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Bladder Outlet Obstruction

Presenter : Dr PASHI Moderator : Prof Munkonge


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


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.

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

urination • Lower urinary tract – bladder and urethra • Obstruction may occur anywhere • More


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 6 th week.




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


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




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.


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


16th week of gestation, the bladder is completely muscularized and the urachus is closed

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

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

Bladder Innervation

Autonomic nervous system

Parasympathetic (S2S4)

Sympathetic (T11L2)

Inhibit parasympathetic to allow detrusor relaxation and expansion

Constrict internal sphincter

Somatic nervous system (pudendal nerve(S1S4)

Control external sphincter

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

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.

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

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.

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


Ureteral peristalsis is overcome

increased hydrostatic pressures are transmitted directly to the nephron

Results in impairment of renal development and function

Pathophysiology of BOO

Pathophysiology of BOO

Pathophysiology of BOO

GFR falls as pressure in the proximal tubule and bowman space increase

After 1224 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.

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.

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


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.


Primary causes :

Anatomical ( congenital or acquired)

functional (congenital or acquired)

Anatomical causes




Functional causes




Congenital urinary anomalies




Posterior urethral valves

Vaginal obstruction

Anterior urethral valves

Urogenital sinus

Posterior urethral polyps

Cloacal abnormalities

Urethral diverticulum, atresia, duplication, stricture




Prune belly syndrome


Acquired urogenital anomalies


Bladder neck fibrosis




Urethral strictures




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.


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

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.

Physical Examination

In the African setting, many children present with complications , due to late presentation and lack of prenatal diagnosis

small stature for age,


gross pitting pedal oedema,

ascites, and

abdominal masses

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.


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.


Haemogram to quantify anaemia. The platelet count may also drop.

Serum biochemistry to assess the electrolytes, urea, creatinine, and

acid-base balance


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.



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)


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.


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

and possible filling defects and urinary incontinence. • A filling phase is important to identify ureterocoele



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.


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


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.



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


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

Posterior Urethral Valves (PUV)


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




PUV classification


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


Type III 5%

Circular diaphragm with a central or eccentric narrow aperture in

membranous urethra

PUV classification

PUV classification
PUV classification

Dewan and Ransley’s challenged Youngs classification; the types are secondary to urethral


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

parallel reinforcements; • Distal ballooning with suprapubic pressure; • traversing the urethral sphincter

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 2550%.

Many foetuses are lost antenatally, and 45% of survivors have renal failure

Other associated anomalies = chromosomal abnormalities, and some

deformations related to the oligohydramnios.

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

PUV Diagnosis - Prenatal


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

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)


PUV Diagnosis - Prenatal

PUV Diagnosis - Prenatal

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



Shunt blockage


Preterm labour

Intrauterine death

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

PUV postnatal


Symptoms of BOO

Poor urinary stream

Palpable bladder

Kidneys may be palpable

Urinary ascites

Listlessness, poor feeding, irritability, failure to thrive

PUV Postnatal


May be asymptomatic

Urinary tract infections

Chronically impaired renal function manifest as poor growth

PUV postnatal

Older child

Urinary tact infections

Voiding symptoms

Growth retardation


endoscopic ablation of the valves is the initial treatment

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

PUV Treatment

Minimises risk of electrolyte disturbance and infection

Primary treatment

bladder drainage


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

Vesicostomy and delayed valve ablation


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 618 months, depending on the

initial indication

the child’s level of renal function

valve ablation, by 6 – 18 months, depending on the • initial indication • the child’s

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)

PUV treatment complications

Damage to sphincters

Urethral strictures


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

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.


Coran Pediatric Surgery 7 th Edition

Essential of Pediatric Urology, 2 nd Edition, Edited by David FM Thomas

Clinical Pediatric Nephrology, 2 nd Edition, Edited by Kanwal K Kher


Langmans medical embryology, 12 th Edition