FRCS in 15

Libby Welcome back to FRCS Urology in Fifteen. Today, prostate cancer. Ryan, this is the biggest topic in the syllabus. What are we actually doing with the fifteen minutes?

Ryan Nine things, and no grade tables read aloud. Screening, and what the trials really show. The diagnostic pathway, which has changed more than people realise, and why the biopsy has moved out of theatre. How risk is grouped now, including a T2 change that catches people out. Who actually needs staging imaging, because that is where men get over-investigated. Why three big trials of surgery against conservative management seem to disagree and do not. When a non-cancer biopsy means you must go back. What has moved in systemic therapy. And what counts as recurrence afterwards, because the two definitions are not interchangeable.

Libby Screening first. If an examiner asks should we screen for prostate cancer, where do I start?

Ryan Start with Wilson and Jungner, the World Health Organisation criteria from nineteen sixty-eight, then show where PSA fails against them. And be specific about which criteria fail, because that is what separates a good answer. The condition is important, it has a long latent phase, and treatment exists, so those pass comfortably. What fails is the test itself: there is no cut-off that is both sensitive and specific. And what also fails is that there is no agreed policy on whom to treat once you have found disease, because a great deal of what you find would never have harmed the man.

Libby And the trials? I can never keep them straight.

Ryan Three, and each contributes something different. ERSPC gave a relative reduction in prostate cancer mortality of about twenty-one per cent at thirteen years, at the cost of substantial overdiagnosis and with no effect on all-cause mortality. PLCO found no mortality difference at all, but its control arm was heavily contaminated by opportunistic testing, so it is really a trial of organised against opportunistic screening rather than screening against none. Say that out loud, because examiners are waiting for it. And CAP, the UK trial, gave a single PSA invitation and found more cancers detected but no mortality benefit at fifteen years.

Libby So what is the synthesis? Because that sounds like three different answers.

Ryan It is one answer. Screening reliably increases detection, moves prostate cancer mortality a little at best, and does not move all-cause mortality. That is precisely why the UK screens nobody as a population and targets instead. The positive counterpoint worth having is IMPACT, which screened men carrying pathogenic BRCA variants and found clinically significant cancer in three point one per cent of BRCA2 carriers against one point three per cent of controls. Genotype, not population, is where targeted screening earns its place.

Libby Diagnostics next. What has actually changed in how we work a man up?

Ryan Two things, and the first is that a man fit for radical treatment now goes straight to multiparametric MRI. No prior outpatient assessment, and no digital rectal examination first, because the DRE adds nothing the MRI will not tell you. That feels wrong to anybody trained to examine before imaging, but the pathway is built that way deliberately.

Libby And the second?

Ryan PSA density now drives the biopsy decision rather than PSA alone, and it is the interaction with the MRI score that matters. For context on what the MRI is buying you: a PI-RADS three lesion yields clinically significant cancer in about twelve to sixteen per cent, a four in about thirty-three, and a five in sixty-six to eighty. PROMIS gave the MRI a negative predictive value of about eighty-nine per cent, so it is genuinely good at telling you who does not need a biopsy, which is the whole reason the pathway was rebuilt around it. And the scan itself is getting simpler: PRIME, in twenty twenty-five, found biparametric MRI, meaning no contrast, non-inferior to full multiparametric within the same patients, twenty-nine point two per cent against twenty-nine point six. The catch is that it depended on strict central quality control, so it is not a licence to drop the contrast everywhere.

Libby You said biopsy has moved out of theatre. That is a big operational change.

Ryan Local anaesthetic transperineal biopsy is the default now, in an outpatient setting, and it is standard care in most English units: a procedure room rather than an operating theatre, and in many centres delivered by specialist nurses. The randomised evidence is what makes it defensible rather than fashionable. TRANSLATE, a UK trial of eleven hundred and twenty-six men, compared it against transrectal biopsy and found Grade Group two or above in sixty per cent against fifty-four, with hospital admission for infection under one per cent against two. Better detection and fewer septic admissions.

Libby Risk stratification. In the UK we use Cambridge Prognostic Groups, but the EAU has its own. How do I hold both?

Ryan Map them onto each other rather than learning two lists. The Cambridge groups run one to five, and they line up roughly with the older language: group one is low risk, group two favourable intermediate, group three unfavourable intermediate, group four high risk, group five very high risk. The EAU low, favourable intermediate and unfavourable intermediate map onto Cambridge one, two and three. Learn the mapping and you can answer in whichever language the examiner uses.

Libby And you said there is a change that catches people out.

Ryan There is, and it is recent. In the twenty twenty-six EAU risk groups, the cT2 substage no longer defines the risk group. T2a, T2b and T2c used to pull a man between categories; now they do not, and the old D'Amico-style any-one-factor table has gone with them. So if you were taught to upgrade someone on the strength of a T2b, that is no longer how it works. One related trap while we are here: defining favourable against unfavourable intermediate by the percentage of positive cores is the NCCN scheme, not the EAU one. Mixing those up is an easy mark to lose.

Libby Once I have the risk group, what am I scanning? I was taught a bone scan for anyone who looked worrying.

Ryan That instinct is what the current position is designed to stop. Staging is driven by risk group now. Low and favourable intermediate disease gets no additional imaging at all, nothing. Unfavourable intermediate and above gets PSMA PET-CT where it is available, and CT with a bone scan where it is not, because PSMA PET is the more sensitive of the two for staging higher-risk disease.

Libby Nothing at all feels bold. What makes it safe?

Ryan The pre-test probability, and the numbers are worth carrying because they make the argument for you. Bone metastasis risk by PSA: under ten, about half a per cent. Ten to twenty, under two per cent. Twenty to fifty, about sixteen per cent. Grade tells the same story: bone scan positivity is around five per cent at Gleason seven or below, against about twenty-eight per cent at Gleason eight. So at the bottom of the range you are scanning two hundred men to find one, and every one of those scans can throw up something equivocal that then needs chasing. The scan is not neutral just because it is non-invasive.

Libby And the nodes, at the time of surgery? There used to be a nomogram cut-off.

Ryan There did, and it has gone, which is the part people have not caught up with. The EAU twenty twenty-six position gives no nomogram risk threshold at all: the old five to seven per cent cut-off for deciding to do a lymph node dissection is simply not there any more. What survives is that if you do perform one, make it extended, that is a strong recommendation. And the counselling is honest: an extended dissection improves staging but has no proven oncological benefit, and it adds real morbidity in lymphocele and lymphoedema. One more, because it is a classic viva question: do not use a nodal frozen section to decide whether to abandon the prostatectomy.

Libby Treatment outcomes. Surgery against conservative management has been studied repeatedly and the trials seem to contradict each other.

Ryan They look like they do, and the resolution is the single most useful thing in this topic. Know them as a set, because their disagreement is an era effect, not a contradiction. SPCG-4 was largely pre-PSA, with palpable disease, and there surgery reduced both prostate cancer mortality and overall mortality. PIVOT randomised men in the PSA era to prostatectomy or observation and found no significant all-cause mortality benefit overall, with surgery helping only where the PSA exceeded ten. ProtecT then randomised screen-detected disease three ways, to monitoring, surgery or radiotherapy, and found no difference in prostate cancer mortality at fifteen years.

Libby So the more recent the trial, the less surgery helps?

Ryan Not quite, and the distinction matters. It is not that surgery stopped working. It is that as the disease being detected got earlier and more indolent, the benefit of treating it immediately shrank towards nothing. Same operation, different disease. That is the line to give, and it explains why active surveillance is the default for Cambridge group one, where ten year prostate cancer mortality is only about two to three per cent.

Libby Re-biopsy. If the histology comes back without cancer, when do I still need to go again?

Ryan This has reversed, and the old answer is now the wrong one. Atypical small acinar proliferation and high-grade PIN do NOT need routine re-biopsy. In contemporary series clinically significant cancer on follow-up is only six to eight per cent, no different from after a benign biopsy, so you manage it like a negative biopsy. The thirty to forty per cent figure people still quote is pre-MRI data, and even there significant cancer was only twelve per cent. What you do say is the NICE line: tell the man his risk is slightly higher. The one finding you must not ignore is intraductal carcinoma without invasive cancer, which marks concurrent high-grade disease, so that is re-biopsy or definitive management.

Libby Anything in between?

Ryan Two things. The MRI, not the benign histology, is what drives a repeat: a negative biopsy with a Likert three or more goes to the MDT with a view to re-biopsy. And then the list you can genuinely ignore, which is worth knowing because ignoring them confidently is what stops unnecessary procedures: high-grade PIN whether single-core or multifocal, atypical adenomatous hyperplasia, proliferative inflammatory atrophy, basal cell hyperplasia, sclerosing adenosis, nephrogenic adenoma, and granulomatous prostatitis after BCG. Low-grade PIN should not even be reported.

Libby What if the MRI was suspicious but the biopsy is negative?

Ryan Then it goes to joint urology and radiology review, and that is the answer they want rather than simply repeating the biopsy reflexively. A Likert or PI-RADS four or five with no atrophy or inflammation on the biopsy suggests you missed the target, so consider immediate re-biopsy, or repeat the MRI at six to twelve months once any inflammation has settled. The review can also regrade the MRI suspicion downwards, which is a legitimate outcome. If the MRI was only equivocal, discharge to the GP with a re-referral PSA threshold set by a senior clinician.

Libby Last one. New agents. What has actually changed recently?

Ryan Two movements. First, PARP inhibitors have moved earlier in the disease, into hormone-sensitive metastatic disease. AMPLITUDE, in twenty twenty-five, showed niraparib with abiraterone and androgen deprivation improves radiographic progression-free survival in men with homologous recombination repair mutations, with a hazard ratio around nought point five two in the BRCA subgroup, and that combination is now approved for BRCA-mutated hormone-sensitive metastatic disease. Previously PARP inhibition was castration-resistant territory only.

Libby And the second?

Ryan Lutetium-177 PSMA, and this one carries a UK trap worth having ready. VISION established it after an androgen receptor pathway inhibitor and a taxane. PSMAfore then showed a progression-free survival benefit in taxane-naive castration-resistant disease, eleven point six months against five point six, but with no significant overall survival benefit, partly because sixty per cent crossed over. The EAU position is to offer it to pretreated patients not fit for docetaxel, and weakly at that. The trap is that NICE does not recommend it on the NHS on cost-effectiveness grounds, so the right answer to what would you give this man in the UK is different from what the trial supports. That gap between trial evidence and NHS availability is a favourite.

Libby We have not touched recurrence. If the PSA starts climbing after treatment, when is that actually a recurrence?

Ryan It depends entirely on which treatment, and mixing the two definitions up is a classic error because they are nothing alike. After a prostatectomy, biochemical recurrence is a PSA of nought point two or more, rising and confirmed. The gland is out, so any measurable PSA means prostate tissue somewhere. After radiotherapy the gland is still in there and still making PSA, so you cannot use a low absolute number. There you use the Phoenix definition, which is the nadir plus two.

Libby Why plus two? That seems arbitrary.

Ryan It is there to stop you calling failure on a bounce. A benign PSA bounce after brachytherapy happens in up to thirty per cent of men, typically somewhere between twelve and twenty-four months, and if you used a tight threshold you would be sending a third of your patients for salvage treatment they do not need. So the plus two is deliberately generous. And when you do have genuine recurrence, restage with PSMA PET, which is far more sensitive than CT and a bone scan at low PSA values.

Libby And what about radiotherapy straight after surgery, for adverse pathology? I was taught adjuvant.

Ryan That has reversed, and it is one of the cleaner practice changes to be able to state. Adjuvant radiotherapy is no longer routine for pT3 disease or positive margins. Early salvage radiotherapy on a rising PSA is preferred for most men, on the strength of RADICALS-RT, RAVES and GETUG, because it gives the same cancer control while sparing radiotherapy entirely to the substantial group who were never going to recur. There is one exception worth naming: node-negative disease with grade group four or five and pT3, with or without a positive margin, where adjuvant radiotherapy is still offered.

Libby Active surveillance. If the ProtecT answer is that monitoring is reasonable, what does monitoring actually consist of?

Ryan PSA at least every six months, digital rectal examination at least yearly, MRI before the confirmatory biopsy, and repeat biopsy every two to three years for up to about ten. And one exclusion worth stating: cribriform or intraductal histology takes a man out of surveillance, because that pattern behaves worse than its grade suggests.

Libby Is it the same protocol for everybody on surveillance?

Ryan No, and that is the modern point. STRATCANS is the stratified model, where the intensity of follow-up is set by the risk tier at first biopsy and the baseline MRI, so a man at the bottom is monitored far more lightly than one at the top of the surveillance range. Surveillance is not one protocol applied uniformly, and saying so shows you understand it is a risk-management strategy rather than a waiting room.

Libby And what actually triggers treatment? That is the bit I would get wrong.

Ryan Biopsy progression. Grade reclassification or volume progression on histology, or patient choice. Not a rising PSA on its own, not a change on MRI on its own, and not a change on examination on its own. Those things trigger more investigation rather than treatment: MRI progression or a PSA doubling time under three years means repeat the MRI and re-biopsy, and then the biopsy decides. There is even a weak recommendation that a low-risk man with a stable MRI and a PSA density under nought point one five may skip the repeat biopsy altogether. Treating on a PSA rise alone is exactly the reflex active surveillance exists to prevent.

Libby Numbers from today.

Ryan Seven. ERSPC, a twenty-one per cent relative reduction in prostate cancer mortality at thirteen years, with no all-cause benefit. PROMIS, MRI negative predictive value about eighty-nine per cent. ASAP and high-grade PIN, six to eight per cent significant cancer on follow-up, so no routine re-biopsy. Cambridge group one, ten-year prostate cancer mortality two to three per cent. Bone metastasis risk by PSA, about half a per cent under ten, rising to about sixteen per cent between twenty and fifty. And recurrence: nought point two after surgery, nadir plus two after radiotherapy.

Libby And the catch to walk out with: the cT2 substage no longer changes the EAU risk group, so stop upgrading men on the strength of a T2b.

Libby Welcome back to FRCS Urology in Fifteen. Today, metastatic prostate and bladder cancer, and the scenarios people run together. Ryan, why those two?

Ryan Because they are the two where the word metastatic hides the most decisions. A candidate hears it and reaches straight for a drug name, when the mark is for something earlier: saying which state the patient is actually in. In prostate the systemic decision hangs on castration status and on metastatic volume. In bladder it hangs on cisplatin fitness and on whether you are treating for cure or for control. Name the state correctly and the regimen follows almost automatically. Name it wrongly and you can be completely fluent and still give the wrong answer.

Libby So the skill is the label, not the drug.

Ryan The label, and knowing which label the guideline is keyed to. Four decisions today. The four states of prostate cancer and why the word changes the drug. High volume against low volume, which is the most examinable split in the whole topic. The three bladder words that get used interchangeably and should not. And metastatic bladder, where the first-line answer has recently inverted and where there is a platinum trap I would put money on being asked.

Libby Start with prostate, because that is where the words multiply fastest.

Ryan Two axes, four states. The first axis asks whether the disease still responds to androgen deprivation, which is castration-sensitive, or whether it is progressing despite castrate testosterone, which is castration-resistant. The second axis asks simply whether there are metastases. Cross those two and you get four boxes, and every prostate systemic recommendation lives in exactly one of them.

Libby Walk me round them.

Ryan Non-metastatic and castration-sensitive is localised or locally advanced disease, and it is still curative intent. Locally advanced means it extends beyond the capsule, so clinical T3 or T4, or node-positive, with no metastases. Non-metastatic castration-resistant is a rising PSA with castrate testosterone and nothing on conventional imaging. Metastatic castration-sensitive is where the intensification trials live. And metastatic castration-resistant is where you work through a sequence whose endpoint is overall survival.

Libby That is a lot of boxes. Which one do people put patients in wrongly?

Ryan They call things castration-resistant that are not. Before you use that word, check the testosterone. Castrate means below one point seven nanomoles per litre, or fifty nanograms per decilitre. A man whose PSA is climbing while his testosterone is not castrate does not have castration resistance. He has a compliance problem or an absorption problem, and the answer is to fix that, not to escalate him to a new drug class.

Libby And locally advanced disease, which is the box people skip. What is the current answer there?

Ryan That it is no longer radiotherapy with hormones alone. For node-negative, non-metastatic disease with at least two of clinical T3 or T4, Gleason eight or above, or a PSA of forty or more, the European recommendation is radiotherapy to the prostate, long-term androgen deprivation, and two years of abiraterone, and that is a strong recommendation on the back of STAMPEDE. If the nodes are positive but there are still no metastases, you widen the radiotherapy to the pelvis and the rest is the same, also strong. So abiraterone is not a metastatic-only drug any more, and that catches people out.

Libby What about the non-metastatic castration-resistant box? That one always sounds like a technicality.

Ryan It is not, and it has a number attached. High risk in that box means a PSA doubling time of ten months or less, and that is not a rule of thumb, it is the enrolment criterion shared by all three of the trials that defined the space: apalutamide in SPARTAN, enzalutamide in PROSPER, darolutamide in ARAMIS. All three improve metastasis-free survival, which is the endpoint for that box, as against overall survival once the disease is metastatic. Treat those men with an androgen receptor pathway inhibitor, not with chemotherapy. And be aware that PSMA PET reclassifies a lot of these men as metastatic, which moves them to a different box entirely.

Libby Now the split you said was the most examinable. High volume against low volume.

Ryan It comes from CHAARTED, and you should be able to say it cold, because it decides two separate things. High volume means visceral metastases, or four or more bone lesions with at least one beyond the axial skeleton and pelvis. That trailing clause is the part people drop. Four lesions all sitting in the spine and pelvis is not high volume. One lesion in the ribs or the long bones, alongside three in the spine, is.

Libby And what does it change?

Ryan Two things in opposite directions. The backbone for everyone with metastatic hormone-sensitive disease is androgen deprivation plus an androgen receptor pathway inhibitor: abiraterone with prednisone, or apalutamide, or enzalutamide, or rezvilutamide, all strong. Docetaxel now only goes in as a triplet, with androgen deprivation plus abiraterone or darolutamide, and that triplet is weighted towards high-volume or de novo disease, because that is where ARASENS and PEACE-1 showed the most benefit. ARASENS gave a hazard ratio of nought point six eight for overall survival, with four-year survival sixty-three per cent against fifty. PEACE-1 gave nought point seven five.

Libby You said opposite directions. What runs the other way?

Ryan Radiotherapy to the primary. In a man whose first presentation is metastatic disease and whose disease is low volume by CHAARTED criteria, you offer androgen deprivation plus prostate radiotherapy, at doses up to the equivalent of seventy-two gray in two gray fractions. That is a strong recommendation, not an option, and it comes from STAMPEDE, where the survival benefit was confined to low-volume disease. So volume pushes you towards the triplet at one end and towards treating the prostate at the other. Those are not interchangeable and the same patient does not get both answers.

Libby Is there a trap in how strongly people sell the triplet?

Ryan Yes, and it is a common one. The doublet carries the strong recommendation. The triplet is a discussion, because doublet outcomes were not significantly different from triplet regimens and docetaxel adds toxicity. Do not present the triplet as the default for everyone with metastases. And the reverse error: androgen deprivation on its own is wrong for de novo metastatic disease in a man who is fit for combination therapy, has a year or more of life expectancy, and accepts the toxicity. Fail any one of those three and androgen deprivation alone becomes the correct answer. Three conditions, and you should say all three out loud.

Libby Bladder next. There are three phrases people use as if they mean the same thing: chemotherapy, chemoradiotherapy and trimodal therapy.

Ryan And they are three different things, so let us separate them. Chemotherapy in muscle-invasive bladder cancer means neoadjuvant cisplatin-based chemotherapy before radical treatment, and it buys an absolute survival benefit of about eight per cent at five years. Chemoradiotherapy means radiotherapy given with a radiosensitiser. Trimodal therapy means all three modalities: a maximal transurethral resection, then concurrent chemoradiotherapy. The resection is part of the treatment, not just the diagnosis, which is why the technique changes if you are planning for it: you debulk maximally rather than just sampling muscle.

Libby Why is the radiotherapy given with chemotherapy rather than alone?

Ryan Because of BC2001, and this is the trial people quote wrongly. Three hundred and sixty patients. Adding fluorouracil and mitomycin C to radiotherapy improved two-year locoregional disease-free survival, sixty-seven per cent against fifty-four, with a hazard ratio of nought point six eight. That is why the standard is chemoradiotherapy and not radiotherapy alone. The catch is that overall survival was not significantly improved: five-year survival forty-eight per cent against thirty-five, hazard ratio nought point eight two, and not significant. It is a locoregional control trial. Claim a survival benefit for it and you have overstated your own evidence.

Libby Can I quote a dose, or is that a lookup?

Ryan You can, and here it is worth it, because the radiosensitiser is a quality metric. The NICE recommendation names two radiosensitiser options, mitomycin with fluorouracil, or carbogen with nicotinamide, which is the BCON regimen. And it gives two dose schedules: sixty-four gray in thirty-two fractions over six and a half weeks, or fifty-five gray in twenty fractions over four weeks. The examinable point is not the arithmetic, it is that a radiosensitiser is expected in the overwhelming majority of cases, so radical radiotherapy without one needs a reason.

Libby So how do I choose between trimodal therapy and cystectomy? Is it a coin toss?

Ryan No, and the honest answer is the one that scores. There is no completed randomised trial against cystectomy. SPARE closed for poor recruitment and none is foreseen, so say that plainly rather than implying equivalence has been proven. The best available comparison is propensity-matched, from Zlotta: seven hundred and twenty-two patients at three centres, all eligible for either treatment. Five-year metastasis-free survival seventy-four per cent against seventy-five, with no difference in cancer-specific or disease-free survival.

Libby That sounds like equivalence to me.

Ryan It is similarity in a retrospective study, and the authors themselves claim similarity rather than superiority. Overall survival actually favoured trimodality, but residual confounding is the obvious explanation and you should say so before anyone asks. The two numbers that make it usable are these: thirteen per cent of the trimodality patients needed a salvage cystectomy, and the selection criteria are strict. Solitary tumour under seven centimetres, no extensive or multifocal carcinoma in situ, no hydronephrosis or at most unilateral, and good bladder function. Offer it outside that and you are not doing what the evidence describes.

Libby And adding immunotherapy to the chemoradiotherapy?

Ryan Investigational, not standard of care. Presenting it as established is a straightforward error. What has entered the standard pathway is perioperative immunotherapy around cystectomy, which is a different thing: NIAGARA gave durvalumab with gemcitabine and cisplatin before surgery and durvalumab after it, with an event-free survival hazard ratio of nought point six eight and overall survival nought point seven five, and it is now NICE-approved for cisplatin-eligible patients.

Libby Move to genuinely metastatic bladder cancer. What is first line now?

Ryan Enfortumab vedotin with pembrolizumab, and it has inverted the whole field. EV-302 gave a median overall survival of about thirty-one and a half months against fifteen point nine for platinum chemotherapy, a hazard ratio of nought point four seven. It roughly doubles survival, and it is chemotherapy-free. The European position is now that platinum combination chemotherapy is the option for people unsuitable for enfortumab vedotin with pembrolizumab, which is the reverse of how everyone learned it.

Libby And if that combination is not available or not suitable?

Ryan Then platinum chemotherapy, gemcitabine with cisplatin if the patient is cisplatin-fit and gemcitabine with carboplatin if not, and then the step people forget: maintenance avelumab in anyone who has not progressed after four to six cycles. JAVELIN Bladder 100 gave overall survival of twenty-one point four months against fourteen point three. That is switch maintenance, so you stop the chemotherapy and start a different drug. It is not continuing the chemotherapy.

Libby You promised a carboplatin trap.

Ryan This is the one I would put money on being asked. Carboplatin is a substitution you may make in the metastatic and palliative setting only. You must not substitute carboplatin in the neoadjuvant, curative setting. There is an explicit strong recommendation against it. So if a man with muscle-invasive disease is cisplatin-ineligible, the answer is not carboplatin before his cystectomy. It is perioperative enfortumab vedotin with pembrolizumab, which in that population gave an event-free survival hazard ratio of nought point four, overall survival nought point five, and a pathological complete response rate of fifty-seven per cent against nine. If that is unsuitable, you proceed straight to cystectomy.

Libby And how do I know whether someone is cisplatin-ineligible in the first place?

Ryan The Galsky criteria, and any one of them is enough. Creatinine clearance below sixty millilitres per minute, performance status of two or worse, grade two or worse hearing loss, grade two or worse peripheral neuropathy, or heart failure of New York Heart Association class three or above. Say any one, because candidates tend to name renal function and stop. Hearing loss and neuropathy are the two that get missed, and they are the two a busy clinic forgets to ask about.

Libby Pull it together.

Ryan Castrate testosterone is below one point seven nanomoles per litre, and you check it before you ever say castration-resistant. High volume by CHAARTED is visceral metastases, or four or more bone lesions with at least one beyond the axial skeleton and pelvis. The triplet is weighted to high-volume and de novo disease, but the doublet of androgen deprivation plus an androgen receptor pathway inhibitor is what carries the strong recommendation. Radiotherapy to the primary helps in low-volume disease only, up to the equivalent of seventy-two gray in two gray fractions. In locally advanced non-metastatic disease with two of three high-risk features, add two years of abiraterone. Non-metastatic castration-resistant high risk means a PSA doubling time of ten months or less, and the endpoint there is metastasis-free survival. BC2001 improved locoregional control, sixty-seven against fifty-four per cent, and did not significantly improve overall survival. Trimodal selection is a solitary tumour under seven centimetres, no extensive or multifocal carcinoma in situ, no hydronephrosis or at most unilateral, and thirteen per cent still needed a salvage cystectomy. Radical radiotherapy gets a radiosensitiser, at sixty-four gray in thirty-two fractions or fifty-five in twenty. EV-302 gave about thirty-one and a half months against fifteen point nine. Maintenance avelumab after four to six cycles of platinum. And carboplatin substitutes for cisplatin in the metastatic setting only, never before a cystectomy.

Libby The word metastatic never finishes a sentence in either of these cancers, so make your first move naming which kind you are looking at. That is FRCS Urology in Fifteen.

Libby Welcome back to FRCS Urology in Fifteen. Today, advanced kidney, upper tract, testicular and penile cancer. Ryan, what ties four such different cancers together?

Ryan That in all four, the systemic decision is keyed to a label underneath the word advanced, and the labels are different in each one. Upper tract is keyed to pathological stage after the nephroureterectomy. Kidney is keyed to a prognostic risk model. Testis is keyed to the IGCCCG risk group. Penile is keyed to node stage. A candidate who reaches for a drug name before naming the label can be completely fluent and still wrong, and in two of these four the commonest error is reaching for an operation when the answer is chemotherapy, or the reverse.

Libby So four decisions, one per cancer.

Ryan Four, and I will tell you each time what happens if you choose wrong. Adjuvant treatment in upper tract disease, where the trial is strong but its survival claim is weaker than people quote. Kidney, where the operation has moved out of the way of the drugs. Testis, where one thing genuinely depends on which side the tumour was and it is not the chemotherapy. And penile, where chemotherapy earns the operation rather than following it.

Libby Upper tract urothelial carcinoma. Chemotherapy, immunotherapy, or both?

Ryan Adjuvant platinum, and the trial is POUT. After a nephroureterectomy, for pathological T2 to T4 disease or node-positive disease, you give four cycles of gemcitabine with cisplatin, or gemcitabine with carboplatin if cisplatin-ineligible, allocated by renal function. Five-year disease-free survival was sixty-two per cent against forty-five, hazard ratio nought point five five. That is a strong recommendation and it is the answer to the question.

Libby Does it improve survival?

Ryan This is where you should be careful, because the honest answer earns more than the confident one. Disease-free survival was the primary endpoint and it was clearly met. Overall survival was a secondary endpoint, the trial closed early and was underpowered for it: five-year overall survival sixty-six per cent against fifty-seven, hazard ratio nought point six eight, with a p value of nought point nought four nine. That is supportive, not definitive, and saying so is the difference between quoting a trial and understanding it.

Libby And if they cannot have platinum?

Ryan Then you discuss adjuvant immunotherapy, nivolumab or pembrolizumab, but only as weak recommendations, and you must add the caveat. The upper tract subgroups within the adjuvant immunotherapy trials did not clearly benefit. So do not carry the bladder wording across to the upper tract as though it were the same organ with a different postcode. In bladder cancer after cystectomy the adjuvant checkpoint recommendation is for nivolumab. In the upper tract there are two separate weak recommendations and a subgroup that did not convince.

Libby Kidney. This is the one where I think the pathway has changed most.

Ryan It has, and the change is that the nephrectomy is no longer first. CARMENA randomised four hundred and fifty patients with intermediate or poor-risk metastatic disease and found sunitinib alone non-inferior to cytoreductive nephrectomy followed by sunitinib, with median overall survival of eighteen point four months against thirteen point nine. The resulting prohibition is strong and it is model-agnostic: do not perform a cytoreductive nephrectomy in poor-risk disease, by either prognostic model.

Libby Does that abolish cytoreductive nephrectomy?

Ryan No, and this is the boundary to get right. It removes it from poor-risk disease. It does not remove it from everyone. In intermediate risk with an asymptomatic primary who needs systemic therapy, you do not operate immediately; you start systemic therapy and then discuss a deferred nephrectomy in those who are benefiting, which is the pattern SURTIME supports. Immediate surgery is still reasonable in someone with good performance status who does not need systemic therapy yet, or in oligometastatic disease where you can achieve complete local treatment.

Libby You keep saying by either model. Does it matter which one I quote?

Ryan It matters more than it sounds. The two models disagree in twenty-three per cent of cases. The older one was built before targeted therapy and the newer one in the targeted-therapy era, which is why the newer one has been used in most recent trials and is the preferred model for practice. So when you assign a risk group, say which model you used. Naming it is not pedantry when nearly a quarter of patients would be scored differently.

Libby And the drugs?

Ryan Combinations have replaced single-agent targeted therapy as first line. In intermediate and poor risk, either ipilimumab with nivolumab, from CheckMate 214 with an overall survival hazard ratio of nought point six three, or an immunotherapy plus targeted therapy doublet. In favourable risk the picture is softer: the doublets, or ipilimumab with nivolumab as an alternative, or single-agent targeted therapy, all weak, because the survival benefit of any combination is less clear there and the decision is driven by progression-free survival and response. One practical point before any of this: offer brain imaging in metastatic patients when you are considering systemic therapy or a cytoreductive nephrectomy.

Libby Testis. I want to ask this the way candidates ask it. Does the chemotherapy depend on which side the tumour was?

Ryan No, and the question is worth taking apart, because something here genuinely does depend on the side and it is not the chemotherapy. The template of a retroperitoneal lymph node dissection depends on the side. The chemotherapy depends on the risk group. Those are two different decisions and conflating them is exactly the error.

Libby Take the template first, then.

Ryan A modified template limits the contralateral dissection below the inferior mesenteric artery, because that is where the contralateral sympathetic fibres and the hypogastric plexus lie. So a right-sided tumour gets a template that preserves the left-sided fibres, and a left-sided tumour the mirror image. The reason the inferior mesenteric artery is the landmark is that the postganglionic fibres can cross the midline, so contralateral clearance below that level is the specific manoeuvre that threatens ejaculation. Nerve-sparing dissection, where you prospectively identify and preserve those fibres, keeps antegrade ejaculation in over ninety-five per cent of selected cases.

Libby And when it goes wrong, what has actually been injured?

Ryan Emission, not erection. Sympathetic, not parasympathetic. Point and shoot: parasympathetic nerves point, sympathetic nerves shoot, and this operation threatens the shoot. Erection is preserved because the cavernous nerves are nowhere near the field. So a man who cannot ejaculate after this operation has a sympathetic injury, and the answer to the examiner is sperm banking before treatment, every time.

Libby Now the chemotherapy. By risk group.

Ryan By IGCCCG risk group. Good risk gets three cycles of BEP, that is bleomycin, etoposide and cisplatin, or four cycles of etoposide and cisplatin if bleomycin is contraindicated. Intermediate and poor risk both get four cycles of BEP. And seminoma has no poor-risk category at all, which is a free mark: for seminoma the thing that makes you intermediate rather than good is non-pulmonary visceral metastases.

Libby What happens to what is left behind afterwards?

Ryan And here the two histologies diverge completely. In non-seminoma you resect every residual mass of one centimetre or more, once the markers have normalised, because about forty per cent contain teratoma and about ten per cent viable tumour, and only around half are pure necrosis or fibrosis. Teratoma is chemoresistant and can grow. In seminoma you observe, and you use FDG-PET only for a residual over three centimetres, at least two months after chemotherapy. PET is not useful below three centimetres, and its positive predictive value is only twenty-three to sixty-nine per cent, so one positive scan should not on its own drive you to operate.

Libby And if the markers are rising rather than falling?

Ryan Then it is salvage chemotherapy, not surgery. Rising markers mean active disease you cannot cut out, and operating into that is the classic wrong answer. The one other thing to have ready is bleomycin lung toxicity: pulmonary fibrosis, so warn the anaesthetist to avoid a high inspired oxygen concentration and fluid overload if that man comes back for a post-chemotherapy dissection.

Libby Last one. Penile cancer, and you said chemotherapy earns the operation.

Ryan Node stage drives everything, and the prognosis makes clear why. Five-year survival is about ninety-two per cent with negative nodes, seventy-three per cent at pathological N1, sixty-one at N2 and thirty-three at N3. The split that matters for systemic therapy is this: for clinically N1 and N2 disease, surgery comes first. For clinical N3, which means a fixed inguinal mass or pelvic nodes, it does not.

Libby So what happens in N3?

Ryan The first question is not what to cut, it is whether the patient is fit for chemotherapy. If he is not, you give chemoradiotherapy. If he is, you give neoadjuvant chemotherapy, cisplatin and taxane based, in preference to upfront surgery, and the regimen to name is TIP: paclitaxel, ifosfamide and cisplatin, with a response rate of around forty to fifty per cent. Then you assess the response, and surgery is what the response earns. A responder goes to inguinal and pelvic lymphadenectomy. Progression leaves the pathway altogether for systemic and palliative treatment.

Libby And bulky N2? You said surgery first for N2.

Ryan Surgery is the strong recommendation for N2, an open radical inguinal lymphadenectomy. Neoadjuvant chemotherapy is a weak alternative specifically where the nodes are bulky or bilateral, and bulky in this context means a high suspicion of extranodal extension. That weak-versus-strong distinction is the examinable part of the whole algorithm: neoadjuvant chemotherapy in N2, the prophylactic pelvic dissection and all of the adjuvant options are discussions, not duties.

Libby When does the pelvis come into it?

Ryan Two triggers on the pathology, and they are a pair: three or more positive inguinal nodes on one side, or extranodal extension. Either one earns an ipsilateral pelvic lymphadenectomy. After that, pathological N2 or N3 is offered adjuvant radiotherapy with or without chemosensitisation, and adjuvant chemotherapy is a discussion if the pelvic nodes are positive. And one timing rule across the whole pathway: complete the inguinal and pelvic surgery within three months of diagnosis, unless you are giving neoadjuvant chemotherapy.

Libby Is there a drug trap here like the carboplatin one?

Ryan There is, and it is my favourite cross-cancer catch of the five. Do not use bleomycin in penile cancer. That is a strong recommendation against, on pulmonary toxicity. And you have just heard me recommend bleomycin, by name, as the B in BEP for metastatic testicular cancer in the same episode. Same drug, standard of care in one germ cell tumour, explicitly forbidden in a squamous cancer two organs away. If you can hold both of those at once you understand that these regimens are not interchangeable between tumours, which is the whole theme.

Libby And where is the evidence going?

Ryan InPACT, which is the first phase three randomised trial in node-positive penile cancer, comparing upfront surgery against neoadjuvant chemotherapy against neoadjuvant chemoradiotherapy. Until it reports, say openly that the multimodal recommendations in node-positive disease are weak precisely because there has never been a randomised comparison. That is not a hedge. It is the correct description of the evidence, and the examiner knows it.

Libby Pull it together.

Ryan POUT: four cycles of adjuvant platinum after nephroureterectomy for pathological T2 to T4 or node-positive disease, five-year disease-free survival sixty-two against forty-five per cent, hazard ratio nought point five five, with overall survival only a secondary endpoint and the trial underpowered for it. If platinum is out, adjuvant immunotherapy is weak and the upper tract subgroups did not clearly benefit. No cytoreductive nephrectomy in poor-risk kidney cancer, by either model, and the two models disagree in twenty-three per cent of cases, so say which one you used. Intermediate risk with an asymptomatic primary starts systemic therapy, and you discuss deferred surgery in responders. Ipilimumab with nivolumab gave an overall survival hazard ratio of nought point six three in intermediate and poor risk. In testis the template depends on the side and the chemotherapy depends on the risk group: BEP three cycles for good risk, four for intermediate and poor, and seminoma has no poor-risk category. Resect non-seminoma residuals of one centimetre or more once markers have normalised; in seminoma use PET only above three centimetres. Rising markers mean salvage chemotherapy, not surgery. Penile five-year survival falls from ninety-two per cent node-negative to thirty-three at pathological N3. Clinical N3 gets neoadjuvant TIP before any surgery, and surgery is what the response earns. Pelvic dissection for three or more positive nodes on one side, or extranodal extension. And never bleomycin in penile cancer.

Libby In all four of these, the first move is to name the label the guideline is keyed to, and only then pick the treatment. That is FRCS Urology in Fifteen.

Libby Welcome back to FRCS Urology in Fifteen. Today, bladder cancer. Ryan, where are we spending the fifteen minutes?

Ryan On eight things, and none of them is a staging table. Reading stage groupings aloud helps nobody. What we are doing instead is the parts that have moved, or that people reliably get wrong: how you image a haematuria patient now, why the chest scan you were taught to order has largely gone, where NICE and the EAU genuinely disagree on follow-up, what counts as BCG failure and what you can offer when it happens, muscle-invasive disease and the chemotherapy trap inside it, first-line metastatic treatment, who needs a second resection, and the upper tract, which behaves differently enough to catch people out.

Libby Start with haematuria, because that is the commonest thing any of us does. What has changed?

Ryan Imaging is risk-stratified now, and that is a genuinely new position. It used to be that suspected bladder cancer meant a CT urogram. Now you split them. Low risk of urothelial cancer, meaning non-visible haematuria, under sixty, non-smoker, no other urological symptoms, gets an ultrasound of kidneys, ureters and bladder, including pre and post-void views. Higher risk gets the CT urogram, and higher risk means age sixty or over, male, a smoker, visible haematuria, previous pelvic radiotherapy, or occupational exposure.

Libby So the young non-smoker with dipstick blood is not getting a CT any more.

Ryan Correct, and that is the practical change. You are sparing a substantial radiation dose and a contrast load in the group whose cancer risk was always low. It is worth having the referral thresholds straight alongside it, because they are what gets a patient in front of you. Suspected cancer pathway referral is visible haematuria at forty-five or over, with no urinary infection, or where it persists after treating one. And then non-visible haematuria at sixty or over, but only when it is unexplained and there is dysuria or a raised white cell count.

Libby You said the chest scan has gone. That one surprises me, because I was taught to stage the chest in high-risk disease.

Ryan So was everybody, and this is the number that changed it. In high-risk non-muscle-invasive disease, the rate of pulmonary metastasis is nought point three per cent. Three in a thousand. You are irradiating a thousand chests to find three, and generating a pile of indeterminate pulmonary nodules that then need following. So there is no routine CT chest for high-risk NMIBC any more.

Libby When do you still do it, then? There must be exceptions.

Ryan Four, and they are worth memorising because this is exactly the kind of thing a viva turns on. Image the chest if the patient is going for radical cystectomy; if the histology is a high-risk subtype, meaning micropapillary or plasmacytoid; if there is lymphovascular invasion; or if muscle invasion is equivocal, so you suspect T2 or worse. And the reason the last one matters is the contrast in the numbers. Once you are into likely muscle-invasive disease, the pulmonary metastasis rate is three point nine per cent, more than ten times higher, and there the chest scan earns its place.

Libby Now the one I always fudge. Follow-up in non-muscle-invasive disease. NICE and the EAU do not agree, do they?

Ryan They do not, and there are three real disagreements rather than a vague sense of difference. The first is duration. NICE discharges low-risk disease at twelve months if there has been no recurrence. The EAU keeps low risk under review for five years. At the other end, NICE lets high-risk follow-up tail off to annual, while the EAU says high risk is explicitly lifelong. That is not a nuance, that is a patient being discharged by one document and followed forever by the other.

Libby Second?

Ryan Cytology. Both agree you do not use it in low or intermediate risk. In high risk, NICE says use cytology; the EAU pairs it with every single cystoscopy. And the third is upper tract imaging, which is the cleanest difference of the three. NICE schedules no routine imaging at all. The EAU builds an annual CT into high-risk follow-up out to five years, then two-yearly after that.

Libby If an examiner asks me which to follow, what is the safe answer?

Ryan Name the difference rather than picking a side, then say which you practise and why. In the UK you follow NICE, and you can add that GIRFT sets no schedule of its own but does say low and intermediate risk do not need routine upper tract surveillance, and that every patient must be given their schedule and clinical nurse specialist contact details. Knowing that the two documents diverge, and exactly where, is what is being tested. Reciting one schedule as though it were the only one is the trap.

Libby BCG failure. I hear the term used very loosely.

Ryan Very, and the first thing to fix is that you cannot call anything a failure until the patient has had adequate BCG. The shorthand is five plus two: at least five of the six induction instillations, and at least two of the three maintenance ones. Or two of six of a second induction. Without that, there is no failure, there is under-treatment, and those are different problems with different answers.

Libby And once they have had adequate BCG, what are the categories?

Ryan Refractory means the disease is still there on treatment: high-grade T1 at three months, high-grade Ta persisting after three months or at six, carcinoma in situ present at three months and still present at six, or any high-grade tumour appearing during maintenance. Relapsing is different and the distinction matters: that is a high-grade recurrence after they completed maintenance, having initially responded. There is also a group the EAU now calls BCG-exposed, which sits between naive and unresponsive, and the point of naming it is that those patients may still benefit from more BCG rather than being written off.

Libby Is there anything that sounds like failure but is not?

Ryan Yes, and it is a common trap. A low-grade recurrence during or after BCG is not BCG failure. It does not carry the same implication and it does not push you towards cystectomy. One more piece of nuance worth carrying: carcinoma in situ present at three months alone is not enough to call refractory, because a further course of BCG produces a complete response in more than half of those patients.

Libby Does cytology help me judge any of this?

Ryan Only in one direction, and people get it backwards. After BCG, cytology has a negative predictive value of ninety-four to ninety-six per cent but a positive predictive value of only about twenty-three. So a negative is genuinely reassuring. A positive one is not diagnostic, it is a prompt to go and look properly. Treat a positive cytology as proof of disease and you will be operating on people who did not need it.

Libby So when BCG genuinely has failed, the old answer was cystectomy. Has that changed?

Ryan It has, and this is the newest material on the topic. TAR-200, marketed as Inlexzo, is an intravesical gemcitabine-releasing system, approved by the FDA in September twenty twenty-five for BCG-unresponsive high-risk non-muscle-invasive disease with carcinoma in situ. In the SunRISe-one trial the overall complete response was eighty-two per cent, with about seventy-nine per cent at three months and around forty-six per cent still in complete response at twelve.

Libby Forty-six per cent at a year. How should I frame that against cystectomy?

Ryan Honestly, which is the right instinct. It is a bladder-preserving option, not a cure guaranteed to hold, and it sits alongside pembrolizumab from KEYNOTE-057 and N-803 combined with BCG. The useful framing for an examiner is that BCG-unresponsive disease used to be a single conversation about removing the bladder, and is now a genuine choice between bladder preservation and cystectomy, with the patient's appetite for surveillance a real part of the decision. Cystectomy remains the standard against which the others are measured.

Libby We have done everything either side of muscle invasion but not the middle. Cisplatin-fit patient, cT2, node negative. What happens?

Ryan Neoadjuvant cisplatin-based chemotherapy before radical cystectomy, and the word neoadjuvant is doing the work. Not adjuvant: giving it first is the preferred sequence if the patient is cisplatin-fit, and it buys an absolute survival benefit of about eight per cent at five years. Cystectomy remains the gold standard operation, and the node dissection should be standard rather than extended, because SWOG one zero one one showed extended dissection adds morbidity without a survival benefit.

Libby And how do I actually decide whether someone is cisplatin-fit? I tend to eyeball it.

Ryan Do not eyeball it, because it is a defined list and it is exactly the sort of thing you can be asked to recite. The Galsky criteria: a patient is cisplatin-ineligible if any one of these is true. Creatinine clearance under sixty millilitres per minute. Performance status of two or worse. Grade two or worse hearing loss. Grade two or worse peripheral neuropathy. Or heart failure of New York Heart Association class three or above. Any single one of those, and cisplatin is off the table.

Libby So the cisplatin-ineligible patient gets carboplatin instead?

Ryan No, and this is the single biggest trap in the topic. Carboplatin belongs in the metastatic, palliative setting, with avelumab maintenance behind it. You do not substitute carboplatin in the neoadjuvant, curative setting. Swapping it in because it is gentler is a mistake that costs the patient their one shot at cure. What the cisplatin-ineligible patient is now offered is perioperative enfortumab vedotin with pembrolizumab, and the results are striking: a complete pathological response in fifty-seven per cent against nine per cent. If that is unsuitable, you go straight to cystectomy.

Libby And the patient who does not want their bladder removed?

Ryan Trimodality bladder preservation, meaning a maximal resection followed by concurrent chemoradiotherapy, but it lives or dies on selection, and being able to state the selection is what marks the answer. Solitary and unifocal disease, cT2 to T3a, no extensive or multifocal carcinoma in situ, no hydronephrosis or at most unilateral, and good bladder function to begin with. Offer it to that patient and it is a genuine alternative. Offer it to a multifocal tumour with a hydronephrotic kidney and you have given them a worse operation and a worse cancer outcome.

Libby Last one. Metastatic disease. I learned gemcitabine and cisplatin.

Ryan That is no longer first line. Enfortumab vedotin with pembrolizumab is, on the strength of EV-302, and the survival difference is not marginal: median overall survival around thirty-one and a half months against sixteen point one with chemotherapy. Close to double, and it holds regardless of whether the patient is cisplatin-eligible, which is what makes it such a decisive result.

Libby Is that what a UK patient actually gets, though?

Ryan Good question, and no, not always, which is exactly the sort of gap examiners probe. NICE technology appraisal one zero nine seven, from September twenty twenty-five, recommends enfortumab vedotin with pembrolizumab only where platinum-based chemotherapy is suitable. So if it is not available or not suitable, you are back to platinum-based chemotherapy, gemcitabine and cisplatin if they are fit, gemcitabine and carboplatin if they are not, followed by maintenance avelumab in anyone who has not progressed. That maintenance step is worth a sentence of its own, from JAVELIN Bladder one hundred: overall survival twenty-one point four months against fourteen point three.

Libby Anything that has come off the list?

Ryan Yes, and knowing a withdrawal is a good way to show you are current. Sacituzumab govitecan has had its indication withdrawn after a negative trial and is no longer recommended. Beyond that, later lines are chosen by what the tumour is carrying rather than by a fixed running order.

Libby Restaging TURBT. Who actually needs a second look?

Ryan Three groups, and it is a clean rule. All T1 tumours. Any incomplete initial resection. And high-grade Ta where there was no detrusor muscle in the specimen. The logic running through all three is the same: you go back when you cannot be confident you know what you are dealing with, or that you removed it.

Libby And who does not need one?

Ryan Primary carcinoma in situ alone does not need a restaging resection, because there is no papillary tumour whose completeness you are doubting. And a high-grade Ta that was completely resected with detrusor confirmed in the specimen does not either. There is also a sensible risk-balanced exception for a frail patient with a smaller high-grade Ta without muscle, where the second anaesthetic may cost more than the information is worth.

Libby When, and by whom?

Ryan Two to six weeks, by a specialist non-muscle-invasive surgeon, and consider photodynamic diagnosis and prostatic urethral biopsies at the same sitting. There is a documentation point examiners like, because it is where the system fails rather than the surgeon: the operative note must say whether the resection was complete and whether detrusor was obtained, and the pathology must say whether detrusor is present. If the note does not say, the next surgeon cannot apply any of the rules we just went through.

Libby We have talked about the bladder all episode. Upper tract disease is five to ten per cent of urothelial cancer. Is it just bladder cancer higher up?

Ryan No, and treating it that way is how people come unstuck. The decision that matters is whether you keep the kidney, and low risk means all five of these are true: unifocal, under two centimetres, low-grade cytology, low-grade biopsy at ureteroscopy, and no invasive appearance on the CT urogram. All five. Any one high-risk feature instead and it is a radical nephroureterectomy with a bladder cuff.

Libby All five is demanding. Is kidney-sparing a real option or a compromise?

Ryan Real, and that is why the criteria are strict rather than indicative: in genuinely low-risk disease survival is similar. The trade is not survival, it is how much looking comes afterwards, including a second look within eight weeks. After a nephroureterectomy, anyone pT2 to T4 or node positive gets adjuvant platinum on the strength of POUT. Quote it precisely: disease-free survival was the primary endpoint and was clearly met, three-year seventy-one per cent against forty-six. Overall survival was secondary, the trial closed early and was underpowered, so the survival signal is supportive rather than definitive.

Libby And you said it behaves differently. Where does that bite?

Ryan In which direction it comes back, and one mechanism makes the whole surveillance pattern obvious: urine flows downstream. After upper tract cancer a bladder recurrence is common, usually within two years, which is why you watch the bladder hard afterwards and why a single dose of intravesical mitomycin goes in after the nephroureterectomy. The other direction is uncommon, two to six per cent, which is why NICE schedules no routine upper tract imaging after bladder cancer. It climbs to ten to twenty-five per cent with carcinoma in situ, high-grade or multifocal disease, or tumour at the trigone or a ureteric orifice.

Libby Numbers from today.

Ryan Six. Pulmonary metastasis in high-risk non-muscle-invasive disease, nought point three per cent, against three point nine once it is likely muscle-invasive. Cytology after BCG, negative predictive value ninety-four to ninety-six per cent, positive predictive value twenty-three. Adequate BCG is five plus two. TAR-200 complete response eighty-two per cent overall, forty-six per cent still responding at twelve months. Neoadjuvant cisplatin, about eight per cent absolute survival benefit at five years, and never carboplatin in that setting. And first-line metastatic survival, thirty-one and a half months against sixteen point one.

Libby And the catch to walk out with: a low-grade recurrence on BCG is not BCG failure, and calling it one sends the patient towards an operation they do not need.

Libby Welcome back to FRCS Urology in Fifteen. Today, kidney cancer and the adrenal mass. Ryan, that is two organs in one episode. How are we splitting it?

Ryan Six on the kidney, three on the adrenal, and nothing that is just a table read aloud. On the kidney: what to do with the small solid mass somebody found by accident, and separately with the cystic one, which is a different problem. When a biopsy actually helps, and the scan that has started to replace it. The one piece of molecular biology that explains why the drugs work, and who should be offered genetic testing. Why taking the kidney out in metastatic disease is no longer automatic. And what first-line systemic treatment looks like now. Then the adrenal: the two questions every incidental lesion has to answer, the one number that lets you stop looking, and the drug order you must never get wrong.

Libby Start with the commonest problem. Three centimetre enhancing mass, found on a scan done for something else. What drives the decision?

Ryan The patient, not the tumour, and that is the shift worth making explicit. Around sixty per cent of kidney cancers are now found incidentally, so you are increasingly treating a picture rather than a person with symptoms. And about twenty per cent of small renal masses are not cancer at all. So the first question is not how do I remove this, it is what does this particular man or woman actually need.

Libby Take me through the branches.

Ryan Three, by fitness. A fit patient gets a partial nephrectomy, which is the gold standard, nephron-sparing, with a radical only where a partial is not technically feasible, so central or hilar or very complex tumours. A frail or comorbid patient with a small tumour goes on active surveillance. And someone unfit for surgery, or with a solitary kidney, bilateral disease or a hereditary syndrome, gets thermal ablation.

Libby Surveillance always makes me nervous. What makes it safe?

Ryan The natural history, and these are the numbers that let you reassure someone honestly. Small renal masses grow slowly, typically two to three millimetres a year, and the risk of metastasis while a lesion is under two centimetres is only about one to two per cent. So you are not gambling, you are exploiting the fact that the disease moves slower than the patient's other problems. You intervene if it grows faster than three to five millimetres a year, if it reaches around four centimetres, or if the patient simply wants it out.

Libby And the limits on ablation?

Ryan Size, and they differ by modality, which is a detail worth having: radiofrequency ablation up to three centimetres, cryoablation up to four. Above those, do not routinely offer it. Accept that local recurrence is higher than with surgery and a repeat may be needed, and counsel for that rather than presenting it as equivalent. One procedural point examiners like: the biopsy is required before ablation, and it is taken at a separate sitting, not at the same time, because you want the histology before you destroy the evidence.

Libby What if the thing on the scan is cystic rather than solid? I know there is a classification but I only half trust myself with it.

Ryan Use the Bosniak system, but learn what it is measuring rather than the five categories, because then you can place a cyst you have not seen described. It is asking one question: how much of this looks like it is growing? The features that count are the walls and septa, how thick they are, how irregular, and above all whether they enhance with contrast. Enhancement is the thread running through the whole thing, because enhancement means blood supply and blood supply means tissue rather than fluid.

Libby So where are the decision points?

Ryan There are really three. A simple cyst, or one with a couple of thin septa, is benign and needs nothing at all. At the other end, a cyst with an enhancing nodule in it carries a malignancy risk around ninety per cent, and you treat that as a renal cancer. The interesting ground is the middle. Minimally thickened enhancing walls or septa puts you at roughly five to ten per cent on the classic figures, and that is surveillance, up to five years, not surgery.

Libby And the category above that?

Ryan Thick or irregular enhancing walls, and here the honest answer has changed. The classic figure is about fifty per cent malignant, so historically you operated. But roughly half of those resections are for lesions of low malignant potential, so you are overtreating about half your patients. The current position offers active surveillance as a reasonable alternative to treating it as a cancer. Being able to say that surgery here overtreats around half the people is precisely the kind of qualification that shows you have read the evidence rather than the table.

Libby Biopsy generally. I was taught renal masses are not biopsied. Has that changed?

Ryan Substantially, and the rule now is that you biopsy when the result will change what you do. So before active surveillance and before ablation, yes. In a young fit patient heading for surgery whatever it shows, no, because it changes nothing. It performs well: diagnostic in about ninety per cent, non-diagnostic in about eight, and sensitivity for malignancy is over ninety-nine per cent. Tract seeding is around one per cent, which is the fear people carry and it is genuinely small.

Libby Where does it let you down?

Ryan Two places, and knowing them is what separates a good answer. Small lesions under two centimetres have a high non-diagnostic rate, so avoid biopsying those. And grade concordance with the final specimen is only modest, around sixty-three per cent, so a biopsy tells you reliably what the tumour is but not reliably how aggressive it is. The bigger limitation is that oncocytoma and chromophobe cannot be reliably separated on a biopsy, and since one is benign and the other is a carcinoma, that uncertainty often drives a resection you might have avoided.

Libby Is there anything that gets round that?

Ryan Yes, and it is a lovely piece of applied biology. A sestamibi scan, which is a nuclear medicine study, and the rule is cold equals cancer. The tracer accumulates in mitochondria. Renal cell carcinoma is mitochondria-poor, so it shows up photopenic, cold. Oncocytoma and chromophobe are packed with mitochondria, so they light up hot. So a hot lesion argues strongly for the benign end of that pair you could not separate on biopsy. It is most useful exactly where biopsy is hardest, in indeterminate or endophytic masses.

Libby You said there is one piece of molecular biology worth knowing. Which?

Ryan The von Hippel-Lindau pathway, because once you have it the entire drug story follows rather than needing to be memorised. The VHL gene sits on the short arm of chromosome three. Its protein has one job worth remembering: it tags hypoxia-inducible factor for degradation. Lose the gene and that factor is no longer being cleared, so it accumulates as though the cell were permanently short of oxygen.

Libby And a cell that thinks it is hypoxic does what?

Ryan Builds blood vessels. It upregulates vascular endothelial growth factor and platelet-derived growth factor, and the tumour becomes intensely angiogenic. That is why clear cell kidney cancer is such a vascular tumour on imaging and at operation, and it is the entire rationale for the anti-VEGF drugs that dominated treatment for years. The same loss happens in most sporadic clear cell tumours, not just the inherited syndrome, which is why the target is so broadly useful. Say that and you have explained the disease, the imaging and the pharmacology in one breath.

Libby Does that mean I should be thinking about inherited disease more often than I do?

Ryan Probably, and there is a trigger list rather than a hunch. Refer for genetic evaluation if the patient is forty-six or younger, if the tumours are bilateral or multifocal, or if there is a first or second-degree relative with kidney cancer. Beyond von Hippel-Lindau, three syndromes are worth recognising because each changes management. Birt-Hogg-Dube gives chromophobe and oncocytic tumours, with skin fibrofolliculomas and lung cysts, so those patients get pneumothoraces. Tuberous sclerosis gives angiomyolipomas, and those respond to mTOR inhibitors, which is a drug you would not otherwise reach for. And fumarate hydratase deficient disease, which comes with cutaneous and uterine leiomyomas, is aggressive: those tumours get immediate surgery, not surveillance. That last one is the exception to everything we said about watching small masses.

Libby Metastatic disease. He has a primary in the kidney and disease elsewhere. Do I take the kidney out?

Ryan Not reflexively, and this is the change people are still catching up with. The trial is CARMENA, and its finding was that cytoreductive nephrectomy was not superior to systemic therapy alone in intermediate and poor-risk metastatic disease. So systemic therapy comes first. In poor-risk disease you do not offer an upfront nephrectomy, and in intermediate-risk disease with an asymptomatic primary who needs systemic treatment, you do not do an immediate one either.

Libby So when does the operation still earn its place?

Ryan Where the primary itself is the problem, so a symptomatic tumour, bleeding or pain, and in selected good-risk patients with low metastatic burden, often after systemic therapy rather than before it. The framing to give is that the operation has moved from the opening move to a considered one. And while we are on operations that have shrunk: a lymph node dissection gives no survival benefit in clinically node-negative disease, so do it for staging when the nodes are clinically positive, not routinely.

Libby And the systemic treatment itself?

Ryan Immunotherapy combinations have replaced single-agent targeted therapy as the standard first line in intermediate and poor-risk disease. You have two shapes: immunotherapy plus immunotherapy, meaning ipilimumab with nivolumab, or immunotherapy plus a targeted agent, such as pembrolizumab with axitinib. Either is reasonable, and the choice is driven by the patient and by how quickly you need a response.

Libby Does that hold for everybody?

Ryan No, and the nuance is worth having because it sounds counterintuitive. In favourable-risk disease the combinations reliably improve progression-free survival and response rate, but the overall survival benefit is much less clear. So in that group some still reasonably consider targeted monotherapy, or even active monitoring, and all of those options carry weak recommendations rather than strong ones. Being able to say the evidence is strongest where the disease is worst is exactly the sort of qualification that marks a good answer.

Libby Anything that has come off the list, or moved?

Ryan Two. Avelumab with axitinib gave a progression-free survival benefit but no overall survival benefit at final analysis, so it is no longer recommended: a good example of why you ask which endpoint moved. And on adjuvant treatment, after surgery for high-risk clear cell disease, pembrolizumab yes, adjuvant targeted agents no. That pair is clean and it is frequently asked.

Libby Over to the adrenal. A lesion turns up on a scan. Where do I start?

Ryan With two questions and only two. Is it functioning, and is it malignant. Every test you order should be answering one of them, and saying that out loud structures the whole answer. For function, everybody gets a one milligram overnight dexamethasone suppression test, without exception, because autonomous cortisol secretion is common and often silent. You add plasma metanephrines unless the imaging is a typical benign adenoma, and you add an aldosterone to renin ratio if they are hypertensive or hypokalaemic.

Libby And the malignancy question?

Ryan Answered largely by density on unenhanced CT, and there is one number that lets you stop. Ten Hounsfield units or less means a lipid-rich adenoma, and that needs no further imaging regardless of size. That last clause is the exam point: people keep chasing a large lesion that has already declared itself benign. Going the other way, four centimetres or more together with a heterogeneous appearance or a density above twenty Hounsfield units goes to the multidisciplinary team and usually to surgery.

Libby And if you think it is an adrenocortical carcinoma?

Ryan Then the approach changes, and this is a clean surgical point. Suspected adrenocortical carcinoma is an open adrenalectomy, not a laparoscopic one, because you are protecting against capsular breach and tumour spillage in a cancer that does very badly once it is seeded. Any functioning lesion also comes out, whatever its size.

Libby Last one, and it is the one I am most afraid of getting wrong in a viva. Phaeochromocytoma.

Ryan Then hold the single rule: never give a beta-blocker before alpha-blockade. Not never give a beta-blocker, but never first. The mechanism is what makes it stick. The tumour is pouring out catecholamines hitting both alpha and beta receptors. Beta activity is doing some vasodilating in skeletal muscle. Block beta first and you strip that away while leaving alpha stimulation completely unopposed, so you get unopposed vasoconstriction and the blood pressure goes through the roof, into a hypertensive crisis. Alpha blockade first, then beta if you still need it for the tachycardia.

Libby Any other adrenal pattern worth carrying?

Ryan One pairing, because the two get confused and the discriminator is simple. Conn's syndrome is hypertension with a low potassium and an alkalosis. Distal renal tubular acidosis, type one, also gives you a low potassium, but the blood pressure is normal, there is a hyperchloraemic acidosis rather than an alkalosis, the urine is inappropriately alkaline, and the patient forms stones. So both give you hypokalaemia, and everything else about them points in opposite directions. Blood pressure and the acid-base picture separate them in one move.

Libby Numbers from today.

Ryan Nine. Around sixty per cent of kidney cancers are incidental, and about twenty per cent of small renal masses are benign. Small masses grow two to three millimetres a year, with a one to two per cent metastatic risk while under two centimetres. Ablation limits: radiofrequency to three centimetres, cryoablation to four. Renal biopsy is diagnostic in ninety per cent with over ninety-nine per cent sensitivity, but grade concordance only sixty-three, and avoid it under two centimetres. Sestamibi, cold equals cancer. On cystic masses, an enhancing nodule is about ninety per cent malignant, while thick irregular enhancing septa are about fifty, where surgery overtreats roughly half. CARMENA, no upfront nephrectomy in poor-risk metastatic disease. Adjuvant pembrolizumab yes, adjuvant targeted agents no. And the adrenal number that lets you stop looking, ten Hounsfield units or less, regardless of size.

Libby And the catch to walk out with: never beta-block a phaeochromocytoma before you have alpha-blocked it.

Libby Welcome back to FRCS Urology in Fifteen. Today, urinary stone disease. Ryan, this is an enormous topic. Where are we spending the fifteen minutes?

Ryan On nine things, and nine only. Not a tour of every classification and every table, because a list of numbers read aloud is no use to anybody. Eight places candidates actually lose marks, each taken properly: the infected obstructed kidney and the stent you should not place, why five to six millimetres decides so much, why you should not believe a patient who tells you the stone has passed, what the medical expulsive therapy evidence really says once you read it, what the PUrE trial changed for lower pole stones, how the rules reverse in pregnancy, why restricting dietary calcium makes things worse, why the anti-inflammatory beats the opiate, and the two stones where the chemistry itself is the treatment.

Libby Start with the one everybody says is the exam favourite. The obstructed, infected kidney.

Ryan An obstructed kidney with signs of infection, or anuria, is a urological emergency. The EAU are unambiguous about that. It needs urgent decompression, either a percutaneous nephrostomy or a retrograde JJ stent, cultures from urine and blood, broad spectrum antibiotics immediately, and resuscitation along sepsis six lines.

Libby So which drainage? That is where I always hesitate.

Ryan Hesitating is the right instinct, because there is no proven winner, and saying so is the correct answer. The EAU strongly recommend decompression but note little evidence favours one route for primary drainage. The STONE trial, that is Stent Or Nephrostomy, compared them directly. The twenty twenty-six EAU position is equal success and equal time to defervescence, with a nephrostomy meaning a longer stay and a stent meaning worse quality of life. So you choose on the patient in front of you. Nephrostomy if the system is heavily infected or frankly pyonephrotic, or if a stent is likely to fail. Stent if retrograde access is straightforward, there is no severe sepsis, or there is an uncorrected coagulopathy, because the retrograde approach is less morbid than going percutaneously.

Libby And the trap?

Ryan The trap is doing too much in one sitting. You do not treat the stone primarily. No ureteroscopy, no shockwave, no PCNL on an infected obstructed system. You drain it, you clear the infection with a full antimicrobial course, and you come back for the stone later. Candidates lose marks by being keen. The keenness is the error.

Libby That is the septic patient though. Does the same caution apply to the ordinary obstructed stone that is not infected?

Ryan No, and this is where a lot of units are still working to the old habit. GIRFT are blunt about it: do not use a temporising ureteric stent as an emergency stop-gap in the patient who is not septic. It feels like the safe, conservative move, but look at what it commits the patient to. A stent now, a second general anaesthetic later to deal with the stone, stent morbidity in between, and clearance pushed weeks down the line. Offer primary treatment instead, shockwave or ureteroscopy, ideally within forty-eight hours of diagnosis if the pain is ongoing or the stone is unlikely to pass. Both should be available acutely, and both should be day case by default.

Libby Let us do size. Everybody memorises that small stones pass. Why is five to six millimetres the number that keeps coming up?

Ryan Because that is where the curve collapses, and understanding that is worth more than the threshold itself. Passage is predicted by size and by location, smaller and more distal pass more easily. Most stones under five millimetres pass, about seventy-five per cent of them, with a median of around seventeen days. At five millimetres and above it is about sixty-two per cent and falling.

Libby But you said the curve collapses, which sounds sharper than that.

Ryan It is sharper, and the Jendeberg nomogram from twenty seventeen shows it properly, because it uses stone width on CT. At zero to three millimetres about ninety-eight per cent pass, at four about eighty-one, at five about sixty-five, at six about thirty-three, and at six and a half or more about nine. So between five and six millimetres you roughly halve the chance of passage. That is not a gentle gradient, it is a cliff, and it is why the decision to watch or intervene changes character across one millimetre.

Libby Does location shift it as much?

Ryan Meaningfully, and in the direction you would expect: a distal stone under five millimetres passes about eighty-nine per cent of the time against about seventy-five per cent for an upper ureteric one. So position moves the odds by roughly the same amount as a millimetre of size does, which is why you should never quote a passage rate from size alone.

Libby Here is one I would have got wrong. The patient rings up and says the pain stopped, I think I passed it. Is that good enough?

Ryan No, and there is a specific paper that tells you how badly wrong it can go. Meltzer, in Urology, twenty twenty, a secondary analysis of the STONE trial cohort. Two hundred and thirty-seven patients with ureteric stones under nine millimetres, mean size under four millimetres, and they compared what the patient said against CT at twenty-nine to thirty-six days. Sensitivity was only forty-seven per cent.

Libby Forty-seven per cent. That is a coin toss.

Ryan For that direction, yes, and it is an asymmetric test, which is the bit worth understanding. Specificity is about eighty-seven per cent and the positive predictive value ninety-four. So if the patient says the stone passed, believe them: only about six per cent still had one. The failure is the other way round. If they say it has not passed, or they do not know, that tells you very little, because the negative predictive value is only about seventy-two per cent.

Libby So being pain free is not clearance.

Ryan Being pain free is not clearance. Confirm it with imaging. And while we are on things that do not exclude a stone, absence of haematuria does not either.

Libby Medical expulsive therapy. I have heard people say EAU and NICE contradict each other on this. Do they?

Ryan That is exactly the thing to get right, because the contradiction is largely manufactured. There is a note in circulation that sets EAU over five millimetres against NICE under ten millimetres, as though those were opposing camps. Read the two sources and they converge. NICE say consider an alpha blocker for distal ureteric stones under ten millimetres. The EAU recommendation is strong, and their evidence discussion is where the over five millimetre figure comes from. Both are off label. The verbs differ in strength, consider against strong, but they are not telling you different things.

Libby Where does the doubt come from then? Because there is real doubt, is there not?

Ryan There is, and it comes from the trials, so quote them properly. SUSPEND, Pickard, in the Lancet, twenty fifteen, over eleven hundred patients, tamsulosin or nifedipine against placebo for stones up to ten millimetres, and it found no difference in need for intervention, time to passage or analgesia. That reads as a flat negative. But about three quarters of those stones were five millimetres or under, and those pass anyway, so it was underpowered for the five to ten millimetre group that actually matters. Its primary outcome was intervention, not CT-proven passage. Note it is a Lancet paper, examiners like catching people out on that.

Libby And the trials that went the other way?

Ryan They point at the same subgroup. Furyk, twenty sixteen, found no overall benefit but a significant benefit in the pre-specified five to ten millimetre group. Ye, in European Urology, twenty eighteen, nearly three and a half thousand patients, expulsion eighty-six per cent against seventy-nine, with the benefit again sitting in stones over five millimetres. Cochrane concludes the same shape. So the honest synthesis, and the one to say out loud, is that alpha blockers do little for small stones that were going to pass, and earn their place in larger distal stones.

Libby Lower pole stones. The classic teaching was shockwave does badly there. Has that survived?

Ryan The direction survived, but the reasoning has moved on, and PUrE is the trial to know now. PUrE first randomised comparison, published in European Urology in twenty twenty-five, four hundred and sixty-one patients with lower pole stones of ten millimetres or less. Flexible ureteroscopy gave a stone-free rate of seventy-two per cent against shockwave at thirty-six. So ureteroscopy doubles your clearance.

Libby Then surely you just do ureteroscopy.

Ryan That is the trap, and it is the whole exam point of the trial. There was no difference in health status between the two arms. The higher stone-free rate did not buy the patient a better outcome that they could feel. And the cost per quality-adjusted life year for ureteroscopy came out around sixty-five thousand pounds, where shockwave had a ninety-nine point nine per cent probability of being cost effective at the twenty thousand pound threshold. So at ten millimetres and under, shockwave, despite losing on stone clearance. Being able to say why a worse stone-free rate can still be the right answer is what separates a good answer from a recited one.

Libby And above ten millimetres?

Ryan It flips, and PUrE answered that too in its second randomisation, lower pole stones ten to twenty-five millimetres. PCNL seventy-one per cent stone-free against flexible ureteroscopy at forty-eight, and this time PCNL was better on health status as well, with an eighty-seven per cent probability of being cost effective. So the rule is clean. Ten millimetres and under, shockwave. Over ten, PCNL. And above twenty millimetres the CROES data show shockwave outcomes falling away sharply, which is the same conclusion arriving from a different direction.

Libby Pregnancy. You have told me before that this is where people fall over.

Ryan Because almost everything you have just learned inverts, and if you answer on autopilot you will get all three wrong. Analgesia reverses. Paracetamol and opioids are first line, and NSAIDs are avoided, because of premature closure of the ductus arteriosus and oligohydramnios. That is the exact opposite of the non-pregnant ladder, where the NSAID is first line and the opioid is not.

Libby Imaging next.

Ryan Imaging reverses too. Ultrasound first, MRI without gadolinium second, and low dose CT only if management actually depends on it. One number defuses the conversation you will have on the ward: even a CT pelvis, at around twenty-five milligray, sits below the fifty milligray threshold, so an indicated scan is never grounds for termination. Treatment reverses as well. Shockwave is absolutely contraindicated and PCNL generally avoided, so you manage conservatively, then stent or nephrostomy if you must, accepting that both encrust and need frequent changes, with definitive treatment usually deferred until after delivery.

Libby Last one, and it is the most counterintuitive. Calcium in the diet.

Ryan Do not restrict it. Patients with calcium stones very reasonably assume that cutting dietary calcium must help, and plenty of clinicians go along with it, and it is wrong. The mechanism is the thing to hold onto, because once you have it you cannot get the advice the wrong way round. Calcium in the gut binds oxalate in the gut. Bound oxalate is not absorbed, it leaves in the stool. Take the dietary calcium away and that oxalate is free to be absorbed, so more oxalate reaches the kidney, and urinary oxalate goes up. You have made the stone-forming risk worse while believing you improved it. So the advice is a normal intake, seven hundred to twelve hundred milligrams a day, not a restricted one. Restrict the oxalate and the salt instead, and keep the fluid up. And once you have that mechanism, a second scenario falls out of it for free. The patient with inflammatory bowel disease, a short bowel, or a bariatric bypass forms oxalate stones for exactly the same reason, arriving from the other direction. Fat is malabsorbed, the calcium in the gut binds to the fat instead of to the oxalate, and the oxalate is left free to be absorbed. Same free oxalate, same rise in urinary oxalate, and it comes with hypocitraturia and a low urine volume on top. So enteric hyperoxaluria is not a separate fact to memorise, it is your calcium rule playing out in someone whose gut has taken the calcium out of the equation for you.

Libby One more, and it is the thing I get asked and fumble. Why is an NSAID first line in colic rather than an opiate?

Ryan Because it treats the mechanism rather than the perception, and once you know the mechanism you cannot get the answer the wrong way round. An acute obstruction raises prostaglandin E2 in the kidney. That prostaglandin dilates the afferent arteriole, so renal blood flow goes up and urine output goes up, and since the outflow is blocked, the pressure inside the collecting system climbs. The pain is that pressure.

Libby So the NSAID lowers the pressure rather than blunting the pain.

Ryan Exactly that. Blocking prostaglandin synthesis reverses the whole sequence: less afferent dilatation, less urine production, lower intrapelvic pressure. And it does two other useful things at the same time, reducing ureteric smooth muscle activity and mucosal oedema. An opiate does none of that. It sits on top of the pain while the pressure carries on. That is why the ladder starts where it does, and it is also why the pregnancy reversal we talked about earlier costs you something real: when you take the NSAID away you are not swapping one painkiller for another, you are giving up the only drug that treats the cause.

Libby Are there stones where the chemistry itself changes what you do, rather than just which device you pick?

Ryan Two, and they sit at opposite ends of the pH scale, which is the neatest way to hold them. Uric acid stones form only in acid urine, below a pH of five point five, and they are the one stone type reliably amenable to oral chemolysis. Alkalinise with potassium citrate and you can genuinely dissolve an existing stone, not merely prevent the next one. Use the right target, though, because there are two of them and that is the examinable bit. Seven point nought to seven point two to dissolve a stone, six point two to six point eight to prevent one. Add allopurinol if the patient is hyperuricaemic. No other stone does that, so do not try it on a calcium stone or on any obstructed or infected system.

Libby And the other end?

Ryan Struvite, the infection stone, magnesium ammonium phosphate. It needs a pH above seven point two, and the mechanism tells you everything else. Urease-producing organisms, Proteus classically, split urea into ammonia, the ammonia drives the pH up, and the salt precipitates out. So the bacteria are not sitting on the stone, they are manufacturing it. These grow fast into staghorns, and the corollary is that medical treatment alone will not do: you need complete clearance, because any residual fragment carries the organism and the whole thing reforms. That is why PCNL is the mainstay for a staghorn, and why the target is stone-free rather than better.

Libby Give me the numbers from today.

Ryan Six numbers. Spontaneous passage at five millimetres, about sixty-five per cent, and at six millimetres about thirty-three, the cliff between them. Patient-reported passage, sensitivity forty-seven per cent, so believe a yes and distrust a no. PUrE first randomisation, flexible ureteroscopy seventy-two per cent stone-free against shockwave thirty-six, with no difference in health status. PUrE second randomisation, ten to twenty-five millimetres, PCNL seventy-one against forty-eight. CT pelvis in pregnancy, about twenty-five milligray, below the fifty milligray threshold. And SUSPEND, over eleven hundred patients, no overall benefit, but three quarters of the stones were five millimetres or under.

Libby And the catch to walk out with: drain the infected obstructed kidney, do not treat the stone at the same sitting, because the keenness is the error.

Libby Welcome back to FRCS Urology in Fifteen. Today, testicular cancer. Ryan, this is a disease we cure, so where do the marks actually go?

Ryan Into eight places where the decision is genuinely difficult, because the cure rate hides how much judgement there is. The impalpable little lesion on a scan, where the question is whether he has to lose a testis at all. The markers, which mislead in both directions. Fertility, which has to be dealt with before anything else. How the risk groups in metastatic disease actually work. Stage one, where the choice is surveillance against treating. What to do with what is left after chemotherapy. Which lumps are not germ cell tumours at all. And why a node dissection threatens ejaculation but not erection.

Libby Start with the one I see most. Scrotal ultrasound for infertility or pain, and there is a small thing in the testis nobody can feel. What now?

Ryan The question has changed, and saying so out loud is the answer. It is no longer is this cancer, it is does this man need to lose a testis to find out. Ultrasound now finds lesions that would never have presented in a lifetime, and a radical orchidectomy for something benign is a real harm: hypogonadism, impaired fertility, and the cost of a cancer pathway he never needed.

Libby So how do I judge the odds before I operate?

Ryan By size, which is the one preoperative predictor that holds up. The smaller and the less palpable, the more likely benign. Virtually all lesions under three millimetres are benign, about eighty-seven per cent of those under five millimetres, and about seventy per cent of those under ten. Surgical series agree: in the largest multicentre series of marker-negative lesions two centimetres or less, only twenty-one of a hundred and forty-seven, so fourteen per cent, were cancer. A cut-off around eight and a half millimetres gave a ninety-five per cent negative predictive value. And the commonest benign answer is a Leydig cell tumour.

Libby Can I lean on the markers being normal?

Ryan No, and this is the trap. Normal markers do not exclude a germ cell tumour. Most pure seminomas never raise alpha-fetoprotein and only a minority raise the beta subunit of human chorionic gonadotrophin, so a clean marker panel tells you very little about a small lesion. What it means in practice is that for a small, impalpable, marker-negative mass you offer testis-sparing surgery with frozen section rather than a radical orchidectomy, and you take the testis only if the frozen section says you must.

Libby Does his history change how suspicious I am?

Ryan It should, and the numbers are more modest than people assume, which is itself worth knowing. An undescended testis carries an absolute risk of roughly one in a hundred and twenty-five if it was unilateral, and about one in forty-five if bilateral. Orchidopexy lowers that risk but does not abolish it, and the normally descended contralateral testis is at raised risk too, which is the part people forget. A first-degree relative confers about a six-fold increase. And if he has germ cell neoplasia in situ in the other testis, that is not a curiosity: roughly half will develop an invasive tumour within five years.

Libby Let us do the markers properly then, because I know there are traps.

Ryan Three that come up repeatedly. The first is the one to have ready: a raised alpha-fetoprotein excludes pure seminoma. If the histology says seminoma and the alpha-fetoprotein is up, you do not believe the histology, you treat him as a non-seminoma. That single rule changes the whole management pathway. The second runs the other way: the beta subunit of human chorionic gonadotrophin is mildly raised in about fifteen to twenty per cent of genuine seminomas, and that does not reclassify anything.

Libby And the third?

Ryan Timing, which is the one people get wrong under pressure. You take markers before the orchidectomy and after it, but they answer different questions. For the risk grouping in metastatic disease you use the pre-chemotherapy values, taken the same day, immediately before chemotherapy starts, not the post-orchidectomy ones. The post-orchidectomy markers do something else: they tell you whether he has residual disease and they guide stage one management. Quote the wrong set and you put the man in the wrong risk group.

Libby Anything about the operation itself?

Ryan One absolute. Never go through the scrotum. Orchidectomy and any biopsy are inguinal, every time, because a trans-scrotal approach seeds the scrotal skin and disrupts the lymphatic drainage, so you convert a disease that drains to the retroperitoneum into one that can drain to the inguinal nodes. You have changed where the cancer goes.

Libby Fertility. I know sperm banking matters, but when exactly?

Ryan Before anything, and at the first consultation rather than once the plan is settled, because the damage is often already done. Spermatogenesis is impaired at diagnosis in a substantial minority of these men, before a drop of chemotherapy. In the largest series, banking semen from over five hundred men before any treatment, about four per cent were azoospermic and roughly thirteen per cent had a million per millilitre or fewer. The safe line for an examiner is that around half of these men have an abnormal semen analysis before treatment starts.

Libby And if he cannot produce a sample, or he is already azoospermic?

Ryan Then onco-TESE, which is surgical sperm retrieval taken from the testis at the same time as the cancer operation. It is the option people forget exists, and the point is the timing: you get one chance at it, while he is already anaesthetised and before any chemotherapy has been given. Raise it at that first appointment, because a man who is told about it after his first cycle has lost the opportunity.

Libby Metastatic disease. Good, intermediate and poor risk. I can never keep the thresholds straight.

Ryan Do not learn it as a grid, learn the two things that move a man down it, and you can reconstruct it. The first is where the disease is: non-pulmonary visceral metastases, so liver, bone or brain rather than lung, push you down a category. The second is how high the markers are, in bands. That is it. Everything else in the table is detail hanging off those two ideas.

Libby And the thing people get wrong?

Ryan Seminoma has no poor-risk category at all. It does not exist. A seminoma is either good risk or, if there are non-pulmonary visceral metastases, intermediate, and that single distinguishing feature is the whole seminoma side of the classification. If you find yourself describing a poor-risk seminoma you have made an error. And the numbers are worth carrying because they show why the grouping matters: good-risk disease has a five-year survival around ninety-five per cent, intermediate around ninety, and poor risk drops to about two thirds.

Libby Does that translate directly into treatment?

Ryan Cleanly, which is why it is worth knowing. Good risk gets three cycles of bleomycin, etoposide and cisplatin. Intermediate and poor risk get four. And one practical warning that examiners like: bleomycin causes pulmonary fibrosis, so if that man comes back for surgery you warn the anaesthetist to avoid a high inspired oxygen concentration and to be careful with fluid.

Libby Stage one disease. Everything is out, the scans are clear. Do I treat him or watch him?

Ryan Watch him, in both histologies, and be able to say why. For stage one seminoma surveillance is preferred outright. For non-seminoma it is also the default, but there the decision is driven by one pathological feature: lymphovascular invasion. That is the key predictor of occult metastatic disease, and it is what splits the group.

Libby So what changes if there is lymphovascular invasion?

Ryan Relapse risk on surveillance runs anywhere from about fourteen to fifty per cent depending on it. If it is absent, surveillance, comfortably. If it is present, you offer either surveillance or a single cycle of chemotherapy, which brings relapse down to around two to three per cent. And be precise here, because there are three wrong answers available: one cycle is preferred over two, and preferred over a node dissection. The reason surveillance remains reasonable even in the high-risk group is that you cure the ones who relapse, so you are choosing between treating everybody a little and treating a minority properly.

Libby What if he is not stage one, but has small nodes in the retroperitoneum?

Ryan For seminoma with low-volume nodes that is where the newest change sits, and it is a good thing to be current on. Chemotherapy or radiotherapy remain standard, but the twenty twenty-six position now also allows a primary nerve-sparing node dissection as an option for nodes three centimetres or less, in high-volume expert centres. The appeal is that it is chemotherapy-free: survival without chemotherapy runs around eighty to eighty-five per cent, and antegrade ejaculation is preserved in ninety to ninety-seven per cent. The honest caveat is that relapses do happen, mostly outside the dissection template, so it is a genuine trade rather than a free win.

Libby After chemotherapy there is still something on the scan. How do I decide what to do with it?

Ryan Entirely differently depending on the histology, and this is a clean pair to hold. In non-seminoma, resect every residual mass of a centimetre or more once the markers have normalised. The reason is teratoma: it is chemoresistant, so chemotherapy will not clear it, and left alone it can keep growing or undergo malignant transformation. When those masses are examined, about forty per cent contain teratoma and around ten per cent viable tumour, so only about half are just necrosis and fibrosis.

Libby And in seminoma?

Ryan Mostly you observe, because residual seminoma usually resolves. If the mass is over three centimetres you can use a PET scan at two months or more after chemotherapy, and the way to quote it is as an asymmetric test. Its negative predictive value is over ninety per cent, so a negative scan is reassuring, but the positive predictive value is only about a quarter to two thirds, so a single positive scan should not by itself send a man to theatre. Below three centimetres the scan is not useful at all.

Libby What if the markers are still climbing?

Ryan Then it is not a surgical problem. Rising markers after chemotherapy mean salvage chemotherapy, not an operation. Operating into active, chemo-sensitive disease that is still progressing is the error, and it is a deliberate distractor because there is a visible mass tempting you to remove it.

Libby Before we finish, are there testicular lumps I should not be treating as germ cell tumours at all?

Ryan Three worth having, and they are common distractors. The first is age-driven: in a man over sixty, the commonest testicular tumour is lymphoma, not a germ cell tumour. So an older man with a testicular mass is a different problem, and reaching reflexively for the germ cell pathway will send you the wrong way.

Libby And the second?

Ryan The Leydig cell tumour, which is the commonest of the sex cord stromal tumours and the commonest benign answer to that small impalpable lesion we started with. It is hormonally active, secreting testosterone or oestrogen, so it can present with gynaecomastia and low libido in an adult, or precocious puberty in a boy. About ten per cent behave malignantly. The histological signature is Reinke crystals. If you want the physiology behind the name: Leydig cells sit between the tubules, are driven by luteinising hormone and make testosterone, whereas Sertoli cells line the tubules, are driven by follicle stimulating hormone and are the nurse cells that form the blood-testis barrier.

Libby And the third?

Ryan Microlithiasis, and this one is a deliberate trap. Isolated testicular microlithiasis, in a man with a normal examination and no other risk factors, is not premalignant. He does not need surveillance ultrasound and he does not need a biopsy. It only carries weight in combination with other risk factors. Putting a healthy man onto an imaging pathway for incidental microlithiasis is the wrong answer, and it is offered to you precisely because it feels cautious.

Libby Last one. Retroperitoneal node dissection and ejaculation. I know they are linked but I could not explain it.

Ryan It is worth being able to, because it is a favourite and the mechanism makes it memorable. The risk is loss of antegrade seminal emission, which gives anejaculation or retrograde ejaculation, and therefore infertility. Erection is preserved, and that is the part people get wrong.

Libby Why is erection spared?

Ryan Because the two functions run on different nerves, and the dissection is only in the territory of one of them. The mnemonic is point and shoot: parasympathetic is point, the erection, carried by the cavernous nerves, which are nowhere near the operative field. Sympathetic is shoot, the emission, and those are the fibres at risk. Specifically the postganglionic sympathetic fibres from the lumbar sympathetic chain, functionally the first and second lumbar levels, coalescing as the hypogastric plexus, which lies right in front of the aortic bifurcation. That is precisely where you are working, which is why the dissection is nerve-sparing wherever possible.

Libby Numbers from today.

Ryan Eight. Small impalpable lesions: about eighty-seven per cent benign under five millimetres, seventy per cent under ten, and an eight and a half millimetre cut-off gives a ninety-five per cent negative predictive value. A raised alpha-fetoprotein excludes pure seminoma, while a mildly raised human chorionic gonadotrophin does not exclude it, in fifteen to twenty per cent of seminomas. Around half of these men have an abnormal semen analysis before any treatment. Seminoma has no poor-risk group, and good-risk survival is about ninety-five per cent against roughly two thirds for poor risk. Stage one non-seminoma with lymphovascular invasion: one cycle of chemotherapy takes relapse from as much as fifty per cent down to two or three. Post-chemotherapy non-seminoma, resect everything a centimetre or more, because forty per cent hold teratoma and ten per cent viable tumour. PET after seminoma only above three centimetres. And in a man over sixty, the commonest testicular tumour is lymphoma.

Libby And the catch to walk out with: rising markers after chemotherapy are a reason for more chemotherapy, not for an operation.

Libby Welcome back to FRCS Urology in Fifteen. Today, benign prostatic hyperplasia and male lower urinary tract symptoms. Ryan, what are we covering?

Ryan We follow the patient's journey, from the clinic door to the operating table. What you want at the first appointment and what you do not. How a flow meter works and how to read the trace, because people do get asked to draw one, and what the number actually means. The medical therapy trials. Then the surgical decision, which is really one trade-off: keeping ejaculation against how long the operation lasts. And the man in chronic retention at the end, where the question is when to operate, not whether.

Libby Start at the clinic door. Man with lower urinary tract symptoms walks in. What do you want?

Ryan Five things, and they are cheap. A history with an IPSS including the quality of life question, and the bands: nought to seven mild, eight to nineteen moderate, twenty to thirty-five severe. A frequency-volume chart of at least three days, which is the one people skip and the one that most often changes the plan. Urinalysis. And since we explain how the flow meter works, it is worth knowing what the dipstick is actually measuring, because it tells you which pad to believe. Nitrite is the specific one: it is positive only when bacteria have reduced dietary nitrate, which also means the urine has to have sat in the bladder long enough for that to happen, so a very frequent voider can be falsely negative. Leucocyte esterase is the sensitive one and the less specific, because it is really just detecting pyuria, and pyuria has plenty of causes that are not infection. Two places not to dip at all: never a catheterised patient, because it is always positive, and not to diagnose infection in a man over sixty-five with non-specific symptoms. A digital rectal examination. And a PSA, but only after counselling and only if it would change management. One caveat on that PSA: if he has been on a five alpha reductase inhibitor for six months or more, double the value before you interpret it for cancer risk, because the drug roughly halves it.

Libby And what do you deliberately not do?

Ryan That is the better half of the question. Creatinine is not routine. You check renal function only if you suspect impairment, so a palpable bladder, nocturnal enuresis, recurrent infection, or a history of renal stones. Imaging and cystoscopy are not routine either, reserved for haematuria, suspected stricture, stones or previous surgery. Ordering everything on everybody is not thoroughness, it is a failure to stratify, and it is marked as such.

Libby Flow rates. Somebody told me they were asked to draw a trace in their exam, so let us take it seriously. How does the machine even work?

Ryan Three methods, and it is a fair question because it is one of the few pieces of kit in urology whose physics you can explain in a sentence each. Gravimetric measures the weight of voided urine accumulating over time and differentiates it. Rotating disc measures the power needed to keep a spinning disc at constant speed as urine lands on it. And capacitance measures the change in capacitance of a dipstick as the fluid rises around it. Gravimetric and rotating disc are the two in common use.

Libby And the shapes? What am I drawing?

Ryan A normal trace is bell-shaped and brief, peaking within the first few seconds, then falling away. Obstruction flattens that bell into a low, prolonged plateau, so the same area is spread over a much longer time. And an intermittent trace, several separate peaks, means either straining or an underactive detrusor rather than obstruction as such. One rule that invalidates everything: the area under the curve is the voided volume, so a trace taken on a small volume cannot be interpreted at all. You need at least a hundred and fifty millilitres for the study to mean anything.

Libby So if the flow is low, he is obstructed. Or is that too simple?

Ryan Too simple, and the numbers let you speak in probabilities rather than absolutes. From the ICS BPH study, a maximum flow under ten millilitres per second means roughly ninety per cent are obstructed. Ten to fifteen, about sixty per cent. Above fifteen, still about thirty per cent. So a good flow does not exclude obstruction, which surprises people.

Libby And the ones with a low flow who are not obstructed?

Ryan About one in ten men with a maximum flow under ten has detrusor underactivity rather than obstruction, and that is the man you must not put through a resection, because you will not fix him and you may make him worse. That single figure is the argument for pressure-flow studies in the equivocal case. Normal flow is also age-dependent, which people forget: over twenty-one millilitres per second under forty, over eighteen between forty and sixty, and over thirteen above sixty.

Libby So who actually gets pressure-flow studies before you operate?

Ryan One idea covers most of it: study the man whose trace you cannot trust or whose story does not fit. A voided volume persistently under a hundred and fifty millilitres, because the trace is not interpretable below that. A maximum flow above ten, where you want obstruction confirmed before committing him to surgery. Age under fifty or over eighty. Suspected detrusor underactivity or predominant storage features. And always study before re-intervening after a treatment that has already failed.

Libby I notice a big residual is not on that list. I thought it was.

Ryan It was, and it came off, which is the change worth knowing. A post-void residual over three hundred millilitres was dropped as an indication for urodynamics in the twenty twenty-six EAU position. It has not become unimportant, it has changed job: it is now the trigger for intermittent catheterisation in the underactive bladder rather than a reason to study him. So the residual still changes what you do, it just no longer sends him for a pressure-flow study on its own.

Libby Medical management. Which trials do I actually need?

Ryan Three, and they say related things. PLESS showed finasteride roughly halved the four-year risk of surgery, from about ten per cent to five, and of retention, from about seven to three. MTOPS showed combination therapy cut clinical progression by about sixty-six per cent, against thirty-four for finasteride and thirty-nine for doxazosin alone. And CombAT showed combination cut retention by about sixty-six per cent and surgery by about seventy, in men with larger prostates.

Libby Is there a single idea running through those?

Ryan Yes, and it is the answer to give rather than three sets of percentages. The alpha blocker treats symptoms quickly and does nothing to the natural history. The five alpha reductase inhibitor works slowly and does change the natural history, shrinking the gland and cutting retention and surgery. Combination does both, which is why it beats either alone on progression. So match the drug to what you are trying to achieve: relief now, or a different trajectory.

Libby And the man whose storage symptoms persist despite the alpha blocker? That is most of my clinic.

Ryan Add an antimuscarinic or a beta-three agonist, but check the residual first, and that caveat is the teaching point. Avoid the antimuscarinic if the post-void residual is over a hundred and fifty millilitres: you are giving a drug that relaxes the detrusor to a man who is already not emptying, and retention is the predictable result. Mirabegron was upgraded to a strong recommendation in twenty twenty-six and is the cleaner choice where antimuscarinics are poorly tolerated. On the dementia question, the July twenty twenty-six MHRA review found the evidence does not confirm bladder anticholinergics cause it, but could not exclude a small risk, so in older men keep the anticholinergic burden low.

Libby Surgery. There are a dozen options now and I find the choice genuinely hard.

Ryan It is one axis, and once you see it the list collapses. Every option trades ejaculatory function against durability, and you are choosing where on that line the man wants to sit. At one end, TURP is the reference standard: seventy to ninety men in a hundred improved, but retrograde ejaculation in fifty to eighty of them. HoLEP is the most effective and the most durable, works at any prostate size, but retrograde ejaculation in seventy-five to eighty-five.

Libby And the ejaculation-preserving end?

Ryan UroLift, with retrograde ejaculation under one in a hundred, done under local anaesthetic as a day case, but it needs the right anatomy and is out if there is an obstructing median lobe. Rezum, nought to three per cent, under local anaesthetic or sedation, though it works by steam so the effect builds over weeks rather than arriving on the table. Both preserve ejaculation far better than a resection, and both ask the man to accept a smaller and slower improvement in return. And keep the newest devices in proportion: iTind's three-year data is fifty patients, which is encouraging but is not the evidence base behind a resection or an enucleation.

Libby Before the numbers, how does prostate size come into it? And somebody framed this to me as cavitating against non-cavitating, which I had not heard.

Ryan That is the better frame, and I would use it. Split the options by whether they remove tissue at all. The cavitating ones, resection, enucleation, vaporisation and Aquablation, take tissue away and leave a cavity, so the improvement is immediate and large and the durability is good, at the cost of ejaculation. The non-cavitating ones, UroLift and Rezum, reshape or retract tissue instead, so they preserve ejaculation but deliver less and hold less well. That single split predicts both the size of the benefit and the side-effect profile, which is why it is a better frame than a list of device names.

Libby And size on top of that?

Ryan Size narrows the field before preference does. Under thirty millilitres, or a tight bladder neck, a bladder neck incision is back on the table and has less ejaculatory dysfunction than a resection. Thirty to eighty is the classic resection range. Above eighty, enucleation or open simple prostatectomy, because a resection there runs long and the bleeding and absorption risks climb.

Libby If we are resecting, I should probably be able to explain TUR syndrome properly rather than just naming it.

Ryan You should, and every feature falls out of one fact: the irrigant. Monopolar resection needs a non-conducting fluid, so it uses one and a half per cent glycine, hypo-osmolar at about two hundred and twenty milliosmoles. Absorb enough and you get a dilutional hyponatraemia. Glycine also breaks down to glyoxylic acid and ammonia, so you can get a hyperammonaemic encephalopathy, and it is itself an inhibitory neurotransmitter in the brain and retina, which is why the patient can have transient visual disturbance with a completely normal fundoscopy. Risk climbs beyond ninety minutes and over about forty-five grams. And the reason you hear about it less is the point: bipolar runs in saline, so there is no hypo-osmolar irrigant to absorb and the syndrome essentially disappears.

Libby Anything the guidelines have changed their mind about?

Ryan Two worth knowing, and both are twenty twenty-six. Aquablation was upgraded from a weak to a strong recommendation for thirty to eighty millilitre prostates. And UroLift keeps its strong recommendation, but the EAU has added a new advisory that you must tell patients retreatment rates are higher than after TURP. That addition is a small thing that tells you exactly where the field's doubt lies, and it leads straight into the numbers.

Libby You said durability is the counterweight. Put numbers on it.

Ryan This is the axis on which the minimally invasive options lose, and being straight about it is what makes the consent conversation honest. Five-year reoperation: TURP and HoLEP in the low single figures, HoLEP as low as one to five per cent. Rezum about four to five. UroLift thirteen point six per cent in the LIFT randomised trial, with real-world rates nearer five to six per cent per year. And prostate artery embolisation is the highest at around twenty per cent.

Libby So how do I put that to a patient without just listing it?

Ryan As a genuine choice rather than a recommendation in disguise. A younger man who cares about ejaculation may rationally accept a one in seven chance of needing something else within five years. A man who wants this dealt with once should have HoLEP and be counselled that retrograde ejaculation is likely. Both are correct answers to different questions, and the examiner is testing whether you know that rather than whether you have a favourite. Two other risks belong in that conversation: permanent incontinence runs one to two per hundred for TURP, HoLEP, GreenLight and Aquablation, and under one per hundred for the preserving options; transfusion is about five per hundred for TURP and Aquablation and one or under for the rest.

Libby Last one. High-pressure chronic retention. Do I resect him?

Ryan Yes, but the question is when, not whether, and the exam point is that you do not operate at presentation. Relieving the outlet is an absolute indication, and these men void well afterwards precisely because the detrusor is demonstrably working, it is the thing generating the pressure. But three arguments say wait.

Libby Go on.

Ryan He is not fit for it: he is uraemic, often hyperkalaemic and acidotic, and about to undergo a post-obstructive diuresis with swings in volume, sodium, potassium and magnesium. Second, his kidney has not finished recovering: creatinine falls over days, but glomerular filtration keeps improving for up to about three months after decompression, so operate early and you operate on a worse kidney than he is going to have. And third, the outcome data, which you should quote carefully. The National Prostatectomy Audit followed nearly four thousand prostatectomies, about twelve hundred of them presenting in retention, and those men carried an excess risk of death against elective surgery. Quote the ninety-day figure, a relative risk of about four point four. The thirty-day risk looks far more dramatic at twenty-six, but the deaths are so few that the interval is enormous, and knowing why you trust one and not the other is the point.

Libby So is the argument that the operation works less well after retention?

Ryan No, and that distinction is the part worth having ready. In that same audit the symptomatic outcome of men operated on after retention was no different from the elective group. The operation works. The argument is entirely about perioperative risk and when you accept it. And the practical corollary is in the data too: men who were catheterised, sent home and readmitted for planned surgery did as well as those kept in. So catheterise, let him recover, bring him back. You are not denying him anything, you are moving the same operation to a safer day.

Libby Does the same argument apply to the low-pressure man with a big residual?

Ryan No, and this is the discriminator an examiner is listening for. Do not carry the argument across. In high-pressure chronic retention the objection is the timing: you will operate, just not today. In low-pressure chronic retention the objection is the operation itself. The detrusor has failed, and a resection does not fix a failed detrusor, so a significant proportion never void and stay catheter-dependent. High pressure is deferred surgery. Low pressure is a conversation about whether to operate at all.

Libby Numbers from today.

Ryan Six. A valid flow needs at least a hundred and fifty millilitres voided. Maximum flow under ten millilitres per second, about ninety per cent obstructed, but one in ten of those has detrusor underactivity instead. MTOPS, combination cut progression by sixty-six per cent. Retrograde ejaculation, fifty to eighty per cent after TURP against under one per cent after UroLift. Five-year reoperation, HoLEP one to five per cent, UroLift thirteen point six, embolisation about twenty. And IPSS: eight to nineteen is moderate.

Libby And the catch to walk out with: a low flow is not proof of obstruction, and the man with an underactive detrusor is the one a resection will not help.

Libby Welcome back to FRCS Urology in Fifteen. Today, urological trauma. Ryan, the one-line version of each organ?

Ryan Renal: grade it, and stability decides, not grade. Bladder: intraperitoneal is repaired, extraperitoneal drained. Urethra: pelvic fracture means a suprapubic catheter or early realignment with delayed urethroplasty, and do not force a catheter. Testis: explore within seventy-two hours and about ninety per cent are salvaged. Five things today: the shock classification and why it misleads, the massive transfusion traps, renal trauma, bladder, and where the two UK and European bodies disagree.

Libby Start with the shock classes.

Ryan Class one is up to fifteen per cent loss, class two fifteen to thirty, class three thirty-one to forty, class four over forty. In a seventy kilogram adult that is up to seven hundred and fifty millilitres, then up to fifteen hundred, then two thousand, then more. But the examinable point is not the table, it is this: blood pressure falls LATE. A normal blood pressure does not exclude significant haemorrhage.

Libby So what moves first?

Ryan Tachycardia and a narrowed pulse pressure, because the diastolic rises with peripheral vasoconstriction. Urine output tracks it well: over thirty millilitres an hour in class one, down to negligible in class four. And base deficit and lactate outperform the vital signs altogether, which is why the current edition puts base deficit in the table: nought to minus two in class one, worse than minus ten in class four.

Libby When does the classification let you down?

Ryan Treat it as a teaching framework rather than a measurement. It is blunted by age, by beta-blockade, by a pacemaker and by athletic fitness. And in pregnancy a substantial volume can be lost before any hypotension appears at all, because the plasma volume is already expanded. Saying that unprompted shows you know the limits of the tool rather than just the tool.

Libby Massive transfusion. What catches people?

Ryan Calcium, and it is now taught as a fourth point alongside the lethal triad, the diamond of death. Citrate in stored blood chelates calcium, so the ionised calcium falls as you transfuse, and that impairs both clotting and myocardial contractility. Keep it above one point nought millimoles per litre. Potassium is the other one: it rises with storage, so hyperkalaemia matters when older units go in fast.

Libby And tranexamic acid?

Ryan One gram over ten minutes, then one gram over eight hours, and the three-hour rule has a sharp edge worth quoting: given beyond that window it does not merely fail to help, it INCREASES mortality. That is a different statement from being ineffective and it is the version that scores.

Libby Damage control?

Ryan Indicated by haemodynamic instability, an established lethal triad, inability to achieve haemostasis, or multiple injuries. Abbreviated laparotomy: stop the tap, pack, temporary closure, resuscitate on intensive care, definitive surgery later.

Libby Renal trauma. What decides?

Ryan Stability, not grade, and say that first. Haemodynamically unstable after resuscitation means emergency laparotomy and a trauma nephrectomy as required. Stable means multiphase CT with arterial AND delayed urographic images, and the delayed phase is the point: it shows collecting system injury, and a single portal-venous phase is not enough. That omission is a common and consequential error.

Libby Then the management by grade.

Ryan Grades one to three are conservative, discharged when the other injuries allow, with analgesia, antibiotics and seven-day open access back to the unit. Grades four to five managed non-operatively get antibiotics, bed rest, monitoring of haemoglobin and renal function, and a repeat CT at forty-eight hours or sooner if they destabilise, with a stent or drain if there is a persistent urine leak on that scan. Active bleeding on CT goes to arteriography with superselective embolisation; if that fails, or it is a penetrating grade five, proceed to surgery.

Libby Which AAST edition am I grading to?

Ryan Know both, and default to twenty eighteen. The EAU Urological Trauma guideline still grades by the twenty eighteen revision, so for an EAU-based answer that is the one you use. If the question names an edition, use that edition.

Libby And the technical point if you do open?

Ryan Gain vascular control before opening Gerota's fascia. Open the fascia first and the tamponade is lost along with the kidney. The other thing worth volunteering is the follow-up, because it is routinely forgotten: outpatient review at eight weeks, renal ultrasound at six weeks unless they had a nephrectomy, and long-term community monitoring of creatinine and blood pressure.

Libby The kidney is the commonest urological organ injured. What should I know about presentation?

Ryan Around ninety percent in the UK are blunt, from road traffic collisions and falls. The degree of haematuria does not correlate with severity, and a major pedicle injury can have no haematuria at all. Each kidney is graded separately.

Libby Give me the twenty eighteen AAST grades.

Ryan Do not learn it as five paragraphs, learn what moves a kidney up it, because then you can place an injury you have never seen described. Three things escalate you. How deep the laceration goes, with a threshold at one centimetre in the twenty eighteen scale. Whether the collecting system is breached, so urine is leaking. And whether the vessels are involved, and if so whether they are still bleeding. Grades one and two are contusions and shallow tears contained by Gerota's fascia; three is a deeper tear or contained vascular injury; four is urine leaking or a segmental vessel gone; five is the shattered kidney or the main artery or vein.

Libby And four and five?

Ryan The twenty eighteen revision did three things, and those are the ones to name: it brought vascular injury properly into the scale, it let active bleeding push an injury up a grade, and it made segmental infarction grade four. Notice the direction of travel there, because it tells you what the scale is for. It is drifting away from describing how torn the kidney looks and towards predicting whether you will have to do something about the bleeding.

Libby So what changed in the twenty twenty-five update?

Ryan It is CT and active-bleeding focused. The laceration threshold rises from one centimetre to two point five centimetres. Urinary extravasation and partial infarction drop from grade four to three, although complete pelviureteric junction disruption stays grade four. Contained vascular injuries, such as pseudoaneurysm, arteriovenous fistula or dissection, are now grade three.

Libby Any new terms?

Ryan A few, and they all point the same way. Haematoma size is now measured explicitly, by the rim distance around the kidney. The shattered kidney becomes the multifragmented kidney, three or more fragments. And the thing that decides whether that multifragmented kidney, or a main vessel injury, is a four or a five is simply whether it is actively bleeding. That is the philosophy of the whole revision: it grades what you will have to do something about, not how bad the pictures look.

Libby Bladder injury. The epidemiology first.

Ryan Bladder injury from blunt trauma is rare, under two per cent, because the bladder sits inside the bony pelvis. Which is why pelvic fractures account for sixty per cent of bladder injuries. Of the injuries themselves, sixty per cent are extraperitoneal, thirty per cent intraperitoneal and ten per cent both.

Libby And the management split?

Ryan Intraperitoneal rupture is always operatively repaired, because urine in the peritoneum causes peritonitis and it will not heal alone: two-layer absorbable closure with catheter drainage. Extraperitoneal is catheter drainage for ten to fourteen days, UNLESS there are complicating features, and those are worth listing: bladder neck involvement, a bone fragment in the bladder wall, an associated rectal or vaginal injury, or the patient is going to laparotomy or internal fixation anyway. Then you repair it. And confirm healing with a cystogram before removing the catheter.

Libby You said the two bodies differ.

Ryan On the cystogram fill volume, and the honest answer is to quote one and name it. The European guidance asks for active retrograde filling with dilute contrast, three hundred to three hundred and fifty millilitres, graded strong. The UK consensus says two hundred to three hundred. Neither is wrong; they are different sources.

Libby Does the difference matter?

Ryan Not as much as the principle both share, which is the thing to say: the bladder must be ACTIVELY filled to a volume that will show a leak. A gravity-filled or under-filled bladder gives a false negative, and a plain CT without retrograde filling misses ruptures altogether. Give the principle, then the number, then whose number it is.

Libby Anything else named specifically?

Ryan One strong European recommendation worth knowing because it is oddly specific: perform cystoscopy to rule out bladder injury during retropubic sub-urethral sling procedures. The trocar passes blind behind the pubis, and the injury is only cheap to fix if you find it on the table. And the general catheterisation rule: do NOT catheterise if a urethral injury is suspected, so blood at the meatus, a high-riding prostate or a perineal haematoma. Retrograde urethrogram first.

Libby Let's move to the ureter.

Ryan Most ureteric injuries are iatrogenic, from gynaecological, colorectal or endoscopic surgery, and they are easily missed, presenting late with fever, ileus, urinoma, fistula or rising creatinine. Diagnose with a delayed-phase CT urogram or retrograde pyelogram, and intraoperatively give indigo carmine or methylene blue if unsure.

Libby The AAST ureteric grades?

Ryan The grading is really measuring two things, and if you hold those you can reason to the repair. How much of the circumference is divided, with fifty per cent as the dividing line between a partial and a substantial injury, and how much length is devascularised, with two centimetres as the line between a clean transection and an avulsion. Those two numbers are exactly what decide whether a stent will do, whether you can join it end to end, or whether you need to bring tissue in from elsewhere.

Libby And repair?

Ryan Low-grade injuries get a stent with or without drainage. A short upper or mid ureteric defect gets a spatulated, tension-free, stented ureteroureterostomy, and a distal injury gets reimplantation with a psoas hitch or Boari flap. Long defects may need a Boari flap, transureteroureterostomy, ileal interposition or autotransplantation. The BAUS consensus says repair immediately if recognised intraoperatively; if recognised late and stenting is not possible, place a nephrostomy and reconstruct at three to six months.

Libby And if the patient is too unwell for a reconstruction?

Ryan Then you do the ureteric version of damage control, and it is a genuinely useful thing to be able to offer in a viva. Ligate the ureter, put in a nephrostomy, and reconstruct later. You have bought a kidney that drains and a patient who survives the night. The same logic applies to an injury found late where a stent will not pass: nephrostomy now, delayed repair at three to six months depending on how contaminated things are.

Libby Onto the urethra. How do posterior and anterior injuries differ?

Ryan Posterior injuries are pelvic fracture urethral injuries from shearing at the bulbomembranous junction. Anterior injuries are classically straddle injuries crushing the bulbar urethra against the pubis. Signs are blood at the meatus, inability to void, a high-riding prostate, and a butterfly perineal haematoma.

Libby Do we catheterise?

Ryan Answer per the source. ATLS and BOAST 14 say do not catheterise and perform a retrograde urethrogram first. The EAU permits a single gentle attempt by an experienced doctor with a sixteen French soft silicone catheter, going suprapubic if it fails.

Libby Remind me of the Goldman classification.

Ryan I would not recite it. The only thing it is really telling you is whether the urogenital diaphragm has been disrupted and whether the bladder neck is involved, because those are what determine continence afterwards and how hard the delayed repair will be. The one fact worth carrying is that the commonest pattern is the combined anterior and posterior injury that disrupts the diaphragm. If an examiner wants the numbered types you can say you would classify it formally on the urethrogram, and that is a better answer than a recited list.

Libby And the management of pelvic fracture urethral injury?

Ryan Urinary diversion with a suprapubic catheter or early endoscopic realignment in selected stable patients, then delayed anastomotic urethroplasty at about three months. The EAU says do not perform immediate urethroplasty within forty-eight hours, because acute open repair carries high rates of stricture, erectile dysfunction and incontinence.

Libby And anterior injuries?

Ryan A partial anterior injury gets a catheter or suprapubic catheter, and many heal. A complete blunt straddle injury gets a suprapubic catheter and delayed urethroplasty. A penetrating anterior injury can have primary repair if clean and stable.

Libby Finally, testicular rupture and penile fracture.

Ryan For testicular rupture, a breach of the tunica albuginea, explore within seventy-two hours for about ninety percent salvage, falling to about thirty percent after seventy-two hours. Ultrasound is about ninety-four percent sensitive for tunica rupture but only an adjunct to clinical judgement, and BAUS favours prompt exploration of large symptomatic haematocoeles too. Penile fracture needs prompt exploration and absorbable closure of the tunica, and urethral injury occurs in ten to twenty percent, so always assess the urethra.

Libby The list.

Ryan Blood pressure falls late; tachycardia and a narrowed pulse pressure come first, and base deficit beats both. Keep ionised calcium above one millimole. Tranexamic acid one gram then one gram, and after three hours it increases mortality. Renal trauma is decided by stability, not grade, and the CT needs a delayed phase. Gain vascular control before opening Gerota's. Pelvic fractures cause sixty per cent of bladder injuries; sixty per cent extraperitoneal, thirty intraperitoneal. Intraperitoneal is repaired, extraperitoneal drained unless complicated. And fill the bladder actively for the cystogram.

Libby A normal blood pressure does not exclude significant haemorrhage, and stability decides the kidney, not the grade. That is FRCS Urology in Fifteen.