Handbook

Subtypes, prognosis, hereditary forms

WHO 2022 classification integrates morphology + immunohistochemistry + molecular findings. Main malignant subtypes: clear-cell (70–80%, VHL/PBRM1/SETD2/BAP1), papillary (13–20%, MET pathway), chromophobe (1–5%, TERT/TP53/PTEN — grade not applicable to this subtype). Aggressive rarities: collecting duct carcinoma, renal medullary carcinoma (SMARCB1-deficient, African ancestry + sickle haemoglobinopathies). Sarcomatoid/rhabdoid change is a dedifferentiation pattern (= ISUP grade 4), not a subtype.

Hereditary RCC ≈5–8% (often underestimated) — von Hippel-Lindau (30–40% lifetime risk), hereditary papillary RCC (100%), Birt-Hogg-Dubé (30%). Suspect with young onset, positive family history, bilateral/multifocal tumours; germline testing trigger age <46. Manage with surveillance/"3cm rule"/nephron-sparing approach — exception: FH-deficient or aggressive SDH-related tumours need immediate radical nephrectomy.

Imaging & the Bosniak classification (2019)

Multiphasic contrast CT is the diagnostic backbone; MRI/CEUS are problem-solving tools (contrast contraindicated, radiation concern, unclear venous thrombus). CT/MRI cannot reliably distinguish oncocytoma from fat-poor AML.

Renal mass biopsy — the evidence

Diagnostic yield 92%; core biopsy sensitivity 99.1%/specificity 99.7%; histotype concordance 90.3%, grade concordance only 62.5% (87% when simplified to low- vs high-grade); tumour seeding risk ≈0.02% (~1 in 5000); complication rate 8.1%, serious complications <1%. Use coaxial core technique (not FNA), aim for ≥2 good cores, biopsy peripherally in larger tumours to avoid necrosis.

Decision-making before treatment

• Life expectancy: do not base treatment on chronological age alone. >10y → active treatment generally worthwhile; 5–10y → individualise; <5y → consider watchful waiting unless symptomatic/aggressive.
• Frailty (Clinical Frailty Scale, ECOG/Karnofsky, G8 screening ≥65y) predicts treatment tolerance better than age.
• Renal function: creatinine/eGFR + albumin-creatinine ratio; nephrology referral if eGFR<60 persisting >3mo, solitary kidney, bilateral tumours, or anticipated postoperative eGFR<45.
• Tumour complexity scored with RENAL (or PADUA/C-index): score 4–6 low complexity (6.4% major complication risk with PN), 7–9 intermediate (11.1%), 10–12 high (21.9%).

EAU recommendations — treatment

No difference in severe CKD at 7y between PN and RN in the EORTC 30904 RCT (eGFR<30: 10% RN vs 6.3% PN). Active surveillance rationale: SRM (cT1a) is benign in 20–30%, malignant ones are often indolent (median growth 0.1–0.3 cm/yr); triggers to intervene are rapid growth >0.5cm/yr, size >4cm, symptoms, or patient preference.

Follow-up after curative treatment

Risk-adapted imaging (CT chest+abdomen+pelvis): ccRCC → Leibovich 2003 score; non-ccRCC → UISS (papillary RCC specifically → VENUSS score). Low-risk: less frequent imaging; high-risk: CT every visit through year 3 then annually/biennially. Functional (renal) follow-up continues independently of oncological imaging.

Before the incision

• Review imaging yourself: confirm side, size/polar location/complexity (RENAL score), map renal arteries (early branching, accessory arteries) and venous anatomy.
• Position: secure flank/lateral decubitus with pressure-point protection; abdomen "hanging off the table"; ports adapted to side, habitus, tumour location — right-sided cases may need liver retraction.

Principal steps

1. Mobilise colon along the line of Toldt, expose Gerota's fascia.
2. Identify ureter/gonadal vein, trace to the hilum (in PN, direct hilar approach is a valid option).
3. Radical: vessel control + circumferential dissection ("5 shades of yellow" landmarks: pericolic fat → perirenal fat → pancreas [left] → perivascular fat → adrenal); control artery before vein.
4. Partial: vessel loop on the main artery even if off-clamp planned; intraoperative ultrasound in every PN (mark cortical boundary, build a 3D depth map, Doppler-test the planned clamped artery) — for endophytic tumours, US is "the operation's navigation system".

Partial nephrectomy — resection & renorrhaphy

• Cold scissors for the main excision plane; avoid excessive monopolar cautery (obscures margin/collecting-system injury); widen the margin rather than maximising preservation if the plane is uncertain.
• Renorrhaphy goals: deep parenchymal haemostasis, close the collecting system if violated, compress the defect without over-ischaemia. Single-layer (faster, less ischaemic, exophytic defects) vs double-layer (deep haemostatic layer + cortical compression); barbed sutures for efficient running closure.
• Early unclamping (remove clamp after the deep layer, before cortical closure) can identify arterial bleeders early and reduce warm ischaemia time.

Perioperative care

Drains: EAU — omitting drains after standard PN/RN does not increase complications and may shorten stay; drain selectively (collecting-system entry, difficult haemostasis, large defect, leak concern).

VTE prophylaxis: after PN with short prophylaxis, VTE 0.6% at 4 weeks / 0.9% at 4 months; after RN, 1% at 4 weeks / 2% at 4 months. Prior VTE is the strongest negative risk factor for both. Open RN, lymph-node dissection and longer stay raise RN-specific risk. LMWH options: enoxaparin, dalteparin, tinzaparin, dosed to weight/eGFR.

Complications

• Early: bleeding/haematoma, AKI, ileus, infection/sepsis, adjacent organ injury — resuscitate, image when stable, get source control; do not watch a deteriorating patient because "the operation went well".
• Late (post-PN): delayed haematuria at 1–3 weeks = pseudoaneurysm/AV-fistula until proven otherwise (work up with CT angiography, treat with selective embolisation); urine leak (drain creatinine > serum) treated with drainage/decompression; urinoma/abscess needs percutaneous drainage ± antibiotics.

Venous tumour thrombus (VTT)

Occurs in ~4–10% of RCC (up to 78% of pT3a). Mayo classification guides surgical planning: T3a = renal vein(s), T3b = below diaphragm, T3c = above diaphragm. Thrombus can progress rapidly — re-image 1–2 weeks before surgery. Surgery is high-risk (mortality 2–10%), individualised approach (open/lap/robotic), refer to a specialised/tertiary multidisciplinary centre. 5-year survival ~36–57% in non-metastatic VTT.

Adjuvant therapy after nephrectomy

KEYNOTE-564 (adjuvant pembrolizumab vs placebo, high-risk ccRCC): DFS benefit (absolute +8%) and OS benefit (+5% at 5y) — but almost 40% of "high-risk" patients still relapse despite treatment, and >50% of them are already cured by surgery alone. Prior TKI-monotherapy adjuvant trials (ASSURE, SORCE, PROTECT, ATLAS) were all negative; S-TRAC showed a DFS (not OS) benefit for sunitinib with high grade 3/4 toxicity.

Metastatic RCC — risk stratification & first-line therapy

15–30% present with metastatic disease; ~20% of localised RCC later relapse. Most common sites: lung, nodes, liver, bone, brain. IMDC/Heng model classifies favourable/intermediate/poor risk from 6 factors: Karnofsky PS, time from diagnosis to systemic therapy, haemoglobin, neutrophils, platelets, corrected calcium.

First-line ccRCC combinations (all phase III positive vs sunitinib): nivolumab+ipilimumab (IO+IO), pembrolizumab+axitinib, nivolumab+cabozantinib, pembrolizumab+lenvatinib (IO+TKI) — pick by risk group and toxicity profile.

Cytoreductive nephrectomy (CN) & metastasis-directed therapy

CARMENA (immediate CN + sunitinib vs sunitinib alone): upfront CN is no longer standard of care for intermediate/poor-risk mRCC in the TKI era. In the modern IO era, retrospective pooled data suggest CN (before or after systemic therapy) is an independent favourable prognostic factor — but selection bias is likely. SURTIME data suggest deferred CN (after ~3 cycles of systemic therapy, in good responders) may outperform upfront CN.

Metastasectomy/SABR: complete metastasectomy associates with longer OS/CSS in selected retrospective series (non-randomised, confounded). Oligometastatic SABR: 1-year local control ~89–90%, severe toxicity ~1%. Do not delay systemic therapy for rapid-progression/high-burden disease.

Prognosis

5-yr recurrence-free survival ~69%, cancer-specific survival ~73%. Independent prognostic factors: stage, grade, lymphovascular invasion, tumour necrosis >10%, tumour architecture, concomitant CIS (in non-muscle invasive disease). Gender and tumour location are not independent factors. Delay to surgery >3 months is associated with worse outcome.

EAU recommendations — RNU technique

Non-negotiable technique principles: avoid entering the urinary tract, avoid instrument–tumour contact, work in a closed system with an endobag for extraction, remove kidney+ureter+bladder cuff en bloc — invasive/large (T3-4 and/or N+/M+) tumours are a contraindication to the minimally-invasive approach (worse outcomes vs open). Endoscopic-only bladder-cuff management is associated with higher intravesical recurrence than formal (trans-/extravesical) excision.

Single instillation: mitomycin C or pirarubicin, given within ~2 hours (up to 10 days) of RNU — relative recurrence reduction ~35% (POP trial-level evidence, O'Brien 2011).

Adjuvant chemotherapy — POUT trial

Adjuvant platinum-based chemotherapy after RNU improved outcomes in locally-advanced UTUC (pT2-T4 and/or pN+); eligibility to cisplatin overall only ~64% given the near-universal post-RNU eGFR decline (>75% fall below 60 mL/min/1.73m² after surgery vs ~50% before) — this is exactly why neoadjuvant chemotherapy (while both kidneys are still present) is being explored (EA8141, iNDUCT trials), though it is not yet a formal guideline recommendation.

Surveillance & low-risk primary chemoablation

• After RNU, high-risk non-infiltrative: cystoscopy+cytology at 3 months then yearly; CT urogram yearly for ≥5 years.
• After RNU, infiltrative: CT urogram twice yearly for 2 years, then yearly.
• After kidney-sparing (low-risk): cystoscopy/URS/in-situ cytology at 3, 6 months then 6-monthly for 2 years then annually; CT urogram at 3, 6 months then yearly.

Epidemiology & pathology

Rare in Europe/USA (0.1–1/100,000), up to 10% of male malignancies in parts of Asia/Africa. Risk factors split into two pathways: HPV-dependent PeIN/SCC (warty, basaloid, mixed subtypes) and HPV-independent PeIN/SCC (usual/papillary or verrucous, linked to phimosis, chronic inflammation, lichen sclerosus). PeIN progresses to invasive SCC at a crude 2–5%/year, up to 33% if left untreated. Men present late — phimosis alone delays diagnosis by ~6 months in 1 in 5 patients.

Staging work-up

• Local: MRI penis in selected cases.
• Inguinal: ultrasound ± FNA in all patients, DSNB for staging.
• Distant: PET-CT (preferred) or CT — only needed once inguinal node metastasis is confirmed, since spread is strictly lymphatic.

EAU recommendations — treatment of the primary

T4/unresectable: induction chemotherapy then surgery, or chemoradiotherapy if non-responder/unsuitable for surgery.

Lymph nodes — the decision that matters most

Pathological nodal staging is the single most important prognostic factor (5-yr CSS: pN0 85–94%, pN1 79–89%, pN2 7–60%, pN3 0–50%; by node count: 1–3 nodes 75%, 4–5 nodes 8.4%, >5 nodes 0%). Occult metastasis risk by primary tumour: G2/pT1a ≈7%, ≥G3/pT1b ≈20–30%.

Metastatic disease

Chemotherapy regimens reported: TIP (median OS ~17 months, mostly used in the neoadjuvant/locally-advanced setting, response rate 50–60%), cisplatin/5-FU (~8 months), TPF (~7–14 months). First-line palliative systemic therapy for distant metastatic disease is platinum-based chemotherapy (Weak). The phase III InPACT trial (neoadjuvant therapy ± prophylactic PLND in advanced penile cancer) completed accrual in 2026.

Risk groups & ladder of care

Risk is set by the 2021 EAU NMIBC scoring model (5-year progression probability <1% to >40%). Extra adverse factors pushing a tumour to very high-risk: CIS of the prostatic urethra, unfavourable histology (micropapillary, nested, plasmacytoid, sarcomatoid, small-cell, neuroendocrine, poorly differentiated), lymphovascular invasion, BCG failure.

BCG-unresponsive disease

Definition (respect it precisely — it identifies who won't benefit from more BCG): any high-grade recurrence after induction + first maintenance round (or two induction rounds) — except a high-grade T1 tumour at 3 months post-induction-only, which already counts as unresponsive; or, in complete responders, any high-grade recurrence within 6 months (Ta/T1) or 12 months (CIS) of the last BCG dose ("BCG-refractory" / "BCG early-relapsing").

Radical cystectomy is genuinely morbid: ~35% complications during primary admission, 39% by 30 days, 60% by 90 days; in-hospital mortality ~2.4%, 90-day mortality ~4.7% — which is exactly why bladder-sparing intensification is being pursued for patients who decline or can't tolerate surgery.

Intensification trials — BCG + immunotherapy

Both positive trials increased immune-related toxicity (grade 3–4 in 14–21%). EAU: discuss the benefits/harms of adding sasanlimab or durvalumab to BCG with maintenance in selected BCG-naïve high- and very-high-risk patients, and discuss all high/very-high-risk cases in a multidisciplinary board when possible.

BCG-unresponsive pipeline: nadofaragene firadenovec (adenoviral gene therapy, FDA-approved, ~53% CIS complete response), TAR-200 (sustained-release intravesical gemcitabine, ~82% CIS CR), pembrolizumab (~41–46% CIS CR), erdafitinib for FGFR-altered papillary disease.

Timing — a genuine prognostic factor

If no neoadjuvant chemotherapy (NAC): OS is significantly worse if TURBT-to-cystectomy exceeds 12 weeks. If NAC is given: keep TURBT-to-NAC-start <8 weeks and NAC-to-cystectomy <6 weeks — both delays independently worsen recurrence-free, cancer-specific and overall survival on multivariable analysis. Good uro-oncology coordination is what actually controls this, not any single decision point.

Lymph node dissection — bigger is not better

Standard PLND template: obturator, external/internal iliac, common iliac up to the ureteric crossing. (Supra-)extended adds presacral, paracaval, interaortocaval, para-aortal nodes to the inferior mesenteric artery.

EAU recommendations — surgery & approach

Robotic vs open cystectomy: similar oncological outcomes (RAZOR, CORAL trials — comparable RFS/OS); robotic approach reduces blood loss/transfusion rate (each transfused unit independently raises bladder-cancer death risk by ~7%) and shortens length of stay, with equivalent PLND quality.

Urinary diversion

Choice: continent orthotopic neobladder, continent cutaneous pouch, or incontinent ileal conduit. Neobladder contraindications: cancer invasion into adjacent organs, eGFR<45, urethral tumour involvement, prior pelvic radiation/bowel disease, severe comorbidity, or inability to manage postoperative self-care. With good technique: daytime continence ~90%, night-time ~82%.

Sexual-sparing procedures — shared decision, MRI-guided

• Men: prostate-sparing techniques give poor oncological results (increased metastatic recurrence risk from occult prostate adenocarcinoma) — prefer neurovascular-bundle preservation instead.
• Women: preserve the anterior vaginal wall/uterus/ovaries when MRI shows no trigone/dorsolateral-wall or uterine invasion — reduces dyspareunia/vaginismus, improves neobladder continence, and avoids the excess cardiovascular/cognitive/osteoporosis risk of surgical menopause. Between 50–80% of patients report receiving little/no counselling on sexual impact before surgery, and 41% of urologists don't routinely discuss organ-sparing options with sexually active patients — this is a counselling gap, not just a technical one.

Prehabilitation & ERAS

Bladder cancer patients are frail by nature (median age 73y, ~40% of ≥65y have renal impairment, sarcopenia in up to 75% of cystectomy patients). Prehabilitation (geriatric/nutritional evaluation, physical activity, respiratory physiotherapy, psychological support, anaemia correction) started 4–6 weeks pre-op, paired with an ERAS protocol (opioid-sparing, tubeless, early feeding/mobilisation), reduces post-op decline below the critical threshold that ERAS alone cannot prevent.

Trimodal therapy (bladder preservation)

Complete TURBT + radiotherapy (IMRT/IGRT) + radiosensitising chemotherapy (platinum/5-FU/MMC/gemcitabine). Late grade>2 GU/GI toxicity only 2–7%; cystectomy for complications ~2%.

Retrospective comparison (Zlotta 2022): OS 78% (TMT) vs 66% (cystectomy) in matched, carefully-selected patients — selection bias means this is not proof of superiority, but it does show TMT is not an inferior fallback when patients are chosen well. Recurrence after TMT: ~1/3 MIBC (→ salvage cystectomy), ~2/3 NMIBC (→ TURBT ± instillations, poor BCG tolerance in a radiated bladder); no impact on 5-year survival; ~34% retain their native bladder at 8 years.

Neoadjuvant chemotherapy

ABC meta-analysis: NAC gives a 5–6% absolute OS benefit at 5–8 years and a 23% reduction in metastasis risk, with no increase in perioperative morbidity/mortality — benefit applies to all fit patients regardless of T stage. Must be cisplatin-based: gemcitabine-carboplatin gives a lower pT0 rate (15.3% vs 24.5% MVAC / 23.9% Gem-Cis) with no proven OS benefit.

VESPER trial (dose-dense MVAC ×6 vs gemcitabine-cisplatin ×4): ddMVAC gave better OS in the neoadjuvant subgroup (HR 0.66); UC histological variants did not predict differential response.

Adjuvant chemotherapy & immunotherapy

Adjuvant chemotherapy alone: no level-1 survival proof (meta-analysis OS benefit at the edge of significance, p=0.049); no role at all if the patient already received NAC.

The "sandwich" era — perioperative chemo-immunotherapy

NIAGARA (perioperative durvalumab + cisplatin/gemcitabine, cisplatin-eligible): 32% reduction in EFS events, 25% reduction in risk of death, +10% pCR rate — durvalumab did not impair the ability to complete surgery. KEYNOTE-905/EV-303 (cisplatin-ineligible) and KEYNOTE-B15/EV-304 (cisplatin-eligible): perioperative enfortumab vedotin + pembrolizumab (EV+P) improved EFS and OS in both populations, with pCR rates of 55.8% and 57.1% respectively (vs 8.6–32.5% for chemotherapy) — without impairing surgical feasibility.

Metastatic urothelial carcinoma — first-line therapy

EV-302/KEYNOTE-A39 established EV+pembrolizumab as the new first-line standard for untreated locally-advanced/metastatic urothelial carcinoma, regardless of cisplatin eligibility: median OS 33.8 vs 15.9 months with platinum-based chemotherapy (HR 0.51 — a 53% reduction in risk of death), with 74% of complete responders maintaining response at 24 months vs 43% with chemotherapy, and benefit consistent across all subgroups (PD-L1 status, liver metastases, renal function, cisplatin eligibility).

Does screening work? The honest answer

ERSPC at 23-year follow-up: 21% relative reduction in PCa-specific mortality (27% after correcting for non-compliance). PLCO was famously negative, but was badly contaminated — 66–90% of the "control" arm had already had a PSA test. Compared to other cancers, PCa's mortality reduction (27%) is actually similar to or better than breast (15–22%) or colon cancer (26%) screening.

EAU recommendations — who and how to test

MRI-first diagnostic pathway

Landmark trials (PRECISION, 4M, Rouvière 2018) all show the same pattern: pre-biopsy multiparametric MRI + targeted biopsy (only, or + limited systematic cores) detects as much or more clinically significant cancer than a full systematic 12-core biopsy, while avoiding 28–49% of biopsies entirely — mostly by skipping men with a negative MRI. Reader expertise matters enormously: detection AUC 0.66 (general radiologist) vs 0.88 (uro-radiologist), and improves from 0.74→0.88 with dedicated training.

Staging

MRI cannot reliably detect microscopic extraprostatic extension and systematically underestimates true tumour volume — it is a local-staging tool, not a volumetric one. For nodal/distant staging, PSMA PET/CT (ProPSMA trial) outperforms conventional CT/bone scan for sensitivity and specificity, but a negative PSMA PET still cannot replace extended PLND in high-risk disease — PSMA misses small (<5.5mm) nodal deposits that ePLND can still remove.

EAU Guidelines on Prostate Cancer 2026, Table 4.3 — EAU risk groups for localised and locally advanced PCa.

Active surveillance vs watchful waiting

Without MRI: include ISUP 1 in AS; ISUP 2 only if low volume (≤3 positive cores, <50% involvement); exclude ISUP 3. Confirmation biopsy within 2 years, then per-protocol every 3 years to 10 years. MRI adds real value — initial PI-RADS score predicts progression, and a negative repeat biopsy halves the risk of future reclassification (useful for tailoring/relaxing follow-up intensity).

GAP3 registry (27,000 men on AS since 2000): safe — 10-year OS 84.1%, 10-year metastasis-free survival 99.4%; by 10 years 20% of low-risk and 31% of intermediate-risk men had crossed over to active treatment.

Triggers to stop AS

Most validated: patient request and biopsy progression (ISUP grade, number of positive cores, % tumour). Others: new comorbidities dropping life expectancy <10y, clinical or MRI progression (cT2→iT3), rising PSA doubling rate.

Focal therapy — not a substitute for AS

Delivery of destructive energy (heat, sound, light, cold, electrical, radiation) to only part of the prostate. Data are still low-quality (mostly small single-centre series, industry-driven, only one RCT — photodynamic therapy vs AS, n=499). Position it as an experimental option in the window between AS and full active treatment for patients who want less morbidity than radical treatment but more action than surveillance — never as a replacement for AS itself. The Dutch ENFORCE-focal RCT is still recruiting.

The ProtecT trial — the sobering one

N=1643, screen-detected localised PCa, randomised to active monitoring vs radical prostatectomy vs radiotherapy+ADT, >15-year follow-up: no significant difference in cancer-specific or overall mortality between the three arms. No QoL difference either — but incontinence and sexual dysfunction were clearly worse in the RP and RT arms. 25% of the active-monitoring group were still alive without any intervention at 15 years.

Radical prostatectomy

Combined analysis of SPCG-4, PIVOT and ProtecT (Vickers 2024): the mortality-reduction benefit of surgery over observation scales with grade — ISUP 1 negligible (0.2% at 15y), ISUP 2 small (<5%), ISUP 3/4 greater (6–9%). Surgeon/hospital volume matters (fewer positive margins, complications, transfusions with more experience). PLND: systematic review shows no oncological benefit of standard or extended PLND over none, with added morbidity — template choice should not be assumed protective.

Continence: driven by bladder-neck preservation and membranous urethral length (MUL, measurable on pre-op MRI) — MUL is significantly associated with continence recovery. Erectile function: nerve-sparing technique (extra-/inter-/intrafascial), avoiding coagulation/traction, with "NeuroSafe" intraoperative margin assessment gaining traction.

Radiotherapy

• Technique: IMRT/VMAT are the current EBRT standards; VMAT is faster with similar biochemical control.
• Dose escalation: 74–80 Gy improves 10-year biochemical control, metastasis and disease-specific mortality vs older lower-dose regimens.
• Hypofractionation: moderate hypofractionation (2.5–3.4 Gy/fraction) with IMRT is safe and equally effective; the CHHiP trial confirmed 60 Gy/20 fractions is as effective and safe as 74 Gy/37 fractions.
• ADT + RT: combined therapy beats RT alone; intermediate-risk optimal duration ~6 months, high-risk 18–24 months (2–3 years).
• Protons: theoretically attractive (Bragg peak sparing of normal tissue) but still experimental — no RCT yet shows a clear clinical advantage over photons.
• Brachytherapy: effective for low/intermediate-risk disease in glands <50cc; less popular now that MRI-guided hypofractionated EBRT is available.

EAU recommendations — high-risk localised & locally advanced disease

Neoadjuvant therapy before prostatectomy — a history of unmet expectations

• 1990s-2000s, neoadjuvant ADT alone: better margins/staging, but no OS benefit and more adverse events — abandoned.
• 2010s-2020s, chemotherapy / early ARPI: 6 cycles of docetaxel before RP gave no survival benefit; phase II ARPI+ADT improved pathological response (pCR/MRD 5-30%), setting up phase III testing.
• 2026, PROTEUS trial (phase III, N=2109, high-risk/locally-advanced PCa): perioperative apalutamide+ADT vs placebo+ADT improved pathological response (composite pCR/MRD 8.9% vs 1.0%) and metastasis-free survival (HR 0.80) — but true pCR was only 5.1%, and the absolute 5-year MFS improvement was <5%.

Managing pN+ after prostatectomy

28% of pN1 patients remain free of biochemical recurrence at 10 years with surgery alone; risk of BCR/ metastasis rises with grade and number of positive nodes. Adjuvant RT adds benefit to ADT in pN1 disease (Touijer 2018: RT+ADT outperforms ADT alone or observation) — and the more positive nodes, the more benefit (each additional positive node raises the relative mortality reduction from adjuvant RT by ~8%; ≥4 positive nodes benefit most).

Biochemical recurrence (BCR) risk stratification

Salvage RT (ESTRO-ACROP): normo-fractionated EBRT + short-term ADT (6 months) for low-risk BCR (PSA<0.7, ISUP<4); + long-term ADT (24 months) for high-risk BCR with ≥10-year life expectancy. FORMULA-509 trial: adding 6 months of ARPI to salvage RT gave an 18.2% absolute improvement at 3 years (NNT=5) — a possible alternative to 24-month ADT.

Defining mHSPC: risk and volume both matter

The mCRPC state has the highest annual progression and mortality rate of any PCa clinical state; average time a patient spends across the whole PCa disease course is ~13 years.

Treating the primary tumour in mHSPC

Systemic therapy for mHSPC — doublet or triplet?

Standard of care has evolved rapidly: ADT alone (2013) → +docetaxel (CHAARTED/STAMPEDE, 2015) → +abiraterone (LATITUDE/STAMPEDE, 2017) → +apalutamide/enzalutamide confirmed (TITAN/ARCHES/ENZAMET, 2019) → triplet ADT+docetaxel+darolutamide (ARASENS, 2022).

Molecular subgroups matter too: the AMPLITUDE trial (niraparib + abiraterone in BRCA-mutated/HRR-mutated mHSPC) reduced the risk of radiographic progression or death by 48% (BRCAm) and 37% (HRRm) — an investigational but promising direction for biomarker-selected intensification.

Supportive care in mHSPC — EAU 2026

mCRPC — sequencing therapy

Treatment choice for CRPC is multifactorial: prior HSPC therapy, response quality/pace of progression on it, known cross-resistance between novel hormonal therapies, molecular features (BRCA1/2), and local approval/reimbursement.

New in 2026: enzalutamide + radium-223 for asymptomatic/mildly-symptomatic bone-only mCRPC without visceral disease (PEACE-3); ¹⁷⁷Lu-PSMA-617 after ARPI+docetaxel for PSMA-avid disease (Strong, VISION), or after ARPI pre-chemotherapy if unfit for docetaxel (Weak, NEW — PSMAfore).

Biomarker-driven add-ons: BRCA1/2 or PALB2 → PARPi + ARPI; MSI-high/dMMR → consider pembrolizumab; high PSMA-avidity → ¹⁷⁷Lu-PSMA-617; aggressive genomics (p53/RB1) → platinum/taxane chemo; bone-only oligoprogression → SBRT.

The clinical picture

Peak incidence 15–40 years. Typical presentation: painless testicular swelling/nodule (a minority present with metastatic symptoms or gynaecomastia). Risk factors: cryptorchidism, testicular dysgenesis syndrome, prior TC or contralateral GCNIS, family history, infertility/impaired spermatogenesis. Two GCNIS-derived tumour families: seminoma and non-seminoma (NSGCT).

EAU recommendations — diagnosis & staging

Tumour markers — must remember

AFP is never elevated in pure seminoma — an elevated AFP means there is a non-seminomatous component regardless of what the histology says.

Orchidectomy & surgical options

• Radical inguinal orchidectomy: standard for diagnosis and local staging. In life-threatening metastatic disease, start chemotherapy first and delay orchidectomy.
• Testis-sparing surgery: consider in selected cases (bilateral tumours, solitary testis, small indeterminate mass with negative markers) in experienced centres — requires frozen section + ≥2 additional biopsies to exclude GCNIS; local recurrence 0–27%.
• Testicular prosthesis — NEW 2026: offer/insert a prosthesis; discuss with every patient undergoing orchidectomy.
• Contralateral GCNIS: discuss biopsy in high-risk men (cryptorchidism, marked atrophy, age <40). GCNIS in a solitary testis → local RT 18–20 Gy (risk: infertility, long-term Leydig-cell insufficiency); 5-year risk of TC with untreated GCNIS ≈50%.

Staging & risk classification

Clinical stage: I = limited to testis (IA no vascular invasion, IB vascular/tunica invasion, IS persistently elevated markers); II = retroperitoneal nodes (IIA <2cm, IIB 2-5cm or >5 nodes, IIC >5cm); III = supradiaphragmatic/visceral spread.

Clinical stage I — surveillance is preferred

~80-85% of stage I seminoma and ~70% of stage I NSGCT are cured by orchidectomy alone.

NSGCT stage IA (no vascular invasion, low risk): relapse ~15%, surveillance preferred. Vascular invasion present (high risk): relapse ~50% — offer one course of BEP, or surveillance after discussion; nerve-sparing RPLND only in highly selected patients.

Principles of first-line treatment

Cisplatin-based combination chemotherapy is the backbone. Three things determine the regimen: histology (seminoma vs non-seminoma have different chemosensitivity and residual-mass biology), IGCCCG prognosis group (defines number of cycles), and — in poor-prognosis disease — marker decline after cycle 1 (unfavourable decline warrants intensification).

Metastatic seminoma

Stage IIA/B (restructured 2026): for nodes ≤3cm with negative markers, de-escalation is now emphasised — nodes <2cm with normal markers can be considered for initial surveillance with early re-evaluation. Option A: nerve-sparing RPLND, expert centres only, may avoid chemo/RT toxicity. Option B: one cycle carboplatin AUC 7 + involved-node RT (30 Gy), or cisplatin-based chemo per IGCCCG, or RT alone. De-escalation strategies (including RPLND) only in high-volume specialised centres (Weak).

Stage IIC and III: primary chemotherapy per IGCCCG (Strong) — good prognosis BEP×3 (or EP×4); residual mass ≥3cm → FDG-PET to assess viability, <3cm PET optional. Intermediate prognosis: BEP×4 (VIP×4 if bleomycin contraindicated).

Metastatic non-seminoma (NSGCT)

Stage IIA/B: marker-positive → start chemotherapy per IGCCCG (BEP×3-4). Marker-negative → CS IIA: nerve-sparing RPLND by an experienced surgeon in a specialised centre is the recommended initial treatment; equivocal nodes <2cm → repeat staging at 6 weeks (shrinking → observe; stable → RPLND for teratoma/undifferentiated tumour; growing with rising markers → BEP).

Stage IIC and III: primary BEP per IGCCCG — intermediate prognosis 4 cycles standard BEP (Strong); poor prognosis 4 cycles BEP, assess marker decline after cycle 1 and consider intensification if unfavourable (Weak, GETUG-13 approach).

Residual masses & salvage therapy

• NSGCT: resect all visible residual masses >1cm once markers are normal/normalising (Strong) — histology splits roughly 10-15% viable cancer, 30-50% teratoma, 40-55% necrosis/fibrosis. FDG-PET is not indicated to restage NSGCT after chemotherapy.
• Seminoma: residual ≥3cm → FDG-PET; PET-positive and stable → repeat PET in 6 weeks or biopsy; growing/PET-positive → salvage therapy. <3cm: PET optional.

Salvage chemotherapy (VIP, TIP, GIP — 4 cycles with G-CSF support) achieves long-term remission in ~50% of relapses after first-line therapy; no RCT compares these regimens directly, and high-dose chemotherapy is an option in expert centres (risk of lethal haematological toxicity).

Special sites & late relapse

Brain metastases: chemotherapy remains effective first-line; consolidation RT at relapse (stereotactic superior to whole-brain); 3-year OS ~48% at diagnosis vs ~27% at relapse. Bone metastases (new §6.3.7 for 2026): an independent predictor of poor outcome in IGCCCG; cisplatin-based chemotherapy first-line as for all poor-prognosis disease; 2-year OS ~75% (seminoma) vs ~36% (non-seminoma).

SWENOTECA population data: late relapse (>2 years) occurs in ~8% of patients, median time to relapse ~7 years, and overall survival after late relapse is only ~50% — the argument for structured, genuinely long-term follow-up rather than discharging patients early.

Why bother? And why it usually doesn't happen

Metabolic screening prevents recurrence (26% at 5 years, 50% at 10 years after a first stone), catches systemic disease early (CKD risk ranges from possible in idiopathic stone formers to very high in primary hyperoxaluria/cystine/struvite), and targets therapy. Yet only ~10% of stone patients actually get one — barriers are clinician confidence, workflow/lab friction, a surgical-centric culture, and weak cost data, not patient refusal.

Timing: no earlier than ~3 weeks after stone-free status, once the patient is metabolically stable, and 8–12 weeks after starting pharmacological prevention (to check it's working).

EAU recommendations — evaluation

High-risk stone formers (~25% of all): recurrent formers, short interval since last stone, metabolic syndrome, polycystic kidney disease, spinal cord injury, strong inheritability (monogenic in 1–11% of adult formers, 12–21% of formers <25 years). Children are inherently high-risk — 2–10% of all stone patients, up to 25% of them <1 year old, 70–80% calcium oxalate, metabolic disorders in 40–60%.

Matching urine chemistry to stone type

Stone-specific prevention

Citrate is a genuinely versatile agent — it complexes ionised calcium and inhibits CaOx/CaP crystal growth, so it's used in calcium stone formers regardless of citraturia, in CaP formers (even though it raises pH), in uric acid formers (target pH 7), and in cystine formers (target pH 7.5–8.0). SGLT2 inhibitors (empagliflozin) are an emerging option for uric acid and calcium stones; lumasiran/nedosiran (RNA interference) target primary hyperoxaluria specifically.

Non-laser energies — pick by stone hardness, not habit

In PCNL: pneumatic is faster on hard stones, ultrasonic faster on soft ones; combined ultrasonic+ballistic ("dual-modality") probes exist (Swiss LithoClast Master, ShockPulse-SE, LithoClast Trilogy) but show no SFR superiority over either energy alone.

Laser lithotripsy — the physics that actually matters clinically

• Ho:YAG: photothermal ablation (stone absorbs light, heats up); scattered beam profile; low-power vs high-power shows no SFR difference, just possibly shorter operative time.
• Thulium fibre laser (TFL): more focused beam; a stream of 50–60 microbubbles creates a vapour channel (vs Ho:YAG's single larger bubble); mechanical force from Ho:YAG bubble collapse reaches 7.5–26 bar vs only 0.6 bar for TFL. No proven SFR superiority over Ho:YAG to date, but possibly higher sepsis rates reported.
• Pulsed Tm:YAG: water is the primary chromophore; photomechanical + photothermal effect; peak power up to 1300–3700W depending on device.

Contact vs non-contact: direct-contact Ho:YAG minimises cavitation bubble formation (energy goes into the stone); non-contact wastes more energy on the cavitation effect ("pop-corning") and ablates less efficiently.

Aetiology & presentation

Presentation: haematuria, frequency, dysuria, suprapubic pain, catheter problems, recurrent UTI, or incidental finding.

EAU recommendations

Real-world data (BLAST registry, EAU Endourology Group): endoscopic surgery is as effective as open, with shorter catheterisation time/convalescence in adults and children; transurethral has a shorter stay than percutaneous. Simultaneous HoLEP + cystolithotripsy adds operative time but not complication risk.

What you're actually protecting against

Deterministic effects (skin, lens, gonads, marrow, GI tract): dose-dependent, a threshold exists, severity rises with dose. Stochastic effects (cancer, heritable/genetic effects): dose-independent probability that rises with dose, no threshold (linear no-threshold model) — estimated ~4% increase in fatal cancer risk per 100 mSv.

Who to protect, and how

Patients, the operator, the whole staff/healthcare team, and the equipment/environment — radiation protection is a shared responsibility. Scatter radiation (produced when the primary beam interacts with the patient), not the primary beam itself, is the main source of exposure to both patient and staff — anything that reduces the patient's dose also reduces the operator's.

Reducing patient dose — the practical checklist

• Pulsed, not continuous, fluoroscopy: same diagnostic performance at a fraction of the dose (e.g. 0.9 vs 2.9 mGy absorbed dose, thick phantom).
• Tight collimation: reduces field size, scatter, and patient dose together — collimating to the area of interest is one of the single highest-yield changes.
• Reduce magnification and increase source-to-image distance where possible — magnification always costs more dose (inverse-square relationship) and more scatter.
• Avoid digital acquisitions (5–10× the dose of fluoroscopy) — use last-image-hold instead of saving extra digital frames.
• Use ultrasound in PCNL whenever feasible — cuts fluoroscopy time substantially (comparative series: ~42–56s with US+fluoro vs fluoro alone).
• Use the audible fluoroscopy-time indicator and watch the cumulative dose display (measured at the interventional reference point, 15cm in front of the iso-centre) — it doesn't account for tube movement, so treat it as a floor, not a ceiling.

Protecting yourself

Structural shielding (room design, fixed barriers) + mobile shielding (screens, ceiling-suspended shields) + personal shielding: lead apron with full front coverage (0.25–0.5mm Pb equivalent) — must; thyroid collar — must; lead glasses when there's eye-scatter risk. Do not wear lead gloves — they increase scatter to the hands and are not actually protective.

How it works, and what predicts success

Shockwaves (spark-gap, piezoelectric, or electromagnetic generator) are focused by a parabolic reflector and coupled into the patient via a bubble-free cushion; high compressive/tensile stress cracks the stone into passable fragments.

• Ramping (start at low energy, progressively increase): success is similar with or without it, but perirenal haematomas are significantly reduced with ramping.
• Stone attenuation >900–1000 HU and skin-to-stone distance >9–10cm both predict worse SFR — check both on the planning CT before committing to SWL.
• Favourable lower-pole anatomy for SWL: infundibulopelvic angle >45°, infundibular width >5mm, infundibular length <2.5mm (i.e. a short, wide, favourably-angled lower pole).

EAU recommendations — best clinical practice

Contraindications: pregnancy, uncompensated bleeding disorder (compensate ≥24h before/48h after), uncontrolled UTI, severe skeletal malformation/obesity preventing targeting, arterial aneurysm near the stone, distal anatomical obstruction. Optimal shock frequency 1.0–1.5 Hz (LE 1a); repeat sessions are feasible within one day for ureteral stones.

Indications & anatomy

Distal and mid-ureteric stones, selected proximal stones, UTUC biopsy, foreign body retrieval. Three physiological narrowings to respect: pelvi-ureteric junction, iliac vessel crossing, vesico-ureteric junction (the ureter is never straight). Semirigid scopes are useful before flexible URS to dilate a narrow ureter — an alternative to pre-stenting, but be careful of injury.

Pre-stenting — the guideline nuance

Safety guidewire: recommended for the majority of ureteroscopic procedures (LE3, GRB) — especially upper ureteral stones, oedema/stricture/abnormal anatomy, encrusted stents, or impacted stones; if bleeding or injury occurs it allows rapid stent placement.

Complications & tips

Even a guidewire can cause damage — respect resistance, don't force it. Post-op care: pain control, stent-symptom and sepsis monitoring, discharge advice, and — as always in stone disease — metabolic prevention follow-up, not just imaging.

Intrarenal pressure (IRP) — why it's the thing to actually watch

High IRP causes backflow/fluid absorption (forniceal rupture, fluid overload, electrolyte imbalance, cardiovascular instability), infectious complications (fever, sepsis), and kidney ischaemia-reperfusion damage. Post-renal-haematoma series: rate 0.45%, mean stone size 1.7cm, managed with transfusion/antibiotics (55%) or percutaneous drainage (28%); prevention = control hypertension, treat pre-op UTI, reduce IRP and operative time. Mean IRP was 81mmHg in patients who developed post-op urosepsis vs 38.5mmHg in controls.

Suction (via access sheath, ureteral catheter, or suction-integrated scope) improves IRP and temperature control, visualisation and SFR while reducing sepsis/bleeding — at the cost of operational complexity and (still) undefined optimal parameters.

Scopes — miniaturisation & single-use

Failed ureteric access without dilatation rises steeply with scope size (9.0Fr 37% vs 7.4Fr 0.9%) — smaller scopes mean less pre-stenting, more primary URS, less post-op stenting, and better suitability for children/small patients. Single-use vs reusable flexible ureteroscopes: no significant difference in infection rate (4.0% vs 4.4%), complications (11.5% vs 11.9%), operative time, length of stay, or SFR (74% vs 74.3%) — cost and sterility-risk profile, not outcome, should drive the choice. Environmental footprint is comparable (single-use LithoVue 4.43 kg CO₂/case vs reusable 4.47 kg CO₂/case).

UTUC endoscopic management & endopyelotomy

"No-touch" technique for UTUC — catch, then pull (kidney) or catch-push-pull (ureter) to avoid direct instrument-tumour contact. For retrograde laser endopyelotomy: know your cut sites by clock-face position (they differ left vs right, and by level — UPJ, proximal/mid/distal ureter, ureteral orifice) to avoid the vessels that cross at each level.

Access — step by step

1. Puncture through a posterior calyx — traverses Brödel's bloodless (avascular) line between the anterior and posterior renal divisions, lowest vascular-injury risk.
2. Bull's-eye technique: site selection with the C-arm at ~30° (posterior calyx orientation), then rotate to 0° to check depth — do not inject contrast at this stage.
3. Advance a hydrophilic guidewire, aiming to cross the UPJ and pass down the ureter as far as possible; if it won't cross, redirect the needle, use an angled/steerable tip, or a "hockey-stick" catheter. Emptying the pelvis or placing a second wire can help find the way; watch for sub-urothelial passage.
4. Exchange for a stiff wire, dilate (one-step to 22-24Fr, or stepwise 16Fr→30Fr) always directing dilation forces toward the ureter, not the hilum.
5. For staghorn stones, consider multiple tracts of different sizes.

Principles that keep it safe

• Never inject contrast before confirming needle depth at 0°.
• Respect the course of the guidewire during dilation — a kinked wire signals a problem, don't push through it.
• Know your instruments' strengths (e.g. flexible nephroscope for hard-to-reach calyces) and have an exit strategy planned before you start.

Prone vs supine — trade-offs, not a winner

Both positions achieve excellent stone-free rates with acceptable safety profiles — position choice should be driven by whether combined retrograde access is wanted, patient anaesthetic risk, and surgeon experience, not by dogma.

ECIRS — endoscopic combined intrarenal surgery

Synergy of RIRS and PNL: simultaneous rigid + flexible instruments, antegrade + retrograde approaches, from the same team. Same indications/contraindications as standard PNL — it's a way of performing PNL, not a separate procedure. The GMSV (Galdakao-Modified Supine Valdivia) position optimally supports it; prone split-leg variants also exist and are in the EAU guidelines since 2023.

Active retrograde ureteroscopy contributes in >50% of ECIRS cases (the "pass-the-ball" technique) — beyond drainage, it lets the surgeon evaluate stone hardness/mobility, distinguish stones from Randall's plaques, decide intraoperatively to switch from ECIRS to RIRS-only, or stop for turbid urine/bleeding. This is endoscopic dynamic anatomy — genuinely different information from the static anatomy on the preoperative CT.

Access under combined guidance: fluoroscopy (biplanar, x/y axis) + ultrasound (depth/third dimension) + endovision — a single inferior-posterior papillary-puncture access is the target in ~93% of contemporary cases, with multiple accesses reserved for complex stones.

Children

Calcium oxalate is the most common stone; hypocitraturia, low urine volume and hypercalciuria predominate — metabolic evaluation is essential in every child, not optional. Presentation varies with age: infants show crying/irritability/vomiting, older children flank pain/haematuria/recurrent UTI — a high index of suspicion is needed.

• Asymptomatic lower-pole stones <7mm: observation is an option in selected cases; alpha-blockers may help distal ureteric stone passage (off-label).
• SWL: first-line for many ureteric stones, SFR 70–90%. Rigid URS SFR 81–98%. Flexible URS/RIRS SFR 76–100%. Choice depends on size, location, anatomy, and local expertise.
• PCNL for stones >2cm or failed SWL/URS: SFR 71–95%, mini-PCNL overall SFR ~97%; miniaturisation reduces morbidity. Open/robotic surgery is rarely needed.

Pregnancy

Requires multidisciplinary care (urologist, obstetrician, radiologist, patient) — untreated urolithiasis is associated with increased maternal and neonatal complications, but every decision balances maternal benefit against fetal safety.

Ureteral stones

Renal stones

Meta-analysis (7 studies/983 patients) driving the 1–2cm lower-pole shift toward endourology: RIRS gives higher SFR and lower retreatment rates than SWL with similar complications (e.g. one RCT: SFR 87% RIRS vs 68% SWL at 3 months, retreatment 8% vs 60%). Still, SWL SFR for stones <10mm reaches 65–91.5%, and pelvic stones <1cm specifically do very well with SWL (85% SFR, 1.2% failure, low cost, no anaesthesia) — don't discard SWL for small, well-located stones just because RIRS wins the head-to-head for lower-pole stones overall.

Sepsis, anuria & medical expulsive therapy

Working through a case, EBU-exam style

A 2-month-old boy: asymmetric scrotum, normal penis, no palpable testis on one side. Incidence of undescended testis (UDT) is 4–6% at birth, falling to ~1% at 1 year as most descend spontaneously in the first months — so the correct next step at 2 months is simply to re-examine after 6 months of age, not to intervene. Examination technique: look at the child first, warm hands, gentle handling, supine and frog-leg position, examine the entire groin/region, compare with the contralateral testis, use lubricant.

If still non-palpable at 9 months: discussing ultrasound/MRI is common in practice but not required by EAU-ESPU guidelines — imaging does not change management. A hypertrophic contralateral testis is a clinically useful sign — it can indicate the ipsilateral testis is non-functioning. Plan surgery for 6–12 months of age.

Under anaesthesia — the actual decision tree

• Repeat the physical exam under general anaesthesia first — this is the true first step of any UDT surgery.
• If palpable now → open orchidopexy.
• If a small firm "nubbin" is palpable in the scrotum → excise it now (already under anaesthesia), or if it was already known from clinic, postponing excision to puberty is a reasonable alternative.
• If still non-palpable → laparoscopy, starting with a single umbilical port to assess the abdominal cavity; empty the bladder first (catheterise before/during surgery).

What's normal, and when circumcision is (or isn't) the answer

Physiological phimosis is normal until puberty. Circumcision is genuinely indicated in posterior urethral valves, CAKUT, and BXO (balanitis xerotica obliterans/lichen sclerosus) — but is formally contraindicated in hypospadias, epispadias, buried penis, and penile curvature, because the foreskin will be needed for the reconstruction.

Penile malformations

Hypospadias surgical goals: normal voiding, preserved sexual function and sensitivity, acceptable glans/skin appearance, and correction of any curvature (orthoplasty) alongside the urethroplasty.

Epispadias is rare, usually part of the bladder exstrophy-epispadias complex. Micropenis = stretched penile length >2 SD below the median for age. Isolated penile curvature: uncommon on its own (ventral → suspect hypospadias, dorsal → suspect epispadias); clinically significant above ~30°; only visible on erection, so photograph it; surgical correction is bracketed by artificial erection testing before and after.

Scrotal malformations

Cryptorchidism

Incidence 1.0–4.6% full-term, up to 45% preterm; bilateral in up to 30% of cases. Undescended (fixed, high position) must be distinguished from retractile testis (overactive cremasteric reflex, pulls up but comes back down) — retractile testes don't need surgery.

Hydrocoele & inguinal hernia

Hydrocoele = fluid between layers of the tunica vaginalis; congenital cause = patent processus vaginalis (acquired hydrocoele instead follows trauma, tumour, or post-varicocele repair). Diagnose with transillumination/ultrasound. Management is not indicated in the first 12 months — most resolve spontaneously as the processus closes. Inguinal hernia, unlike hydrocoele, is an indication for surgery.

Neurogenic bladder

Most often caused by myelomeningocele (spinal dysraphism). Level of the spinal lesion correlates poorly with actual bladder/sphincter function — you cannot predict function from the MRI level, you have to test it. Goals: protect kidney function long-term, avoid UTI, improve continence when appropriate/desired.

Clean intermittent catheterisation (CIC) is the most important first-line treatment — proactive approach, started ASAP after birth, with urodynamics before hospital discharge (or within 3 months) specifically to catch detrusor-sphincter dyssynergia and poor compliance early, reducing VUR/hydronephrosis risk. Not mandatory if the sphincter is synergic with complete, low-pressure emptying.

Pharmacotherapy: anticholinergics from the neonatal period improve compliance and reduce pressure/contractions (watch for cognitive/behavioural side effects); intradetrusor botulinum toxin is off-label in most countries, effect wanes over 3–6 months as new synapses form, does not cross the blood-brain barrier (no CNS effects), but antibody formation is possible.

Don't forget to discuss sexuality at the appropriate age — this is an explicit take-home message, not an afterthought.

Congenital lower urinary tract obstruction — posterior urethral valves (PUV)

PUV is the most frequent cause; usually bilateral (unlike upper-tract obstruction). Prenatally: a thick-walled bladder predicts PUV better than a dilated posterior urethra alone; falling 2nd-trimester amniotic fluid, raised bladder pressure, and the "pop-off" phenomenon (unilateral high-grade VUR protecting the contralateral kidney) are all relevant. Mortality in severe prenatal presentations 60–80%; of survivors, 1/3 eventually reach end-stage kidney disease.

Serum creatinine nadir >0.85 mg/dL correlates with poor long-term prognosis (LE 2a). Despite everything done right, roughly 20% of PUV patients still progress to ESRD — this is a lifelong surveillance disease, not a one-time fix.

Symptom groups & work-up

Storage (altered sensation, frequency, nocturia, urgency, incontinence), voiding (hesitancy, intermittency, slow/split stream, straining, terminal dribble) and post-micturition symptoms (incomplete emptying, dribble) are the three buckets — OAB is a storage-symptom syndrome, and its diagnosis is clinical, not urodynamic.

Treatment ladder

Treatment goals — the "PICK" framework

Neuro-urological management is not just about dryness: Pleasure (sexuality, quality of life), Independence (self-catheterisation over carer-dependent care where feasible), Continence, and — the priority that overrides the rest — protecting Kidney function. A proactive approach (early urodynamic assessment, early CIC) protects the upper tracts even when the patient is not yet symptomatic.

Clean intermittent catheterisation — the backbone of management

CIC (Lapides, 1970s) is clean, not sterile, done 4–6×/day by patient or carer. It's the most important first-line treatment for detrusor–sphincter dyssynergia and poor bladder compliance — the goal is avoiding kidney damage by keeping the bladder a low-pressure reservoir, which reduces the risk of VUR and hydronephrosis. Antimuscarinics/anticholinergics and intradetrusor botulinum toxin A are added on top of CIC to improve compliance and reduce detrusor pressure/contractions when CIC alone is not enough; conservative treatment is maintained for as long as it remains adequate before escalating to reconstructive surgery.

When conservative treatment isn't enough

Bladder augmentation (bowel segment ± catheterisable channel ± bladder neck procedure) is reserved for persistent poor compliance/high pressure despite CIC and pharmacotherapy — it carries a high complication burden (stones, metabolic disruption, malignancy risk, need for lifelong surveillance), so it is a last resort, not a default. Continent catheterisable channels (Mitrofanoff) and urinary diversion are options when transurethral CIC is not feasible.

• Autonomic dysreflexia — a life-threatening, sudden hypertensive crisis triggered by a noxious stimulus below a spinal lesion at or above T6 (classically bladder overdistension). Recognise it (headache, sweating, bradycardia, severe hypertension), remove the trigger (empty the bladder), and treat the blood pressure — this is an emergency, not a nuisance symptom.
• Long-term surveillance risks specific to neurogenic bladder: higher lifetime risk of bladder stones and of bladder cancer (especially with long-term indwelling catheters and chronic inflammation) in spinal cord injury patients — this drives the lifelong video-urodynamic and upper-tract imaging follow-up that neuro-urological patients need, for the rest of their lives, regardless of whether they feel well.

Vesico-vaginal fistula (VVF)

In high-resource settings the dominant cause is gynaecological surgery (~90%, chiefly hysterectomy); in resource-limited settings it is overwhelmingly obstetric (obstructed labour, ~90%). UK data: roughly 1 VVF per 400–2,000 hysterectomies. Assessment combines clinical exam, CT IVU (to exclude hydronephrosis/ureterovaginal fistula), and — if equivocal — a 3-swab test, cystogram, or cystoscopy under anaesthesia; biopsy any radiotherapy-associated fistula before assuming it's simple.

Surgical principles: excise the fistula margins/tract, close under no tension, and interpose healthy vascularised tissue (classically a modified Martius labial fat pad flap). Route: vaginal repair is preferred whenever feasible (higher closure rate, faster recovery); abdominal/laparoscopic/robotic access is reserved for simultaneous ureteric reimplantation, clam cystoplasty, or other concurrent bowel surgery. A 2019 systematic review found 94% closure with vaginal repair vs 84% abdominal; adding a Martius flap improves simple-repair success from ~75% to ~90%+ and appears to reduce dyspareunia and recurrent USUI. Early repair (within the 2–3 week post-injury window) does as well as delayed repair in expert hands, though obstetric fistulae are conventionally allowed to settle first.

Complications: stress incontinence (1–55%, mainly after obstetric fistula), vaginal stenosis/dyspareunia, ureteric injury, tethered vagina syndrome. Global burden: obstetric fistula affects >2 million women worldwide, with 50,000–100,000 new cases per year, disproportionately young (73% <20 years) and first-pregnancy patients — the Goh (2004) and Waaldijk (1995) systems are the two classifications in use for grading complexity.

Urethral diverticulum

Arises from obstruction/infection of the periurethral (Skene's) glands, dissecting within the periurethral fascia; more common in Afro-Caribbean women and after childbirth (though 20% are nulliparous). Iatrogenic causes include TVT/TVT-O placement, urethral bulking agents, and instrumentation. Presents with recurrent UTI, post-void dribbling, dyspareunia, or a palpable anterior vaginal wall mass.

Diagnosis: MRI is the best test for diverticular anatomy (configuration, size, number of connections); video-urodynamics assesses concurrent bladder/continence function; ultrasound is cheap but operator-dependent and can miss small (<2cm) or complex/circumferential diverticula.

Treatment ladder: conservative management (leave alone) carries ongoing risk of infection, stones, and cancer in up to 9% over time, and needs annual exam+MRI if chosen. Endoscopic incision/fulguration has only small, short-follow-up case series behind it. Open excision with a tension-free 3-layer closure ± Martius fat pad interposition is the reference standard: cure in 80–100% depending on diverticulum configuration (simple > horseshoe > circumferential), but new stress incontinence in up to 33%, persistent USUI in up to 73%, and urethrovaginal fistula/urethral stricture in up to 15% — patients need clear counselling that continence problems are a real trade-off of cure.

Epidemiology & aetiology

Incidence 229–627 per 100,000 men (≈1.7 million men in Europe), mean age 45, rising sharply >55 years. 92% are anterior urethral (47% bulbar, 18% meatal). Causes: iatrogenic (32–79% of cases — instrumentation, prior urethral/BPO surgery, radiation; long-term catheterisation carries an 8.7% stricture risk vs 3.4% for <3 weeks), external trauma (bulbar from straddle injury/blunt trauma; membranous from pelvic-fracture deceleration injury), infectious (gonococcus/chlamydia/ mycoplasma urethritis — 1–5% of strictures in high-income countries vs up to 50% in low-income settings), and inflammatory (lichen sclerosus — involves the urethra in 20% of cases and causes nearly half of panurethral strictures; risk factors are no circumcision, metabolic syndrome, and smoking).

Diagnosis & treatment ladder

Uroflowmetry and cystoscopy screen for stricture; retrograde urethrography is recommended before any reconstructive surgery to map length/location. MRI adds periurethral tissue detail but is expensive and less available; ultrasound (with saline instillation) is cheap, radiation-free and can show spongiofibrosis, but is operator-dependent.

Pelvic fracture urethral injury (posterior urethral distraction defect): if the obstruction is complete, do not attempt endoluminal realignment — refer to a specialist centre for delayed repair (resect all fibrosis/scar, combined transpubic/abdominal approach); if incomplete, an endoluminal attempt is reasonable once. Complications to counsel for: recurrent stricture, urethral misalignment, erectile dysfunction, incontinence.

Epidemiology, mechanism & classification

SUI affects 17–45% of women >40 in high-income countries; BMI>30 roughly doubles the risk. Risk factors: vaginal delivery, obesity, smoking/chronic cough, ageing, family history. Mechanistically, SUI is multifactorial rather than one lesion — urethral hypermobility from deficient support (DeLancey's hammock theory) and intrinsic sphincter deficiency (from trauma, radiotherapy, prior pelvic surgery, neurological disease, or ageing) sit on a continuum rather than being a strict either/or.

A standing cough test is more sensitive for SUI than a supine one (100% vs 76%) — do it standing. Red flags on history (pain, haematuria, recurrent UTI, voiding symptoms, continuous leak suspicious of fistula) warrant early referral rather than routine work-up.

Is urodynamics needed?

Performing urodynamics in uncomplicated SUI that is clear from history and exam is not necessary — a high-quality RCT (n=630) found urodynamics changed the clinical diagnosis in 56% of women but did not change 12-month surgical outcomes, and a Cochrane review found urodynamics reduced surgery rates without changing treatment outcomes within trial populations. Reserve it for SUI with associated storage symptoms, unclear incontinence type, suspected voiding dysfunction, or associated POP/prior SUI surgery.

Treatment ladder

Terminology & basic work-up

LUTS (symptoms) may be caused by BPO (obstruction), which is usually due to BPE (enlargement), which is usually driven by BPH (the histological hyperplasia) — a patient can have any of these without the others. Prostate volume alone is a poor predictor of obstruction.

Progression risk rises with prostate volume >30mL (3×), Qmax<12mL/s (4×), moderate–severe symptoms (4×), and age 70–79 (8×). Baseline PSA independently predicts future prostate growth (PLESS study) — both PSA and volume carry prognostic, not just diagnostic, information.

Medical treatment ladder

Indications

Absolute: recurrent/refractory urinary retention, overflow incontinence, recurrent UTIs, bladder stones or diverticula, treatment-resistant macroscopic haematuria from BPH/BPE, upper-tract dilatation due to BPO (± renal insufficiency). Relative: bothersome LUTS refractory to medical management.

EAU recommendations by technique

Greenlight (532nm) laser vaporisation performs comparably to TURP up to 24 months (180W systems) or 60 months (80–120W systems) across multiple RCTs, with a lower transfusion rate but a signal towards more reinterventions in meta-analysis — an option, not a universal replacement. Open/simple prostatectomy remains the most effective option for very large glands (IPSS improves 63–86%, Qmax +375%) but carries the highest morbidity: transfusion 7–14%, incontinence <10%, bladder-neck stenosis/stricture 3–5%. Prostate artery embolisation is still emerging/investigational — roughly 21% reintervention rate at 2 years; "one size does not fit all" is the honest summary across all these options.

Choosing between TURP variants

Anatomy, physiology & assessment

The urethral sphincter has an internal smooth-muscle layer (involuntary, resting tone) and an external striated layer (voluntary, recruited under stress) — a horseshoe shape with no direct attachment to levator ani, first anatomically described by Henle (1855). Resting urethral closure pressure is roughly 60cmH₂O at baseline, rising further with skeletal-muscle recruitment during abdominal stress. Radical prostatectomy damages this system directly, with reported SUI rates of 5–48% across series.

Assessment: classify as SUI, UUI or mixed, and rule out overflow incontinence/nocturnal enuresis. Validated tools: ICIQ-UI Short Form, bladder diary/frequency-volume chart, 24-hour pad-weight test. A commonly used (though not formally validated) severity split is <200g/24h mild, 200–400g moderate, >400g severe. The posterior urethral repositioning test (manually repositioning the urethra during cystoscopy/exam) can suggest whether a sling is likely to help versus whether sphincter damage predominates.

Treatment ladder

Definition & why it matters

ED is the persistent or recurrent inability to attain and/or maintain an erection sufficient for satisfactory sexual performance. It is common (≈52% of men >40y) and shares its risk-factor profile with cardiovascular disease almost exactly — obesity, smoking, sedentary lifestyle, dyslipidaemia, diabetes/metabolic syndrome.

Causes, by category

• Vascular: CVD, hypertension, diabetes, hyperlipidaemia, smoking, pelvic surgery/radiation
• Neurological: MS, Parkinsonism, stroke, spinal cord disease, polyneuropathy, pelvic/retroperitoneal surgery
• Hormonal: hypogonadism, hyperprolactinaemia, thyroid disease, Cushing's
• Anatomical/structural: Peyronie's disease, penile fracture, congenital curvature, hypo-/epispadias
• Drug-related: antihypertensives (diuretics, β-blockers), antidepressants, antipsychotics, antiandrogens, opioids
• Psychogenic: loss of libido, performance anxiety, relationship issues, depression

Diagnosis

Every patient: comprehensive sexual/medical history, validated questionnaire (IIEF, EHS), focused physical exam, and labs (glucose, lipid profile, total testosterone) to catch reversible risk factors.

Specialised testing — only if:

• Lifelong (primary) ED without acquired organic disease
• Young patient after pelvic/perineal trauma who could be a vascular-surgery candidate
• Penile deformity (Peyronie's) or complex psychiatric/endocrine disease
• Patient request or medico-legal indication

EAU recommendations — treatment

Treatment ladder

Post-radical prostatectomy ED

Incidence 15–95% depending on nerve-sparing status, age, baseline EF, comorbidity and surgeon experience. Penile rehabilitation aims to keep cavernosal oxygenation up (35–40 → 75–100 mmHg during erection) to prevent smooth-muscle loss that starts as early as month 2 post-op. PDE5i effective in 35–75%, daily ≈ on-demand; combine with vacuum/traction to preserve length; injections often still needed.

Congenital penile curvature (CPC)

Rare (<1%), from disproportionate tunica-albuginea development, usually ventral, not associated with urethral malformation. Diagnosis is clinical (history + exam during erection / auto-photography, sometimes after an ICI test dose). Treatment is surgical plication (Nesbit, 16-dot, Yachia, Essed-Schröeder, Shaeer), with or without degloving/neurovascular bundle elevation.

Peyronie's disease (PD)

Acquired fibrotic disorder of the tunica albuginea, incidence 0.4–11%, typical onset 50–60y. Likely mechanism: repetitive microtrauma → abnormal wound healing, on a genetic fibrotic predisposition (4–26% of PD patients also have Dupuytren's contracture). Risk factors: diabetes, hypertension, dyslipidaemia, ischaemic heart disease, ED, smoking, heavy alcohol use, low testosterone, pelvic surgery.

Two phases — get this distinction right

• Active (acute): painful erections, palpable nodule, deformity still changing. Pain resolves spontaneously in ~90% within 12 months.
• Stable (chronic): curvature unchanged and pain-free for ≥3 months.

Natural history of the curvature itself: worsens in 21–48%, stabilises in 36–67%, improves in only 3–13% — true spontaneous resolution is uncommon. Psychological burden is significant: about half of men with PD have moderate-to-severe depressive symptoms.

Work-up

• Peyronie's Disease Questionnaire (PDQ) — psychological/physical symptoms, pain, bother
• Focused history to separate active vs. stable disease
• Exam: stretched/erect length, curvature, plaque; extend to hands (Dupuytren) and feet (Ledderhose)
• IIEF / ICI test for erectile function; penile Doppler US before any surgical planning

EAU recommendations

Surgery is reserved for stable disease (≥3–6 months, or >9–12 months from onset) with functional impairment. Outcome data: straightening >85–97% across techniques; shortening (any) 22–69%, clinically significant >1 cm in 3–9%; de-novo ED 3–10% after shortening procedures, up to 50% after lengthening/grafting; satisfaction 83–94%.

Three flavours — tell them apart fast

Ischaemic priapism

Definition: painful rigid erection >4h with little/no cavernosal arterial inflow — >95% of all priapism. Causes: idiopathic, sickle cell disease (29–42% across all ages), haematological dyscrasias, malignancy, drugs (ICI, PDE5i, antipsychotics, α-blockers).

Diagnosis

• History + exam: corpora rigid and tender, glans soft, severe pain
• CBC; corporal blood gas from aspiration (hypoxic, hypercapnic, acidotic)
• Colour duplex US before aspiration; MRI if smooth-muscle viability needs assessing

EAU recommendations — management

Non-ischaemic (high-flow) priapism

Cavernosal artery laceration → AV fistula, almost always from blunt perineal/penile trauma; onset can be delayed 2–3 weeks after the injury. Not painful, not an emergency — untreated it can still cause ED over time.

• 1st: conservative — ice, site-specific perineal compression (US-guided)
• 2nd: selective arterial embolisation — success 61.7–83.3%, ED risk 0–33.3%; temporary material preferred initially, repeat embolisation is reasonable
• Last resort: surgical fistula ligation — highest ED risk of the three options

Stuttering (recurrent) priapism

Short, repeated painful episodes, mostly in sickle cell disease; goal is prevention, not just acute treatment.

Acute episodes are managed as ischaemic priapism. Penile prosthesis is a last resort for medically refractory cases.

Definitions

• Infertility: no spontaneous pregnancy after 12 months of unprotected intercourse.
• Unexplained infertility (couple): normal tubal patency, ovulation and semen analysis — 20–30% of couples.
• Idiopathic male infertility: no relevant history, normal exam/endocrine/genetic work-up, but abnormal semen parameters — 30–40% of male-factor cases; thought to involve oxidative stress, environmental endocrine disruption, and unidentified genetic/epigenetic factors.

Aetiology snapshot

Work-up

Basic: history + risk factors, physical exam, semen analysis. Advanced (as indicated): scrotal ultrasound, hormones, genetic testing, extended sperm testing (DNA fragmentation, ROS).

Semen analysis — the 5 things to get right

1. Abnormal semen parameters ≠ infertility — a semen analysis alone never proves or excludes it; only the couple's combined fertility potential does.
2. One analysis is never enough — repeat if the first is abnormal (WHO 6th edition methodology).
3. Results vary a lot — recent fever/illness, abstinence variation, etc.
4. Respect abstinence: 2–7 days.
5. Collect close to the lab; if transported, keep between 20–37 °C.

Azoospermia = no spermatozoa after centrifugation (3,000g/15min) on phase-contrast microscopy of the pellet. Leukocytospermia (>1×10⁶ WBC/mL) → semen culture to look for male accessory-gland infection.

Hormonal pattern-matching

EAU recommendations — genetics & imaging

AZFc microdeletion: sperm can be found in 50–75% of retrieval attempts. AZFa or AZFb (complete): 0% — do not attempt TESE. Klinefelter syndrome (most common sex-chromosome abnormality): TESE/mTESE succeeds in up to 50% despite azoospermia.

Varicocelectomy

Present in 15% of men generally, 25% with abnormal semen, 35–44% with primary and 45–81% with secondary infertility. Treating a clinical varicocele produces a large positive effect on sperm concentration, total count, motility and morphology vs. untreated men — improvement takes ~2 spermatogenic cycles (~64 days each), pregnancy typically 6–12 months post-op.

Microsurgical inguinal/subinguinal approach has the lowest recurrence (0.4%) and complication rate of all techniques (vs. 2.6–29% for open/laparoscopic/radiological approaches) — the EAU panel does not issue a formal recommendation on technique, but the evidence favours microsurgery.

Obstructive azoospermia — location dictates the fix

Whenever a reconstructive seminal-tract surgery is attempted, sperm retrieval for cryopreservation should always be attempted at the same time as a fallback.

Sperm retrieval for ART

• Obstructive azoospermia: MESA / PESA / TESA / TESE — any technique works because sperm production is normal; choose reconstruction first if the couple has time, or go straight to retrieval + ICSI if ovarian reserve is limited or reconstruction isn't feasible.
• Non-obstructive azoospermia: TESE/microdissection-TESE (mTESE). mTESE gives higher retrieval and fewer complications than conventional TESE — considered the optimum approach.
• Complete AZFa or AZFb microdeletion → do not attempt retrieval (0% yield).

Vasectomy

WHO recommends the No-Scalpel Vasectomy (NSV) technique with fascial interposition, which markedly reduces failure rate; thermal cautery preferred over electrocautery (fewer granulomas). Pregnancy rate 0–2% (most <1%).

No increased risk of: antisperm-antibody disease, prostate cancer, sexual dysfunction, cardiovascular disease, or reproductive hormone changes. Semen analysis at 8–16 weeks confirms azoospermia/success.

Definition & classification

A clinical syndrome combining symptoms (with or without signs) and biochemical testosterone deficiency — neither alone is sufficient for diagnosis.

Testosterone measurement — the traps

• Measure total testosterone in the morning (07:00–10:00), fasting, confirmed on ≥2 occasions.
• SHBG shifts change how informative total T is: SHBG ↑ (ageing, hyperthyroidism, liver disease, smoking, HIV) can make total T look normal while free T is low → missed hypogonadism. SHBG ↓ (obesity, hypothyroidism, insulin resistance, Cushing's, NAFLD) can make total T look low while free T is normal → false hypogonadism.
• Do not use direct immunoassay free-T — inaccurate; use SHBG + albumin-based calculated free T instead.
• EAU 2026: free-T threshold of 220 pmol/L (6.4 ng/dL) is useful specifically when total T sits in the grey zone of 8.0–11.0 nmol/L.

Late-onset hypogonadism (LOH) — what you'll actually see in clinic

EMAS data: healthy men lose ~0.4%/year total T and ~1.3%/year free T with age — mostly from falling Leydig cell mass, not disease. Obesity and metabolic comorbidity, not age itself, drive most of the clinically relevant decline.

Symptoms: specific — reduced libido, ED, fewer spontaneous/morning erections, reduced vigorous activity; less specific — fatigue, low mood, sleep disturbance, hot flushes.

Testosterone replacement therapy (TRT)

Contraindications and monitoring: EAU Guidelines on Sexual & Reproductive Health 2026, §3.5.9 "Summary of evidence and recommendations on safety and monitoring in testosterone therapy".

• Do not give testosterone to eugonadal men, or to men wanting fertility (it suppresses spermatogenesis) — use gonadotropin therapy instead if fertility is desired, especially in secondary hypogonadism.
• Combination TRT + PDE5i outperforms PDE5i alone for moderate-severe ED with concurrent hypogonadism.
• Low-risk prostate cancer after radical prostatectomy: TRT may be considered (weak) only after ≥1 year of undetectable/very low PSA monitoring — counsel on limited long-term safety data.
• Formulations: gel, buccal, nasal spray, transdermal patch, IM/SC injection, subdermal implant — gel or long-acting injectable favoured for the best safety profile; gel preferred to start in higher-risk patients (easier to stop).

Monitoring schedule

Haematocrit ≥54% at any point → reduce dose, switch formulation, or perform venesection.

The 2026 reclassification

The EAU panel has dropped "uncomplicated / complicated" in favour of a symptom-based split:

• Localised UTI (cystitis): frequency, urgency, suprapubic pain — no systemic signs. Applies to all sexes; male sex alone is no longer treated as a risk factor (only prostatic involvement is).
• Systemic UTI: fever, chills, tachycardia, hypotension, confusion — with or without local symptoms. Includes pyelonephritis, acute prostatitis, urosepsis.

Risk factors to screen for regardless of category: infancy, frailty, anatomical/functional abnormality, catheters, stones, obstruction, immunosuppression, neuro-urological disease, recent instrumentation, resistant organisms, pregnancy/pelvic organ prolapse.

Pocket Guidelines 2026, Table 1 (localised/systemic signs & symptoms) and Table 2 (UTI risk factors).

Asymptomatic bacteriuria (ABU)

≥10⁵ CFU/mL, confirmed on 2 consecutive samples in women / 1 in men, without symptoms.

Cystitis

Diagnose women without systemic risk factors on history alone (dysuria/frequency/urgency + no vaginal discharge) — culture is not routinely needed unless: systemic infection suspected, symptoms persist/recur by 4 weeks, atypical presentation, high resistance risk, or pregnancy.

Pocket Guidelines 2026, Table 3 — suggested regimens for antimicrobial therapy in cystitis.

Do not use aminopenicillins or fluoroquinolones for cystitis (Strong).

Recurrent cystitis (≥3/year or ≥2/6 months)

• No extensive routine work-up (cystoscopy, US) in women <40y without risk factors (Weak)
• Vaginal oestrogen in post-menopausal women (Strong)
• Methenamine hippurate (Strong); cranberry products (Strong, but evidence quality is low/contradictory)
• D-mannose, probiotics, herbal combinations (Weak, mixed evidence)
• Continuous or post-coital antibiotic prophylaxis once non-antibiotic options have failed (Strong)
• Self-start short antibiotic course for reliable, well-informed patients (Strong)

Pyelonephritis

Fever >38°C, flank pain, nausea/vomiting, CVA tenderness. Urinalysis + culture + susceptibility + imaging (exclude an urgent urological problem, e.g. obstruction) — all Strong.

Pocket Guidelines 2026, Table 4 (oral regimens) and Table 5 (parenteral regimens) for pyelonephritis.

Do not use nitrofurantoin, oral fosfomycin, or pivmecillinam for pyelonephritis — none reach adequate tissue levels.

Systemic UTI & catheter-associated UTI

• Empirical IV: amoxicillin + aminoglycoside, OR 2nd-gen cephalosporin + aminoglycoside, OR a 3rd-gen cephalosporin (Strong).
• Ciprofloxacin only if local resistance <10% and beta-lactams/aminoglycosides are contraindicated or not tolerated (Strong) — avoid fluoroquinolones in urology inpatients or after FQ use in the last 6 months (Strong).
• CA-UTI: don't culture asymptomatic catheterised patients; don't use pyuria or cloudy/odorous urine alone as a diagnostic trigger; remove/replace the catheter before starting antibiotics; hydrophilic-coated catheters and minimal catheterisation duration reduce risk; no routine antibiotic prophylaxis for catheter placement, removal, or intermittent self-catheterisation.

Urosepsis: the EAU chapter is under full revision (2027 edition) — in the interim, follow the Surviving Sepsis Campaign 2021. Key actions in the first hour: cultures, fluid resuscitation, broad-spectrum antimicrobials; source control (e.g. decompressing an obstructed infected kidney) is the single most important step for survival.

Bacterial prostatitis

NIH classification: I acute bacterial (ABP), II chronic bacterial (CBP), IIIa/b chronic pelvic pain syndrome (inflammatory/non-inflammatory), IV asymptomatic inflammatory.

• Never perform prostatic massage in suspected ABP (Strong) — treat as a systemic UTI.
• CBP diagnosis: Meares–Stamey 2- or 4-glass test (Strong); do not rely on ejaculate culture alone (Weak).
• CBP treatment: fluoroquinolone 4–6 weeks first-line (Strong); macrolide/tetracycline if intracellular organism identified; metronidazole for T. vaginalis.

Pocket Guidelines 2026, Table 8 — antimicrobial therapy for chronic bacterial prostatitis.

Acute epididymitis

Rule out testicular torsion first — sudden severe pain demands urgent exploration, not antibiotics.

Fournier's gangrene & fungal UTI

Fournier's gangrene: necrotising fasciitis of the perineum/genitalia, mortality ~20%. Type I polymicrobial (most common), II Group A Streptococcus, III gas gangrene (Clostridium). Broad-spectrum antibiotics on presentation + surgical debridement within 24h, with a mandatory second-look/re-debridement at 24h (both Strong). Divert urine/faeces if the rectum is involved.

Fungal UTI: mostly presents as localised cystitis. Fluconazole-susceptible: 200 mg/day PO ×2 weeks. Fluconazole-resistant: amphotericin B deoxycholate, flucytosine, or caspofungin, adjusted for renal function. Replace indwelling catheters/stents where present (Weak).

Pocket Guidelines 2026, Table 9 (Fournier's regimens) and Table 12 (fungal UTI regimens).

Peri-procedural antibiotic prophylaxis

Pocket Guidelines 2026, Table 13 — antimicrobial prophylaxis prior to urological procedures.

General principles

Trauma is the leading cause of death under 45y and the 4th overall. Evidence base is inherently thin — mostly case series, almost no RCTs — so many recommendations rest on expert consensus rather than high-level evidence.

• ATLS primary survey first: Airway, Breathing, Circulation, Disability, Exposure.
• Damage control (unstable patient): (1) rapid haemorrhage/contamination control → (2) ICU resuscitation (temperature, coagulation, oxygenation) → (3) definitive reconstruction once stable. Guards against the lethal triad: hypothermia + coagulopathy + acidosis.
• Trauma-centre centralisation cuts mortality by ~25% and length of stay by 4 days.

Renal trauma

Most commonly injured GU organ (young males, M:F 3:1). Blunt ~80% (MVA, falls, violence), penetrating ~20%, plus iatrogenic (PCNL, biopsy, SWL).

Bilateral injuries: upgrade one grade (up to grade III).

Imaging

CT indications: visible haematuria; microscopic haematuria + hypotension; rapid deceleration; direct flank trauma/rib or thoraco-lumbar fracture; penetrating trauma; any child with microhaematuria. Three-phase CT: arterial (30–45s, vascular injury/active extravasation), nephrographic (parenchymal contusion/laceration), delayed (5–10 min, collecting-system injury). Red flags: medial haematoma (vascular injury), medial urine extravasation (UPJ injury), no contrast enhancement (arterial injury).

Conservative management is preferred for grade I–III almost always, grade IV if stable, grade V possibly if parenchymal and stable — ~90% of grade IV and ~50% of grade V blunt injuries are managed without surgery. Embolisation success: 95% (III), 89% (IV), 52% (V); prevents nephrectomy in ~70% of cases and is not associated with AKI. Operative indications: instability refractory to resuscitation, grade V vascular/penetrating injury, expanding/pulsatile peri-renal haematoma. Nephrectomy rates by grade: 1% (III), 12% (IV), 55% (V) — nephrectomy after high-grade trauma roughly doubles mortality risk, so preserve parenchyma whenever haemorrhage can be controlled another way. 80–90% of urinary extravasation heals spontaneously — drain only if symptomatic (fever, worsening pain, infection, AKI), not routinely.

Ureteral trauma

Rare (1–2.5% of urinary tract trauma) but overwhelmingly iatrogenic (~80%, mostly gynaecological surgery). Do not rely on haematuria — present in only ~70% of cases and has no pathognomonic signs; delayed presentation is common (fever, sepsis, flank pain, excess drain output, anuria).

Repair principles: debride to healthy tissue, spatulate the ends, place an internal stent, close watertight with absorbable suture, place an external drain, and wrap the repair in omentum/peritoneum. In the unstable patient: tie off, place a nephrostomy, and repair later (damage-control ureter).

Bladder trauma

Intraperitoneal (~40%, dome rupture from a sudden rise in intravesical pressure — the weakest, most mobile part of the bladder) vs. extraperitoneal (~55%, usually with a pelvic fracture).

Rationale for operating on intraperitoneal injuries: urine free in the peritoneum can progress to peritonitis, intra-abdominal sepsis and death — extraperitoneal leaks do not carry that risk and heal on catheter drainage alone in ~85% by day 10.

Urethral trauma

Cardinal sign: blood at the meatus (posterior injury 37–93%, anterior >75%). Bulbar urethra is the most commonly injured site overall, mostly from iatrogenic catheterisation (13.4/1000 catheterisations) or straddle injury. Posterior urethral injury (PFUI) accompanies unstable pelvic fractures (1.54% of pelvic fractures, up to 66% with additional major injuries, 5–33% mortality) or penetrating trauma (mostly gunshot).

Diagnosis: retrograde urethrogram, or cystoscopy — superior for penile-fracture-related and female urethral injuries, and doesn't require moving the patient.

Diversion: suprapubic catheter (US-guided) is a reliable default; one gentle transurethral attempt is acceptable if position is confirmed. Life-threatening injuries (ABCDE) always take priority over urethral management.

Genital trauma

Penile fracture

Tunica albuginea tear of the erect penis — sexual intercourse (46%), forced flexion (21%), masturbation (18%), rolling over (8%). Classic triad: audible "snap/pop", immediate detumescence, rapidly expanding ("eggplant") haematoma. Concomitant urethral/corpus spongiosum injury in 10–22%.

Immediate surgical exploration and repair gives the lowest rate of long-term sequelae. Conservative management carries 35% fibrosis/angulation and up to 62% ED — this is not a "watch and wait" injury.

Testicular trauma

Testicular rupture occurs in ~50% of direct blunt scrotal trauma (compression against the pubis, ~50 kg force). Ultrasound is highly sensitive/specific for rupture (heterogeneous echo pattern, loss of contour definition) — but if the picture is equivocal, explore anyway.

Early exploration (<3 days) preserves the testis in ~90% of cases vs. ~50% when surgery is delayed — this mirrors the penile-fracture lesson: early operative management, not observation, protects the organ.