GC213 Why Do You Wet Your Bed All The Time Paediatric Urology
Pediatric nocturnal enuresis is the involuntary passage of urine during sleep in children beyond the age of expected bladder control, often due to maturational delay in bladder capacity, arousal mechanisms, or nocturnal vasopressin secretion.
Why Do You Wet Your Bed All the Time? — Paediatric Urology
Lecture Map
This lecture is a rapid-fire tour of paediatric urology — a discipline that spans the kidney, ureter, bladder, urethra, and external genitalia in children. The anchor clinical scenario is a child who wets the bed, but the deck goes far beyond enuresis to cover the full scope of conditions a medical student must recognize: antenatal hydronephrosis, vesico-ureteric reflux (VUR), posterior urethral valves (PUV), UTI workup for underlying anomalies, prepuce/phimosis/circumcision, and buried penis. [1]
- Classify paediatric urinary incontinence and distinguish Primary Monosymptomatic Nocturnal Enuresis (PMNE) from Non-Monosymptomatic Enuresis (NMNE).
- Take a structured history and perform a focused physical examination for a child with wetting.
- Manage PMNE with behavioural measures, enuresis alarm, and desmopressin.
- Recognize causes of non-monosymptomatic and continuous incontinence (neurogenic bladder, ectopic ureter, PUV, detrusor overactivity).
- Approach UTI in children — identify those at risk for underlying urological anomalies and order appropriate investigations.
- Understand VUR: pathophysiology, grading, and treatment principles.
- Understand antenatal hydronephrosis and its differential diagnosis.
- Recognize PUV as the most common cause of obstructive uropathy leading to renal failure in newborn boys.
- Differentiate physiological non-retractile foreskin from true phimosis (BXO); know indications and contraindications for circumcision.
- Know about buried penis and alternatives to circumcision.
The scope of paediatric urology covers: Kidney (PUJO, duplication anomalies, cystic kidney diseases), Ureter (VUJO, VUR), Bladder (neurogenic bladder, other voiding dysfunction, PUV), Scrotum (undescended testis, testicular torsion/acute scrotum, varicocele), Penis/Prepuce (hypospadias, chordee, buried penis), Disorder of Sex Development, Enuresis/voiding disorders, and others (stones, trauma, oncological conditions, exstrophy). [1]
This is the most commonly tested "list" question — examiners love asking "Name common paediatric urological conditions."
Presenting Complaints in Paediatric Urology
Five main presenting complaints: (1) Wetting, (2) UTI, (3) Antenatal hydronephrosis, (4) Penile/prepuce conditions, (5) Perineal conditions. [1]
Why this matters: These five complaints form the clinical entry points. The lecture is structured around them. Most children are seen either because antenatal ultrasound detected something, they had a UTI, or they're wetting.
High-Yield Definitions from Lecture
From first principles: By age 5, most children have achieved daytime and nighttime urinary continence. Before age 5, wetting is considered physiological. The cutoff of 6 months for "dry" distinguishes primary from secondary — the logic is that if a child has been consistently dry for 6 months, their bladder control circuits were mature, so something has gone wrong (stress, UTI, diabetes, constipation) to cause secondary enuresis.
ICCS Terminology Reference (From Lecture Appendix)
The lecture appends a detailed ICCS (International Children's Continence Society) terminology table. Key terms for exam purposes: [1]
| Category | Term | Definition |
|---|---|---|
| Storage | Increased frequency | > 8 voids/day |
| Decreased frequency | < 3 voids/day | |
| Urinary incontinence | Involuntary leakage of urine | |
| Continuous incontinence | Constant urine leak day and night | |
| Intermittent incontinence | Leakage in discrete amounts | |
| Daytime incontinence | Intermittent incontinence while awake | |
| Enuresis | Intermittent incontinence exclusively during sleeping | |
| Urgency | Sudden compelling need to void | |
| Nocturia | Child wakes at night to void | |
| Voiding | Hesitancy | Difficulty initiating voiding |
| Straining | Needs Valsalva to initiate/maintain voiding | |
| Weak stream | Observed weak flow | |
| Intermittency | Stop-start micturition | |
| Dysuria | Burning/discomfort during micturition | |
| Other | Holding maneuvers | Strategies to postpone voiding or suppress urgency |
| Post-micturition dribble | Involuntary leakage immediately after voiding | |
| Spraying/splitting of stream | Urine passes as spray rather than single stream |
Three critical questions to answer: [1]
- How old is the patient? Greater or less than 5 years
- Continuous vs intermittent urinary incontinence
- Wet only at night vs other daytime symptoms (urgency, daytime incontinence, BBD i.e. constipation/bowel incontinence)
Why these three questions?
- Age < 5 → likely physiological immaturity; no further workup needed in most cases.
- Continuous incontinence → structural anomaly (ectopic ureter draining below sphincter, epispadias, exstrophy) → refer specialist immediately.
- Night-only without daytime symptoms = monosymptomatic enuresis (usually benign, self-limiting). Daytime symptoms = non-monosymptomatic → suggests bladder dysfunction, neurogenic cause, or other pathology → needs investigation.
The aim is to differentiate Primary Monosymptomatic Enuresis (PMNE) vs Non-Monosymptomatic Enuresis (NMNE). [1]
Classification Flowchart (From Lecture Slide)
Paediatric Urinary Incontinence ≥ 5 years old: [1]
Continuous → Refer Specialist
Intermittent → splits into:
- Daytime urinary incontinence
- Enuresis (night only) → Monosymptomatic NE vs Non-Monosymptomatic NE
- Monosymptomatic → Primary vs Secondary
- Primary Monosymptomatic Nocturnal Enuresis (PMNE) = the most common and most benign category
Key Distinction
A very common exam trap: students confuse "enuresis" with "urinary incontinence." Remember: enuresis = night time ONLY. If the child also wets during the day, it is NOT monosymptomatic enuresis. [1]
4. History and Physical Examination
Specific questions to ask: [1]
- Holding maneuvers (squatting, leg crossing — suggests the child is trying to suppress detrusor contractions)
- Symptoms of urgency/frequency
- Constipation or bowel incontinence (BBD — bladder-bowel dysfunction — is extremely common and must be treated first)
- Behavioural problems, e.g. ADHD, neurological problems
Additional history points from senior notes [2]:
- Number of wet episodes per night and per week, timing
- Any previous dry period (primary vs secondary)
- Fluid intake habits, especially before bed
- Family history (50% have positive family history — genetics plays a role)
- Sleep quality (OSA association)
- Triggers for secondary enuresis: stress (parental divorce, birth of sibling), stool retention, infrequent daytime voiding
Physical examination: [1]
- Abdomen: palpable bladder, impacted stool
- Perineum: labial adhesion, ectopic ureteric opening, ureterocele
- Back: ? Spina bifida occulta (look for sacral dimple, hairy patch, lipoma)
- Lower limbs: limb weakness, increased jerk (signs of upper motor neuron lesion → neurogenic bladder)
Why examine the back? The spinal cord controls the micturition reflex via the sacral micturition centre (S2-S4). Spina bifida occulta can disrupt these nerves silently. A hairy tuft, sacral dimple, or skin discolouration over the lower spine should raise suspicion.
Why check perianal sensation and lower limb reflexes? If the child has a neurogenic bladder from a spinal cord lesion, you'd expect altered perianal sensation, absent anal wink, and potentially upper motor neuron signs in the legs.
5. Tools of Evaluation
Bladder diary: [1]
- Enuresis chart: minimum of 7 continuous nights of recording
- Frequency/volume chart: minimum of 48 hours of recording of volume voided and volume intake
Bowel diary: 7-day diary using Bristol Stool Scale [1]
Why diaries? They objectively quantify the problem, identify patterns (e.g., massive fluid intake before bed, infrequent daytime voiding, constipation), and are essential to distinguish PMNE from NMNE.
Other urodynamic tools: [1]
- Uroflow and residual urine (non-invasive; measures flow pattern and post-void residual — a staccato pattern suggests dysfunctional voiding)
- Ultrasound of urinary system (non-invasive; checks for structural anomalies, hydronephrosis, bladder wall thickening)
- Invasive urodynamics (bladder catheterization — suprapubic or transurethral — plus rectal catheter to measure abdominal pressure; used for neurogenic bladder or refractory cases)
6. Primary Monosymptomatic Nocturnal Enuresis (PMNE)
PMNE — The Most Important Condition in This Lecture
Key facts: [1]
- ONLY wet at night, NO other symptoms
- Most common type — accounts for ~80% of all enuretic children
- Epidemiology: 15–20% of 5-year-olds (UK), 3.5% of 4–12-year-olds (HK), male > female
- Natural course: resolution with age for most children, but some wet till adults
- Associations: ADHD, OSA
- Most of them DO NOT need investigations
PMNE is a multifactorial condition. Three main mechanisms contribute:
- Nocturnal polyuria — Failure to produce adequate ADH (vasopressin) at night → excessive urine production exceeds bladder capacity during sleep. This is why desmopressin works.
- Small functional bladder capacity — The bladder cannot hold the normal volume of urine produced overnight. This is why the alarm works (conditions the child to wake before the bladder is full).
- Failure to arouse from sleep — Maturational delay in the cortical mechanism that should wake the child when the bladder is full. [2]
Genetics: ~50% have a positive family history. If one parent had enuresis, the child has a 44% risk; if both parents had it, the risk is 77%. [2]
When a previously dry child starts wetting again, consider: [2]
- Lifestyle factors (increased fluid before bed)
- Stress/psychosocial (new sibling, parental divorce, school bullying)
- UTI
- Diabetes mellitus / Diabetes insipidus (polyuria)
- Constipation / BBD
- Obstructive uropathy
7. Management of PMNE
Behavioural modification: [1]
- Fluid restriction 2 hours before bed
- Increase daytime fluid intake (to ensure adequate hydration but shift intake away from evening)
- Timed voiding (regular toilet schedule during the day)
- Void before bed
- Treat constipation if present
- Bedwetting diary (records enuresis pattern)
- Star chart (reward system — positive reinforcement for dry nights)
Why behavioural first? These are non-pharmacological, zero-risk interventions. Many children improve with simple measures alone. Treating constipation is crucial because a loaded rectum compresses the bladder, reducing functional capacity.
Enuresis alarm: makes sound/vibrate/light when the sensor is wet. [1] From 'void in bed' to 'wake up to void' — a behavioural therapy. Kids would wake up to void BEFORE they pee in bed. [1]
What the alarm diagram shows: underwear moisture sensor linked to a bedside/wireless unit that sounds when wet — conditioning from “void in bed” to “wake to void,” not a drug. [1]
Mechanism: Classical conditioning. Over weeks, the child learns to associate bladder fullness with waking up, eventually waking before the alarm triggers. This is most effective in children with small functional bladder capacity. [1]
Desmopressin (DDAVP): [1]
- Anti-diuretic hormone analogue
- Reduces night-time urine production
- Most efficient in children with nocturnal polyuria
- Tablet or fast-melting form
- Restrict night-time fluid intake (essential — risk of hyponatraemia if excess fluid with DDAVP)
- Trial of at least 2–6 weeks
- Good response → continue up to 3 months
Safety Warning
Always restrict fluid intake when using DDAVP. DDAVP reduces renal water excretion. If the child drinks excess fluid on top of DDAVP, they can develop water intoxication / hyponatraemia — potentially causing seizures. This is the most important counselling point. [1]
DDAVP response: [1]
- 30–70% patients achieve dry nights
- 50% report relapse after stopping
- Gradual withdrawal reduces relapse
- Large bladder capacity > 70% estimated → increased efficacy
Alarm response: [1]
- 2/3 achieve no NE for 14 consecutive days
- 50% have no recurrence
- Small bladder capacity → increased efficacy
| Feature | DDAVP | Alarm |
|---|---|---|
| Mechanism | Reduces urine production | Conditions waking response |
| Best for | Nocturnal polyuria, large bladder capacity | Small functional bladder capacity |
| Success rate | 30–70% dry nights | 66% dry for 14 days |
| Relapse rate | ~50% (reduced by gradual withdrawal) | ~50% remain dry long-term |
| Onset of effect | Rapid (days) | Slow (weeks to months) |
If the above is not successful → review the diagnosis (i.e., reconsider whether this is truly PMNE or whether there's an underlying cause being missed). [1]
A lot of different causes — Neurogenic vs Non-neurogenic: [1]
- Continuous urinary incontinence → anatomical anomalies (ectopic ureter, epispadias)
- Neurogenic cause → neurogenic bladder (spina bifida, transverse myelitis)
- Other non-neurogenic causes: detrusor overactivity, stress incontinence, giggle incontinence, post-void dribbling, dysfunctional voiding [1]
Differentiating Key Causes
| Cause | Key Features | Mechanism |
|---|---|---|
| Ectopic ureter | Continuous wetting between normal voids; often in duplex system | Upper moiety ureter inserts below sphincter (in girls) |
| Posterior urethral valve | Boys only; weak stream, UTI, bilateral hydronephrosis | Obstructive valves in posterior urethra |
| Exstrophy | Obvious at birth — bladder exposed on anterior abdominal wall | Failure of abdominal wall closure |
| Neurogenic bladder | Back signs (spina bifida), lower limb weakness, bowel incontinence | Disrupted sacral micturition centre |
| Detrusor overactivity | Urgency, frequency, urge incontinence | Involuntary detrusor contractions during filling |
| Dysfunctional voiding | Staccato flow, incomplete emptying, recurrent UTI | Habitual contraction of external sphincter during voiding |
| Giggle incontinence | Incontinence triggered by laughter only | Likely brainstem-mediated detrusor contraction |
Causes: [1]
- Congenital: neural tube defects (spina bifida, myelomeningocele, anorectal malformations)
- Acquired: trauma, tumour, anoxic brain injury, extensive pelvic surgery
Initial diagnosis: establish diagnosis and type of problem on urodynamic studies Treatment: depends on symptoms and findings on urodynamic study [1]
Why urodynamics matter in neurogenic bladder: The bladder can be:
- Overactive (high-pressure) — risk of upper tract damage if not treated (high intravesical pressure transmits to kidneys → reflux nephropathy → renal failure)
- Underactive (low-pressure, large capacity, poor emptying) — risk of UTI, overflow incontinence
Treatment may include:
- Clean intermittent catheterization (CIC) — the mainstay
- Anticholinergics (e.g., oxybutynin) — to reduce detrusor overactivity
- Botulinum toxin injection to detrusor
- Augmentation cystoplasty — in refractory cases
- Monitoring upper tracts with regular ultrasound and renal function tests
Complications of Neurogenic Bladder (Exam-Relevant — See 2023 SAQ Q8)
- Recurrent UTIs (urinary stasis, incomplete emptying)
- Upper urinary tract damage / Hydronephrosis (high-pressure bladder → VUR → reflux nephropathy)
- Renal failure (end-stage from chronic damage)
- Urinary stones (urinary stasis, recurrent infection → struvite stones)
- Bladder cancer (long-term catheterization, chronic inflammation → squamous cell carcinoma)
Conditions causing urinary stasis that predispose to UTI: [1]
- VUR
- Urinary obstruction: PUJO, VUJO
- Bladder dynamic problem: neurogenic bladder
- Others: stones
Workup After Paediatric UTI
Workup: [1]
- Urinalysis and urine culture
- Aim: identify those at risk of having underlying urological anomalies
Subsequent workups: [1]
- USG urinary system (non-invasive first-line imaging)
- MCUG (micturating cystourethrogram — gold standard for VUR and PUV)
- DMSA (dimercaptosuccinic acid scan — detects renal scarring/differential function)
- Radionuclide scans (e.g., MAG3 for drainage/obstruction assessment)
When to investigate after UTI? Guidelines generally recommend:
- All children < 6 months with first UTI → USG + consider MCUG
- Children > 6 months with atypical/recurrent UTI → USG; MCUG if recurrent or abnormal USG
- DMSA at 4–6 months after acute UTI to assess for renal scarring
11. Vesico-Ureteric Reflux (VUR)
VUR: abnormal retrograde urine flow from bladder to upper urinary tract [1]
- Primary vs Secondary
- 1% prevalence
- Reflux nephropathy (repeated reflux of infected urine → renal scarring → chronic kidney disease)
Treatment: [1]
- Conservative
- Antibiotic prophylaxis
- Surgery: endoscopic (Deflux injection) or operative ureteric reimplantation
The normal vesico-ureteric junction (VUJ) has an oblique intramural tunnel through the bladder wall. When the bladder fills and pressure rises, the tunnel compresses the ureter shut (like a valve), preventing reflux. In primary VUR, the intramural tunnel is too short (congenital), so the valve mechanism fails.
| Grade | Description |
|---|---|
| I | Reflux into ureter only |
| II | Reflux into renal pelvis, no dilatation |
| III | Mild dilatation of ureter and pelvis |
| IV | Moderate dilatation, blunting of fornices |
| V | Severe dilatation, tortuous ureter, papillary impressions lost |
What the VUR grade panel shows: five MCUG-style drawings I→V with progressive ureteral/calyceal filling and dilatation (V = tortuous megaureter + clubbed calyces), plus a contrast MCUG of bladder filling the upper tracts — grade drives expectant vs endoscopic/open repair. [1]
Low-grade (I–III) → often resolves spontaneously with growth (the intramural tunnel lengthens). Antibiotic prophylaxis to prevent UTI while waiting.
High-grade (IV–V) or breakthrough UTIs despite prophylaxis → surgical intervention.
Surgery: [1]
- Endoscopic 'Deflux' injection (bulking agent injected under the ureteric orifice to create a valve mechanism — minimally invasive)
- Ureteric reimplantation (open/MIS) (the ureter is reimplanted with a longer submucosal tunnel)
Common causes of antenatal hydronephrosis: [1]
- Transient hydronephrosis (most common — resolves spontaneously)
- PUJO (pelvi-ureteric junction obstruction)
- VUJO / megaureter
- PUV (posterior urethral valve)
- VUR
Grading systems: Urinary Tract Dilatation (UTD) System, Society for Fetal Urology (SFU) [1]
Clinical approach: Antenatal USG detects dilatation → postnatal USG after 48 hours of life (not immediately — the neonate is relatively dehydrated in the first 48 hours, which may underestimate hydronephrosis) → further investigation based on severity and laterality.
13. Posterior Urethral Valve (PUV)
Antenatal: [1]
- Urinary ascites
- Keyhole sign (on antenatal USG — dilated bladder with dilated posterior urethra creates a keyhole appearance)
- Bilateral hydronephro-ureterosis
Postnatal: [1]
- Respiratory distress due to pulmonary hypoplasia (oligohydramnios from poor fetal urine output → lung underdevelopment)
- Urinary retention
Urinary symptoms: [1]
- Weak stream
- Voiding dysfunction ("Valve Bladder")
- UTI
Why does PUV cause pulmonary hypoplasia? The valves obstruct urine outflow → the bladder distends → bilateral ureteric obstruction → reduced fetal urine output → oligohydramnios → fetal lungs need amniotic fluid for normal development (breathing movements in utero) → pulmonary hypoplasia.
Investigations: [1]
- Ultrasonography (bilateral hydronephrosis, thick-walled bladder, dilated posterior urethra)
- MCUG — dilated posterior urethra (diagnostic)
- Endoscopy — diagnosis and valve ablation
Management: [1]
- Severe cases: bladder drainage (catheter), stabilization
- Definitive: endoscopic valve ablation
- Long-term sequelae: bladder dysfunction ("valve bladder"), renal impairment [1]
Valve bladder: Even after successful valve ablation, the detrusor may remain abnormal (thick, poorly compliant) because it developed under chronic high pressure in utero. These children need lifelong urological follow-up for bladder function and renal function monitoring.
14. Prepuce, Phimosis, and Circumcision
Phimosis ≠ Non-retractile foreskin [1]
| Age | Retractile Foreskin |
|---|---|
| Newborn | 0–4% |
| 1 year | 50% |
| 4 years | 90% |
Non-retractable foreskin at birth is NORMAL. Glans can't be exposed ≠ phimosis. [1]
From first principles: The inner prepuce is naturally adherent to the glans at birth (preputial adhesions). These gradually lyse spontaneously. Attempting forceful retraction causes trauma, scarring, and secondary phimosis. Only when there is a pathological scarred, non-retractile preputial ring should the term "phimosis" be used.
Absolute: phimosis, paraphimosis (inability to pull forward retracted foreskin), traumatic foreskin injury [1] Relative: recurrent balanitis [1] Non-medical: religious, social [1] Controversial: prevent UTI, carcinoma, HIV [1]
Contraindications: hypospadias, micropenis, webbed penis, buried penis [1]
Why is circumcision contraindicated in hypospadias?
In hypospadias, the urethral meatus opens on the ventral surface of the penis rather than the tip. The foreskin is needed as tissue for the surgical repair (urethroplasty). Circumcising before repair removes this valuable tissue graft source. The same logic applies to buried penis — the foreskin is needed for reconstruction.
Alternatives: [1]
- Steroid cream (topical betamethasone 0.05% applied to tight foreskin for 4–8 weeks — softens and thins the preputial ring)
- Preputial stretching (gentle manual stretching, often combined with steroid cream)
- Preputioplasty (surgical widening of the preputial ring without removing the foreskin)
An apparent absence of penis exists when it lacks its proper sheath of skin, lies buried beneath the integument of the abdomen or scrotum. (Keyes, 1919) [1]
Key points:
- The penis is of normal size but hidden beneath suprapubic fat or abnormal skin attachments
- Circumcision is contraindicated (and can worsen the problem — "buried penis post circumcision") [1]
- Treatment: foreskin reconstruction / degloving and skin redistribution [1]
Ectopic ureter (extra-vesical): duplex system; wetting in between normal voids [1] Obstruction: posterior urethral valve [1] Anomalies: exstrophy [1]
Ectopic ureter explained: In a duplex kidney, the upper moiety ureter may insert ectopically — in girls, it may insert below the external sphincter (into the vagina or vestibule), causing constant dribbling between normal voids. In boys, the ectopic ureter always inserts above the external sphincter, so it doesn't typically cause incontinence.
Exam Intelligence
| Trap | Correct Answer | Why Students Get It Wrong |
|---|---|---|
| "Enuresis" includes daytime wetting | No — enuresis = night time ONLY | Confusing "enuresis" with "urinary incontinence" |
| Non-retractile foreskin in a 2-year-old = phimosis | No — physiological at this age (50% retractile at 1 year, 90% by 4 years) | Not knowing the natural history of foreskin retractability |
| Circumcision is indicated for all non-retractile foreskins | No — consider steroid cream, stretching, preputioplasty first | Over-treating a physiological finding |
| Circumcision for hypospadias | Contraindicated — foreskin needed for repair | Not knowing that foreskin is a tissue source |
| PMNE always needs investigations | No — most do NOT need investigations | Over-investigating a benign condition |
| DDAVP can be given with unlimited fluids | No — must restrict fluid to avoid hyponatraemia | Not knowing the mechanism of DDAVP |
| PUV occurs in girls | No — PUV is a disease of boys only (posterior urethra anatomy) | Not recalling the anatomy |
| Ectopic ureter causes incontinence equally in boys and girls | No — continuous incontinence mainly in girls (ectopic insertion below sphincter) | Not knowing the anatomical difference |
- PMNE management stepwise: Behavioural → Alarm OR DDAVP → If fail, review diagnosis
- PUV = most common obstructive uropathy causing renal failure in newborn boys
- Keyhole sign on antenatal USG = PUV until proven otherwise
- MCUG is the investigation for VUR and PUV
- DMSA is for renal scarring
- True phimosis = BXO (only 1% of boys)
- VUR treatment: conservative (prophylactic antibiotics) → endoscopic Deflux → ureteric reimplantation
High Yield Summary
-
Enuresis = night-time ONLY intermittent incontinence.
- Primary = never dry > 6 months. Secondary = previously dry > 6 months.
-
PMNE
- (Primary Monosymptomatic Nocturnal Enuresis): ~80% of enuretic children; 15–20% of 5-year-olds; M > F; associations: ADHD, OSA; most do NOT need investigations.
-
Three key questions
- for evaluation: Age ≥ 5? Continuous vs intermittent? Night-only vs daytime symptoms?
-
PMNE Management
- Behavioural modification → Enuresis alarm (best for small bladder capacity) → DDAVP (best for nocturnal polyuria, large bladder capacity) → If fail, review diagnosis.
-
DDAVP
- Restrict fluids to avoid hyponatraemia. Trial 2–6 weeks. Gradual withdrawal reduces relapse.
-
Continuous incontinence → anatomical (ectopic ureter, epispadias, exstrophy) → refer specialist.
-
Neurogenic bladder
- Congenital (spina bifida) or acquired (trauma). Diagnose with urodynamics. Complications: UTI, hydronephrosis, renal failure, stones.
-
PUV
- Most common obstructive uropathy → renal failure in newborn boys. Keyhole sign on antenatal USG. MCUG diagnostic. Endoscopic valve ablation. Long-term "valve bladder."
-
VUR
- 1% prevalence. Reflux nephropathy risk. Treatment: conservative → Deflux → reimplantation.
-
Non-retractile foreskin at birth is NORMAL.
- True phimosis = BXO (1%). Circumcision contraindicated in hypospadias, buried penis. Alternatives: steroid cream, stretching, preputioplasty.
Active Recall - Lecture Notes
[1] Lecture slides: GC 213. Why do you wet your bed all the time Paediatric urology.pdf (all pages) [2] Senior notes: Adrian Lui Pediatrics Notes.pdf (p. 338 — Enuresis section) [3] Lecture slides: Pediatric urology.pdf (scope and overview) [4] Senior notes: Maksim Surgery Notes.pdf (Paediatric urology section p. 4) [5] Senior notes: Block A - Abdominal distension_ ascites and cirrhosis.pdf (obstructive uropathy in AKI context) [6] Senior notes: Ryan Ho Critical Care.pdf (p. 25 — AKI and post-renal causes) [7] Senior notes: Block A – Nephrology Data Interpretation.pdf (obstructive nephropathy) [8] Senior notes: Block A - Glomerular and Tubulo-interstitial Diseases and Acute Kidney Injury.pdf (hematuria DDx) [9] Lecture slides: GC 209. Urinary incontinence and overactive bladder.pdf (adult OAB context) [10] Lecture slides: GC 210. Urinary tract infection.pdf (UTI workup) [11] AOS material: AOS - Paeds.pdf (paediatric MCQ questions) [12] Past papers: 2023 Fourth Summative SAQ.pdf (Q8 — spinal cord injury and neurogenic bladder complications)
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