum;
• a small hole adjacent to the verumontanum
• an oblique membrane with the distal attachment
lying anteriorly
• paramedian parallel reinforcements;
• Distal ballooning with suprapubic pressure;
• traversing the urethral sphincter

47. PUV Incidence
• Incidence is between 1 in 5000 - 8000 male births
• Few familial cases recorded, including in siblings, but no established
genetic predisposition
• Represent 10% of urological anomalies detected by prenatal U/S in Europe
• Accounts for less than 1% of antenatally diagnosed hydronephrosis
• Overall mortality is 25–50%.
• Many foetuses are lost antenatally, and 45% of survivors have renal failure
• Other associated anomalies = chromosomal abnormalities, and some
deformations related to the oligohydramnios.

48. PUV symptoms
• Severe obstruction leads to intrauterine renal failure and fetal death
in utero or soon after birth from potters syndrome.
• Less severe obstruction allows the fetus to survive, but if not detected
early leads to
• Septic complications from UTI and
• metabolic abnormalities caused by renal failure

49. PUV Diagnosis - Prenatal
Fetus
• Prenatal U/S detects 80% of cases, 50% between 16-20 weeks
• Obstruction develop at 7 wks GA and are detectable by U/S by 14 wks

50. PUV Diagnosis – Prenatal U/S features
• Bilateral upper tract dilatation
• Persistently distended full bladder
Predictors of poor functional outcome an early-onset renal failure
• Detection before 24 weeks’ gestation
• Bladder wall thickening
• Echo-bright kidneys (renal dysplasia)
• Oligohydramnios

51. PUV Diagnosis - Prenatal

52. PUV Treatment
• Fetus treatment
• Vesicoamniotic shunting
• Intrauterine valve ablation
• Fetal intervention still controversial because diagnosis is difficult and
benefits are difficult to ascertain
• Fetal intervention carries high risk of mortality 43%
• Early diagnosis ensures early treatment and minimises risk of
infection

53. .
Complications
• Shunt blockage
• Migration
• Preterm labour
• Intrauterine death

54. PUV postnatal
• Neonate
• Symptoms of BOO
• Poor urinary stream
• Palpable bladder
• Kidneys may be palpable
• Urinary ascites
• Listlessness, poor feeding, irritability, failure to thrive

55. PUV Postnatal
• Infant
• May be asymptomatic
• Urinary tract infections
• Chronically impaired renal function manifest as poor growth

56. PUV postnatal
• Older child
• Urinary tact infections
• Voiding symptoms
• Growth retardation
• Treatment
• endoscopic ablation of the valves is the initial treatment

57. PUV postnatal diagnosis
• U/S – dilation of prostatic urethra and thickening of bladder wall amd
also hydronephrosis
• VCUG – dilated prostatic urethra, valve leaflets, detrusor hypertrophy,
bladder diverticula, bladder neck hypertrophy, narrow penile urethra
stream and probably incomplete emptying
• Renal scan – assess kidney function

58. PUV Treatment
• Minimises risk of electrolyte disturbance and infection
• Primary treatment
• bladder drainage
• Antibiotics
• Correction of metabolic disturbances
• Urethral or suprapubic drainage
• Transurethral valve ablation definitive RX – incision at 4 and 8 o’ clock
• Post op catheterisation only when significant intra op bleeding but
may be left for 1 or 2 days

59. • Vesicostomy and delayed valve ablation
• Indication
• markedly impaired renal function, especially
• deteriorating despite catheterisation,
• gross bilateral vesicoureteric reflux.
• Stoma created at the apex of the bladder to
minimise risk of prolapse
• Closure done after valve ablation, by 6–18
months, depending on the
• initial indication
• the child’s level of renal function

60. PUV treatment
• Urinary leaks due to high intravesical pressure
• Urinary ascites and perinephric collections or ‘urinomas’ usually
respond to a short period of bladder drainage.
• Large or persistent perirenal collections may require ultrasound-
guided percutaneous aspiration or open drainage (in combination
with open nephrostomy)

61. PUV treatment complications
• Damage to sphincters
• Urethral strictures
• haemorrhage

62. Patent Urachus
• Associated with drainage of urine from the umbilicus.
• Suspect Clear drainage from the umbilicus
• Investigate the urinary tract for bladder outlet obstruction in which the
urachus is functioning as a relief valve
• A patent urachus may be approached either through the umbilicus or
through an infraumbilical incision.
• It is important to identify all the umbilical structures for a definitive
diagnosis.
• The patent urachus is ligated and transected at the level of the bladder;
broad-based connections are closed in two layers with absorbable sutures

63. Urethral Polyps
• Urethral polyps are fibromuscular epithelial structures with
transitional epithelium covering the surface.
• They may occur either in the posterior or anterior urethra.
• In either position, they may cause hematuria, urgency, or obstructive
symptoms.
• Bladder ultrasound may show the polyps in the posterior urethra but
VCUG and cystoscopy are diagnostic and excision through the
cystoscope is usually curative.
• Polyps can present as congenital obstructing lesions with all of the
characteristics of bladder outlet obstruction.

64. References
• Coran Pediatric Surgery 7th Edition
• Essential of Pediatric Urology, 2nd Edition, Edited by David FM Thomas
• Clinical Pediatric Nephrology, 2nd Edition, Edited by Kanwal K Kher
MD
• Langmans medical embryology, 12th Edition