• You ask me any Urology question - just like in a real viva
• I'll give you a structured, examiner-level answer drawn from authoritative sources
• After each answer, I can also tell you what follow-up questions an examiner might ask next, so you can keep drilling
• Feel free to ask about any topic: renal, bladder, prostate, stones, oncology, paediatrics, trauma, andrology - anything goes

• Think out loud - examiners want to follow your reasoning, not just hear the answer
• Use systematic frameworks (anatomy first, then pathophysiology, then management)
• When unsure, say what you do know and build from there

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Quick Reference - What the Examiner Wants to Hear

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• Inflammatory diseases (prostatitis, TB of urinary tract, epididymo-orchitis)
• Andrology (male infertility, priapism)
• Trauma (kidney, bladder, urethra)
• Diagnostic methods (CT/MRI, uroflowmetry, PSA, cystoscopy)
• Wilms tumour, ureter tumours

1. Differential Diagnosis of Hematuria - causes by anatomical origin, workup, AUA guidelines
2. Renal Colic - pathophysiology, 3 sites of narrowing, investigations, management
3. Acute Pyelonephritis - organisms, clinical features, investigations, treatment
4. Acute Urinary Retention - causes, management, TWOC
5. Renal Cell Carcinoma - subtypes, classic triad, paraneoplastic syndromes, diagnosis, staging, treatment
6. BPH - LUTS symptoms, IPSS, diagnosis, medical and surgical treatment
7. Urolithiasis - stone types table, pathogenesis, treatment (ESWL, URS, PCNL)
8. Bladder Cancer - staging (NMIBC vs MIBC), diagnosis, treatment (BCG, cystectomy)
9. Urosepsis - Sepsis-3 criteria, Sepsis 6 bundle, emergency decompression
10. Acute Scrotum Syndrome - differential table, testicular torsion emergency, time-to-salvage rates

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Topic 1: Differential Diagnosis of Hematuria

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First Step - Exclude Pseudohematuria

• Foods: beetroot, rhubarb
• Drugs: rifampicin, phenazopyridine, nitrofurantoin
• Myoglobinuria (rhabdomyolysis)
• Haemoglobinuria

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Causes - Organized by Anatomical Origin

Upper Tract (Kidney & Ureter)

• Renal cell carcinoma
• Urothelial carcinoma of renal pelvis/ureter
• Nephrolithiasis / ureterolithiasis
• Acute pyelonephritis / renal abscess
• Glomerulonephritis (IgA nephropathy is the most common worldwide)
• Polycystic kidney disease
• Renal trauma
• Renal papillary necrosis (seen in diabetes, sickle cell, analgesic abuse)
• Renal tuberculosis

Lower Tract (Bladder, Prostate, Urethra)

• Bladder cancer - most common cause of painless gross hematuria in patients >50 years
• Cystitis (bacterial, radiation-induced, cyclophosphamide-induced)
• BPH / benign prostatic enlargement
• Prostate cancer
• Urethritis
• Urethral caruncle (post-menopausal women)

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Key Clinical Clues

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Risk Factors for Urological Malignancy

• Age >35-50
• Smoking (single biggest modifiable risk factor for bladder cancer)
• Industrial chemical exposure: aniline dyes, benzene, aromatic amines (rubber/dye workers)
• Cyclophosphamide chemotherapy
• Pelvic radiation
• Chronic indwelling catheter
• Analgesic abuse (phenacetin)
• Schistosoma haematobium infection (causes squamous cell carcinoma of bladder)

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Workup (AUA Guidelines)

1. Urinalysis with microscopy + urine culture (exclude UTI)
2. Cystoscopy - mandatory in adults >35 with gross hematuria or significant microscopic hematuria
3. Upper tract imaging - CT urogram is the gold standard (evaluates kidneys, ureters, bladder)
4. Urine cytology - highly specific for high-grade cancer and CIS, but low sensitivity for low-grade tumours

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Examiner's Key Point

Painless gross hematuria in a patient over 50 is bladder cancer until proven otherwise. Always take a smoking history. A dipstick alone is insufficient to diagnose or exclude true hematuria - microscopy is required.

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Topic 2: Renal Colic

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Pathophysiology

1. Stone lodges at a point of ureteric narrowing
2. Proximal ureter and renal pelvis dilate (hydronephrosis)
3. Increased intraluminal pressure activates prostaglandin release
4. Prostaglandins increase ureteric peristalsis → smooth muscle spasm → colicky pain
5. Pain is visceral, transmitted via T11-L2 (explains loin-to-groin radiation)

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Three Sites of Physiological Ureteric Narrowing

1. Pelviureteric junction (PUJ)
2. Crossing of the iliac vessels (pelvic brim)
3. Vesicoureteric junction (VUJ) - most common site of impaction

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Clinical Presentation

• Sudden severe loin-to-groin pain - radiates to ipsilateral testicle/labia majora
• Patient is restless, writhing - cannot find a comfortable position
  • This distinguishes renal colic from peritonitis, where the patient lies still
• Nausea and vomiting
• Haematuria (macro or micro) in ~90% of cases
• Urinary frequency/urgency if stone is near the VUJ
• Fever = danger sign - suggests concurrent infection in an obstructed system → urological emergency

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Investigations

Urine

• Dipstick/microscopy: haematuria (absent in ~10% - does not exclude a stone)
• Urine culture: mandatory to exclude infection

Bloods

• FBC, U&E, creatinine, CRP
• Serum calcium, urate, phosphate (metabolic workup for stone type)
• Clotting if intervention planned

Imaging

• Hyperdense calcific focus in ureter
• Proximal hydroureter and hydronephrosis
• Renal enlargement
• Perinephric fat stranding (hallmark of acute obstruction)

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Stone Radiolucency - Important for Viva

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Management

Acute Pain Relief

• NSAIDs (diclofenac, ketorolac) - FIRST LINE
  • Mechanism: reduce prostaglandin synthesis → decrease ureteric spasm and renal pelvic pressure
  • Superior to opioids for renal colic
• Opioids (morphine, pethidine): second-line if NSAIDs contraindicated (renal impairment, peptic ulcer)
• Anti-emetics: metoclopramide, ondansetron

Medical Expulsive Therapy (MET)

• Alpha-1 blockers (tamsulosin 0.4mg OD): relax smooth muscle of distal ureter → facilitate stone passage
• Recommended for distal ureteric stones ≤10mm
• Increases spontaneous passage rate and reduces time to passage

Spontaneous Passage Rates

• Stones ≤5mm: ~90% pass spontaneously
• Stones 5-10mm: ~50% pass (MET recommended)
• Stones >10mm: unlikely to pass - intervention usually required

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Indications for Urgent Intervention ("Stone does not wait")

1. Infected obstructed kidney (fever + obstruction) - emergency decompression with ureteric stent OR percutaneous nephrostomy (PCN)
2. Solitary or transplanted kidney with obstruction
3. Bilateral ureteric obstruction
4. Acute kidney injury (AKI)
5. Refractory pain or vomiting despite analgesia
6. Social reasons (pilot, solo parent, etc.)

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Definitive Surgical Treatment

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Differential Diagnosis of Renal Colic (Viva trap!)

• Ruptured/leaking AAA (aortic aneurysm) - pulsatile mass, haemodynamic instability, older patient
• Acute appendicitis (right-sided)
• Ovarian torsion / ectopic pregnancy (women of reproductive age)
• Acute pyelonephritis
• Musculoskeletal pain
• Herpes zoster (pain precedes rash)

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Examiner's Key Point

An infected obstructed kidney is a urological emergency. It cannot be managed with antibiotics alone - the obstruction MUST be relieved urgently with either a ureteric stent or percutaneous nephrostomy, regardless of how unwell the patient is. Antibiotics without drainage will not clear the sepsis.

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Topic 3: Acute Pyelonephritis

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Pathogenesis

Route of infection:

• Ascending (most common): Bacteria colonize the perineum → urethra → bladder → ascend via ureters to kidney
• Haematogenous (less common): Bloodborne seeding, classically with Staphylococcus aureus

Predisposing factors:

• Female sex (short urethra, proximity to anus)
• Urinary tract obstruction (stone, stricture, BPH)
• Vesicoureteric reflux (VUR) - especially in children
• Diabetes mellitus
• Pregnancy
• Urinary catheterization / instrumentation
• Immunosuppression (HIV, transplant, steroids)
• Structural anomalies (horseshoe kidney, duplex system)
• Neurogenic bladder

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Causative Organisms

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Clinical Features

Classic triad:

1. Fever (≥38°C) with rigors/chills
2. Loin/flank pain (unilateral or bilateral)
3. Costovertebral angle (CVA) tenderness on palpation

Additional symptoms:

• Dysuria, frequency, urgency (LUTS present in ~60% - absent in many)
• Nausea, vomiting
• Abdominal pain (can mimic GI pathology - appendicitis, cholecystitis)
• Malaise, anorexia

In special populations:

• Elderly/immunocompromised: Atypical presentation - confusion, no fever, only mild symptoms
• Pregnant women: Higher risk of preterm labour; must treat aggressively
• Children: Non-specific symptoms - fever, poor feeding, vomiting, irritability

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Investigations

Urine

• Dipstick: Positive leucocyte esterase + nitrites (gram-negative bacteria)
• Microscopy: Pyuria (WBCs, often in clumps), bacteriuria
• WBC casts - highly specific for renal parenchymal involvement (pyelonephritis vs cystitis)
• Urine culture (midstream clean catch): Positive in >80%; ~20% have <10⁵ CFU/mL (still significant with symptoms)
• Always send before starting antibiotics

Blood tests

• FBC: Leukocytosis with neutrophilia
• CRP/ESR: Elevated
• U&E/Creatinine: May show AKI in severe cases
• Blood cultures (×2): Positive in ~20%; always take before antibiotics

Imaging

• Renal ultrasound: First-line; excludes obstruction, hydronephrosis, abscess; may show enlarged hyperechoic kidney
• CT abdomen with contrast: Indicated if:
  • No clinical improvement after 48-72 hours of treatment
  • Suspected abscess or emphysematous pyelonephritis
  • Diagnostic uncertainty
  • CT shows "striated nephrogram" - wedge-shaped areas of reduced enhancement

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Severity Classification

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Management

Uncomplicated (outpatient - mild/moderate):

• Oral fluoroquinolone (ciprofloxacin 500mg BD × 7 days) - first-line where resistance rates <10%
• Alternatives: co-amoxiclav, trimethoprim-sulfamethoxazole (if sensitivity confirmed)
• Adequate hydration
• Review urine culture at 48-72 hours and adjust if needed

Complicated / Severe (inpatient):

• IV fluids for resuscitation
• IV broad-spectrum antibiotics:
  • Ceftriaxone 1-2g OD, OR
  • Co-amoxiclav (piperacillin-tazobactam if resistant organisms suspected)
  • Carbapenem (meropenem) if ESBL or multidrug-resistant organism
• Step down to oral once clinically improving and afebrile for 24-48h
• Total course: 10-14 days

No improvement after 48-72 hours:

• Repeat imaging (CT) to exclude:
  • Obstruction not previously seen
  • Developing abscess
  • Resistant organism
  • Emphysematous pyelonephritis

Complicated pyelonephritis with obstruction:

• Emergency ureteric stent or percutaneous nephrostomy - same principle as infected obstructed kidney

Abscess drainage:

• Small (<3cm): antibiotics alone may suffice
• Large (>3cm): Percutaneous drainage under USS/CT guidance ± nephrectomy if non-responsive

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Complications

• Septicaemia / Urosepsis - most serious acute complication
• Acute kidney injury - usually reversible with treatment
• Renal abscess / carbuncle formation
• Emphysematous pyelonephritis (diabetics)
• Chronic pyelonephritis → renal scarring → hypertension → chronic kidney disease
• Papillary necrosis (in diabetics, sickle cell)
• Perinephric abscess - infection breaks through renal capsule

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Chronic Pyelonephritis

• Repeated episodes of acute pyelonephritis → progressive renal scarring
• Often associated with VUR (especially in children)
• Imaging: small scarred kidney with focal cortical thinning, calyceal clubbing ("thyroid-like" appearance on IVU)
• Can lead to hypertension and CKD
• Management: treat underlying cause (VUR - anti-reflux surgery in children), long-term low-dose prophylactic antibiotics

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Examiner's Key Points

• E. coli causes 80% of cases via ascending route
• WBC casts in urine sediment are highly specific for renal parenchymal infection
• Always send blood cultures AND urine culture before starting antibiotics
• If no improvement at 48-72 hours - image again (CT) to exclude abscess or obstruction
• Emphysematous pyelonephritis is a diabetic emergency - gas in the kidney on CT, often requires nephrectomy

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Topic 4: Acute Urinary Retention (AUR)

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Two Types - Know the Difference

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Causes

In Men (most common overall cause = BPH)

In Women (less common overall)

In Both Sexes

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Clinical Features

• Severe suprapubic pain and distension
• Absolute inability to void despite strong urge
• Palpable and percussable tender bladder above the pubic symphysis
• Bladder volume typically 300-800ml (can exceed 1L in chronic/overflow retention)
• Agitation, sweating
• In neurological AUR - may be painless (no sensation)

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Key Examination Findings

• Suprapubic mass (distended bladder)
• Dull to percussion suprapubically
• Tender on palpation
• DRE in men: enlarged smooth rubbery prostate (BPH) vs hard/nodular (cancer) vs exquisitely tender boggy (prostatitis)
• Neurological exam: perianal sensation, anal tone, lower limb power/reflexes → exclude cauda equina syndrome

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Cauda Equina Syndrome - NEVER MISS

• Bilateral leg weakness/numbness
• Saddle anaesthesia (perineum, inner thighs, genitalia)
• Reduced anal tone
• Back pain

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Investigations

• Urine dipstick + culture: exclude UTI/haematuria
• Bloods: U&E, creatinine (assess for renal impairment from chronic obstruction)
• Bladder scan (portable ultrasound): confirms urinary retention non-invasively (>300ml post-void = retention)
• PSA: after catheterization (wait 4-6 weeks as catheterization falsely elevates PSA)
• Renal USS: if renal impairment - exclude bilateral hydronephrosis
• Uroflowmetry + post-void residual: after catheter removal/TWOC

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Immediate Management

Step 1: Catheterize

• Urethral catheterization (14-16Fr Foley catheter) - first-line
• Use anaesthetic lubricating gel (e.g. lidocaine gel)
• Document residual volume drained

If urethral catheter fails:

• Try a Tiemann-tipped catheter (curved tip, for BPH/false passages)
• Flexible cystoscopy-guided catheter
• Suprapubic catheter (SPC) - inserted percutaneously above the pubic symphysis under USS guidance; used when urethral catheterization is impossible (stricture, trauma) or contraindicated

Clot Retention:

• 3-way (triple lumen) catheter with continuous bladder irrigation (CBI) using normal saline
• Evacuate clots manually via bladder syringe before starting irrigation

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Post-Catheterization Care

Post-obstructive Diuresis

• After relieving large volume retention, kidneys may produce massive diuresis (>200ml/hr)
• Caused by: osmotic diuresis (retained urea), impaired tubular reabsorption, ANP release
• Monitor: hourly urine output, fluid balance, U&E, creatinine
• Replace ~50-75% of urine output with IV fluids to avoid hypovolaemia and electrolyte imbalance
• Self-limiting in most cases

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Trial Without Catheter (TWOC)

• Attempted after 24-48 hours of catheterization (allows bladder/detrusor to recover)
• Alpha-blocker (tamsulosin 0.4mg OD) started 24-48h before TWOC - relaxes smooth muscle of bladder neck, significantly improves TWOC success rate
• TWOC is successful if patient voids adequately with post-void residual <100ml
• TWOC success rates:
  • Precipitated AUR: ~60-70%
  • Spontaneous AUR: ~30-40%

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Definitive Management (After Failed TWOC or Recurrent AUR)

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Chronic Urinary Retention

• Low-pressure chronic retention: Large residual (>300ml), painless, no discomfort - patient adapts; may present with overflow incontinence ("dribbling")
• High-pressure chronic retention: Back-pressure causes bilateral hydronephrosis and renal impairment; palpable bladder, hypertension
  • Monitor closely after catheterization for post-obstructive diuresis
  • Do NOT rapidly decompress in high-pressure chronic retention - gradual drainage

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Examiner's Key Points

• Always exclude cauda equina syndrome - this is a neurosurgical emergency
• Start tamsulosin before TWOC to improve success rates
• Post-obstructive diuresis is a real risk after draining a large volume - monitor fluid balance and electrolytes
• Spontaneous AUR has a worse prognosis than precipitated AUR - more likely to need TURP
• In acute prostatitis causing AUR, a suprapubic catheter is preferred over urethral catheter (less painful, avoids worsening inflammation)

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Topic 5: Renal Cell Carcinoma (RCC)

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Epidemiology

• Peak incidence: 6th-7th decade
• Male : Female = 2:1
• ~5% are hereditary; majority are sporadic
• Incidence is rising - largely due to incidental detection on cross-sectional imaging

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Risk Factors

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Histological Subtypes - Know These

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Clinical Presentation

Classic Triad (present in only ~10% of patients today):

1. Painless gross haematuria
2. Loin/flank pain
3. Palpable abdominal/flank mass

When all three are present together, suspect advanced disease

How most RCCs present today:

• Incidentally discovered on USS or CT done for another reason ("incidentaloma") - accounts for ~50-60% of cases
• Haematuria alone
• Symptoms from metastases (bone pain, cough, neurological symptoms)
• Paraneoplastic syndrome

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Paraneoplastic Syndromes - High-Yield Viva Topic

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Patterns of Spread

• Direct: Into perinephric fat, adrenal gland, adjacent organs
• Venous (characteristic of RCC): Extension into renal vein → IVC thrombus → right atrium
  • IVC involvement is a hallmark of RCC - seen in ~10%
  • Can cause right heart failure, pulmonary emboli
• Lymphatic: Para-aortic/paracaval lymph nodes
• Haematogenous metastases:
  • Lungs (most common) - "cannonball" metastases on CXR
  • Bone (lytic lesions)
  • Liver
  • Brain
  • Contralateral kidney
  • Thyroid (RCC is the most common tumour to metastasize to the thyroid)

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Investigations

Initial

• Urine dipstick/microscopy: haematuria
• Bloods: FBC (polycythaemia or anaemia), U&E, LFTs (Stauffer syndrome), calcium, LDH, ESR
• Urine cytology: typically negative (not a urothelial tumour)

Imaging

Bosniak Classification (Cystic Renal Lesions):

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Staging - TNM System

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Treatment

Localised Disease (T1-T2, N0M0)

• Partial nephrectomy preserves renal function - important for solitary kidney, bilateral tumours, CKD, young patients

Locally Advanced (T3-T4)

• Radical nephrectomy ± lymph node dissection ± IVC thrombectomy (if IVC involved)
• IVC thrombus requires cardiothoracic surgery input if above diaphragm

Metastatic RCC (mRCC)

• Cytoreductive nephrectomy: Removing the primary tumour in the setting of metastatic disease may improve outcomes in selected patients
• Metastasectomy: Surgery or ablation for solitary metastasis (especially lung, brain)
• Radiotherapy: Palliative - for bone and brain metastases

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Prognosis

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Examiner's Key Points

• Most RCCs are now found incidentally - the classic triad is present in only ~10%
• Paraneoplastic syndromes: polycythaemia (EPO), hypercalcaemia (PTHrP), Stauffer syndrome (liver dysfunction that reverses after nephrectomy)
• IVC thrombus is a hallmark of RCC - can extend into the right atrium
• "Cannonball" metastases in the lungs on CXR = think RCC
• RCC is resistant to chemo and radiotherapy - treatment is surgery (localised) or targeted/immunotherapy (metastatic)
• VHL gene mutation on chromosome 3p25 → clear cell RCC

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Topic 6: Benign Prostatic Hyperplasia (BPH)

BPH is NOT premalignant - it does not increase the risk of prostate cancer.

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Anatomy Reminder

• Transition zone (~5-10% of gland) - site of BPH
• Peripheral zone (~70%) - site of most prostate cancers
• Central zone (~25%) - surrounds the ejaculatory ducts

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Pathophysiology

• Driven by DHT (dihydrotestosterone) - converted from testosterone by 5-alpha reductase (type 2) in prostatic stromal cells
• DHT binds androgen receptors → stimulates cell proliferation
• Age-related increase in oestrogen:androgen ratio also plays a role
• Results in both static obstruction (enlarged gland physically compresses urethra) and dynamic obstruction (increased alpha-1 adrenoceptor-mediated smooth muscle tone in prostate and bladder neck)

This explains the two drug targets: 5-alpha reductase inhibitors (static) and alpha-blockers (dynamic)

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Epidemiology

• Histological BPH present in:
  • ~20% of men aged 40
  • ~70% of men aged 60
  • ~90% of men aged 80
• Only ~50% of men with histological BPH develop clinical symptoms

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Clinical Manifestations - LUTS

Voiding (Obstructive) Symptoms - caused by bladder outlet obstruction:

• Hesitancy - difficulty initiating stream
• Weak/poor stream - reduced flow rate
• Intermittency - stream starts and stops
• Straining - needs to push/Valsalva to void
• Incomplete emptying - feeling bladder not fully empty
• Post-micturition dribble - terminal dribbling

Storage (Irritative) Symptoms - caused by detrusor overactivity:

• Frequency - voiding more often than every 2 hours
• Nocturia - waking at night to void (≥2 times is significant)
• Urgency - sudden compelling desire to void
• Urge incontinence - leakage associated with urgency

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International Prostate Symptom Score (IPSS)

Always mention the IPSS in the viva - examiners love it

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Complications of Untreated BPH

• Acute urinary retention (AUR)
• Chronic urinary retention → overflow incontinence
• Recurrent UTIs (stagnant residual urine)
• Bladder stones (from stagnant urine + infection)
• Bladder diverticula (increased voiding pressure)
• Bilateral hydronephrosis → back-pressure nephropathy
• Chronic kidney disease / renal failure
• Haematuria (from dilated prostatic vessels)

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Diagnosis

History

• IPSS questionnaire
• Duration of symptoms, impact on quality of life
• Drug history (anticholinergics, alpha-agonists worsen symptoms)
• Sexual function (ED often coexists)

Examination

• Digital Rectal Exam (DRE):
  • BPH: enlarged, smooth, rubbery, non-tender, symmetrical prostate; median sulcus preserved or obliterated
  • Prostate cancer: hard, irregular, nodular, asymmetric; loss of median sulcus
  • Prostatitis: exquisitely tender, boggy
• Suprapubic palpation (distended bladder in retention)
• Neurological exam (exclude neurogenic cause)

Investigations

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Treatment

1. Conservative (Mild symptoms - IPSS ≤7)

• Watchful waiting with lifestyle modifications:
  • Reduce caffeine and alcohol (diuretics and bladder irritants)
  • Reduce fluid intake in evenings (reduces nocturia)
  • Double voiding (void, wait, void again)
  • Bladder retraining
  • Treat constipation
  • Review medications

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2. Medical Treatment (Moderate symptoms - IPSS 8-19)

Alpha-1 Adrenoceptor Blockers (Alpha-blockers)

• Examples: Tamsulosin (0.4mg OD), alfuzosin, doxazosin, terazosin
• Mechanism: Block alpha-1 receptors in prostate smooth muscle and bladder neck → reduce dynamic obstruction → improve urine flow
• Onset: Days to weeks (fast)
• Effect: Improve Q-max by ~1.5-2ml/s, reduce IPSS by ~30-40%
• Side effects: Postural hypotension, retrograde ejaculation (especially tamsulosin), dizziness, nasal congestion
• Note: Tamsulosin is uro-selective (alpha-1a) → less hypotension
• First-line for moderate LUTS

5-Alpha Reductase Inhibitors (5-ARIs)

• Examples: Finasteride (5mg OD), dutasteride (0.5mg OD)
• Mechanism: Inhibit conversion of testosterone → DHT → reduce static component → shrink prostate volume by 20-30%
• Onset: Takes 3-6 months to show benefit
• Effect: Reduce prostate volume, reduce AUR risk, reduce need for surgery
• Best for: Large prostates (>40g / >30ml) or elevated PSA
• Important: Reduce PSA by ~50% - must double the PSA reading to get true value; failure of PSA to fall by 50% on 5-ARI → suspect prostate cancer
• Side effects: Erectile dysfunction, decreased libido, ejaculatory disorders, gynaecomastia, teratogenic (women must not handle crushed tablets)

Combination Therapy

• Alpha-blocker + 5-ARI superior to monotherapy for large prostates
• MTOPS and CombAT trials: combination reduces risk of AUR and need for surgery more than either drug alone
• First-line for large prostate + moderate-severe symptoms

Other Agents

• Antimuscarinics (solifenacin, oxybutynin): for storage/OAB symptoms; caution - can precipitate AUR in BOO
• Beta-3 agonist (mirabegron): for OAB component; safer than antimuscarinics in terms of retention risk
• PDE-5 inhibitors (tadalafil 5mg OD): approved for LUTS/BPH; also treats coexisting ED

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3. Surgical Treatment (Severe symptoms / complications / failed medical therapy)

Indications for Surgery:

• IPSS >20 / severe symptoms not responding to medication
• Recurrent AUR
• Recurrent UTIs
• Bladder stones secondary to BPH
• Renal impairment from obstruction
• Bladder diverticula
• Patient preference

TURP - Transurethral Resection of Prostate

• Gold standard endoscopic procedure
• Resectoscope passed via urethra; prostate chips resected using diathermy loop
• Tissue sent for histology (may incidentally find prostate cancer in ~10%)
• Outcomes: improves Q-max by ~150%, IPSS by ~70%
• TURP Syndrome - classic complication:
  • Absorption of glycine (hypotonic irrigating fluid) through open venous sinuses
  • Causes dilutional hyponatraemia (Na⁺ can drop to <120 mmol/L)
  • Features: confusion, bradycardia, hypertension, visual disturbances, pulmonary oedema, seizures
  • Treatment: Stop procedure; IV hypertonic saline (3% NaCl) if Na⁺ <120; furosemide
  • Bipolar TURP and laser procedures use normal saline → eliminate TURP syndrome risk

Other Surgical Options

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Complications of TURP

• TURP syndrome (see above)
• Retrograde ejaculation (~80%) - semen goes into bladder rather than out; infertile but not impotent
• Erectile dysfunction (~5-10%)
• Urinary incontinence (<1% - external sphincter damage)
• Urethral stricture (late complication)
• Bleeding (primary, reactionary, secondary)
• UTI
• Bladder neck contracture (late)

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Examiner's Key Points

• BPH = hyperplasia (not hypertrophy) of the transition zone; NOT premalignant
• Two mechanisms of obstruction: static (enlarged gland) and dynamic (smooth muscle tone) - explains two drug classes
• 5-ARIs reduce PSA by 50% - always double the PSA value in a patient on finasteride/dutasteride
• TURP syndrome = dilutional hyponatraemia from glycine absorption - confusion, bradycardia, visual disturbance
• Retrograde ejaculation occurs in ~80% after TURP - warn patients pre-operatively
• Combination therapy (alpha-blocker + 5-ARI) is superior for large prostates

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Topic 7: Urolithiasis (Urinary Stone Disease)

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Etiology and Pathogenesis

Core Mechanism - Three Steps:

1. Supersaturation - urine becomes oversaturated with lithogenic substances
2. Nucleation - crystals form around a nidus (cell debris, foreign body, bacteria)
3. Crystal growth and aggregation - crystals enlarge and aggregate into a stone

Factors promoting stone formation:

• Low urine volume (dehydration, low fluid intake, hot climate)
• High concentration of lithogenic substances (hypercalciuria, hyperoxaluria, hyperuricosuria)
• Low concentration of inhibitors (low citrate, low magnesium)
• Abnormal urinary pH (acidic urine → uric acid stones; alkaline urine → calcium phosphate, struvite stones)
• Urinary stasis (obstruction, anatomical anomalies)
• Infection (urease-producing bacteria → struvite stones)

General Risk Factors:

• Male sex (M:F = 3:1 for calcium stones)
• Age 20-50 years (peak)
• Family history
• Hot climate / occupation (outdoor workers, military)
• High protein, high sodium, low calcium diet
• Inflammatory bowel disease (increased oxalate absorption)
• Hyperparathyroidism
• Gout
• Anatomical: horseshoe kidney, PUJ obstruction, medullary sponge kidney
• Medications: loop diuretics, acetazolamide, calcium supplements, vitamin D excess, indinavir (HIV drug → radiolucent stones)

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Stone Composition - Know All Five Types

1. Calcium Oxalate (~70% of all stones)

• Most common type
• Radio-opaque (visible on plain X-ray)
• Two subtypes:
  • Monohydrate (whewellite): hard, spiky, more common; resistant to ESWL
  • Dihydrate (weddellite): softer, mulberry-shaped; responds better to ESWL
• Causes: hypercalciuria (most common), hyperoxaluria, hypocitraturia, low urine volume
• Hypercalciuria causes:
  • Absorptive (increased GI calcium absorption)
  • Resorptive (primary hyperparathyroidism)
  • Renal leak (defective tubular reabsorption)

2. Calcium Phosphate (~5-10%)

• Radio-opaque
• Associated with: renal tubular acidosis (RTA type 1), hyperparathyroidism, alkaline urine

3. Uric Acid (~10%)

• Radiolucent on plain X-ray - NOT visible on KUB; seen on CT
• Associated with: gout, hyperuricosuria, low urinary pH (<5.5), myeloproliferative disorders, dehydration, high purine diet
• Unique: can be dissolved with urinary alkalinization (potassium citrate, sodium bicarbonate → raise urine pH to 6.5-7)

4. Struvite / Magnesium Ammonium Phosphate (~10%)

• Radio-opaque (can be very dense)
• Almost always associated with urease-producing bacteria (Proteus, Klebsiella, Pseudomonas, Staphylococcus)
• Mechanism: urease splits urea → ammonia → alkaline urine → supersaturation with magnesium ammonium phosphate
• Form staghorn calculi - fill the entire renal collecting system
• More common in women (more UTIs)
• Require complete stone removal + antibiotics to prevent recurrence

5. Cystine (~1%)

• Weakly radio-opaque (ground glass appearance)
• Caused by cystinuria - autosomal recessive defect in renal tubular transport of dibasic amino acids (Cystine, Ornithine, Lysine, Arginine - "COLA")
• Presents in young patients; highly recurrent
• Resistant to ESWL (very hard stones)
• Treatment: high fluid intake, urinary alkalinization, D-penicillamine or tiopronin (chelating agents)

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Summary Table

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Clinical Manifestations

Renal/Upper Ureteric Stone:

• Loin pain (dull, constant ache) from capsular distension
• Haematuria
• May be asymptomatic (renal calculus without obstruction)

Ureteric Stone (Renal Colic - covered in Topic 2):

• Sudden severe loin-to-groin colicky pain
• Haematuria
• Nausea/vomiting
• Urinary symptoms if near VUJ

Bladder Stone:

• Suprapubic pain worse at end of micturition (stone rolls onto trigone)
• Terminal haematuria
• Interrupted stream (stone acts as ball-valve)
• Recurrent UTI
• Most bladder stones in adults are secondary (BPH → stasis → stone formation)

Urethral Stone:

• Acute urinary retention or reduced stream
• Perineal/penile pain
• Haematuria

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Complications of Urolithiasis

• Obstruction → hydronephrosis → renal impairment
• Infected obstructed kidney → urosepsis (emergency)
• AKI (bilateral stones or solitary kidney)
• Chronic kidney disease (recurrent obstruction + infection → scarring)
• Recurrent UTIs
• Bladder dysfunction (chronic bladder stones)
• Renal papillary necrosis (chronic obstruction)
• Ureteric stricture (after instrumentation or prolonged stone impaction)
• Squamous cell carcinoma of renal pelvis (rare, from chronic stone irritation)

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Metabolic Evaluation

• 24-hour urine collection: volume, calcium, oxalate, uric acid, citrate, phosphate, pH, creatinine
• Serum: calcium, phosphate, urate, bicarbonate, creatinine, PTH (if hypercalcaemia)
• Stone analysis (sent from retrieved stone or post-intervention fragments)

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Treatment

Conservative Management

• High fluid intake (>2.5 litres/day, urine output >2L/day) - cornerstone of prevention
• Dietary advice:
  • Reduce salt and animal protein (reduce urinary calcium and urate)
  • Normal calcium intake (low calcium diet paradoxically INCREASES oxalate absorption)
  • Reduce oxalate-rich foods (spinach, rhubarb, nuts, chocolate) for calcium oxalate stones
  • Reduce purines (red meat, offal, seafood) for uric acid stones
• Medical expulsive therapy (MET): tamsulosin for distal ureteric stones ≤10mm

Medical Prevention (Targeted by Stone Type)

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Surgical Treatment

Extracorporeal Shock Wave Lithotripsy (ESWL)

• External shock waves focused on stone using fluoroscopy/USS guidance
• Fragments stone into small pieces passed spontaneously
• Best for: Renal stones ≤2cm, upper ureteric stones; calcium oxalate dihydrate or calcium phosphate stones
• Poor results: Hard stones (cystine, calcium oxalate monohydrate), lower pole stones, stones in obstructed/abnormal systems
• Contraindications: Pregnancy, bleeding disorders, obstruction distal to stone, aortic aneurysm adjacent to stone, pacemaker (relative)
• May require multiple sessions; steinstrasse (stone street) - fragments pile up in ureter - complication

Ureteroscopy (URS) + Holmium Laser Lithotripsy

• Rigid/semi-rigid ureteroscope for distal ureter; flexible ureteroscope for proximal ureter and kidney
• Holmium:YAG laser fragments stone; fragments removed with Nitinol basket
• Highest stone-free rate for ureteric stones
• Ureteric stent left post-procedure (removed at 1-2 weeks)
• Contraindication: active UTI (treat first)

Percutaneous Nephrolithotomy (PCNL)

• Percutaneous access through flank skin into renal collecting system under USS/fluoroscopic guidance
• Nephroscope passed through tract; stone fragmented (ultrasonic, pneumatic, or laser) and removed
• Best for: Large renal stones (>2cm), staghorn calculi, failed ESWL/URS, lower pole stones
• Complications: Bleeding (may need transfusion or angioembolization), sepsis, pneumothorax (upper pole puncture), injury to adjacent organs

Open / Laparoscopic Surgery

• Rarely needed in modern practice
• Indications: complex anatomy, failed endoscopic approaches, simultaneous reconstruction (e.g. PUJ obstruction + stone)

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Surgical Treatment Summary

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Examiner's Key Points

• Uric acid stones are radiolucent on plain X-ray but visible on CT - the only stone type that can be dissolved medically with urinary alkalinization
• Struvite stones = urease-producing bacteria (remember Proteus) + alkaline urine = staghorn calculi; more common in women
• Cystinuria is autosomal recessive - "COLA" amino acids affected; presents young; very hard stones resistant to ESWL
• Low dietary calcium paradoxically increases stone risk by increasing oxalate absorption - always advise normal calcium intake
• Infected obstructed kidney = emergency decompression (stent or nephrostomy) regardless of stone size

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Urinary Stone Types - Quick Reference Comparison Table

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Radio-opacity Cheat Sheet

VISIBLE on plain X-ray (KUB):
  ✅ Calcium oxalate   (most common - remember this one)
  ✅ Calcium phosphate
  ✅ Struvite          (staghorn - very dense)
  ⚠️ Cystine          (faintly visible - "ground glass")

NOT visible on plain X-ray:
  ❌ Uric acid         (radiolucent - need CT to see it)

ALL stones are visible on CT regardless of type

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Urinary pH Cheat Sheet

Acidic urine (pH <5.5) → Uric acid stones form
Alkaline urine (pH >7)  → Struvite + Calcium phosphate form
Normal/any pH           → Calcium oxalate + Cystine

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"Most Likely" Summary for Viva Scenarios

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Memory Aids

• "COLA" for Cystine = Cystine, Ornithine, Lysine, Arginine (all affected in cystinuria)
• "Proteus causes Problems" = Proteus → urease → struvite → staghorn
• "Uric acid = Unique" = only stone you can dissolve with medication
• "Staghorn = She" = struvite staghorn more common in women

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Topic 8: Bladder Cancer

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Epidemiology

• Male : Female = 3:1
• Peak incidence: 65-70 years
• More common in developed countries
• ~75% present as non-muscle invasive disease
• High recurrence rate - requires lifelong surveillance

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Histological Types

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Risk Factors

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Pathology

Growth Patterns:

• Papillary - frond-like projections into bladder lumen; most common; tends to be lower grade
• Flat (CIS - Carcinoma in Situ) - flat, high-grade intraepithelial lesion; velvety red mucosa; highly aggressive
• Solid/sessile - more likely to be high grade and invasive

Grade:

• Low grade - well-differentiated; tends to recur but rarely progresses to invasion
• High grade - poorly differentiated; high risk of muscle invasion and metastasis; CIS is always high grade

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Staging - TNM (THE Most Important Concept)

The Critical Division:

• Non-Muscle Invasive Bladder Cancer (NMIBC): Ta, T1, CIS → ~75% at presentation → treated endoscopically
• Muscle-Invasive Bladder Cancer (MIBC): T2 and above → ~25% → needs radical treatment

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Clinical Manifestations

Cardinal Symptom:

• Painless frank (gross) haematuria - present in ~80% of patients
  • Typically intermittent, can be single episode
  • Painless = no infection = must investigate regardless of whether it resolves

Other symptoms:

• Irritative LUTS (frequency, urgency, dysuria) - especially with CIS or large tumour
• Obstructive symptoms - if tumour involves bladder neck or ureteric orifices
• Unilateral hydronephrosis / flank pain - ureteric orifice involvement
• Pelvic pain - locally advanced disease
• Bone pain, weight loss, fatigue - metastatic disease
• Leg oedema - lymph node obstruction

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Diagnosis

1. Urine Tests

• Urine dipstick + microscopy: haematuria
• Urine cytology:
  • High specificity for high-grade tumours and CIS (~90% sensitivity for high grade)
  • Poor sensitivity for low-grade tumours (~20-30%)
  • Cells shed into urine - look for malignant urothelial cells
• Urine NMP22, BTA stat, FISH (UroVysion): newer biomarkers; adjunct to cytology

2. Imaging

• CT Urogram (CTU): gold standard for upper tract evaluation and bladder lesion detection; staging in muscle-invasive disease
• Ultrasound: can detect large bladder tumours but misses small/flat lesions and CIS
• MRI pelvis (mpMRI/VI-RADS scoring): best for assessing depth of muscle invasion (T staging) pre-operatively
• CT chest/abdomen/pelvis: staging for MIBC

3. Cystoscopy - THE Definitive Investigation

• Flexible cystoscopy: outpatient/day case; diagnostic; visualizes bladder mucosa
• Rigid cystoscopy under GA + TURBT: both diagnostic AND therapeutic
  • Bimanual examination under anaesthesia (EUA): palpable mass = T3/T4
  • Resection of all visible tumour to detrusor muscle
  • Must include detrusor muscle in specimen (to assess T stage)
  • Blue light cystoscopy (HAL/hexvix): photosensitizing agent makes tumour cells fluoresce pink; detects CIS and satellite lesions missed by white light - increases detection rate by ~20%

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Risk Stratification of NMIBC

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Treatment

Non-Muscle Invasive Bladder Cancer (NMIBC)

Step 1: TURBT (all patients)

• Complete resection of all visible tumour
• Re-TURBT at 4-6 weeks for:
  • T1 tumours (to confirm staging and ensure complete resection)
  • Any tumour where no muscle in specimen
  • Large/multifocal tumours

Step 2: Intravesical Therapy

• Live attenuated Mycobacterium bovis
• Instilled into bladder via catheter
• Triggers local immune response (T-cell mediated) against tumour cells
• Reduces recurrence and progression to muscle invasion
• Contraindicated if: active UTI, traumatic catheterization, immunosuppressed, active TB

Step 3: Surveillance Cystoscopy

• Lifelong cystoscopic surveillance
• High risk: cystoscopy at 3 months, 9 months, then annually
• Low risk: cystoscopy at 3 months, 12 months, then annually for 5 years

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Muscle-Invasive Bladder Cancer (MIBC)

Standard Treatment: Neoadjuvant Chemotherapy + Radical Cystectomy

• Given BEFORE surgery
• Downstages tumour, treats micrometastases
• Improves survival by ~5-8% at 5 years

• Removal of bladder, perivesical fat, regional lymph nodes
• In men: prostate and seminal vesicles also removed
• In women: uterus, ovaries, anterior vaginal wall also removed
• Requires urinary diversion

Urinary Diversion Options

Alternative: Bladder-Preserving Trimodality Therapy (TMT)

• TURBT + radiotherapy + radiosensitizing chemotherapy (cisplatin/5-FU)
• For patients unfit for cystectomy or who refuse surgery
• 5-year survival ~50% for selected patients (comparable to cystectomy in some series)
• Bladder preserved in ~50% long-term

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Metastatic Bladder Cancer

• First-line: Cisplatin-based chemotherapy (GC: gemcitabine + cisplatin) - if fit
• Cisplatin-ineligible: Carboplatin-based or immunotherapy
• Second-line / Maintenance: Immune checkpoint inhibitors:
  • Pembrolizumab (anti-PD1) - approved second-line
  • Atezolizumab (anti-PD-L1)
• Erdafitinib: FGFR inhibitor for FGFR2/3 mutations
• Palliative radiotherapy for bone/bleeding

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Patterns of Spread

• Direct: Perivesical fat → prostate, uterus, rectum, pelvic sidewall
• Lymphatic: Obturator → internal/external iliac → common iliac → para-aortic nodes
• Haematogenous: Liver, lungs, bone, adrenal glands

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Prognosis

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Examiner's Key Points

• Painless gross haematuria in a smoker over 50 = bladder cancer until proven otherwise - always investigate
• Urine cytology is highly sensitive for high-grade disease and CIS, but poor for low-grade tumours
• TURBT specimen MUST contain detrusor muscle - otherwise cannot stage the tumour
• BCG is immunotherapy, not chemotherapy - it works via T-cell mediated immune response; contraindicated in active UTI or immunosuppression
• CIS (Tis) is flat, high-grade, and always treated as high risk despite being "in situ" - it has high progression potential
• Immediate post-operative mitomycin C within 6 hours of TURBT reduces recurrence in low-risk disease
• Schistosoma haematobium causes squamous cell carcinoma, not TCC

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Topic 9: Urosepsis

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Understanding the Spectrum - Key Definitions (Sepsis-3, 2016)

Mortality of septic shock exceeds 40%

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Common Urological Sources

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Causative Organisms

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Pathophysiology

UTI / Urological source
        ↓
Bacteria enter bloodstream (bacteraemia)
        ↓
Bacterial products (LPS from gram-negative, LTA from gram-positive)
        ↓
Activate pattern recognition receptors (TLR-4)
        ↓
Massive cytokine release (TNF-α, IL-1, IL-6) → "Cytokine storm"
        ↓
Systemic vasodilation + increased vascular permeability
        ↓
Hypotension + tissue hypoperfusion + microvascular thrombosis
        ↓
Multi-organ dysfunction (kidneys, lungs, liver, heart, coagulation)
        ↓
Septic shock → Death

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Recognition - Clinical Features

Early Sepsis:

• Fever (>38°C) or hypothermia (<36°C) - hypothermia is a BAD sign
• Tachycardia (HR >90)
• Tachypnoea (RR >20)
• Altered mental status / confusion
• Rigors
• Flank pain / suprapubic pain (urological source)

Septic Shock:

• Hypotension (SBP <90 or MAP <65) despite fluid resuscitation
• Cold, clammy peripheries (vasoconstriction)
• Oliguria (<0.5ml/kg/hr)
• Mottled skin / cyanosis
• Reduced GCS

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Screening Tools

qSOFA (Quick SOFA) - Bedside screening outside ICU:

• Altered mentation (GCS <15)
• RR ≥ 22 breaths/min
• SBP ≤ 100 mmHg

SOFA Score (full):

• Increase of ≥2 from baseline = sepsis

NEWS2 (National Early Warning Score):

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Investigations

Immediate (before antibiotics):

• Blood cultures ×2 (peripheral, different sites) - BEFORE antibiotics
• Urine culture + microscopy (midstream or catheter specimen)
• Urethral catheterization - allows urine culture AND urine output monitoring

Bloods:

Imaging:

• Renal USS (urgent): hydronephrosis? obstruction? - the single most important imaging step
• CT abdomen/pelvis (contrast): if obstruction suspected and USS equivocal; identifies source (abscess, emphysematous pyelonephritis, obstructing stone)
• CXR: exclude pneumonia as source; assess pulmonary oedema

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Management - The Sepsis 6 / Hour-1 Bundle

"Sepsis 6" - to be completed within 1 hour:

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Antibiotic Choice

Empirical (before cultures):

• Piperacillin-tazobactam (Tazocin) 4.5g IV TDS - broad-spectrum, covers gram-negative including Pseudomonas
• Meropenem / Ertapenem - if ESBL suspected, hospital-acquired, prior resistant organism
• Add vancomycin/teicoplanin if MRSA suspected or gram-positive source likely
• Gentamicin: can be used as single dose in sepsis (but nephrotoxic - monitor levels, avoid in renal impairment)

De-escalation:

• Review cultures at 48-72 hours
• Switch to narrow-spectrum antibiotic guided by sensitivities
• Switch to oral when clinically improving, afebrile, tolerating oral medications

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THE Critical Urological Principle - Obstruction Must Be Relieved

Antibiotics alone are NOT sufficient if there is an obstructed infected urinary system. Pus under pressure cannot be sterilized with antibiotics - it must be drained.

Emergency Decompression Options:

• Both are equally effective
• PCN preferred if: very unwell patient, failed retrograde stenting, complex anatomy
• JJ stent preferred if: less unwell, anatomically straightforward

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Septic Shock Management (Beyond Sepsis 6)

Vasopressors (if hypotension persists after 30ml/kg fluids):

• Noradrenaline (norepinephrine) - first-line vasopressor; alpha-1 agonist; raises MAP
• Vasopressin - add if high-dose noradrenaline needed
• Dobutamine - add if cardiac dysfunction/low cardiac output (inotrope)
• Target MAP ≥65 mmHg

Steroids:

• Hydrocortisone 200mg/day IV - if refractory septic shock despite adequate fluids and vasopressors
• Addresses relative adrenal insufficiency

Glycaemic control:

• Target blood glucose 6-10 mmol/L
• Insulin infusion if persistent hyperglycaemia

Renal Replacement Therapy (RRT):

• If severe AKI with fluid overload, hyperkalaemia, metabolic acidosis
• Continuous haemofiltration (CVVH) in ITU

DVT Prophylaxis:

• LMWH (enoxaparin) + compression stockings once bleeding risk assessed

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Complications of Urosepsis

• Acute kidney injury (AKI) - most common organ affected in urosepsis
• ARDS (acute respiratory distress syndrome) - lung injury from cytokine storm
• DIC (disseminated intravascular coagulation) - coagulation cascade dysregulation → bleeding + thrombosis
• Multi-organ dysfunction syndrome (MODS) - liver, heart, CNS involvement
• Death - mortality 20-40% for sepsis; >40% for septic shock

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Prognosis Markers

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Examiner's Key Points

• Sepsis-3 definition: organ dysfunction (SOFA ≥2) from dysregulated host response to infection - NOT just fever + tachycardia
• Serum lactate is the most important single marker - >2 = tissue hypoperfusion; >4 = critical
• Antibiotics within 1 hour - each hour of delay increases mortality
• Obstructed infected kidney = EMERGENCY - must decompress (stent or PCN) alongside antibiotics - antibiotics alone will fail
• Noradrenaline is the first-line vasopressor in septic shock
• Blood cultures BEFORE antibiotics - always
• Procalcitonin is specific for bacterial infection and useful for guiding antibiotic duration

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Topic 10: Acute Scrotum Syndrome

The golden rule: Testicular torsion must be excluded in every patient with acute scrotal pain until proven otherwise.

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Differential Diagnosis - Overview

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1. Testicular Torsion - THE Emergency

Mechanism:

• Twisting of the spermatic cord → venous occlusion first → arterial occlusion → ischaemia → infarction
• Predisposed by "bell-clapper deformity" - abnormally high attachment of tunica vaginalis allowing testis to rotate freely within it
• Bell-clapper deformity is bilateral in ~80% → contralateral orchiopexy always required

Epidemiology:

• Bimodal age distribution:
  • Neonatal torsion (extravaginal - occurs in utero or perinatally)
  • Peripubertal torsion (intravaginal - peak 12-18 years; accounts for 65%)
• Can occur at any age; uncommon but possible in adults

"Time is Testicle" - Salvage Rates

This is the most important table in scrotal emergency medicine

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Clinical Features of Testicular Torsion:

• Sudden onset severe scrotal pain - may wake patient from sleep
• Nausea and vomiting (visceral pain response)
• Lower abdominal pain (referred via spermatic cord - T10-L1 dermatome)
• No urinary symptoms
• No fever (initially)
• Prior similar episodes that resolved spontaneously (intermittent torsion)

• Absent cremasteric reflex - single most important sign
  • Cremasteric reflex: stroking inner thigh → ipsilateral testis rises
  • Absent in torsion due to cord twisting abolishing reflex arc
• High-riding testis - spermatic cord shortens as it twists
• Horizontal lie of testis ("transverse lie") - bell-clapper position
• Swollen, tender, indurated testis
• Scrotal erythema and oedema (late sign)
• Prehn's sign: lifting testis relieves pain in epididymo-orchitis but NOT in torsion (unreliable - do not rely on it)

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Investigations:

• Doppler ultrasound: Absent or reduced blood flow to testis; useful if diagnosis uncertain and patient stable
  • Sensitivity ~88%, specificity ~90% - NOT 100%; can miss early torsion
  • A normal Doppler does NOT exclude torsion if clinical suspicion is high
• Urine dipstick: Usually normal in torsion (pyuria suggests epididymo-orchitis)
• Bloods: Usually normal; may show mild leucocytosis

If in doubt - explore the scrotum. A negative exploration is far better than a missed torsion.

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Management - Emergency Surgical Exploration:

Pre-operative:

• IV access, analgesia (IV morphine + anti-emetic)
• Consent for bilateral orchiopexy ± orchidectomy
• NBM, mark operating site
• Manual detorsion can be attempted while awaiting theatre:
  • Rotate testis "like opening a book" (lateral to medial, i.e. outward rotation)
  • Left testis: rotate clockwise; Right testis: rotate anti-clockwise
  • Partial relief does NOT exclude torsion - still needs surgical exploration
  • Temporary measure only

Surgical Exploration:

1. Midline scrotal raphe incision (allows access to both sides)
2. Deliver affected testis, untwist spermatic cord
3. Wrap in warm swabs - observe for 15 minutes for viability
4. Viable testis (pink, bleeding): Bilateral orchiopexy - 3-point fixation with non-absorbable sutures (fixes testis to scrotal wall preventing re-torsion)
5. Non-viable testis (black, necrotic): Orchidectomy + contralateral orchiopexy
   • Prosthetic testis can be offered later for cosmesis

Contralateral orchiopexy is ALWAYS performed - bell-clapper deformity is bilateral; the other testis is equally at risk

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2. Torsion of Testicular Appendage (Appendix Testis)

• Small embryological remnant (Müllerian duct) at upper pole of testis
• Most common cause of acute scrotum in prepubertal boys (7-12 years)

• More gradual onset than testicular torsion
• Less severe pain
• Tenderness localized to upper pole of testis
• "Blue dot sign" - infarcted appendage visible as blue/black dot through scrotal skin at upper pole (pathognomonic; present in ~20%)
• Normal cremasteric reflex
• Doppler: normal or increased blood flow

• Conservative in most cases: analgesia (NSAIDs), scrotal support, reassurance
• Resolves spontaneously over 5-10 days as appendage infarcts and fibrosises
• Surgery if diagnosis uncertain or pain not settling

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3. Epididymo-orchitis

Causes by Age:

Clinical Features:

• Gradual onset scrotal pain (hours to days) - unlike sudden onset in torsion
• Fever, rigors
• Urethral discharge (STI-related)
• Dysuria, frequency (UTI-related)
• Positive cremasteric reflex - present (distinguishes from torsion)
• Prehn's sign positive - lifting testis relieves pain (epididymis decompresses)
• Tender, swollen epididymis (posterolateral) ± testis
• Scrotal erythema, warmth
• Reactive hydrocele may develop

Investigations:

• Urine dipstick + culture
• Urethral swab + STI screen (Chlamydia, gonorrhoea NAAT)
• Doppler USS: Increased blood flow (hyperaemia) to epididymis/testis - opposite of torsion
• Bloods: Raised WBC, CRP

Management:

• STI-related (<35 yrs): Doxycycline 100mg BD × 10-14 days (Chlamydia) + single dose ceftriaxone IM (gonorrhoea)
• Non-STI (>35 yrs): Quinolone (ciprofloxacin 500mg BD) or trimethoprim × 14 days; treat underlying UTI/obstruction
• Scrotal support, analgesia (NSAIDs), bed rest
• Partner notification and treatment if STI-related
• Complications: Epididymal abscess (needs drainage), chronic epididymitis, infertility, testicular atrophy

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4. Fournier's Gangrene - Don't Miss This

• Rapidly spreading scrotal/perineal erythema, oedema, necrosis
• Crepitus on palpation (subcutaneous gas from anaerobes) - pathognomonic
• Severe systemic sepsis (fever, tachycardia, hypotension)
• Foul-smelling discharge
• Pain often disproportionately severe initially, then decreases as nerves are destroyed

• CT perineum/pelvis: gas tracking along fascial planes (more extensive than clinical exam suggests)
• Bloods: LRINEC score (Lab Risk Indicator for Necrotizing Fasciitis) - CRP, WBC, Hb, Na, creatinine, glucose

• Emergency wide surgical debridement - remove ALL necrotic tissue; often extensive
• IV broad-spectrum antibiotics (piperacillin-tazobactam + metronidazole + gentamicin)
• ITU admission, resuscitation
• Repeat debridement every 24-48 hours until clean margins
• Hyperbaric oxygen therapy (adjunct)
• Reconstructive surgery (skin grafting) after infection controlled
• Urinary diversion (suprapubic catheter) if urethra involved

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Clinical Decision-Making - Torsion vs Epididymo-orchitis

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Examiner's Key Points

• Every acute scrotum = testicular torsion until proven otherwise
• Absent cremasteric reflex is the single most important clinical sign of testicular torsion
• Salvage is ~100% if operated within 6 hours - do NOT wait for imaging if suspicion is high
• Bell-clapper deformity is bilateral - always perform contralateral orchiopexy even if that side is normal
• Blue dot sign at the upper pole = torsion of appendix testis (not a surgical emergency)
• Fournier's gangrene = crepitus + necrosis + systemic sepsis → emergency debridement; mortality 20-40%
• Orchitis from mumps virus is haematogenous (not ascending) - occurs 4-8 days after parotitis; can cause infertility

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Summary: All 10 High-Yield Topics Completed ✅

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Section: Inflammatory Diseases - Remaining Topics

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Topic 11: Prostatitis

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Classification - NIH Classification System (Know All 4 Categories)

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Category I: Acute Bacterial Prostatitis

Organisms:

• E. coli (~80%), Klebsiella, Pseudomonas, Enterococcus
• STI-related in young men: Chlamydia, Gonorrhoea

Clinical Features:

• Systemically unwell - fever, rigors, malaise
• Perineal/pelvic/low back pain
• LUTS - dysuria, frequency, urgency, hesitancy
• Possible AUR (inflamed prostate compresses urethra)
• DRE: exquisitely tender, boggy, warm prostate
• WARNING: Vigorous DRE/prostatic massage is CONTRAINDICATED in acute prostatitis - risk of bacteraemia/sepsis

Investigations:

• Urine culture (midstream)
• Blood cultures (if systemically unwell)
• Bloods: FBC (leukocytosis), CRP, U&E
• PSA: markedly elevated (not useful for cancer in this context - wait 4-6 weeks after treatment)
• Transrectal USS: only if abscess suspected (fluctuant mass on DRE, failure to improve)

Management:

• Mild/moderate (oral): Fluoroquinolone (ciprofloxacin 500mg BD) - excellent prostatic penetration; 4 weeks
• Severe (IV): IV ceftriaxone ± gentamicin; step down to oral when improving; total 4-6 weeks
• Analgesia (NSAIDs), adequate hydration
• If AUR: suprapubic catheter preferred over urethral catheter (less painful, avoids worsening)
• Complications: Prostate abscess (needs transrectal or transperineal drainage), chronic prostatitis, sepsis, AUR

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Category II: Chronic Bacterial Prostatitis

• Most common cause of recurrent UTIs in men
• Same organism cultured on repeated occasions
• Symptoms: perineal discomfort, post-ejaculatory pain, LUTS, recurrent UTIs
• DRE: may be normal or mildly tender
• Diagnosis: Meares-Stamey 4-glass test or 2-glass test (pre- and post-massage urine)
• Treatment: Fluoroquinolone × 4-6 weeks (ciprofloxacin or levofloxacin); alpha-blockers for LUTS
• High relapse rate; may need long-term low-dose suppression

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Category III: Chronic Pelvic Pain Syndrome (CPPS)

• Most common form of prostatitis (~90%)
• Pelvic/perineal pain >3 months duration
• No bacterial pathogen identified
• Poorly understood - possible neurogenic, autoimmune, or myofascial mechanism
• Symptoms: pelvic/perineal pain, dysuria, post-ejaculatory pain, sexual dysfunction
• Treatment: multimodal - alpha-blockers (tamsulosin), NSAIDs, 5-ARIs, antibiotics (trial), physiotherapy (pelvic floor), psychological support, gabapentin/pregabalin (neuropathic pain)

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Examiner's Key Points

• Vigorous DRE is contraindicated in acute prostatitis - risk of bacteraemia
• Fluoroquinolones are first-line - best prostatic penetration
• If AUR complicates prostatitis - use suprapubic catheter, not urethral
• CPPS (Category III) is the most common form - no bacteria, poorly understood, multimodal treatment

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Topic 12: Epididymitis and Orchitis

Quick Summary:

• <35 yrs: Chlamydia/Gonorrhoea → doxycycline + ceftriaxone

• 35 yrs: E. coli/gram-negatives → ciprofloxacin × 14 days

• Doppler USS: increased blood flow (hyperaemia)

• Mumps orchitis - most important form
  • Occurs 4-8 days after parotitis
  • Haematogenous spread (not ascending)
  • 20-30% of post-pubertal males with mumps develop orchitis
  • Bilateral in ~30% → risk of infertility (oligospermia/azoospermia)
  • Treatment: supportive (analgesia, scrotal support, ice packs); no antiviral
  • Prevention: MMR vaccine
• Autoimmune orchitis, granulomatous orchitis (TB, sarcoid) - rare

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Topic 13: Renal Abscess and Carbuncle

• Renal abscess: Collection of purulent material within the renal parenchyma
• Renal carbuncle: Coalescence of multiple small cortical abscesses into a single larger abscess (historically referred to cortical abscess from haematogenous S. aureus)

Pathogenesis:

• Haematogenous route: S. aureus from skin infection (furuncle, IV drug use) → cortical abscess
• Ascending route: Complicated UTI / pyelonephritis → corticomedullary abscess (E. coli, gram-negatives)

Clinical Features:

• Fever, rigors, flank pain persisting despite antibiotic treatment
• Should be suspected when pyelonephritis fails to improve after 48-72h of antibiotics
• Flank tenderness, palpable mass (large abscess)
• Psoas irritation: hip held in flexion (psoas abscess extension)

Investigations:

• CT abdomen with contrast: Gold standard - thick-walled ring-enhancing collection; perinephric extension
• USS: Hypoechoic collection; used for drainage guidance

Management:

• Antibiotic choice: S. aureus (flucloxacillin/MRSA → vancomycin); gram-negatives (as per pyelonephritis)
• Duration: 4-6 weeks IV/oral antibiotics

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Topic 14: Tuberculosis of the Urinary Tract

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Pathogenesis

• Primary pulmonary TB → haematogenous spread to kidneys (bilateral seeding)
• Renal cortex is the initial site (rich blood supply)
• Forms granulomas → caseous necrosis → cavitation → "putty kidney" (dystrophic calcification)
• Spread down collecting system → ureter (strictures) → bladder (fibrosis, contracted bladder) → epididymis (most common genital site) → testis

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Clinical Features - "The Great Masquerader"

Symptoms:

• Sterile pyuria - the classic hallmark (pus cells in urine with negative routine culture)
• Haematuria (macro or micro)
• Frequency, dysuria, nocturia (cystitis-like)
• Flank pain
• Systemic: weight loss, night sweats, low-grade fever, malaise
• Often insidious/asymptomatic until advanced disease
• Epididymal swelling (beaded, irregular epididymis) in genital TB

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Investigations

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Treatment

Anti-TB Chemotherapy - Standard Regimen (RIPE):

• 2 months intensive phase: Rifampicin + Isoniazid + Pyrazinamide + Ethambutol (RIPE)
• 4 months continuation phase: Rifampicin + Isoniazid
• Total: 6 months

Side effects to know:

Surgical Complications Requiring Intervention:

• Ureteric strictures: Balloon dilatation or ureteric stenting; open reconstruction (ureteroplasty) if severe
• Contracted bladder (capacity <100ml): Augmentation cystoplasty (bladder augmented with ileal segment)
• Non-functioning kidney (destroyed by disease): Nephrectomy
• Epididymal abscess: Surgical drainage or epididymectomy

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Examiner's Key Points

• Sterile pyuria (pyuria + negative standard urine culture) = TB until proven otherwise
• Send 3 early morning urine specimens for AFB culture - highest yield
• CT urogram: moth-eaten calyces, ureteric strictures, putty kidney, small contracted bladder
• Golf-hole ureteric orifices on cystoscopy = TB
• Ethambutol → optic neuritis; Isoniazid → peripheral neuropathy (give B6); Rifampicin → orange urine

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Section: Andrology

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Topic 15: Male Infertility

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Causes - Classified as Pre-testicular, Testicular, Post-testicular

Pre-testicular (Endocrine/Hormonal) ~1-2%:

• Hypogonadotropic hypogonadism (low FSH, LH, testosterone)
• Kallmann syndrome (GnRH deficiency + anosmia)
• Hyperprolactinaemia (prolactinoma)
• Anabolic steroid / exogenous testosterone use (suppresses FSH/LH → azoospermia)
• Systemic illness (liver disease, renal failure, thyroid disorders)

Testicular (Primary Gonadal Failure) ~70-80%:

• Idiopathic - most common (no identifiable cause)
• Varicocele - most common identifiable/correctable cause (~40% of infertile men)
• Cryptorchidism (undescended testis) - heat damage to spermatogenesis
• Klinefelter syndrome (47,XXY) - most common genetic cause; azoospermia; small firm testes; gynaecomastia; tall stature
• Orchitis (mumps, autoimmune)
• Chemotherapy / radiotherapy
• Testicular torsion (previous)
• Y chromosome microdeletions (AZF regions - AZFa, AZFb, AZFc)

Post-testicular (Obstructive) ~10-20%:

• Vasectomy (most common cause of obstructive azoospermia)
• Epididymal obstruction (post-epididymitis, Young syndrome)
• Ejaculatory duct obstruction
• Congenital bilateral absence of vas deferens (CBAVD) - associated with cystic fibrosis (CFTR mutation)
• Retrograde ejaculation (semen enters bladder; seen with TURP, diabetes, alpha-blockers)

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Diagnosis

History:

• Duration of infertility, previous pregnancies (partner's fertility)
• Sexual history (frequency, timing, erectile/ejaculatory dysfunction)
• Past medical: orchitis, STIs, cryptorchidism, testicular surgery/torsion
• Drugs: anabolic steroids, chemotherapy, sulfasalazine (reversible azoospermia), antihypertensives
• Social: smoking, alcohol, heat exposure (hot baths, laptops, tight clothing), occupational toxins

Examination:

• Secondary sexual characteristics (body hair, voice, gynaecomastia)
• Testicular volume (Prader orchidometer): normal >15ml; small testes = poor spermatogenesis
• Varicocele (standing + Valsalva): "bag of worms" feel; left side >>right (left gonadal vein drains into left renal vein at 90°)
• Epididymis (full/tender = obstruction), vas deferens (absent = CBAVD)
• DRE (ejaculatory duct obstruction)

Investigations:

---

Treatment

Specific treatments:

Assisted Reproduction:

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Examiner's Key Points

• Varicocele is the most common correctable cause of male infertility
• Klinefelter (47,XXY) is the most common genetic cause - small firm testes, gynaecomastia, raised FSH/LH, low testosterone
• CBAVD = absent vas deferens + CFTR mutation → always test for cystic fibrosis
• Raised FSH = primary testicular failure (testes not responding to FSH)
• Low FSH + low testosterone = pre-testicular/hypothalamic-pituitary cause
• Anabolic steroids suppress FSH/LH → azoospermia (usually reversible)

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Topic 16: Priapism

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Classification - Three Types

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Causes

Ischaemic Priapism:

• Sickle cell disease - most common cause in children; sickled cells occlude corporal sinusoids
• Haematological malignancies (leukaemia, lymphoma)
• Drugs: intracavernosal injections (alprostadil/PGE1 - most common in adults), antipsychotics (chlorpromazine, quetiapine), antidepressants (trazodone), antihypertensives, cocaine
• Idiopathic (~50%)

Non-Ischaemic (High-Flow) Priapism:

• Perineal/penile trauma → fistula between cavernosal artery and lacunar space → unregulated flow
• Painless; not an emergency

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Pathophysiology of Ischaemic Priapism:

Venous outflow obstruction
        ↓
Blood stasis in corpora cavernosa
        ↓
O₂ consumption without replenishment
        ↓
Hypoxia + acidosis + hypercapnia
        ↓
Smooth muscle necrosis → fibrosis → erectile dysfunction

After 4-6 hours: smooth muscle damage begins After 24 hours: permanent ED likely After 48-72 hours: near-certain irreversible ED

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Diagnosis

• Clinical: Rigid corpora cavernosa + flaccid glans (corpus spongiosum not involved)
• Cavernosal blood gas aspiration: differentiates ischaemic (dark, deoxygenated blood) from high-flow (bright red, oxygenated)
  • Ischaemic: pO₂ <30mmHg, pCO₂ >60mmHg, pH <7.25
  • Normal/High-flow: pO₂ >90mmHg
• Colour Doppler USS: absent cavernosal artery flow = ischaemic; high-flow fistula = non-ischaemic

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Management

Ischaemic Priapism - Stepwise:

• Corporal aspiration of blood via 19G butterfly needle in corpora cavernosa (2 o'clock or 10 o'clock position at base of penis)
• Aspirate 20-50ml dark blood; irrigate with normal saline
• Detumescence occurs in ~30%

• Phenylephrine (alpha-1 agonist) - first-line; most selective, least cardiovascular side effects
• Dilute in normal saline; inject every 3-5 minutes × up to 1 hour
• Monitor BP and HR (risk of hypertension/reflex bradycardia)
• Adrenaline / metaraminol - alternatives

• If aspiration + phenylephrine fails
• Creates fistula between corpus cavernosum and corpus spongiosum or glans
• Types:
  • Distal shunts (first-line surgical): Winter (core biopsy through glans), Ebbehoj, Al-Ghorab
  • Proximal shunts: Quackels (cavernosus-spongiosus), Grayhack (cavernosus-saphenous vein)
• If all shunts fail → immediate penile prosthesis insertion (within 2 weeks is easier before fibrosis)

Sickle Cell Priapism:

• Additional measures: IV hydration, oxygen, analgesia, blood transfusion/exchange transfusion
• Hydroxyurea for prevention of recurrent episodes

Non-Ischaemic Priapism:

• Not an emergency; can observe
• Selective arterial embolization (interventional radiology) - first-line
• Surgical ligation if embolization fails

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Examiner's Key Points

• Ischaemic priapism = painful + deoxygenated blood on aspiration = emergency
• Non-ischaemic = painless + oxygenated blood = arteriovenous fistula from trauma = NOT emergency
• Phenylephrine is the intracavernosal drug of choice (alpha-1 selective, safest cardiovascular profile)
• Time matters: after 24 hours, permanent ED is likely; after 48 hours, near-certain
• Sickle cell disease is the most common cause in children

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• Trauma section (kidney, bladder, urethra)
• Urological Emergencies (already covered renal colic, AUR, urosepsis, acute scrotum - remaining: acute renal failure, emergency obstructive uropathy)
• Tumours (Wilms tumour, ureter tumours, prostate cancer)
• Diagnostic Methods (CT/MRI, uroflowmetry, cystoscopy, PSA)

Section: Urological Emergencies (Remaining)

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Topic 17: Acute Renal Failure in Urology (Acute Kidney Injury - AKI)

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KDIGO Staging of AKI

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Classification - Pre-renal, Renal, Post-renal

Pre-renal AKI (most common overall ~55%):

• Reduced renal perfusion
• Causes: hypovolaemia (haemorrhage, dehydration, burns), heart failure, sepsis, hepatorenal syndrome, NSAIDs/ACEi (reduce GFR)
• Urine sodium <20 mmol/L; urine osmolality >500 mOsm/kg (kidneys conserving)
• Reversible with fluid resuscitation

Intrinsic Renal AKI (~40%):

• Direct damage to kidney parenchyma
• Acute tubular necrosis (ATN) - most common intrinsic cause
  • Ischaemic (prolonged pre-renal → tubular hypoxia)
  • Nephrotoxic (aminoglycosides, contrast, NSAIDs, cisplatin, myoglobin/rhabdomyolysis)
• Glomerulonephritis, vasculitis, interstitial nephritis, myeloma cast nephropathy
• Urine sodium >40 mmol/L; urine osmolality <350 mOsm/kg (kidneys cannot concentrate)

Post-renal AKI (Obstructive - Most Relevant to Urology ~5%):

• Bilateral obstruction OR unilateral obstruction in solitary/transplant kidney
• Must be excluded in ALL patients with AKI - it is the most reversible cause
• Causes:
  • Bilateral ureteric obstruction (stones, retroperitoneal fibrosis, pelvic malignancy - cervical, prostate, colorectal)
  • BPH / prostate cancer (bladder outlet obstruction → bilateral hydronephrosis)
  • Ureteric strictures
  • Neurogenic bladder
  • Posterior urethral valves (children)
  • Blood clots, sloughed papillae
  • External compression: retroperitoneal lymphadenopathy, retroperitoneal fibrosis

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Urological Causes of AKI - Key Scenarios

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Clinical Features

• Oliguria (<400ml/day) or anuria (<100ml/day)
• Fluid overload: peripheral oedema, pulmonary oedema, hypertension, raised JVP
• Uraemia: nausea, vomiting, confusion, pericarditis ("uraemic frost" in severe)
• Hyperkalaemia - most dangerous acute complication → cardiac arrhythmia → death
• Metabolic acidosis
• Anaemia (reduced EPO production)
• Distended bladder (palpable/percussable) if bladder outlet obstruction

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Investigations

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Life-Threatening Complications - AEIOU Indications for Emergency RRT

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Hyperkalaemia Management (Urological Emergency)

1. IV Calcium gluconate (10ml of 10%) - cardioprotective; stabilizes cardiac membrane; immediate effect; does NOT lower K⁺
2. IV Insulin + Dextrose (10 units actrapid + 50ml 50% dextrose) - shifts K⁺ into cells; onset 15-30 min
3. Salbutamol nebuliser (10-20mg) - beta-2 agonist; shifts K⁺ into cells; adjunct
4. Calcium resonium (sodium polystyrene sulfonate) - oral/PR resin; removes K⁺ from gut; slower
5. Sodium bicarbonate - if severe metabolic acidosis; shifts K⁺ intracellularly
6. Dialysis/haemofiltration - definitive if above measures fail; FASTEST at removing K⁺

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Management of Post-renal AKI

Immediate:

1. Bladder catheterization if bladder outlet obstruction (most common/quickest fix)
2. Bilateral ureteric stents (JJ stents) - if bilateral ureteric obstruction
3. Bilateral percutaneous nephrostomies - if stenting not possible or very unwell for GA
4. Monitor for post-obstructive diuresis (as covered in Topic 4)

Ongoing:

• Fluid balance, daily U&E/creatinine
• Avoid nephrotoxins (NSAIDs, aminoglycosides, contrast - use DECT/non-contrast CT)
• Treat underlying cause (malignancy, stone)
• Renal team input - may need RRT if no recovery

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Examiner's Key Points

• Post-renal AKI is the most reversible cause - USS kidneys in EVERY AKI to exclude obstruction
• Hyperkalaemia is the most immediately life-threatening complication - calcium gluconate first (cardioprotective), then shift K⁺ into cells (insulin/dextrose, salbutamol)
• ECG changes in hyperkalaemia: peaked T waves → prolonged PR → widened QRS → sine wave → VF/asystole
• Post-obstructive diuresis after catheterization of chronic retention - monitor and replace fluids carefully
• Malignant ureteric obstruction (bilateral) from pelvic cancer = bilateral nephrostomies to restore renal function before oncological treatment

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Topic 18: Emergency Conditions in Obstructive Uropathy

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Classification by Level of Obstruction

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Emergency Scenarios in Obstructive Uropathy

1. Infected Obstructed Kidney (Pyonephrosis)

• Definition: Infected, obstructed, dilated collecting system filled with purulent urine (pus in the kidney)
• Causes: Obstructing ureteric stone + superimposed infection (most common); malignant obstruction + UTI
• Clinical features: Fever, rigors, loin pain, AKI, septic shock
• Imaging: USS/CT - hydronephrosis + debris/echogenic material in collecting system (pus)
• Management:
  • Emergency percutaneous nephrostomy (PCN) preferred (avoids GA; direct drainage)
  • OR retrograde ureteric stent under antibiotic cover
  • IV broad-spectrum antibiotics (piperacillin-tazobactam)
  • ICU if septic shock
  • Treat underlying cause (stone removal) once infection controlled

2. Bilateral Ureteric Obstruction + AKI

• Causes: Bilateral stones, retroperitoneal fibrosis, bilateral malignant obstruction (pelvic cancers)
• Retroperitoneal fibrosis (RPF): Periaortic fibrotic mass encases and medially displaces ureters
  • CT: soft tissue mantle around aorta
  • Cause: idiopathic (IgG4-related disease), drugs (methysergide, beta-blockers), malignancy, post-radiation
  • Treatment: ureteric stenting; corticosteroids for IgG4-related; ureterolysis (surgical release)
• Management of bilateral obstruction: Bilateral PCN or bilateral JJ stents; urgent oncology referral if malignancy

3. AUR with Renal Failure (High-Pressure Chronic Retention)

• Covered in Topic 4 and Topic 17
• Key point: gradual decompression; watch for post-obstructive diuresis

4. Ureteric Injury (Iatrogenic)

• Most common urological complication of pelvic surgery (hysterectomy, colorectal surgery)
• Types: Ligation, kinking, transection, ischaemia
• Presentation: Flank pain, fever, AKI, urinary leak (ureterovaginal fistula)
• Diagnosis: CT urogram; IVU; retrograde pyelogram
• Management:
  • Early (<48h): surgical repair (primary anastomosis, reimplantation)
  • Delayed (>48h): percutaneous nephrostomy first → definitive repair at 6-12 weeks
  • Boari flap / psoas hitch: for distal ureteric defects
  • Ileal ureter: for long-segment defects

5. Posterior Urethral Valves (PUV) - Paediatric Emergency

• Most common cause of severe obstructive uropathy in male neonates/infants
• Congenital membrane at level of verumontanum obstructs posterior urethra
• Detected antenatally (bilateral hydronephrosis on USS), or neonatal poor stream/urosepsis
• Renal dysplasia from in utero back-pressure
• Management: Endoscopic valve ablation (cystoscopy); temporary vesicostomy if unfit for endoscopy
• Long-term: risk of CKD, bladder dysfunction, renal transplant

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Examiner's Key Points

• Pyonephrosis (pus in obstructed kidney) = emergency PCN under antibiotic cover
• Retroperitoneal fibrosis: medial deviation of ureters on CT/IVU; IgG4-related disease; treat with steroids + stenting
• Iatrogenic ureteric injury at hysterectomy: PCN first if delayed presentation; repair at 6-12 weeks
• Posterior urethral valves: most common severe lower urinary obstructive lesion in male neonates; treat with endoscopic valve ablation

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Section: Tumours of the Urinary and Reproductive Systems (Remaining)

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Topic 19: Wilms Tumour (Nephroblastoma)

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Epidemiology

• Accounts for ~90% of childhood kidney tumours
• Most cases sporadic; ~10% bilateral
• M:F = 1:1
• Associated with overgrowth syndromes and congenital anomalies

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Associated Syndromes - High-Yield Viva

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Pathology

• Classically contains 3 elements: blastemal + stromal + epithelial (triphasic histology)
• Favourable histology (~90%): absence of anaplasia → good prognosis
• Unfavourable histology (~10%): diffuse anaplasia → poor prognosis; resistant to chemotherapy

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Clinical Features

Symptoms:

• Smooth, non-tender abdominal mass - most common presentation; often discovered by parent bathing child
• Abdominal pain (if haemorrhage into tumour)
• Haematuria (macro or micro) - less common than RCC in adults
• Hypertension (renin secretion by tumour)
• Fever, malaise, weight loss

Signs:

• Flank/abdominal mass - smooth, firm, does NOT cross the midline (unlike neuroblastoma which does)
• Hypertension (~25%)
• Varicocele (left-sided - IVC/renal vein involvement)

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Investigations

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Staging (COG/SIOP System)

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Treatment

North American approach (COG - Children's Oncology Group):

• Primary nephrectomy first (without pre-operative chemotherapy) → then adjuvant therapy based on stage/histology

European approach (SIOP - International Society of Paediatric Oncology):

• Pre-operative chemotherapy first (vincristine + actinomycin D × 4 weeks) → then nephrectomy → adjuvant therapy
• Advantage: reduces tumour size/spillage risk; allows tumour response assessment

Treatment by Stage (general):

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Prognosis

• Excellent overall - one of the great success stories of paediatric oncology
• Stage I-II favourable: >95% 5-year survival
• Stage III-IV favourable: ~85-90%
• Unfavourable histology (anaplasia): ~55-70%

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Wilms vs Neuroblastoma - Viva Distinction

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Examiner's Key Points

• Wilms tumour = most common renal malignancy in children; peak 3-4 years; smooth non-tender flank mass
• WAGR syndrome: Wilms + Aniridia + Genitourinary anomalies + intellectual Retardation = WT1 gene deletion
• Triphasic histology: blastemal + stromal + epithelial
• Distinguish from neuroblastoma: Wilms does NOT cross midline; normal catecholamines; older child
• Excellent prognosis - >95% survival for stages I-II with favourable histology
• Bilateral (Stage V) = nephron-sparing surgery to preserve renal function

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Topic 20: Tumours of the Ureter

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Epidemiology

• Rare - account for ~5% of all urothelial tumours
• Renal pelvis : ureter = 2:1
• M:F = 3:1; peak age 70-80 years
• Strongly associated with bladder urothelial carcinoma - synchronous or metachronous

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Risk Factors

• Smoking (as for bladder cancer)
• Analgesic abuse / aristolochic acid (herbal remedies - Balkan nephropathy)
• Lynch syndrome (HNPCC) - strongest genetic association; autosomal dominant; MLH1/MSH2 mutations; 15x increased risk of UTUC
• Occupational chemical exposure
• Chronic urinary tract inflammation/stones
• Previous bladder TCC

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"Field Change" Theory

• Synchronous bilateral upper tract tumours
• Concurrent bladder TCC
• Metachronous tumours (new tumours appearing at other sites)
• Lifetime cystoscopic surveillance required even after UTUC treatment

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Clinical Features

• Haematuria (gross or microscopic) - most common symptom (~75%)
• Flank/loin pain (obstruction of ureter)
• Hydronephrosis (obstruction)
• Palpable flank mass (advanced)
• Incidental finding on CT/USS
• Passage of clots (elongated/worm-shaped - upper tract origin)

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Investigations

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Staging

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Treatment

Low-risk UTUC (low grade, small, unifocal):

• Ureteroscopic laser ablation (nephron-sparing endoscopic treatment)
• Topical BCG or mitomycin via retrograde instillation
• Close surveillance with ureteroscopy

High-risk UTUC (high grade, large, multifocal, hydronephrosis, positive cytology):

• Radical nephroureterectomy (RNU) - gold standard
  • Removes kidney, entire ureter, and bladder cuff (small cuff of bladder around ureteric orifice)
  • Bladder cuff excision is mandatory (leaving ureteric stump = risk of stump recurrence)
  • Laparoscopic approach preferred
• Lymph node dissection if high-risk/invasive
• Neoadjuvant cisplatin-based chemotherapy (same as bladder cancer) for muscle-invasive UTUC

Adjuvant intravesical mitomycin C:

• Single instillation post-RNU reduces bladder recurrence

Metastatic UTUC:

• Cisplatin-based chemotherapy (GC regimen)
• Immunotherapy (pembrolizumab) second-line

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Post-treatment Surveillance

• Lifelong cystoscopy (bladder recurrence in ~30% after RNU)
• Contralateral ureteroscopy
• CT urogram annually

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Examiner's Key Points

• UTUC is part of a field change - entire urothelium at risk; always check bladder with cystoscopy
• Lynch syndrome (HNPCC) = strongest genetic predisposition; MLH1/MSH2 mutations
• "Goblet sign" on retrograde pyelogram = ureteric TCC (vs smooth filling defect from stone)
• Radical nephroureterectomy with bladder cuff excision is gold standard for high-risk UTUC
• Bladder cuff must be excised - leaving a ureteric stump risks stump recurrence
• ~30% develop bladder TCC after RNU - lifelong cystoscopic surveillance mandatory

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Topic 21: Prostate Cancer

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Epidemiology

• Most common male cancer in the UK/USA
• Predominantly a disease of older men (rare <50 years; median diagnosis age ~66)
• M:F - only men
• Risk factors: age, Black African/Caribbean ethnicity (2-3x higher risk, more aggressive), family history (1st degree relative - 2x risk; BRCA2 mutation - high risk), high-fat Western diet

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Pathology

• Adenocarcinoma ~95% - arises from peripheral zone (~70%), transition zone (~30%)
• Other types: ductal adenocarcinoma, neuroendocrine/small cell (aggressive)
• Gleason grading system:
  • Histological grading based on glandular architecture
  • Two most predominant patterns scored 1-5 each; added together
  • Gleason score = primary pattern + secondary pattern (e.g. 3+4=7)
  • Modern reporting uses Grade Groups (GG) 1-5:

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Clinical Features

Localised disease (often asymptomatic):

• Incidental finding on PSA screening or TURP histology
• DRE: hard, irregular, nodular prostate; loss of median sulcus; asymmetry

Locally advanced disease:

• LUTS (obstructive and irritative) from urethral involvement
• Haematuria, haematospermia
• Erectile dysfunction
• Ureteric obstruction → AKI

Metastatic disease:

• Bone pain - most common presenting symptom of metastatic prostate cancer
  • Osteoblastic (sclerotic) bone metastases - characteristic (unlike most other cancers which are lytic)
  • Spine (most common), pelvis, femur, ribs
• Pathological fractures
• Spinal cord compression - back pain + leg weakness + urinary/faecal incontinence → neurological emergency
• Weight loss, anaemia, fatigue
• Lower limb oedema (lymph node obstruction)

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PSA (Prostate-Specific Antigen)

• Serine protease produced by prostatic epithelium; organ-specific (not cancer-specific)
• Normal: <4 ng/mL (age-specific ranges used)
• Causes of elevated PSA:
  • Prostate cancer
  • BPH
  • Prostatitis
  • Urinary retention
  • Post-catheterization
  • Post-DRE (minimal effect)
  • Post-TRUS/biopsy (significant rise)

PSA derivatives:

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Diagnosis

Biopsy Pathway:

1. Elevated PSA or abnormal DRE
2. mpMRI prostate (multiparametric MRI) - FIRST before biopsy in most guidelines
   • T2W + DWI + DCE sequences
   • PI-RADS scoring (1-5):
     • PI-RADS 1-2: very low/low probability of clinically significant cancer
     • PI-RADS 3: equivocal
     • PI-RADS 4-5: likely/highly likely clinically significant cancer → proceed to biopsy
3. Prostate biopsy:
   • Transperineal (TP) biopsy (preferred): needle inserted through perineum skin under local anaesthesia; no risk of rectal sepsis; higher detection rate
   • Transrectal ultrasound (TRUS) guided biopsy: needle through rectum; risk of rectal sepsis/septicaemia; largely replaced by TP approach
   • MRI-targeted (fusion) biopsy: combines mpMRI targets with systematic biopsy; highest cancer detection rate

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Staging

TNM:

Risk Stratification (EAU/NCCN):

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Treatment - Localised Prostate Cancer

Low risk / very low risk:

• Active surveillance (AS): PSA monitoring, repeat mpMRI, repeat biopsy at intervals; curative treatment deferred unless progression
  • Suitable for GG1 (Gleason 6), T1-T2a, PSA <10

Localised (any risk) - Curative Intent:

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Treatment - Advanced/Metastatic Prostate Cancer

Androgen Deprivation Therapy (ADT) - Backbone of Advanced Treatment:

• Prostate cancer is androgen-dependent → deprive testosterone → tumour regression
• Methods:
  • Surgical castration (bilateral orchidectomy): Immediate, permanent, cheap; psychological impact
  • LHRH agonists (leuprorelin, goserelin): Monthly/3-monthly SC implants; cause initial testosterone surge ("flare") → give anti-androgen first (bicalutamide) for 2-4 weeks to block flare
  • LHRH antagonists (degarelix): No flare; immediate testosterone suppression
  • Anti-androgens (bicalutamide, enzalutamide): Block androgen receptor at prostate

Castrate-Resistant Prostate Cancer (CRPC):

• Disease progresses despite castrate testosterone levels (<50 ng/dL)
• Treatment:
  • Enzalutamide - next-generation anti-androgen (blocks AR more potently)
  • Abiraterone - inhibits CYP17A1 (androgen synthesis in adrenal glands and tumour); must give with prednisolone
  • Docetaxel - chemotherapy; improves survival in metastatic CRPC
  • Cabazitaxel - second-line taxane
  • Radium-223 (Xofigo) - alpha-emitting radiopharmaceutical; for bone-dominant metastatic CRPC; reduces skeletal events
  • PARP inhibitors (olaparib, rucaparib) - for BRCA1/2 or homologous recombination repair defects

Spinal Cord Compression - Emergency:

• High-dose IV dexamethasone immediately (reduces oedema)
• Urgent MRI spine (whole spine)
• Oncology + neurosurgery/spinal surgery referral
• Radiotherapy to affected levels
• Surgical decompression if single level, good prognosis, fit for surgery

Bone Metastases Management:

• Bisphosphonates (zoledronic acid IV): reduce skeletal-related events, bone pain
• Denosumab (anti-RANKL): superior to bisphosphonates for prevention of skeletal events
• Radiotherapy for painful bone metastases
• Pathological fracture: orthopaedic fixation

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Prognosis

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Examiner's Key Points

• Prostate cancer arises from the peripheral zone; BPH from the transition zone
• Gleason/Grade Group system: GG1 (3+3) = low risk; GG5 (9-10) = very high risk
• PSA is organ-specific NOT cancer-specific; BPH, prostatitis, and instrumentation all raise PSA
• mpMRI before biopsy; PI-RADS 4-5 = proceed to biopsy
• Osteoblastic (sclerotic) bone metastases are characteristic of prostate cancer
• ADT flare: LHRH agonists cause initial testosterone surge - cover with anti-androgen (bicalutamide) for first 2-4 weeks
• Spinal cord compression = emergency: IV dexamethasone immediately + urgent MRI
• Abiraterone blocks CYP17A1 (adrenal androgen synthesis) - must give with prednisolone to prevent adrenal insufficiency
• BRCA2 mutation = high risk of aggressive prostate cancer + eligible for PARP inhibitors

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Section Summary - Topics Covered This Round

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• Trauma (kidney, bladder, urethra, combined)
• Diagnostic Methods (CT/MRI, uroflowmetry, PSA examination, cystoscopy, urinalysis)
• General topics (dysuric disorders, pain syndrome, differential diagnosis of flank pain)

Section: Trauma of the Genitourinary System

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Topic 22: Renal Trauma

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Epidemiology

• Blunt trauma accounts for ~90% (road traffic accidents, falls, contact sports, assaults)
• Penetrating trauma ~10% (stab wounds, gunshot wounds - higher in USA)
• Right and left kidneys equally affected
• Children more vulnerable - kidneys relatively larger, less perirenal fat, weaker abdominal muscles, incomplete ossification of ribs

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Mechanism of Injury

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AAST (American Association for the Surgery of Trauma) Grading

Grades I-III = minor injuries (~90%); Grades IV-V = major injuries (~10%)

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Clinical Features

Symptoms:

• Haematuria - cardinal sign (present in ~80-90%)
  • Important caveat: Degree of haematuria does NOT correlate with injury severity
  • Renal pedicle avulsion (Grade V) can present with microscopic or NO haematuria
• Flank pain, loin tenderness
• Nausea, vomiting

Signs:

• Flank bruising / ecchymosis (Grey Turner's sign - retroperitoneal haematoma)
• Loin/flank tenderness, guarding
• Palpable flank mass (large haematoma)
• Signs of haemodynamic instability (tachycardia, hypotension) in major injury
• Fractured lower ribs (10, 11, 12) or transverse process fractures → associated renal injury

Associated injuries:

• Liver, spleen (right vs left respectively)
• Bowel, pancreas, great vessels
• Spinal fractures
• Chest injuries (pneumothorax, haemothorax)

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Investigations

When to Image (CT indication criteria):

• Gross haematuria after any trauma → always image
• Microscopic haematuria + hypotension (SBP <90) → always image
• Significant deceleration mechanism (high-speed RTA, fall >6m)
• Penetrating trauma to flank/abdomen
• Paediatric patients: any haematuria (lower threshold)
• Suspected major injury regardless of haematuria

Microscopic haematuria alone in haemodynamically stable adult after blunt trauma has low yield - imaging may be deferred, but clinical judgement required

Imaging:

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Management

Principles:

• Haemodynamic stability determines management approach
• Renal preservation is the goal whenever safely possible
• Most renal injuries (Grades I-III) are managed conservatively

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Haemodynamically Stable Patient:

• Conservative management (non-operative):
  • Bed rest until gross haematuria clears
  • Adequate analgesia
  • Strict fluid balance, serial haematocrit monitoring
  • IV antibiotics if collecting system injury
  • Repeat CT at 48-72h if clinical deterioration
  • Avoid NSAIDs (impair renal perfusion, inhibit platelet function)
  • Activity restriction until haematuria resolves; no contact sports for 4-6 weeks
  • Success rate >95% for Grade I-III

• Selected Grade IV injuries can be managed conservatively with close monitoring
• Urinary extravasation: Most resolve spontaneously; if persistent → ureteric stent
• Vascular injuries (segmental): Angioembolization (selective)

• Shattered kidney or pedicle injury in stable patient: Angioembolization if segmental; or surgical exploration
• Devascularized kidney: warm ischaemia tolerated <90 min; revascularization rarely successful if delayed presentation

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Haemodynamically Unstable Patient:

1. IV access × 2, aggressive fluid resuscitation
2. Activate massive transfusion protocol (MTP): 1:1:1 ratio (packed red cells : FFP : platelets)
3. If isolated renal injury causing instability → emergency exploration and nephrectomy
   • Intraoperative one-shot IVU before nephrectomy (10ml/kg IV contrast, plain film at 10 min) - confirms functioning contralateral kidney
4. Renal reconstruction (renorrhaphy) if sufficient viable tissue and patient stable enough
5. Damage control: pack and leave → ICU resuscitation → return to theatre 24-48h

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Indications for Surgical Exploration

Blunt trauma: Retroperitoneal haematomas are generally NOT explored if stable (Gerota's fascia tamponades bleeding); Penetrating trauma: All Zone II (perirenal) haematomas are explored

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Minimally Invasive Interventions:

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Complications

Early:

• Haemorrhage (primary, secondary - delayed haemorrhage at 1-2 weeks from pseudoaneurysm)
• Urinary extravasation → urinoma formation
• Infection / abscess

Late:

• Renal artery stenosis → renovascular hypertension ("Page kidney" - external compression of kidney by fibrotic capsule causing renin-mediated hypertension)
• Post-traumatic hydronephrosis (PUJ stricture)
• Arteriovenous fistula (pulsatile bruit, haematuria months after trauma or iatrogenic injury)
• Loss of renal function / atrophy
• Renal abscess

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Examiner's Key Points

• Haematuria is the cardinal sign but does NOT correlate with injury severity - Grade V pedicle injuries can have minimal haematuria
• CT with delayed phase is essential to detect urinary extravasation (Grade IV)
• Haemodynamically stable = conservative management for Grades I-III; unstable = surgery/damage control
• One-shot IVU before emergency nephrectomy = confirms contralateral kidney function
• Page kidney = perinephric haematoma/fibrosis → external compression → renin-mediated hypertension
• Penetrating retroperitoneal haematomas must be explored; blunt haematomas are generally not explored if stable

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Topic 23: Trauma of the Bladder

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Epidemiology

• ~2% of all abdominal trauma
• ~90% associated with pelvic fractures
• ~10% of pelvic fractures have associated bladder injury
• Penetrating bladder injuries less common in civilian trauma

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Mechanism and Types

Blunt Trauma:

• Pelvic fracture → bony fragments directly lacerate bladder wall (most common mechanism)
• Sudden compressive force on full bladder → intraperitoneal rupture (bladder dome - thinnest part)
• Seat belt injury / steering wheel injury

Penetrating Trauma:

• Stab/gunshot through lower abdomen or pelvis

Iatrogenic:

• TURBT (transurethral resection - most common iatrogenic cause)
• Gynaecological surgery (hysterectomy, caesarean section)
• Colorectal surgery
• Cystoscopy
• Trocar placement (laparoscopy)

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Classification - Two Main Types

1. Intraperitoneal Rupture (IP) - ~40%

• Mechanism: Blunt force on distended/full bladder → dome ruptures → urine leaks into peritoneal cavity
• Site: Bladder dome (only part covered by peritoneum)
• Presentation: Lower abdominal pain, distension, inability to void, peritonism (urine peritonitis)
• CT finding: Free fluid (urine) in peritoneum, around bowel loops; contrast in peritoneal cavity on delayed CT
• Treatment: Emergency surgical repair (laparotomy or laparoscopic) - intraperitoneal urine causes chemical and bacterial peritonitis

2. Extraperitoneal Rupture (EP) - ~60%

• Mechanism: Direct laceration from pelvic fracture bone fragments; or blunt force on empty bladder
• Site: Anterolateral wall
• Presentation: Haematuria, difficulty voiding, perineal/scrotal ecchymosis, pelvic haematoma
• CT finding: Contrast extravasation confined to perivesical space (flame-shaped); does NOT enter peritoneal cavity
• Treatment: Conservative - urethral catheter drainage × 10-14 days → repeat cystogram → remove catheter when healed

3. Combined IP + EP:

• Rare; requires surgical repair

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Diagnosis

Clinical suspicion:

• Gross haematuria after trauma + pelvic fracture = bladder injury until proven otherwise
• Inability to void post-trauma
• Never catheterize blindly if urethral injury suspected first (see Topic 24)

Investigations:

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Management

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Complications

• Urine leak/urinoma if not adequately repaired/drained
• Vesicovaginal fistula (gynaecological surgery complication)
• Vesicointestinal fistula (colorectal surgery/radiation)
• Bladder outlet obstruction (stricture)
• Recurrent UTIs
• Bladder capacity reduction (fibrosis)

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Examiner's Key Points

• Gross haematuria + pelvic fracture = bladder injury until proven otherwise; always do CT cystogram
• Intraperitoneal rupture = bladder dome + full bladder + blunt force = surgical emergency
• Extraperitoneal rupture = pelvic fracture fragments = conservative catheter drainage
• Active bladder filling (350ml contrast via catheter) is essential for CT cystogram - passive filling from IV contrast is insufficient and will miss injuries
• Drainage film on conventional cystogram is mandatory - contrast hidden behind full bladder may only be seen after drainage

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Topic 24: Trauma of the Urethra

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Anatomical Division - Critical for Understanding Urethral Injuries

Male Urethra (20cm):

• Posterior urethra: Prostatic urethra + membranous urethra (passes through urogenital diaphragm)
• Anterior urethra: Bulbar urethra + penile (spongiosa) urethra + fossa navicularis

Female Urethra (4cm):

• Much shorter; entirely "posterior" equivalent
• Injuries less common but can occur with pelvic fractures

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Posterior Urethral Injuries

Mechanism:

• Almost exclusively associated with pelvic fractures (especially straddle fractures, "butterfly" fractures of pubic rami)
• Shearing force at the prostatomembranous junction (where urethra is fixed by urogenital diaphragm)
• Prostate displaced superiorly by haematoma

Clinical Features - Classic Triad:

1. Blood at the urethral meatus - most important sign; present in ~75%
2. Inability to void / urinary retention
3. High-riding/floating prostate on DRE (prostate displaced superiorly by perineal haematoma; may be difficult to feel)

Other signs:

• Perineal bruising/haematoma
• Scrotal haematoma (butterfly bruising)
• Pelvic fracture on X-ray/CT

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Anterior Urethral Injuries

Mechanism:

• Straddle injury - most common (fall astride a bar/bicycle crossbar/fence; compresses bulbar urethra against inferior pubic rami)
• Penile fracture with associated urethral injury
• Iatrogenic: urethral catheterization, cystoscopy, TURP
• Penile constriction rings, sexual trauma
• Direct penetrating trauma

Clinical Features:

• Blood at urethral meatus
• Perineal haematoma - "butterfly haematoma" confined to Colles' fascia (does NOT spread to thighs as fascia attaches to pubic rami and deep fascia of thigh)
• Urinary retention
• Penile/scrotal swelling

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GOLDEN RULE OF URETHRAL INJURY

If blood at the urethral meatus is present, DO NOT pass a urethral catheter blindly. A urethral injury must be excluded first with a retrograde urethrogram. Blind catheterization can convert a partial tear into a complete disruption.

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Diagnosis

Retrograde Urethrogram (RUG):

• Gold standard for urethral injury
• Technique: 14Fr Foley catheter inserted 1-2cm into meatus; balloon inflated with 1-2ml; contrast injected under fluoroscopy
• Findings:
  • Partial tear: Some contrast passes into bladder; extravasation at injury site
  • Complete disruption: No contrast reaches bladder; large extravasation
• Always perform before catheterization if urethral injury suspected

CT urethrogram:

• Can be combined with CT pelvis for associated injuries

Flexible cystoscopy:

• Can assess urethral injury and guide catheter placement

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Classification - Goldman Classification (Posterior Urethral Injuries)

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Management

Posterior Urethral Injury (Pelvic Fracture-Associated):

• DO NOT pass urethral catheter blindly
• Suprapubic catheter (SPC) - immediate bladder drainage; inserted above pubic symphysis under USS guidance
• Manage life-threatening associated injuries (haemorrhage, pelvic stabilization)

• Acute haematoma and tissue oedema make anatomy unclear
• Risk of worsening erectile dysfunction and incontinence
• Delayed urethroplasty has better outcomes when performed in specialized centre

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Anterior Urethral Injury:

• SPC if urinary retention or significant injury
• Small partial tears: urethral catheter carefully guided over guidewire

• Small partial tears: Urethral catheter × 2-3 weeks → spontaneous healing
• Complete disruption: Urethroplasty (excision + primary anastomosis for bulbar urethra; substitution urethroplasty with buccal mucosal graft for penile urethra)
• Iatrogenic strictures: Optical urethrotomy (incision of stricture) or formal urethroplasty

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Long-Term Complications of Urethral Injury

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Penile Fracture - Brief Coverage

• "Popping/cracking" sound followed by immediate detumescence
• Rapid swelling and bruising
• Aubergine deformity - purple/black swollen penis, often deviated away from tear
• Haematoma under Buck's fascia (confined to penis) or Colles' fascia if Buck's fascia torn
• Urethral injury in ~10-38% (blood at meatus, haematuria)

• Emergency surgical repair - evacuation of haematoma + primary closure of tunica albuginea tear
• If urethral injury → repair or SPC
• Delayed repair → higher rates of penile curvature/Peyronie's disease

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Combined Genitourinary Trauma

Principles when multiple GU structures injured:

1. Life-threatening injuries first (vascular, solid organ haemorrhage)
2. Urinary diversion (SPC) if lower tract injured
3. Staged repair - immediate damage control; definitive reconstruction when stable
4. Involve relevant specialists: urology, orthopaedics (pelvic ring), vascular, colorectal if needed

Pelvic Fracture + Urethral + Bladder Injury:

• SPC for bladder drainage
• Pelvic ring stabilization (external fixator)
• Retrograde urethrogram
• CT cystogram
• Delayed reconstruction

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Full Trauma Section Summary Table

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Examiner's Key Points - Trauma Section

Kidney:

• Haematuria does NOT correlate with injury severity - pedicle avulsion can have NO haematuria
• Delayed CT phase essential for urinary extravasation
• One-shot IVU before nephrectomy confirms contralateral kidney

Bladder:

• IP rupture = dome + full bladder + blunt = surgery
• EP rupture = pelvic fracture = catheter drainage
• Active filling (350ml contrast) required for CT cystogram

Urethra:

• Blood at meatus = DO NOT catheterize blindly = get urethrogram first
• Posterior urethra = pelvic fracture = SPC + delayed urethroplasty
• Anterior urethra = straddle injury = butterfly haematoma
• Complications of posterior urethral injury: stricture, ED, incontinence ("the terrible triad")

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• Diagnostic Methods (CT/MRI in urology, uroflowmetry, PSA, cystoscopy, urinalysis, urodynamics)
• General topics (symptoms of urological diseases, pain syndrome, dysuric disorders, differential diagnosis of flank pain)

Section: General Urology Topics

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Topic 25: Symptoms of Urological Diseases

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1. Lower Urinary Tract Symptoms (LUTS)

Storage (Irritative) Symptoms:

Voiding (Obstructive) Symptoms:

Post-micturition Symptoms:

• Post-micturition dribble
• Sensation of incomplete emptying

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2. Urinary Incontinence

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3. Pain in Urology

Renal/Ureteric Pain:

• Originates from renal capsule stretch or ureteric spasm
• Loin pain - dull, constant ache → distension of renal pelvis (obstruction, pyelonephritis)
• Renal colic - severe, colicky, loin-to-groin radiation → ureteric stone
• Radiation to ipsilateral testis/labia majora (T10-L2 dermatome)

Bladder Pain:

• Suprapubic pain, worse as bladder fills, relieved by voiding → interstitial cystitis
• Suprapubic pain + LUTS → cystitis, bladder stone
• Strangury: painful desire to void with only small amounts passed (severe bladder irritation)

Prostatic Pain:

• Perineal, rectal, lower back pain
• Post-ejaculatory pain
• Acute prostatitis: exquisite perineal pain + systemic sepsis

Scrotal/Testicular Pain:

• Acute sudden pain → torsion (emergency)
• Gradual + fever → epididymo-orchitis
• Dragging/aching discomfort → varicocele, hydrocele, epididymal cyst
• Referred testicular pain from ureteric stone (T10)

Penile Pain:

• Dysuria → UTI, urethritis, herpes
• Pain on erection → Peyronie's disease, phimosis
• Priapism → ischaemic type (painful)

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4. Changes in Urine

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5. Sexual and Reproductive Symptoms

• Erectile dysfunction (ED): Inability to achieve/maintain erection sufficient for intercourse
• Premature ejaculation: Most common male sexual dysfunction
• Retrograde ejaculation: Semen enters bladder (post-TURP, diabetes, alpha-blockers) → cloudy post-orgasm urine
• Haematospermia: Blood in semen → usually benign (prostatitis, seminal vesicle cyst); if persistent/age >40 → exclude prostate cancer
• Anejaculation: Failure to ejaculate (neurological, psychological)

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Topic 26: Pain Syndrome in Urological Diseases

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Acute vs Chronic Urological Pain

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Pain Pathways in Urology

Visceral Pain (kidney, ureter, bladder):

• Transmitted via autonomic fibres (sympathetic T10-L2)
• Poorly localized, deep, cramping
• Referred pain pattern:
  • Kidney → loin
  • Upper ureter → loin + ipsilateral iliac fossa
  • Mid-ureter → iliac fossa (mimics appendicitis on right)
  • Lower ureter / VUJ → groin, scrotum/labia, inner thigh
  • Bladder → suprapubic, perineum

Somatic Pain (external genitalia, urethra):

• Transmitted via somatic nerves (pudendal nerve S2-4)
• Well-localized, sharp
• Scrotal skin pain, urethral pain, perineal pain

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Key Pain Syndromes

Renal Colic (covered in Topic 2)

Interstitial Cystitis / Bladder Pain Syndrome (BPS):

• Chronic suprapubic pain related to bladder filling
• Urinary urgency/frequency without infection
• Pathology: epithelial dysfunction (leaky urothelium), mast cell infiltration
• Diagnosis: exclusion of infection + cystoscopy (Hunner ulcers in ~10%; glomerulations)
• Treatment: dietary modification (avoid caffeine, alcohol, acidic foods), amitriptyline, pentosan polysulfate, intravesical dimethyl sulfoxide (DMSO), hydrodistension, cyclosporine, neuromodulation, cystoplasty (last resort)

Chronic Pelvic Pain Syndrome (CPPS):

• Covered in Topic 11 (Prostatitis Category III)
• Affects both men (prostatitis-associated) and women (interstitial cystitis, pelvic floor dysfunction)
• Multimodal management: analgesia, alpha-blockers, physiotherapy, psychological support

Peyronie's Disease:

• Fibrous plaque formation in tunica albuginea of penis
• Causes penile curvature, pain on erection, shortening
• Acute phase (<12-18 months): pain + progressive deformity → colchicine, vitamin E, intralesional verapamil/collagenase
• Stable phase: surgical correction (Nesbit plication for mild curvature; plaque incision + graft for severe; penile prosthesis if ED)

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Topic 27: Dysuric Disorders in Urology

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Causes of Dysuria

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Strangury

• Extreme form of dysuria: painful, frequent, urgent desire to urinate with only small amounts passed
• Causes: severe cystitis, bladder stone on trigone, bladder cancer (especially CIS), severe urethritis
• Associated with suprapubic/perineal pain and haematuria

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Approach to Dysuria in the Viva

Young sexually active woman:

• Most likely: cystitis (E. coli) → urine culture + empirical trimethoprim/nitrofurantoin

Sexually active young adult (any sex):

• Consider: STI (Chlamydia, gonorrhoea) → urethral swab + NAAT + STI screen

Man with dysuria + perineal pain + fever:

• Acute prostatitis → urine + blood cultures + fluoroquinolone

Older man with dysuria + obstructive symptoms:

• BPH/prostate cancer → DRE + PSA + urine flow rate

Painless haematuria + dysuria/frequency in older patient:

• Bladder cancer (CIS) → cystoscopy + urinary cytology

Post-radiotherapy patient with dysuria:

• Radiation cystitis → check for secondary infection; intravesical treatments; hyperbaric oxygen for severe haemorrhagic radiation cystitis

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Topic 28: Differential Diagnosis of Flank Pain

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Differential Diagnosis - Systematic Approach

Urological Causes (most common):

Vascular Causes - Must Not Miss:

Musculoskeletal:

Gastrointestinal:

Gynaecological (women):

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Systematic Approach to Flank Pain in the Viva

Step 1: Is the patient haemodynamically stable?
        → If NO: consider ruptured AAA, ectopic pregnancy, massive renal haemorrhage
        → EMERGENCY management first

Step 2: Is there haematuria?
        → Yes + colicky pain = STONE (most likely)
        → Yes + fever = pyelonephritis or infected stone
        → Yes + no pain = cancer until proven otherwise

Step 3: Is there fever?
        → Yes = infection (pyelonephritis, renal abscess, infected stone)

Step 4: What is the character of pain?
        → Colicky = stone
        → Constant dull = tumour, hydronephrosis, cyst
        → Tearing = vascular (AAA)
        → Dermatomal = herpes zoster

Step 5: Age and sex?
        → Young woman = consider ectopic, ovarian pathology, UTI
        → Older man = stone, cancer, AAA
        → Child = Wilms tumour, PUJ obstruction

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Red Flags in Flank Pain - Never Miss

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Examiner's Key Points

• Always exclude AAA in older patient with flank pain - lack of haematuria and pulsatile mass are key distinguishing features from renal colic
• Herpes zoster causes flank pain BEFORE the rash appears - a classic diagnostic trap
• PUJ obstruction: Dietl's crisis = intermittent severe loin pain after high fluid intake; classic in young adults
• Renal infarction: flank pain + haematuria + source of emboli (AF, endocarditis) → CT angiogram shows absent nephrogram
• Renal vein thrombosis: associated with nephrotic syndrome (hypercoagulable state) + membranous nephropathy

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Topic 29: Physical Examination in Urology

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General Examination

• Build, nutritional status, pallor (anaemia from chronic disease/haematuria/renal failure)
• Oedema (renal failure, nephrotic syndrome, lymph node obstruction)
• Hypertension (renal disease, renal artery stenosis, RCC)
• Lymphadenopathy (malignancy spread)
• Gynaecomastia (liver disease, Klinefelter, testicular tumour, drug side effects)

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Abdominal Examination

Inspection:

• Distended bladder (suprapubic fullness)
• Nephrostomy tubes, stomas, scars (previous urological surgery)
• Transplant kidney scar (iliac fossa)

Palpation - Kidney:

• Bimanual palpation (ballottement): one hand posteriorly in loin, one anteriorly - push forward with posterior hand
• Normal kidneys usually not palpable (except thin patients and right kidney)
• Enlarged kidney: Hydronephrosis, polycystic kidney, RCC, Wilms tumour
• Distinguishing renal mass from spleen/liver:
  • Kidney: resonant to percussion (bowel in front), ballottable, moves with respiration, cannot get above it on right (vs spleen: dull, not ballottable, can get above it)
• Transplant kidney: Right iliac fossa, non-ballottable, tender if rejection

Palpation - Bladder:

• Normal bladder not palpable (empties below pubic symphysis)
• Palpable suprapubic mass + dull to percussion = distended bladder (retention)
• Dull to percussion (full of urine) vs ovarian cyst/fibroid (different origin)

Percussion:

• Renal angle tenderness (punch tenderness/fist percussion) = pyelonephritis, perinephric abscess
• Suprapubic dullness = full bladder

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Genital Examination

Male:

• Penis: Phimosis (non-retractable foreskin), paraphimosis (retracted foreskin stuck behind glans - emergency), meatal stenosis, penile lesions, Peyronie's plaques, urethral discharge
• Scrotal contents:
  • Inspect: asymmetry, skin changes, oedema
  • Palpate each testis separately: size, consistency, tenderness
  • Normal: testis smooth, homogeneous, ~4x3cm; epididymis posterior
  • Hydrocele: fluid anterior to testis; transilluminates; cannot get above it
  • Varicocele: "bag of worms" above testis; L>R; disappears lying flat; present on Valsalva
  • Epididymal cyst: separate from testis, transilluminates, at upper pole
  • Testicular tumour: hard, non-tender, does NOT transilluminate; replace testis sensation with dull heaviness

Digital Rectal Examination (DRE):

• Patient in left lateral position or standing bent forward
• Assess: anal tone, rectal mucosa, prostate
• Normal prostate: Smooth, firm, rubbery, walnut-sized, bilobed with central sulcus
• BPH: Enlarged, smooth, rubbery, symmetrical, non-tender, sulcus may be obliterated
• Prostate cancer: Hard, nodular, irregular, asymmetric, may be fixed
• Prostatitis: Exquisitely tender, warm, boggy

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Examination of External Genitalia in Female

• Inspect urethral meatus (caruncle, prolapse, meatal stenosis)
• Perineum: scarring from childbirth, skin conditions
• Prolapse: ask patient to cough/strain (cystocele = anterior wall bulge; rectocele = posterior; uterine prolapse = cervix descends)
• Stress incontinence: demonstrate on coughing
• Bimanual examination: uterine/adnexal masses (pressing on bladder)

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Section: Diagnostic Methods

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Topic 30: Urinalysis in Urology

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Components of Urine Dipstick

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Urine Microscopy

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Urine Culture

• Midstream clean catch (MSU): Routine; >10⁵ CFU/mL = significant bacteriuria
• Catheter specimen (CSU): >10⁴ CFU/mL = significant
• Suprapubic aspirate (SPA): Any growth = significant (gold standard)
• Early morning urine (EMU) × 3: TB culture (Löwenstein-Jensen medium)
• Sensitivity testing (C&S): Guides antibiotic choice

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Urine Cytology

• Voided urine or bladder washings
• High sensitivity for high-grade TCC and CIS (~90%)
• Poor sensitivity for low-grade tumours (~20-30%)
• Positive cytology → proceed to cystoscopy regardless of other findings
• Paris classification for reporting (benign, atypical, suspicious, malignant)

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24-Hour Urine Collection (Metabolic Stone Workup)

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Topic 31: Functional Methods of Kidney Examination

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Glomerular Filtration Rate (GFR)

• Gold standard: Inulin clearance (inulin freely filtered, not secreted or reabsorbed)
• Practical: Creatinine clearance (Cockcroft-Gault formula) or eGFR (CKD-EPI equation)
• eGFR used clinically: calculated from serum creatinine, age, sex
• CKD stages based on eGFR:

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Isotope Renal Studies (Nuclear Medicine)

DTPA (Diethylenetriamine pentaacetic acid) Scan:

• Dynamic renal scan - assesses GFR and drainage
• Filtered by glomeruli; not reabsorbed
• Used for: split renal function (% contribution of each kidney), assessment of obstruction (MAG3 preferred)

MAG3 (Mercaptoacetyltriglycine) Scan:

• Dynamic renal scan - assesses renal perfusion + tubular secretion + drainage
• Better for obstructed/poorly functioning kidneys
• Diuresis renogram (MAG3 + furosemide): distinguishes true obstruction from dilated but unobstructed system
  • F15 protocol: furosemide at 15 min; rapid washout = no obstruction; delayed/no washout = obstruction
• Used for: PUJ obstruction diagnosis, post-pyeloplasty follow-up, renal transplant assessment

DMSA (Dimercaptosuccinic acid) Scan:

• Static renal scan - assesses cortical function and scarring
• Taken up by proximal tubular cells; remains in cortex
• Used for:
  • Split renal function (most accurate method)
  • Renal scarring (post-pyelonephritis/VUR in children)
  • Ectopic kidney/horseshoe kidney identification
  • Confirm functioning renal tissue

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Topic 32: Instrumental and Radiological Diagnostic Methods

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Cystoscopy

Flexible Cystoscopy:

• Outpatient procedure under local anaesthesia (urethral lubricant with lignocaine)
• 16Fr flexible scope
• Indications: Haematuria investigation, bladder tumour surveillance, ureteric orifice assessment, bladder stone/foreign body detection, urethral assessment
• Findings: Normal mucosa (smooth pink), tumours (papillary fronds, solid masses), CIS (red velvety patches), stones, trabeculation (BPH-related), diverticula, ureteric orifice abnormalities

Rigid Cystoscopy (under GA/spinal):

• Better optics and working channel
• Allows TURBT, biopsy, ureteric catheterization, stent insertion

Blue Light Cystoscopy (HAL - hexaminolevulinate):

• Photosensitizing agent instilled intravesically 1 hour before
• Absorbed preferentially by tumour cells → protoporphyrin IX → fluoresces pink/red under blue light
• Increases detection of CIS and satellite lesions by ~20-25%
• Used for: initial TURBT, recurrence surveillance in high-risk patients

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Retrograde Pyelogram (RGP)

• Contrast injected via ureteric catheter passed cystoscopically
• Indications: CT equivocal upper tract findings, allergy to IV contrast, ureteric filling defect characterization
• Shows: filling defects (TCC = goblet sign; stone = smooth filling defect), strictures, ureteric anatomy pre-stenting
• Risk: UTI, ureteric perforation

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Antegrade Pyelogram / Nephrostogram

• Contrast injected via existing nephrostomy tube
• Assesses collecting system, site of obstruction, fistula

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Uroflowmetry

• Non-invasive measurement of urine flow rate
• Patient voids into flow meter after attending with comfortably full bladder (voided volume must be >150ml for reliable result)

Key Parameters:

Flow Curve Patterns:

• Normal: Bell-shaped curve with Q-max >15ml/s
• BPH/Obstruction: Prolonged, low plateau curve
• Urethral stricture: Box-shaped plateau curve
• Straining: Multiple peaks (detrusor + abdominal effort)
• Detrusor overactivity: Interrupted flow

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Urodynamics (Pressure-Flow Study)

• Gold standard for diagnosing bladder outlet obstruction and detrusor dysfunction
• Intravesical pressure catheter + rectal pressure catheter (subtracted = detrusor pressure)
• Bladder filled at controlled rate; voiding phase assessed
• Detrusor pressure at Q-max (PdetQmax):
  • High PdetQmax + low Q-max = bladder outlet obstruction (BPO)
  • Low PdetQmax + low Q-max = impaired detrusor contractility
  • High PdetQmax + high Q-max = normal/detrusor overactivity

Components:

• Cystometrogram (CMG): Filling phase - measures bladder compliance, sensation, detrusor overactivity
• Pressure-flow study: Voiding phase - obstruction vs detrusor failure
• Video urodynamics: Combines fluoroscopy + urodynamics; for complex cases (VUR, neurogenic bladder)

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CT and MRI in Urology

CT Urogram (CTU):

• Three phases:
  1. Non-contrast: stones, calcifications, baseline
  2. Nephrographic phase (100s): renal masses, vascularity
  3. Delayed/excretory phase (10-15 min): collecting system, ureters, bladder
• Indications: Haematuria workup (gold standard), renal/ureteric stones, staging of urological malignancies, trauma, upper tract assessment

CT KUB (Non-contrast):

• Detects stones >95%; perinephric stranding; hydronephrosis
• No contrast required

MRI Prostate (mpMRI):

• Sequences:
  • T2-weighted: anatomical detail; zones of prostate; capsule integrity
  • Diffusion-weighted imaging (DWI): cell density; restricted diffusion = cancer
  • Dynamic contrast enhancement (DCE): vascularity; early enhancement = cancer
• PI-RADS scoring 1-5: standardized reporting of cancer likelihood
• Pre-biopsy MRI is now standard of care before prostate biopsy

MRI Pelvis (Bladder/Staging):

• VI-RADS scoring: Assesses muscle invasion in bladder cancer (T staging)
• Better soft tissue contrast than CT for local staging

MRI Abdomen (Renal):

• IVC thrombus extent in RCC
• Characterization of complex cystic lesions (Bosniak)
• CT contrast contraindicated (renal failure, allergy)

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Examination of the Prostate Gland - PSA and DRE

PSA Interpretation:

PSA Velocity: >0.75 ng/mL/year = suspicious for cancer

Free:Total PSA Ratio: <10-15% = cancer more likely (BPH produces more free PSA)

PSA density: >0.15 = cancer more likely

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Emergency Diagnostic Methods in Urology

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Complete Topic Coverage - Final Summary

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1. Create a rapid revision cheat sheet of all topics as a single downloadable reference?
2. Quiz you with viva-style questions to test retention?
3. Deep dive into any specific topic you feel less confident about?

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What's inside the 2-page PDF:

• Section A - General Urology: LUTS classification, pain syndromes, dysuria, flank pain DDx, physical exam findings
• Section B - Haematuria & Renal Colic: key rules, workup, management
• Section C - Inflammatory Diseases: table covering pyelonephritis, prostatitis, epididymo-orchitis, renal abscess, TB, urosepsis
• Section D - Urolithiasis: all 5 stone types comparison table + surgical treatment ladder
• Section E - Urological Emergencies: AUR, AKI, testicular torsion (time-to-salvage), obstructive uropathy
• Section F - Tumours: RCC, bladder cancer, Wilms, UTUC, prostate cancer in a single table
• Section G - Andrology: male infertility causes/treatment, priapism types

• Section H - BPH: pathophysiology, IPSS, medical/surgical treatment, TURP syndrome
• Section I - Trauma: kidney/bladder/urethra/penile fracture in one table
• Section J - Diagnostics: urinalysis casts, renal scans, uroflowmetry, mpMRI, PSA rules
• Section K - Master Memory Aids: all mnemonics (COLA, WAGR, RIPE, AEIOU, etc.)
• Section L - Right Test for the Right Question: rapid imaging reference table
• Red Flags Box - 8 never-miss emergency scenarios

Urosepsis Viva Quiz

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Question 1

"A 68-year-old man presents to A&E with a 6-hour history of rigors, fever of 39.2°C, right loin pain, and confusion. His blood pressure is 88/60 mmHg and heart rate is 118 bpm. He has a known right ureteric stone on previous imaging. How do you define what this patient has, and what is your immediate management?"

Feedback on Question 1 — Score: 6/10 ✅ Good foundation, needs refinement

• Correctly identified septic shock (hypotension + tachycardia + fever)
• Correctly identified the urological source (obstructed infected kidney)
• Mentioned IV fluids, IV antibiotics, and decompression - the three pillars
• Recognised qSOFA criteria

1. Definition of septic shock (Sepsis-3): Don't just say "septic shock" - define it precisely for the examiner:
   • Sepsis = life-threatening organ dysfunction (SOFA ≥2) from dysregulated host response to infection
   • Septic shock = sepsis + vasopressor requirement to maintain MAP ≥65 mmHg + lactate >2 mmol/L despite adequate fluid resuscitation
   • This patient's qSOFA = 3/3 (confusion = AMS, RR not given but BP ≤100 + AMS already = ≥2) → high risk
2. Sepsis 6 Bundle - be specific about ALL 6 actions within 1 hour:
   • Give O2, Blood cultures ×2 BEFORE antibiotics, IV antibiotics, IV fluid bolus 30ml/kg, Serum lactate, Catheterize + monitor urine output
3. Antibiotic choice - name the drug: piperacillin-tazobactam (Tazocin) IV is first-line
4. Critical point you nearly missed: "Decompression" is correct but be precise - NOT stone removal. In a septic patient you do NOT attempt definitive stone treatment. You do emergency drainage only (PCN or ureteric stent). Stone removal comes weeks later when infection is cleared.
5. Why antibiotics alone fail - the examiner wants to hear you say: "Pus under pressure cannot be sterilised with antibiotics alone - the obstruction must be relieved to source control the infection."

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Model Answer for Q1:

"This patient has uroseptic shock - defined as sepsis with persistent hypotension requiring vasopressors to maintain MAP ≥65 and lactate >2 mmol/L despite resuscitation. His qSOFA score is at least 2 (altered consciousness + SBP ≤100). The source is an infected obstructed right kidney from his known ureteric stone - pyonephrosis. I would immediately activate the Sepsis 6 bundle within one hour: high-flow oxygen, two sets of blood cultures before antibiotics, IV piperacillin-tazobactam, 30ml/kg crystalloid fluid bolus, serum lactate measurement, and urethral catheterization to monitor urine output targeting >0.5ml/kg/hr. If he remains hypotensive despite fluids, I would start noradrenaline as the first-line vasopressor. Most critically, I would arrange emergency upper tract decompression - either a percutaneous nephrostomy or retrograde ureteric stent. Antibiotics alone will not clear this infection while the kidney remains obstructed - source control is mandatory."

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Question 2 - Follow Up

"You order a serum lactate. It comes back at 5.2 mmol/L. What does this tell you, and does it change your management?"

Feedback on Question 2 — Score: 5/10 ⚠️ Partially correct, some important errors

• Correctly identified lactate >4 = critical / high mortality
• Mentioned tissue hypoperfusion - correct concept
• Steroids - partially correct (but the indication is wrong - see below)
• Recognised need for further monitoring

❌ Error 1: RRT is NOT the next step

• Refractory acidosis (pH <7.1)
• Refractory hyperkalaemia
• Fluid overload not responding to diuretics
• Symptomatic uraemia

❌ Error 2: Steroids - wrong indication stated

• Hypotension persisting despite adequate fluid resuscitation AND vasopressors - not just a high lactate alone
• This patient hasn't yet received full resuscitation, so steroids are premature at this point

❌ Error 3: "Another blood screen to find other bacteria"

✅ What the examiner wanted to hear:

1. Lactate >4 = severe tissue hypoperfusion = very high mortality marker - the 1-hour bundle becomes even more urgent
2. Repeat lactate at 1-2 hours - if clearance <10% = inadequate resuscitation
3. Escalate vasopressors - noradrenaline if not already started; target MAP ≥65
4. The MOST important action remains - emergency decompression of the obstructed kidney - this is the source and no amount of resuscitation will be sufficient without removing it
5. ITU referral - this patient needs ICU-level monitoring
6. Steroids: Hydrocortisone 200mg IV/day - only if hypotension refractory to fluids AND vasopressors (not yet at that stage necessarily)
7. RRT: Only if AEIOU criteria met - not yet indicated

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Model Answer for Q2:

"A lactate of 5.2 mmol/L indicates severe tissue hypoperfusion and carries very high mortality - this places him firmly in septic shock. It tells me my resuscitation needs to be maximal and urgent. I would ensure 30ml/kg IV crystalloid has been given and start noradrenaline immediately targeting MAP ≥65 mmHg. I would recheck the lactate at 1-2 hours - if it fails to clear by at least 10%, resuscitation is inadequate. I would refer urgently to ITU. However, the most important intervention that will actually turn this patient around is emergency decompression of the obstructed kidney - no amount of fluid or antibiotics will clear this infection while pus remains under pressure. If hypotension persists despite adequate fluids and vasopressors, I would add hydrocortisone 200mg IV daily for relative adrenal insufficiency. RRT would only be considered if he develops refractory acidosis below pH 7.1, severe hyperkalaemia, or fluid overload unresponsive to diuretics - not at this stage."

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Question 3 - Escalating difficulty

"The ITU team asks you - as the urologist - what your preferred method of decompression is in this patient, and why. The patient is drowsy with a GCS of 13 and BP is still 80/50 despite 2 litres of fluid. What do you choose and what are the risks?"