Tag Archive for: urologist brisbane

A kidney tumour larger than 3 cm: what does it mean?

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By Dr Jo Schoeman | Patient information | September 2026

Finding a kidney mass can be frightening. The first question is whether it is cancer; the next is whether it is confined to the kidney. A mass measuring 3.1 cm is not automatically advanced cancer. If a renal cell carcinoma (RCC) is no more than 4 cm and remains within the kidney, it is classified as T1a. A tumour over 4 cm but no more than 7 cm, still confined to the kidney, is T1b. Lymph-node and distant spread are assessed separately. Some kidney masses are benign, and imaging alone cannot always tell us which. [1–3]

How might it present?

Many tumours are discovered by chance during an ultrasound or CT scan for another problem. Others cause blood in the urine, persistent pain in the side or back, or occasionally a palpable lump. Unexplained weight loss, fatigue, anaemia or fever warrant assessment, although they have many possible causes. The combination of blood in the urine, pain and a palpable mass is uncommon. Visible blood in the urine should always be investigated; a kidney mass does not rule out another source of bleeding. [2]

What investigations are needed?

  • Dedicated imaging: A multiphase contrast CT of the kidneys and abdomen shows whether the lesion enhances, its exact position, its relationship to major blood vessels and the collecting system, and whether there are enlarged nodes or signs of spread. Chest imaging completes staging; its extent is tailored to the tumour and clinical circumstances. MRI may clarify an uncertain lesion or suspected tumour extension into a vein, or be useful when CT contrast is unsuitable. A complex kidney cyst needs its own imaging assessment. [2]
  • Blood and urine tests: Kidney function (creatinine and eGFR), a full blood count and other tests guided by the clinical picture help assess fitness for treatment and preserve kidney function. Urine testing may identify infection or another cause of bleeding. [2]
  • Biopsy: A needle biopsy can be useful if its result will change management, particularly before ablation or drug treatment without prior tissue diagnosis. A typical surgically removable solid mass does not always need a biopsy beforehand. A biopsy can occasionally be inconclusive. [2]
  • Further staging: Bone or brain scans are generally reserved for relevant symptoms or suspected advanced disease. Routine PET scans and bone scans are not recommended for initial RCC staging. [2]

The team should review the images, kidney function, other medical conditions and the patient’s priorities together. An indeterminate mass should not be labelled definitively as RCC before appropriate assessment.

A note about my practice: I no longer perform nephrectomies. I can assess your kidney mass, discuss the findings and treatment options with you, and, if an operation is appropriate, refer you to a colleague who performs kidney surgery. We can also arrange input from a multidisciplinary team where needed.

Treatment when the tumour is confined to the kidney

Partial nephrectomy removes the tumour while preserving the rest of the kidney. This is generally preferred for T1 cancers when technically feasible, particularly if kidney function is reduced or there is only one functioning kidney. It can be performed by robotic, laparoscopic or open surgery according to tumour complexity and surgical expertise. Risks include bleeding, urine leak, infection, reduced kidney function and, occasionally, the need to remove the whole kidney. [1]

Radical nephrectomy removes the kidney and may be appropriate when a safe partial nephrectomy is not feasible, particularly with a larger or more complex tumour. Robotic or laparoscopic surgery offers an approach to the operation; it does not change the underlying choice between partial and radical removal. [1]

Active surveillance may suit selected people with a small, slow-growing mass, competing health risks or a strong preference to defer treatment. It involves planned scans and a clear trigger to reconsider treatment. A tumour just above 3 cm needs a particularly careful discussion because the room for further growth before 4 cm is limited. Thermal ablation, such as cryoablation or radiofrequency or microwave ablation, may suit selected small tumours, especially when surgery is unsuitable; a biopsy is recommended before ablation. Local recurrence and the possible need for repeat treatment should be discussed. [1, 2]

Stereotactic ablative radiotherapy (SABR) is also being used in specialist centres for selected patients with localised RCC who cannot undergo surgery. It is a distinct option from routine radiation after an operation, and its long-term comparative evidence continues to mature. [1]

What if lymph nodes look enlarged?

An enlarged node on a scan is suspicious, not proof of cancer; inflammation can also enlarge nodes. The team considers the appearance and site of the nodes, whether there is disease elsewhere and whether tissue confirmation will change treatment. If nephrectomy is planned, visibly enlarged regional nodes may be removed for diagnosis and staging. Removing normal-looking nodes routinely has not been shown to improve survival for organ-confined RCC. The survival benefit of removing involved nodes is uncertain. [1]

Confirmed regional node involvement is a substantial change in risk even if the kidney tumour is small. It calls for multidisciplinary discussion about whether all visible disease can be removed, whether postoperative drug treatment is appropriate, and how closely to monitor. Nodes beyond the regional area, or spread to organs such as the lung or bone, may represent metastatic disease and require a different plan. Surgery on the kidney is not automatically the best first step when cancer is widespread. [1, 3]

When does immunotherapy help?

For selected patients with clear-cell RCC at higher risk of recurrence after complete surgery, a course of pembrolizumab may lower recurrence risk and has shown an overall survival benefit in the KEYNOTE-564 study. The eligible groups include some patients with confirmed regional node involvement and no distant metastases. A 3–4 cm node-negative tumour confined to the kidney would not usually qualify based on size alone. The final pathology, stage and overall health matter. [1, 4]

If cancer has spread and cannot all be removed, initial treatment for clear-cell RCC often combines immune checkpoint drugs with each other (nivolumab plus ipilimumab) or combines immunotherapy with an oral targeted drug (for example, pembrolizumab plus axitinib, pembrolizumab plus lenvatinib, or nivolumab plus cabozantinib). The best regimen depends on risk group, other illnesses, kidney function, previous treatment and the specific cancer subtype. Papillary and other non-clear-cell cancers may need different approaches. Availability and subsidy in Australia should be checked for the individual indication. [1]

Immunotherapy can cause serious inflammation of the bowel, lungs, liver, kidneys or hormone-producing glands; targeted drugs can cause high blood pressure, diarrhoea, fatigue and other adverse effects. Some immune effects can persist after treatment ends. Benefits and risks need an individual discussion with a medical oncologist. [1, 4]

Is chemotherapy useful?

Conventional cytotoxic chemotherapy is generally ineffective for the common types of RCC and is not standard treatment for ordinary clear-cell RCC. Rare subtypes, including collecting duct and renal medullary carcinoma, are exceptions in which chemotherapy may have a role. A cancer arising from the lining of the renal pelvis (upper-tract urothelial carcinoma) is a different disease with different chemotherapy options; establishing the diagnosis matters. [1]

Does radiation offer a benefit?

Radiotherapy is not routinely given after nephrectomy to prevent recurrence of localised RCC. Its clearest established role is treating specific problems from spread, such as painful bone lesions, brain metastases or symptoms from another site. Precisely targeted radiation may also control selected limited metastases or treat a primary tumour in someone unsuitable for surgery. Whether it adds benefit to systemic therapy or surgery in an individual case depends on the site, number and behaviour of lesions and is best decided with radiation oncology input. It should not be presented as a standard substitute for an operable partial nephrectomy. [1, 5]

Questions worth asking at your consultation

  1. Is this definitely a solid enhancing kidney tumour, and what is its exact size and location?
  2. Is the disease confined to the kidney? Are any nodes merely enlarged, or proven to contain cancer?
  3. Can we safely preserve part of the kidney? What is my current kidney function?
  4. Would a biopsy change the plan?
  5. If the cancer is clear-cell and higher risk, would adjuvant pembrolizumab be suitable?
  6. Would drug treatment or targeted radiation offer a benefit in my particular situation?

Seek prompt medical attention for heavy bleeding with clots, inability to pass urine, severe persistent pain, or sudden neurological symptoms. This article is general information and cannot replace review of your scans and pathology at a multidisciplinary meeting.

References

  1. European Association of Urology. EAU Guidelines on Renal Cell Carcinoma: Disease Management. 2026.
  2. European Association of Urology. EAU Guidelines on Renal Cell Carcinoma: Diagnostic Evaluation. 2026.
  3. European Association of Urology. EAU Guidelines on Renal Cell Carcinoma: Staging and Classification Systems. 2026.
  4. National Cancer Institute. Adjuvant Keytruda improves kidney cancer survival, reporting updated KEYNOTE-564 outcomes. 2024.
  5. National Cancer Institute. Renal Cell Cancer Treatment (PDQ), Health Professional Version. Accessed September 2026.

Prostate cancer with kidney failure: is surgery, focal therapy or radiation the right choice?

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A patient guide by Dr Jo Schoeman

A diagnosis of prostate cancer is unsettling. Having chronic kidney disease or needing dialysis can make treatment decisions feel even harder. The reassuring point is that kidney failure does not automatically rule out treatment. The best choice depends on the cancer, the degree of kidney impairment, other medical conditions and, crucially, whether a kidney transplant is planned.

What does Gleason 3+4 mean?

Gleason 3+4=7 is Grade Group 2 prostate cancer. Most of the sampled tumour has pattern 3, with a smaller component of pattern 4. It is generally less concerning than Gleason 4+3=7, but “3+4” alone cannot tell us whether immediate treatment is needed.

I would review the PSA and PSA density, examination, MRI findings, number and length of positive biopsy cores, percentage of pattern 4, any cribriform or intraductal cancer, and whether disease is confined to the prostate. Kidney function, dialysis schedule, life expectancy and transplant eligibility are considered alongside these findings. Some men have favourable intermediate-risk cancer; others have features that make definitive treatment more appropriate. Staging scans are selected according to overall risk rather than biopsy grade alone. [1,2]

Could active surveillance be reasonable?

Yes, for selected men with small-volume, favourable Grade Group 2 cancer. Surveillance means scheduled PSA tests, clinical review, MRI where useful and repeat biopsy when indicated. It keeps treatment available if the cancer changes. It is a particularly meaningful option when another serious illness makes the harms of immediate treatment more likely to outweigh its benefit. It does, however, require a patient who can attend follow-up and accepts a small increased risk of progression compared with immediate treatment. [1,2]

If kidney disease or other illnesses substantially limit life expectancy, watchful waiting may be more appropriate: care focuses on symptoms rather than routine testing intended to trigger curative treatment. This is a separate decision from active surveillance. [1]

Can radical prostatectomy or robotic surgery be performed?

Often, yes. Chronic kidney disease and dialysis are not automatic contraindications to radical prostatectomy. Robotic assisted surgery may offer less blood loss and a shorter hospital stay than open surgery in selected patients, but it still involves general anaesthesia, abdominal insufflation and a head-down operating position. Advanced kidney disease increases the importance of planning for bleeding, infection, fluid and electrolyte balance, medication dosing and postoperative kidney injury. Population studies find higher complication rates in patients with chronic kidney disease, particularly advanced disease; individual risk varies considerably. [3,4]

Before an operation I would coordinate with the nephrologist, anaesthetist and, where relevant, dialysis team. We would assess cardiovascular health, haemoglobin, potassium, anticoagulants, residual kidney function and the timing of dialysis. Surgery also carries the usual risks of urinary leakage or incontinence, erectile dysfunction, infertility, blood clots and possible need for further cancer treatment. Whether a robotic approach is feasible depends on the patient and the surgical team; it is not automatically a safer choice for every person with kidney failure. [1,3,4]

Is focal therapy a better option?

Not simply because the kidneys are failing. Focal therapy treats the visible cancer-bearing portion of the prostate, using a technique such as focused ultrasound, cryotherapy or another ablative method. It may appeal to men hoping to reduce urinary or sexual side effects, but the cancer can be present elsewhere in the gland, and longer-term cancer control is less certain than for established whole-gland treatments. Further MRI, biopsies and sometimes repeat treatment are necessary.

The AUA/ASTRO guideline notes a lack of high-quality comparisons with surgery, radiation and surveillance. European guidance restricts focal treatment to settings with careful prospective follow-up, such as a trial or registry. Kidney disease alone does not establish that focal treatment is preferable. In a suitable patient it can be discussed with a specialist who explains uncertainty, access, costs and a clear follow-up plan. [1,2]

Is radiotherapy an option?

Yes. External beam radiotherapy avoids major surgery and usually does not expose the kidneys directly when treating a prostate confined to the pelvis. Options include moderately shortened courses and, for selected men, more condensed schedules or brachytherapy. The radiation oncologist will tailor treatment to the cancer and urinary function. Depending on whether the disease is favourable or unfavourable intermediate risk, a course of androgen deprivation therapy (ADT) may also be advised; ADT has its own effects on energy, muscle, bone and metabolic health. [1,2]

Radiotherapy may cause temporary urinary frequency, burning or bowel upset; longer-term urinary, bowel or erectile effects are also possible. Existing urinary obstruction and kidney transplant anatomy can change planning. In a transplant recipient, the graft and ureter may sit in the pelvis, so radiation dose constraints require particular attention. Dialysis, by itself, does not make prostate radiation impossible. [1,2]

What if a kidney transplant is planned?

This is a central part of the discussion. A transplant team may need to know whether the cancer is under surveillance or has been treated, its estimated risk of progression and the proposed follow-up. The presence of prostate cancer does not automatically mean that transplantation must wait for a fixed number of years; transplant eligibility is individual and should be discussed directly with the transplant team. A transplanted kidney in the pelvis also affects the planning of later pelvic surgery or radiotherapy. [5]

How do we decide?

Option When it may fit Main trade-off
Active surveillance Low-volume, favourable Grade Group 2 disease Regular testing and a possibility of later treatment
Robotic radical prostatectomy Fit patient seeking definitive local treatment Anaesthetic and surgical risks, with continence and erectile side effects
Radiotherapy Patient seeking definitive treatment without prostate removal Urinary, bowel and sexual effects; ADT may be needed
Focal therapy Carefully selected patient after discussion of uncertainty Less established long-term cancer control and ongoing biopsies
Watchful waiting Limited life expectancy or major competing health risks Treats symptoms if they arise rather than aiming for cure

There is no universal winner between robotic surgery and radiation for Gleason 3+4 cancer with kidney failure. A multidisciplinary discussion involving urology, radiation oncology, nephrology and the transplant team, if applicable, helps align cancer control with kidney health and the patient’s priorities.

This article offers general information and cannot determine treatment for an individual patient. Decisions require review of the pathology, imaging, kidney function and overall health.

References

  1. European Association of Urology. EAU Guidelines on Prostate Cancer: Treatment. Accessed September 2026.
  2. American Urological Association and American Society for Radiation Oncology. Clinically Localized Prostate Cancer Guideline. 2022.
  3. Post-surgical outcomes of patients with chronic kidney disease and end stage renal disease undergoing radical prostatectomy: 10-year results from the US National Inpatient Sample. 2019.
  4. The Effect of Chronic Kidney Disease on Adverse In-Hospital Outcomes at Radical Prostatectomy. 2025.
  5. Kidney Disease: Improving Global Outcomes. KDIGO Clinical Practice Guideline on the Evaluation and Management of Candidates for Kidney Transplantation. 2020.

Urethral bulking for stress urinary incontinence: a first procedure or an option after a sling?

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Leaking urine when you cough, laugh, exercise or lift something is called stress urinary incontinence (SUI). It differs from urgency incontinence, when a sudden need to pass urine leads to leakage. Some women have both. Identifying which symptom is most troublesome matters because an injection aimed at SUI will not reliably treat urgency.

Urethral bulking involves placing small deposits of material into the wall of the urethra, usually through a fine instrument passed into the urethra. The deposits help the urethra close when pressure rises. You may hear this described as periurethral bulking, although many contemporary injections are delivered through the urethra into its surrounding wall. This is generally a day procedure under local anaesthesia or sedation/general anaesthesia, depending on the circumstances. It does not place a sling or mesh tape.

Could bulking be my first procedure?

Yes. After a trial of pelvic floor muscle training and discussion of other conservative measures, bulking can be chosen as a first procedure for appropriately assessed SUI. It may appeal to someone seeking a shorter procedure and recovery, or wishing to avoid a sling. It is also an option when a larger operation or anaesthetic carries additional risk. It is not usually the first treatment before conservative care. USANZ’s 2026 position statement lists bulking alongside autologous fascial slings, colposuspension and synthetic midurethral slings among the standard options that should be discussed. UGSA’s patient information stresses its lower success and frequent need for repeat treatment. [1–3]

Bulking, synthetic midurethral sling surgery, a sling made from the patient’s own fascia, and colposuspension have different benefits and risks. A donated-tissue (allograft) sling is distinct from a sling made from your own tissue (autograft) and from a synthetic mesh sling; the strength and duration of evidence for each are different. No single procedure is best for every woman. [1,4]

How effective and durable is it?

The realistic aim is often less leakage, rather than guaranteed dryness. Success figures change substantially depending on whether researchers count complete dryness, improvement, satisfaction, or avoidance of further treatment. UGSA’s patient leaflet quotes about 40–50% cure or improvement and reports that approximately 30% need a further injection within two years. These are broad counselling figures, not a prediction for an individual. [2]

Some women remain improved for years, but repeat injections or another operation may be needed. In a randomised comparison of polyacrylamide hydrogel injection and synthetic tension-free vaginal tape for primary SUI, the tape achieved better objective continence at one year (negative cough test 95.0% versus 66.4%). The five-year follow-up did not establish that injection was non-inferior to tape. The EAU similarly advises that bulking is generally less effective than slings or colposuspension for cure, and that repeat injection is likely. These findings do not mean everyone should have a tape: the value of a less invasive procedure and the acceptability of a possible repeat treatment are personal considerations. [4–6]

What if I still leak after a sling?

Bulking can be considered for persistent leakage soon after a sling or recurrent leakage after an initial period of improvement. It can sometimes reduce leakage without placing another sling. A 2022 systematic review of 11 studies after synthetic midurethral sling failure reported a pooled 75% cure-or-improvement rate, but also pooled failure and further-operation rates of 32% and 25%. The studies differed considerably in their patients, products, follow-up and definitions of success; the 75% figure should not be presented as a personal chance of cure. An American Urogynecologic Society clinical practice statement also recognises bulking as an option after a sling. [7,8]

After an allograft sling, the same clinical possibility exists, but the published post-sling bulking evidence is mainly about synthetic midurethral slings. We should not simply transfer those success figures to donated-tissue slings. The precise graft, previous surgery and examination findings should guide an individual discussion.

An injection should not be used to mask a sling complication. Before offering more treatment, I would review the original operation, check urine and bladder emptying, examine for prolapse, scarring and vaginal exposure, and assess whether leakage occurs with coughing or with urgency. Cystoscopy, a bladder diary, pad testing or urodynamics may be appropriate, especially after previous surgery, mixed symptoms, pain, blood in the urine or difficulty emptying. A tape or graft causing obstruction, exposure, erosion, infection or pain may require its own assessment and treatment. [1,3,7]

Is it safe? What are the side effects?

Most reported problems are short lived, but no injection is risk free. Possible effects include:

  • burning when passing urine and a little blood in the urine;
  • urinary tract infection;
  • temporary difficulty emptying the bladder, occasionally requiring short-term catheterisation;
  • new or persisting urgency symptoms; and
  • incomplete benefit, recurrence or the need for another injection or operation.

Less commonly, there may be persistent pain, a collection or infection at the injection site, or a reaction or complication related to the particular material. Risks also depend on anaesthesia, previous surgery and the chosen product. Emptying should be checked before discharge. Seek prompt assessment if you cannot pass urine, develop fever, worsening pain or heavy bleeding. [2,4,8]

Choosing a treatment

The first step is to confirm the type and severity of leakage and clarify your goals: complete dryness, meaningful improvement, shorter recovery, avoiding mesh, or avoiding the likelihood of repeat treatment. Pelvic floor therapy remains an initial option. When a procedure is appropriate, we can compare bulking with sling and colposuspension procedures using your examination findings, health history and preferences. If you have already had a sling, the reason for the continuing leakage deserves a fresh assessment before choosing another procedure.

This page is general education, not a recommendation for a particular product or a promise of a result. Treatment, including its material, risks, costs and alternatives, should be discussed during an individual consultation.

References

  1. Urological Society of Australia and New Zealand (USANZ). Surgical Treatment of Stress Urinary Incontinence: Position Statement Pol 054, version 2.0. Approved 9 May 2026.
  2. Urogynaecological Society of Australasia (UGSA). Urethral Bulking: Patient Information.
  3. UGSA. Stress Urinary Incontinence: Patient Resources.
  4. European Association of Urology. Guidelines on Non-neurogenic Female Lower Urinary Tract Symptoms: Disease Management, section 4.2.4.c.2.c.
  5. Itkonen Freitas A-M, et al. Tension-free vaginal tape surgery versus polyacrylamide hydrogel injection for primary stress urinary incontinence: a randomised clinical trial. Journal of Urology. 2020.
  6. Itkonen Freitas A-M, et al. Tension-free vaginal tape versus polyacrylamide hydrogel injection for stress urinary incontinence: five-year follow-up. NEJM Evidence. 2025.
  7. Braga A, et al. Urethral bulking agents for the treatment of recurrent stress urinary incontinence: a systematic review and meta-analysis. Maturitas. 2022. doi:10.1016/j.maturitas.2022.05.007.
  8. American Urogynecologic Society. Urethral Bulking: Clinical Practice Statement. Urogynecology. 2024. doi:10.1097/SPV.0000000000001548.

Tranexamic Acid for Radiation Cystitis: Benefits, Duration and Important Risks

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Blood in the urine after pelvic radiotherapy can be frightening. It may appear months or even many years after treatment for prostate, bladder, rectal or gynaecological cancer. One possible cause is radiation cystitis: delayed injury to the bladder lining and its small blood vessels.

Tranexamic acid is sometimes considered when bleeding is troublesome. It can help stabilise blood clots, but it does not repair the radiation injury itself and it is not suitable for every patient. In urinary tract bleeding, preventing a clot from dissolving may reduce bleeding but may also allow a larger clot to obstruct the bladder or ureter. Careful patient selection and medical supervision are therefore essential.

Seek urgent medical attention if you cannot pass urine, are passing large clots, feel faint or breathless, develop fever or flank pain, or the bleeding is heavy or worsening.

What is radiation cystitis?

Radiotherapy can cause progressive damage to the bladder’s small blood vessels. These vessels may become fragile and bleed easily. Patients may experience visible haematuria, urinary frequency, urgency, pain or recurrent clot retention.

Radiation cystitis should not be assumed simply because a patient has previously received radiotherapy. Infection, urinary stones, recurrent or new cancer, kidney disease and medication-related bleeding must also be considered. Assessment may include urine testing and culture, a full blood count, renal function, imaging of the upper urinary tract and cystoscopy. Biopsy is used selectively because irradiated tissue heals poorly.

How does tranexamic acid work?

The body normally breaks down blood clots through a process called fibrinolysis. Tranexamic acid blocks the binding of plasminogen and plasmin to fibrin, slowing this breakdown. It is therefore an antifibrinolytic medicine: it helps a clot remain in place rather than acting as a blood-clotting factor itself.

For radiation cystitis, tranexamic acid is intended to control active bleeding. It does not remove abnormal radiation-induced blood vessels, reverse fibrosis or prevent future bleeding once the medicine is stopped.

How effective is it for radiation cystitis?

The evidence is limited. Tranexamic acid has been used for haematuria from several causes, and a small randomised emergency-department study found that intravenous treatment reduced the amount of bladder irrigation required to clear the urine. However, it did not significantly reduce haemoglobin loss or transfusion requirements. Importantly, this study included mixed causes of haematuria and was not designed specifically for radiation cystitis.

The Canadian Urological Association best-practice report concluded that evidence was insufficient to make a formal recommendation for tranexamic acid in radiation-induced haemorrhagic cystitis. Later narrative reviews have reached a similar conclusion. Intravesical tranexamic acid, placed directly into the bladder, has shown encouraging results in small emergency-department studies of gross haematuria, but evidence specific to radiation cystitis is still inadequate and this remains a specialist, non-standard use.

In practice, tranexamic acid may be considered as a temporary adjunct in selected patients while the cause and severity of bleeding are assessed, or while more definitive treatment is arranged. It should not delay bladder washout, clot evacuation, cystoscopic treatment, hyperbaric oxygen therapy, embolisation or other appropriate care when these are required.

How long can tranexamic acid be used?

There is no well-supported universal duration for radiation cystitis. The Australian product information for oral tranexamic acid describes treatment of haematuria while blood remains macroscopically visible, but radiation cystitis is a recurrent condition and that instruction should not be interpreted as approval for indefinite therapy.

For this indication, treatment is generally best regarded as a short, medically supervised course for an active bleeding episode. The exact dose and duration depend on:

  • whether bleeding is mild, ongoing or causing clot retention;
  • whether the source is the bladder or upper urinary tract;
  • kidney function, because tranexamic acid is largely eliminated in the urine;
  • previous blood clots, cardiovascular risk and pro-thrombotic medicines;
  • anticoagulant or antiplatelet therapy; and
  • the response to treatment and need for definitive therapy.

There is no good evidence supporting continuous long-term tranexamic acid as prophylaxis for recurrent radiation cystitis. If bleeding has not clearly improved within a short course, recurs promptly after treatment, or requires repeated courses, the diagnosis and management plan should be reassessed. Longer or repeated use should occur only under specialist supervision, with renal function and thrombotic risk reviewed.

Patients should not start, extend, repeat or stop prescribed tranexamic acid without discussing it with their treating clinician.

Important side effects

Common or less serious adverse effects may include:

  • nausea, vomiting, diarrhoea or abdominal discomfort;
  • headache, dizziness or fatigue; and
  • muscle or joint discomfort.

Potentially serious adverse effects include:

Blood clots

Deep-vein thrombosis, pulmonary embolism, stroke, heart attack and other arterial or venous thromboses are uncommon but potentially serious. Risk assessment is particularly important in patients with an active or previous clot, known thrombophilia, active malignancy, prolonged immobility or concurrent pro-thrombotic medication.

Urgent assessment is required for new unilateral leg pain or swelling, sudden chest pain, shortness of breath, coughing blood, weakness on one side, difficulty speaking or sudden severe headache.

Clot retention and urinary obstruction

Tranexamic acid may stabilise clots within the urinary tract. This can contribute to painful bladder clot retention. It is particularly concerning when bleeding arises from a kidney or ureter, because a clot may obstruct the ureter and cause flank pain, hydronephrosis or loss of kidney function. Upper-tract haematuria therefore warrants particular caution and specialist assessment.

Kidney impairment

Most tranexamic acid is excreted unchanged through the kidneys. The dose must be reduced when renal function is impaired; accumulation increases the risk of toxicity, including neurological adverse effects. Significant renal impairment may make treatment inappropriate or require a substantially altered regimen.

Seizures

Seizures are a recognised, dose-related risk, reported particularly with high intravenous doses and when the medicine accumulates in renal impairment. A history of seizures requires careful consideration.

Visual disturbance

Rare visual effects, including altered colour vision, have been reported. New visual symptoms require prompt review and usually discontinuation pending medical advice. Ophthalmic monitoring may be considered when prolonged treatment is unavoidable.

Severe allergy

Facial or throat swelling, wheeze, breathing difficulty or a widespread blistering rash requires emergency care.

Who may not be suitable for treatment?

Tranexamic acid may be contraindicated or require particular caution in people with:

  • active thromboembolic disease or a substantial history or risk of thrombosis;
  • significant kidney impairment;
  • upper urinary tract bleeding or suspected ureteric obstruction;
  • a history of seizures;
  • acquired disturbances of colour vision;
  • disseminated intravascular coagulation unless managed by an experienced clinician; or
  • hypersensitivity to tranexamic acid.

Medication review is essential. Anticoagulants and antiplatelet agents can worsen bleeding, but stopping them may cause stroke, pulmonary embolism, heart attack or coronary-stent thrombosis. They should not be stopped merely because haematuria develops without an individual risk assessment involving the prescribing clinician. Likewise, combining tranexamic acid with pro-thrombotic medicines requires caution.

Where does it fit in the management pathway?

Management is guided by severity. Initial care may include resuscitation, correction of significant anaemia or coagulopathy, a large-bore catheter, manual washout and continuous bladder irrigation. Cystoscopy permits clot evacuation, exclusion of tumour and cautery or laser treatment of bleeding areas.

For persistent or recurrent radiation cystitis, options may include intravesical agents, hyperbaric oxygen therapy, selective arterial embolisation and, rarely, urinary diversion or cystectomy. Hyperbaric oxygen is one of the better-studied treatments because it aims to improve tissue oxygenation and new blood-vessel formation rather than merely suppressing an episode of bleeding.

Tranexamic acid may have a role as a bridge or adjunct in a carefully selected patient. Its value must always be balanced against the danger of thrombosis and urinary tract obstruction.

The take-home message

Tranexamic acid can reduce haematuria in some patients, but evidence specifically for radiation cystitis is weak. It is not a cure and should usually be used only for a short, active bleeding episode under medical supervision. There is no established safe or effective duration for continuous long-term use in radiation cystitis. Kidney function, clotting history, the anatomical source of bleeding and concurrent medication must be reviewed before treatment.

Visible haematuria after radiotherapy always deserves proper investigation, particularly if it is recurrent, contains clots or is accompanied by difficulty passing urine.

This article provides general information and does not replace individual medical advice. Tranexamic acid is a prescription medicine in Australia; its use for radiation cystitis must be individualised by the treating clinician.

References

  1. Goucher G, Saad F, Lukka H, Kapoor A. Canadian Urological Association Best Practice Report: Diagnosis and management of radiation-induced hemorrhagic cystitis. Can Urol Assoc J. 2019;13(2):15–23. doi:10.5489/cuaj.5788
  2. Moharamzadeh P, Ojaghihaghighi S, Amjadi M, Rahmani F, Farjamnia A. Effect of tranexamic acid on gross hematuria: a pilot randomized clinical trial study. Am J Emerg Med. 2017;35(12):1922–1925. doi:10.1016/j.ajem.2017.09.012
  3. Abramowitz D, et al. Clinical management of radiation cystitis: a narrative review. AME Med J. 2021;6:30. Clinical management of radiation cystitis
  4. Choi H, et al. Impact of intravesical administration of tranexamic acid on gross hematuria in the emergency department: a before-and-after study. Am J Emerg Med. 2023;68:118–122. doi:10.1016/j.ajem.2023.03.010
  5. Pfizer Australia. Cyklokapron (tranexamic acid) Australian Product Information. Current product information should be checked through the Therapeutic Goods Administration or the sponsor before prescribing. Australian product information
  6. DailyMed. Tranexamic acid injection—prescribing information. US National Library of Medicine. DailyMed drug labelling
  7. Chauncey JM, Wieters JS. Tranexamic Acid. In: StatPearls. Updated 2025. NCBI Bookshelf

 

Prostate Artery Embolisation: Who May Benefit, Important Caveats, and Can It Be Done After Radiotherapy?

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Lower urinary tract symptoms: poor flow, hesitancy, incomplete emptying, frequency, urgency and nocturia, are common as men age. When benign enlargement of the prostate (BPH) is genuinely responsible, treatment may include lifestyle measures, medication, minimally invasive procedures or surgery. Prostate artery embolisation (PAE) is one option that may be considered for appropriately assessed patients.

PAE is not simply a “smaller TURP”. It works differently, is performed by an experienced interventional radiologist, and has a different balance of benefits, limitations and risks. The most important question is not whether the prostate looks large, but whether prostatic obstruction is actually causing the patient’s symptoms.

What is prostate artery embolisation?

PAE is a minimally invasive, image-guided procedure. A small catheter is introduced through an artery, usually at the wrist or groin, and guided into the arteries supplying the prostate. Tiny permanent particles or, in selected expert practice, a liquid embolic agent are delivered to reduce blood flow to the hyperplastic prostate tissue. This causes controlled ischaemia, gradual shrinkage of the transition zone and reduced compression of the urethra.

The procedure can often be performed without a general anaesthetic and does not require instruments to pass through the urethra. Improvement, when it occurs, is usually progressive rather than immediate and may take several weeks or months. Results vary, and some men obtain little benefit or require another treatment.

Regulatory note for Australian readers: The TGA regulates therapeutic goods, including medicines and medical devices; it does not “approve” or endorse a medical procedure or an individual health service. References to PAE in this article should not be interpreted as TGA endorsement. Any embolic agent, catheter or other medical device used must be lawfully supplied in Australia and used in accordance with its applicable regulatory status, intended purpose and clinical governance requirements.

Important Wesley Hospital research

Associate Professor Nicholas Brown, an interventional radiologist affiliated with The University of Queensland and I-MED Radiology at The Wesley Hospital, led the following Australian studies of PAE.

The P-EASY ADVANCE randomised controlled trial, published in BJU International in 2024, compared PAE with combined tamsulosin and dutasteride therapy in 39 treatment-naïve men with enlarged prostates, moderate-to-severe symptoms and obstructed or equivocal urodynamic studies. At follow-up, 63% of men treated with PAE were urodynamically unobstructed, compared with 28% receiving medication. Within this study population and follow-up period, the PAE group had greater improvements in prostate volume, urinary flow, incomplete emptying, overall symptom score and quality of life. The trial was small, the estimates should not be generalised to every patient, and larger comparative trials with longer follow-up are required.

The follow-up P-EASY PLUS study, published in BJU International in 2025, assessed 105 men at a mean of 18 months. Mean prostate volume fell by 30.6%, total symptom scores improved by 55%, quality-of-life scores improved by 65.9%, and maximum urinary flow increased by 5 mL/second. Among the 57 men who completed paired urodynamic testing, the proportion classified as obstructed fell from 66.7% to 29.8%. No major procedural complication or new urinary incontinence was reported in this cohort; new retrograde ejaculation occurred in 2%. These are group-level study outcomes and do not guarantee an individual result. The authors noted that longer-term comparative research is required.

The P-EASY ADVANCE publication received the BJUI Global Prize for 2026. This statement describes the publication award only; it is not a patient-outcome claim, regulatory endorsement or guarantee of treatment effectiveness.

Author disclosure: I, Dr Joseph Schoeman, was a co-author of both Wesley Hospital studies. I performed some of the urodynamic studies for this article. Readers should take this relationship into account when considering the discussion. The results are reported with their limitations and placed alongside independent guidelines, randomised trials and systematic reviews. No patient testimonial or individual outcome has been used in this article.

Who may be a good candidate?

PAE may be considered when a man has:

  • bothersome moderate-to-severe urinary symptoms attributable to benign prostatic obstruction;
  • an enlarged prostate, particularly a moderately large or very large gland;
  • inadequate relief, unacceptable adverse effects or a preference not to take long-term medication;
  • a wish to avoid transurethral or more invasive surgery;
  • increased anaesthetic or surgical risk;
  • a preference for an option with lower reported rates of ejaculatory dysfunction or urinary incontinence in some studies, while recognising that these complications can still occur;
  • catheter-dependent urinary retention where obstruction from BPH is considered reversible and bladder contractility is adequate; or
  • recurrent or refractory bleeding shown to arise from the prostate in selected circumstances.

Current European Association of Urology guidance recommends offering PAE to men with moderate-to-severe LUTS due to benign prostatic obstruction who want a minimally invasive option and accept that outcomes may be less optimal than TURP. The American Urological Association also permits PAE as a treatment option when performed by appropriately trained clinicians, but grades the evidence as conditional.

What assessment is needed before PAE?

A large prostate does not prove obstruction, and urinary symptoms are not always caused by the prostate. Appropriate assessment may include:

  • symptom and quality-of-life scoring;
  • urinalysis and urine culture when indicated;
  • PSA assessment and prostate-cancer evaluation appropriate to age and risk;
  • digital rectal examination;
  • urinary flow rate and post-void residual measurement;
  • ultrasound or MRI assessment of prostate size and anatomy;
  • cystoscopy where haematuria, urethral stricture, bladder-neck pathology, stones or bladder disease is suspected;
  • urodynamic studies when the diagnosis is uncertain, symptoms are mixed, bladder contractility may be poor, or prior pelvic treatment has complicated the picture; and
  • CT or MR angiographic assessment of pelvic arterial anatomy, renal function and contrast risk when requested by the interventional radiologist.

The best decisions are generally made jointly by a urologist and an experienced PAE interventional radiologist.

Potential advantages of PAE

Potential advantages include:

  • no prostate tissue resection and usually no general anaesthetic;
  • day-stay or short hospital admission in many patients;
  • lower reported rates of major bleeding and transfusion than some operative procedures in comparative studies;
  • low reported, but not zero, rates of urinary incontinence;
  • a lower reported likelihood of retrograde ejaculation than with TURP or enucleation procedures in available studies;
  • usefulness in some very large prostates and medically complex patients; and
  • preservation of later surgical options if symptoms persist or recur.

Caveats: what PAE may not do as well

Compared with TURP or endoscopic enucleation, PAE generally produces a less immediate and less pronounced improvement in urinary flow and objective relief of obstruction. A Cochrane review found that short-term symptom improvement may be similar to TURP, but the certainty of evidence was low and retreatment may be more likely after PAE. Meta-analyses and longer-term randomised data generally show stronger objective improvement after TURP. Comparisons across studies must be interpreted cautiously because patient selection, technique, follow-up and outcome definitions differ.

PAE also does not provide prostate tissue for histology. Prostate cancer must therefore be considered and investigated before treatment rather than assumed to be excluded by a fall in prostate size or PSA afterward.

Technical success depends heavily on operator experience. Prostatic arteries are tiny, variable and sometimes severely atherosclerotic. Embolic material can rarely reach non-target vessels supplying the bladder, rectum or penis. Pre-procedure vascular imaging and cone-beam CT can reduce this risk but add iodinated contrast exposure and ionising radiation.

Side effects and complications

Common short-term effects form part of a post-embolisation syndrome and may include pelvic or perineal discomfort, urinary frequency and urgency, dysuria, fatigue, nausea, low-grade fever or a small amount of blood in the urine or semen. Temporary difficulty passing urine and the need for a catheter can occur.

Less common complications include urinary infection, access-site bruising or haematoma, contrast reaction, kidney injury, arterial injury, prostate infection or abscess, and passage of necrotic prostate tissue. Rare but important complications of non-target embolisation include ischaemic injury to the bladder, rectum or penis. Severe skin injury from fluoroscopic radiation is also rare but is a recognised procedural concern, particularly during prolonged or technically difficult cases.

Contraindications and reasons to pause

PAE is generally unsuitable, or requires correction and specialist review first, when there is:

  • an active urinary tract or systemic infection;
  • suspected or untreated prostate or bladder cancer requiring diagnostic clarification;
  • symptoms predominantly caused by urethral stricture, bladder-neck contracture, bladder stone, neurogenic dysfunction, overactive bladder or another non-BPH condition;
  • a poorly contractile or decompensated bladder unlikely to empty even if outlet resistance is reduced;
  • severe pelvic arterial atherosclerosis, occlusion, tortuosity or anatomy that prevents safe selective catheterisation;
  • an uncorrectable bleeding disorder;
  • a severe iodinated-contrast allergy that cannot be safely managed;
  • significant renal impairment where contrast risk is unacceptable; or
  • inability to tolerate arterial access, fluoroscopy or the required aftercare.

Small prostate size is not an absolute prohibition, but it makes careful confirmation of the cause of obstruction particularly important and may reduce the likelihood of benefit. A prominent obstructing median lobe is not automatically a contraindication in experienced hands, although prostate anatomy should be considered alongside all alternative treatments.

Can PAE be performed after prostate radiotherapy?

Potentially yes, but prior pelvic or prostate radiotherapy is not a routine indication, and the decision must be individualised. It is neither sensible to call radiotherapy an automatic absolute contraindication nor appropriate to assume that PAE will relieve every post-radiation urinary symptom.

After radiotherapy, poor flow, urgency, frequency, pain, retention or bleeding may result from:

  • persistent benign prostatic obstruction;
  • radiation cystitis and reduced bladder capacity;
  • detrusor overactivity or poor bladder contractility;
  • urethral stricture or bladder-neck stenosis;
  • prostate-cancer recurrence or progression;
  • infection, stones or clot retention; or
  • a combination of these problems.

PAE is most likely to help only when a meaningful component of the problem is supplied by vascular, enlarged prostate tissue or confirmed prostatic obstruction. It will not correct a urethral stricture, a scarred bladder neck, radiation cystitis, a small fibrotic low-capacity bladder or detrusor failure.

Evidence specifically studying PAE for BPH-type obstruction after completed radiotherapy is sparse. Most major BPH trials did not establish a dedicated post-radiotherapy evidence base. Radiotherapy can also alter pelvic tissues and small blood vessels, making angiographic anatomy and tissue response less predictable. For that reason, these patients should be assessed in a multidisciplinary setting and often benefit from cystoscopy, flow and residual testing, imaging and formal urodynamics before treatment.

PAE has been studied in men with prostate cancer and is being investigated before radiotherapy to reduce gland size and urinary symptoms. Embolisation has also been used for refractory bleeding of prostatic origin, including bleeding associated with malignancy or radiation. However, embolisation for life-threatening radiation-related haematuria may target vesical or other pelvic arteries and is a different clinical problem from PAE for benign outlet obstruction. These two indications should not be confused.

In a post-radiotherapy patient, PAE may therefore be reasonable when:

  1. recurrent cancer, infection and urethral or bladder-neck stenosis have been excluded or appropriately managed;
  2. investigations demonstrate an enlarged, vascular prostate with genuine outlet obstruction;
  3. bladder function is adequate enough to benefit from reducing resistance;
  4. pelvic arterial anatomy permits safe selective embolisation; and
  5. the patient understands that outcome data are limited and that further treatment may still be required.

How does PAE compare with surgery?

There is no universally “best” procedure. TURP, GreenLight laser, HoLEP or other enucleation procedures usually provide faster and more complete mechanical relief of obstruction. PAE is less invasive and some comparative studies report fewer ejaculatory or perioperative adverse effects; however, symptom relief can be slower, objective improvement may be smaller and retreatment may be more likely.

The right option depends on prostate size and configuration, the severity and cause of symptoms, bladder function, cancer risk, medical fitness, sexual priorities, arterial anatomy, previous pelvic treatment and the patient’s tolerance for the possibility of later retreatment.

The take-home message

PAE is an available treatment option for selected men with symptomatic benign prostatic obstruction. The Wesley Hospital P-EASY studies contribute Australian randomised and urodynamic data on symptoms, quality of life and obstruction, but their findings should be considered with the study designs, sample sizes, follow-up and declared author relationships.

It remains essential to diagnose the cause of symptoms before treating the scan. PAE is not a cure for every urinary problem and does not replace cancer assessment, cystoscopy or urodynamics when these are clinically indicated. After radiotherapy, PAE may be technically and clinically possible, but the evidence is limited and patient selection must be particularly rigorous.

References and further reading

  1. Brown N, et al. P-EASY ADVANCE: a randomised controlled trial of prostate embolisation versus medication for BPH. BJU International. 2024. doi: 10.1111/bju.16479.
  2. Brown N, et al. P-EASY PLUS: preliminary and follow-up urodynamic studies. BJU International. 2025. doi: 10.1111/bju.16808.
  3. Mark P, Brown NI, Ormiston WEL. Current considerations in prostate artery embolisation. CVIR Endovascular. 2026;9:45. doi: 10.1186/s42155-026-00689-5.
  4. European Association of Urology. Guidelines on the Management of Non-neurogenic Male LUTS: Disease Management. Current online edition accessed September 2026.
  5. Sandhu JS, et al. Management of Lower Urinary Tract Symptoms Attributed to BPH: AUA Guideline Amendment 2023. Journal of Urology. 2024;211:11–19. doi: 10.1097/JU.0000000000003698.
  6. Jung JH, et al. Prostatic arterial embolisation for the treatment of lower urinary tract symptoms in men with BPH. Cochrane Database of Systematic Reviews. 2022. Cochrane evidence summary.
  7. Müllhaupt G, et al. Prostatic artery embolisation versus TURP for benign prostatic obstruction: long-term outcomes of a randomised trial. European Urology. 2024. PubMed record.
  8. Zumstein V, et al. Prostatic artery embolization versus standard surgical treatment for LUTS secondary to BPH: systematic review and meta-analysis. European Urology Focus. 2019;5:1091–1100. doi: 10.1016/j.euf.2018.09.005.
  9. Parikh N, et al. Prostate artery embolization in the setting of prostate cancer. Seminars in Interventional Radiology. 2025. Full text.
  10. Kably I, et al. Prostatic artery embolization in refractory haematuria of prostatic origin. Techniques in Vascular and Interventional Radiology. 2020. PubMed record.
  11. Therapeutic Goods Administration. Advertising health services that involve therapeutic goods. Updated 18 June 2026.
  12. Therapeutic Goods Administration. General requirements for advertising therapeutic goods to the public. Updated 11 March 2025.
  13. Australian Health Practitioner Regulation Agency. Advertising guidelines and other guidance. Accessed 22 September 2026.

Australian publication and advertising statement

This article is intended as balanced disease and treatment education. It does not advertise a named embolic product, catheter, medicine or device; offer an inducement; use testimonials; promise a cure; or claim that PAE is safe, risk-free, superior or effective in every case. Mention of the TGA, Ahpra, professional guidelines, a hospital, a journal or an award does not imply endorsement of this article, the author or the treatment.

Clinical claims are linked to identified publications and should be reviewed when the article is updated. Any future addition of brand names, booking prompts, prices, before-and-after images, patient stories, sponsored links or manufacturer-supplied material may change the regulatory character of the page and should undergo a fresh compliance review.

This article provides general information current at the stated review date and is not personal medical advice. It does not establish a doctor–patient relationship. Benefits and risks differ between individuals. Suitability for PAE should be decided after assessment by appropriately qualified clinicians, commonly including a urologist and an interventional radiologist. Patients should seek urgent medical care for inability to pass urine, fever or sepsis symptoms, severe pain, heavy bleeding or clot retention.

PAE BJU article

Blood in the Urine After Radiotherapy: Understanding Radiation Cystitis

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Pelvic radiotherapy is an important and often highly effective treatment for prostate, bladder, rectal and gynaecological cancers. However, radiation can leave the small blood vessels and lining of the bladder fragile. Months or even many years later, this may cause urinary symptoms or bleeding known as radiation cystitis. When bleeding is prominent, the condition is also called radiation-induced haemorrhagic cystitis.

Most episodes can be controlled, but visible blood in the urine must never simply be attributed to previous radiotherapy. Infection, urinary stones, recurrent cancer and a new bladder or upper urinary tract cancer must first be considered.

Seek urgent medical care if you cannot pass urine, are passing large clots, feel faint or short of breath, develop fever or severe pain, or have heavy ongoing bleeding.

What causes radiation cystitis?

Radiotherapy damages cancer cells, but the bladder may receive some radiation because it lies close to the treatment area. Early inflammation can make the bladder lining swollen and irritable. Late injury is different: progressive damage to small blood vessels causes reduced oxygen supply, scarring and fragile abnormal vessels called telangiectasia. These vessels may bleed with little provocation.

Radiation damage can also reduce bladder capacity and elasticity. In severe cases, ulceration, fibrosis, fistula formation or obstruction may occur.

When does it present?

Radiation-related bladder problems have two broad patterns:

  • Acute radiation cystitis occurs during radiotherapy or within the first few weeks or months. Frequency, urgency, burning and pelvic discomfort are common; substantial bleeding is less usual. Symptoms often settle after treatment finishes.
  • Late radiation cystitis generally begins more than six months after radiotherapy and may appear years or even decades later. The Canadian Urological Association review notes pathological vascular changes from about 6–12 months, with new symptoms reported as long as 20 years after treatment.

The risk varies with radiation dose and field, treatment technique, previous pelvic surgery, smoking, vascular disease, diabetes and combined cancer treatments.

How can it present?

Presentation ranges from microscopic blood found on a urine test to recurrent heavy bleeding with clots. Symptoms may include:

  • pink, red or cola-coloured urine;
  • small or large blood clots;
  • urinary frequency, urgency, burning or bladder pain;
  • interrupted flow or complete retention when clots obstruct the outlet;
  • tiredness, dizziness or breathlessness from anaemia; and
  • a small, painful or poorly compliant bladder in advanced disease.

Bleeding may be intermittent. A clear urine sample between episodes does not exclude radiation cystitis.

Does anticoagulant or antiplatelet therapy matter?

Anticoagulants such as warfarin, apixaban, rivaroxaban or dabigatran, and antiplatelet drugs such as aspirin or clopidogrel, do not create radiation cystitis. They can, however, make bleeding from its fragile vessels more prolonged or severe. Excess anticoagulation, impaired kidney function, drug interactions and combined anticoagulant–antiplatelet therapy can further increase bleeding risk.

These medicines may be preventing a stroke, heart attack, pulmonary embolus or thrombosis of a coronary stent. Do not stop them yourself. During significant bleeding, the urologist, emergency team and the clinician responsible for the medication should jointly balance:

  • the severity of bleeding and haemoglobin fall;
  • the reason for treatment and the risk of thrombosis if it is interrupted;
  • the last dose, kidney function and, for warfarin, the INR;
  • whether a temporary hold, reversal or dose adjustment is justified; and
  • when and how treatment should safely restart.

Importantly, anticoagulant or antiplatelet use does not remove the need to investigate haematuria. It may reveal bleeding from an otherwise silent bladder or upper-tract tumour.

How is haematuria investigated after radiotherapy?

Assessment is tailored to the patient and severity, but commonly includes:

  1. History and examination: radiation site, dose and timing; cancer history; smoking; infection symptoms; bleeding pattern; and all medicines.
  2. Urine testing: urinalysis and culture. Urine cytology may be appropriate in selected patients, but it does not replace cystoscopy.
  3. Blood tests: full blood count, kidney function and coagulation studies. Severe or ongoing bleeding may require group-and-screen or crossmatch.
  4. Imaging of the upper urinary tracts: usually CT urography when appropriate; ultrasound or alternative imaging may be chosen when contrast or radiation exposure is unsuitable.
  5. Cystoscopy: inspection of the urethra and bladder to identify typical diffuse telangiectasia, exclude a tumour, evacuate clots and sometimes cauterise bleeding vessels. Suspicious areas require biopsy, performed carefully because irradiated tissue heals poorly.

A stepwise approach to treatment

Treatment depends on the rate of bleeding, clot retention, anaemia, bladder function, medical fitness and local expertise. No single treatment suits every patient.

1. Stabilisation and bladder drainage

Heavy bleeding may require hospital admission, intravenous fluids, correction of anaemia or clotting abnormalities, and blood transfusion when clinically necessary. A large three-way catheter permits manual clot washout and continuous bladder irrigation with saline. Persistent clots may require cystoscopic evacuation under anaesthesia.

Treat a proven urinary infection, but antibiotics do not treat sterile radiation injury. Medication contributing to bleeding should be reviewed collaboratively rather than stopped automatically.

2. Cystoscopy and endoscopic haemostasis

Cystoscopy can confirm the diagnosis and exclude malignancy. Focal bleeding may be treated with diathermy, laser or another endoscopic coagulation technique. This is often effective initially, although diffuse disease may recur and repeated aggressive cautery can worsen scarring or perforation risk.

3. Intravesical and systemic options

Options used for persistent or recurrent bleeding include:

  • Alum bladder irrigation: may control bleeding relatively quickly, but recurrence is possible. It requires caution in substantial kidney impairment because aluminium toxicity can occur.
  • Hyaluronic acid, sometimes combined with chondroitin sulphate: aims to restore the bladder’s protective lining. Evidence suggests benefit for haematuria and urinary symptoms, but treatment is gradual and is not suitable for an unstable major bleed.
  • Oral sodium pentosan polysulphate: has limited, slower-onset evidence. Long-term exposure also requires discussion of pigmentary maculopathy and eye monitoring.
  • Other agents have been reported, but supporting evidence is generally limited.

Formalin can rapidly seal bleeding vessels but may cause severe pain, bladder contraction, reflux, ureteric damage, fistula or systemic complications. It is therefore reserved for life-threatening or otherwise uncontrollable bleeding, used at the lowest effective concentration by experienced teams after the upper tracts have been assessed and protected.

4. Hyperbaric oxygen therapy

Hyperbaric oxygen therapy (HBOT) is one of the best-studied treatments for persistent late radiation cystitis. The patient breathes 100% oxygen in a pressurised chamber. This increases tissue oxygen levels and encourages new blood-vessel growth and healing in chronically oxygen-deprived bladder tissue; it is not simply a short-lived attempt to “oxygenate the blood.”

How effective is it?

The evidence is encouraging, although success definitions and patient populations vary:

  • A meta-analysis cited by the Canadian Urological Association included 602 patients with at least one year of follow-up; 84% achieved partial or complete resolution of haematuria.
  • The multicentre randomised RICH-ART trial found a clinically meaningful improvement in patient-reported urinary symptoms after HBOT compared with standard care. At five years, 48 of 70 followed patients (68.6%) met the study’s responder definition, and the mean improvement among responders remained substantial. This supports durability for many—but not all—patients.
  • HBOT is not guaranteed. Some patients have incomplete improvement, relapse, or still require endoscopic or more invasive treatment. Earlier referral after recurrent bleeding may be preferable to waiting until the bladder is severely fibrotic or the patient has needed repeated transfusions.

How long does it take?

A usual course is 30–40 weekday sessions, sometimes more. Each treatment commonly involves approximately 80–90 minutes breathing oxygen at pressure, although total chamber time is longer. In practical terms, treatment usually takes six to eight weeks. Benefit may develop during the course and continue over subsequent weeks or months as tissue healing progresses.

HBOT is unsuitable or requires specialist assessment in some circumstances. An untreated pneumothorax is an absolute contraindication. Ear or sinus pressure injury, temporary visual change, claustrophobia and, rarely, oxygen-related seizure can occur. Lung disease, certain chemotherapy drugs, implanted devices and difficulty equalising ear pressure require individual review. Availability and daily travel are practical limitations.

5. Arterial embolisation

For ongoing significant bleeding despite less invasive measures, selective or super-selective embolisation can block the bleeding arterial supply. Modern targeted techniques reduce, but do not eliminate, risks such as pelvic pain, tissue ischaemia and non-target embolisation. It can be valuable in frail patients who are poor candidates for major surgery.

When should urinary diversion be considered?

Urinary diversion is a last-resort, potentially life-saving strategy, not an early treatment for uncomplicated bleeding. It should be discussed in a multidisciplinary setting at an experienced centre when there is:

  • life-threatening, transfusion-dependent or recurrent clotting haematuria despite endoscopic treatment, HBOT, appropriate intravesical therapy and/or embolisation;
  • a severely contracted, painful, non-functional bladder with intolerable frequency or poor storage;
  • fistula, necrosis, major outlet or ureteric damage, or progressive upper-tract deterioration;
  • repeated admissions and unacceptable loss of quality of life; or
  • inability to control bleeding safely by less invasive means.

Options include nephrostomy tubes or ureteric occlusion as temporary or palliative measures; cutaneous ureterostomy; or an ileal conduit. Diversion without removing the bladder may be considered in a very high-risk patient, but the retained irradiated bladder can continue to bleed, become infected or painful, and may later require surgery. Cystectomy with diversion provides definitive removal of the diseased bladder but is a major operation. Previous radiation makes tissue planes, healing and bowel surgery more difficult, so complication and mortality rates are substantially higher than for routine cystectomy.

The decision should incorporate the patient’s cancer status, cardiovascular and respiratory fitness, frailty, kidney and bowel function, previous operations, goals of care and willingness to manage a stoma or external drainage.

The practical message

Radiation cystitis may appear long after the original cancer treatment and can range from mild intermittent haematuria to a medical emergency. Blood-thinning medication may worsen the episode, but it should neither be blamed as the sole cause nor stopped without a coordinated medical plan. A careful evaluation to exclude malignancy and other treatable causes comes first.

Management is progressive: stabilisation and irrigation, cystoscopic treatment, selected bladder therapies, HBOT and embolisation before major diversion surgery. HBOT offers worthwhile, durable improvement for many appropriately selected patients, but requires a substantial weekday treatment commitment. Diversion is reserved for a devastated bladder or bleeding that remains dangerous despite comprehensive treatment.

References

  1. Goucher G, Saad F, Lukka H, Kapoor A. Canadian Urological Association Best Practice Report: Diagnosis and management of radiation-induced hemorrhagic cystitis. Can Urol Assoc J. 2019;13(2):15–23. doi:10.5489/cuaj.5788
  2. Oscarsson N, Müller B, Rosén A, et al. Radiation-induced cystitis treated with hyperbaric oxygen therapy (RICH-ART): a randomised, controlled, phase 2–3 trial. Lancet Oncology. 2019;20(11):1602–1614. doi:10.1016/S1470-2045(19)30494-2
  3. Abramowitz DJ, Warner JN. Clinical management of radiation cystitis: a narrative review. AME Med J. 2021;6:9. doi:10.21037/amj-20-62
  4. Liem X, Saad F, Delouya G. A practical approach to the management of radiation-induced hemorrhagic cystitis. Drugs. 2015;75:1471–1482. doi:10.1007/s40265-015-0443-5
  5. Smit SG, Heyns CF. Management of radiation cystitis. Nat Rev Urol. 2010;7:206–214. doi:10.1038/nrurol.2010.23
  6. AUA/SUFU. Microhematuria Guideline (2020; amended 2025). American Urological Association. AUA guideline
  7. Oscarsson N, Rosén A, Müller B, et al. Radiation-induced cystitis treated with hyperbaric oxygen therapy (RICH-ART): long-term follow-up of a randomised controlled, phase 2–3 trial. EClinicalMedicine. 2025;83:103214. doi:10.1016/j.eclinm.2025.103214
  8. Yang TK, Wang YJ, Li HJ, et al. Efficacy and safety of hyperbaric oxygen therapy for radiation-induced hemorrhagic cystitis: a systematic review and meta-analysis. J Clin Med. 2024;13(16):4724. doi:10.3390/jcm13164724

This article provides general information and does not replace individual medical advice. Treatment availability and suitability vary. Visible haematuria, particularly with clots or difficulty passing urine, requires prompt medical assessment.

Cxbladder Urine Testing for Urothelial Cancer: Diagnosis, Surveillance, Accuracy and Pitfalls

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Bladder cancer surveillance can feel repetitive: another cystoscopy, another urine sample and another anxious wait. This has driven interest in urine-based molecular tests that may help identify patients at very low risk of recurrent urothelial carcinoma.

One such platform is Cxbladder. It is sometimes informally called “Cx View,” but the established commercial name is Cxbladder. The version designed for patients who already have a history of urothelial cancer is Cxbladder Monitor.

Cxbladder can provide useful additional information, particularly when the clinical question is whether cancer is unlikely to be present. However, it is not a stand-alone diagnosis, does not show where a tumour is located and should not automatically replace cystoscopy, imaging or biopsy.

What is the Cxbladder test?

Cxbladder is a non-invasive laboratory test performed on voided urine. It measures the expression of five messenger RNA biomarkers associated with urothelial carcinoma:

  • IGFBP5
  • HOXA13
  • MDK
  • CDK1
  • CXCR2

The result is calculated using a proprietary algorithm. Depending on the particular Cxbladder assay, clinical variables may also be incorporated into risk assessment.

The test looks for a molecular signal shed into urine by urothelial cancer cells. It does not provide a picture of the bladder, determine tumour size or location, reliably assign stage or grade, or replace histopathological examination.

The different Cxbladder tests are not interchangeable

The name “Cxbladder” covers several tests developed for different clinical settings.

Cxbladder Triage

This is designed primarily to help identify patients with haematuria who have a low probability of urothelial cancer. It prioritises sensitivity and negative predictive value, accepting lower specificity.

Cxbladder Detect

This is intended to help identify urothelial cancer in patients undergoing diagnostic evaluation, such as those presenting with haematuria. It is not specifically designed for post-treatment surveillance.

Cxbladder Monitor

This is designed for patients with a previous diagnosis of urothelial carcinoma who are undergoing surveillance for recurrence. It is the most relevant assay for follow-up after treatment of non-muscle-invasive bladder cancer (NMIBC).

Newer or region-specific Cxbladder combinations may use different algorithms and thresholds. Performance figures from one assay should not be transferred uncritically to another.

How is the sample collected?

The patient provides a voided urine sample into the supplied collection system. No catheter is normally required. The sample is stabilised and sent to a specialised laboratory for analysis.

Collection instructions must be followed carefully. Insufficient urine, incorrect handling, contamination, excessive delay or failure to use the correct collection container may produce an invalid or unreliable result. A repeat sample may occasionally be required.

What role can Cxbladder have in initial diagnosis?

For a patient with visible or microscopic haematuria, Cxbladder may help refine the estimated probability of urothelial cancer. A low-risk result can be reassuring, especially in a carefully selected lower-risk patient.

However, haematuria can be caused by bladder cancer, upper-tract urothelial cancer, renal cancer, urinary stones, infection, benign prostate bleeding and other conditions. A urine biomarker cannot evaluate all these causes. Depending on age, symptoms and risk factors, the patient may still require cystoscopy and upper-tract imaging.

Current guideline-based haematuria assessment is risk stratified. Urine markers may support shared decision-making in selected patients, but should not delay investigation of visible haematuria or replace a complete assessment in a patient at significant risk.

How may Cxbladder Monitor be used in surveillance?

After treatment of NMIBC, conventional surveillance may include:

  • cystoscopy;
  • urine cytology in selected intermediate- and high-risk patients;
  • upper-tract imaging when indicated; and
  • biopsy or TURBT when a suspicious lesion is found.

Cxbladder Monitor may be added to this pathway to help identify patients with a low probability of recurrent disease. In selected lower-risk situations, a negative result may support extending the interval to cystoscopy or avoiding an additional cystoscopy, provided this forms part of a urologist-directed protocol.

A positive result does not prove that a recurrence is present. It usually means that further assessment, commonly cystoscopy, and sometimes cytology, enhanced cystoscopy, imaging or biopsy is warranted.

The test should be used particularly cautiously in patients with previous high-grade disease, carcinoma in situ (CIS), recent positive cytology, new haematuria, concerning symptoms or a history suggesting a high risk of progression. Missing high-grade recurrence carries much greater consequences than postponing a procedure in a genuinely low-risk patient.

How accurate is Cxbladder Monitor?

Published validation data have generally shown that Cxbladder Monitor is better at ruling out recurrence than confirming it.

Across key validation studies, reported performance has been approximately:

  • sensitivity: 91–93%;
  • negative predictive value (NPV): 96–97%;
  • specificity: approximately 34–39%; and
  • positive predictive value (PPV): approximately 21% in some validation cohorts.

One comparative study reported sensitivity of 91% and NPV of 96% for Cxbladder Monitor, outperforming cytology, NMP22 and UroVysion FISH for sensitivity in that study population. Another validation reported sensitivity of 93% and NPV of 97%.

These results need careful interpretation.

What does a negative predictive value of 97% mean?

In a study population similar to the one in which that figure was measured, about 97 of every 100 patients with a negative result did not have a detected recurrence, while approximately three could still have disease.

It does not mean the test is “97% accurate” in every patient. NPV changes with the underlying prevalence of recurrence. It will usually look higher in a low-risk population and lower when recurrence is common.

Why is the positive predictive value relatively low?

When specificity is low, many patients with a positive result will not have cancer confirmed on the subsequent assessment. A positive test is therefore a prompt to investigate, not a cancer diagnosis.

Does it detect high-grade disease better?

Urine-based biomarkers often perform better for biologically active high-grade tumours than for very small low-grade recurrences. Nevertheless, no negative urine test can guarantee that high-grade tumour or CIS is absent. Study populations also differ in the proportions of low-grade, high-grade and recently treated patients, making direct comparisons difficult.

Important pitfalls

1. A negative result can be falsely reassuring

False negatives occur. Small, low-volume or intermittently shedding tumours may release too little RNA into the urine. A diluted or poorly collected sample may also reduce the signal. A negative result must not override visible haematuria, positive cytology, a suspicious cystoscopy or a high-risk clinical history.

2. A positive result is not proof of cancer

Because Monitor is deliberately designed to be sensitive, specificity is modest. A positive result may lead to cystoscopy or biopsy that finds no tumour. The test cannot identify the lesion’s location, stage or grade.

3. Infection, inflammation and recent instrumentation complicate interpretation

Urinary infection, stones, bleeding, recent cystoscopy, catheterisation, TURBT, intravesical BCG or chemotherapy can alter urinary cellular material and the clinical context. Cxbladder includes an inflammatory-associated marker intended to reduce this “background noise,” but real-world confounding is not eliminated. Testing should be timed and interpreted by the treating urologist.

4. The test does not examine the upper urinary tract

Urothelial cancer may arise in the ureter or renal pelvis. A urine result cannot localise a tumour or replace CT urography, ureteroscopy or other upper-tract evaluation when clinically indicated.

5. It does not replace pathology

Only tissue examination can determine tumour grade, assess invasion and guide definitive treatment. Cxbladder is a risk-stratification tool rather than a histological diagnosis.

6. Performance may not generalise perfectly

Some studies were supported by or involved investigators connected with the test manufacturer. Many validation cohorts were enriched for particular risk groups and may not reflect every Australian practice. Independent prospective studies, longer follow-up and trials showing that biomarker-guided surveillance preserves oncological outcomes are especially important.

7. “Fewer cystoscopies” is not the same as “no cystoscopies”

Real-world studies suggest that Cxbladder Monitor can reduce cystoscopy frequency in selected low-risk patients. This should not be extrapolated to high-risk NMIBC or used to abandon risk-based surveillance. Cystoscopy remains the direct method of inspecting the bladder and permits immediate biopsy or resection planning.

8. Cost and access vary

Availability, laboratory turnaround time, out-of-pocket cost and reimbursement vary by location and insurer. Australian patients should confirm current access and costs with their urologist and testing provider before collection.

How does it compare with urine cytology?

Urine cytology is highly specific for high-grade urothelial carcinoma but has limited sensitivity, particularly for low-grade tumours. Cxbladder Monitor generally has higher reported sensitivity and NPV, but substantially lower specificity.

The tests therefore answer slightly different questions:

  • cytology: a clearly positive result strongly raises concern for high-grade disease;
  • Cxbladder Monitor: a negative result may help identify a low probability of recurrence; and
  • cystoscopy: directly visualises the bladder and remains central to surveillance.

Combining information may be more useful than treating any one result in isolation.

What do international guidelines say?

Major guidelines acknowledge that urinary molecular markers are improving, but remain cautious about their routine use as complete substitutes for cystoscopy.

  • The AUA/SUO NMIBC guideline states that urinary biomarkers should not replace cystoscopic evaluation during surveillance. Markers may be used in selected settings, including assessment of an equivocal cytology result or response to intravesical BCG.
  • The EAU NMIBC guideline recognises that molecular urine tests may have a future role in reducing cystoscopy frequency, particularly in lower-risk surveillance, but notes that evidence and prospective implementation data remain insufficient for a universal marker-driven schedule.
  • Guideline recommendations evolve as new trials emerge; decisions should be based on the patient’s individual recurrence and progression risk rather than the availability of a test alone.

A practical, balanced approach

Cxbladder Monitor is most helpful when the question is: “Is recurrence sufficiently unlikely that we can safely reduce or postpone an invasive investigation in this particular patient?”

It is less useful as a stand-alone answer to: “Does this patient definitely have cancer, where is it, and how aggressive is it?”

For a carefully selected patient with previous low-risk NMIBC, no new symptoms and a negative Monitor result, a biomarker-informed surveillance plan may reduce unnecessary cystoscopies. For a patient with previous CIS or high-grade tumour, positive cytology, visible haematuria or a suspicious finding, conventional investigation should not be deferred because of a negative urine test.

The result is best interpreted alongside tumour history, grade and stage, time since treatment, cystoscopy findings, cytology, imaging and the patient’s preferences.

References

  1. Kavalieris L, O’Sullivan P, Frampton C, et al. Performance characteristics of a multigene urine biomarker test for monitoring for recurrent urothelial carcinoma in a multicenter study. J Urol. 2017;197(6):1419–1426. PubMed search
  2. Lotan Y, O’Sullivan P, Raman JD, et al. Clinical comparison of noninvasive urine tests for ruling out recurrent urothelial carcinoma. Urol Oncol. 2017;35(8):531.e15–531.e22. PubMed search
  3. O’Sullivan P, Sharples K, Dalphin M, et al. A multigene urine test for the detection and stratification of bladder cancer in patients presenting with hematuria. J Urol. 2012;188(3):741–747. PubMed search
  4. Li KD, McLennan MT, Barocas DA, et al. Cxbladder Monitor testing to reduce cystoscopy frequency in patients with bladder cancer. J Urol. 2023. PubMed
  5. Konety B, Shore N, Kader AK, et al. Evaluation of Cxbladder and adjudication of atypical cytology and equivocal cystoscopy. Eur Urol. 2019;76(2):238–243. PubMed search
  6. Darling D, Luxmanan C, O’Sullivan P, et al. Clinical utility of Cxbladder for the diagnosis of urothelial carcinoma. Adv Ther. 2017;34:1087–1096. PubMed search
  7. Breen V, Kasabov N, Kamat AM, et al. A holistic comparative analysis of diagnostic tests for urothelial carcinoma: a study of Cxbladder Detect, UroVysion FISH, NMP22 and cytology. BMC Med Res Methodol. 2015;15:27. Full text
  8. Harvey JC, et al. Analytical validation of Cxbladder Detect, Triage, and Monitor assays for detection and management of urothelial carcinoma. Diagnostics. 2024;14(18):2061. Full text
  9. Holzbeierlein JM, Bixler BR, Buckley DI, et al. Diagnosis and treatment of non-muscle invasive bladder cancer: AUA/SUO guideline. American Urological Association; amended 2024. AUA guideline
  10. European Association of Urology. EAU Guidelines on Non-Muscle-Invasive Bladder Cancer. Current online edition. EAU guideline
  11. Barocas DA, Lotan Y, Matulewicz RS, et al. Updates to microhematuria: AUA/SUFU guideline. J Urol. 2025. PubMed

This article provides general information and does not replace personalised medical advice. Surveillance should be tailored to the original tumour’s stage and grade, prior treatment, current symptoms and the individual’s risk of recurrence and progression.

How a Stroke Can Affect Bladder Function

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A cerebrovascular accident (CVA), more commonly called a stroke, can affect much more than movement and speech. It can also disrupt the communication between the brain and bladder, leading to urgency, urinary leakage, difficulty emptying the bladder or a combination of these problems.

Bladder difficulties are common after stroke, particularly during the early stages of recovery. They can cause embarrassment, interfere with rehabilitation, disturb sleep and increase the risks of falls, skin problems and urinary tract infection. Fortunately, many patients improve as the brain recovers, and persistent symptoms can usually be managed with an individualised bladder rehabilitation and treatment plan.

How does the brain normally control the bladder?

The bladder stores urine at a low pressure until it is convenient to empty. This depends on coordinated communication between:

  • The frontal lobes, which help recognise bladder filling and suppress urination until an appropriate time.
  • Deeper brain centres involved in bladder sensation and behavioural control.
  • The pontine micturition centre in the brainstem, which coordinates contraction of the bladder with relaxation of the urinary sphincter.
  • The spinal cord and peripheral nerves that carry messages between the brain, bladder and sphincter.

A stroke may interrupt one or more of these pathways. The resulting bladder problem depends on the location and extent of the stroke, the patient’s previous bladder function and the presence of other conditions such as prostate enlargement, diabetes, constipation or reduced mobility.

What bladder problems can occur after a stroke?

Urgency and urge urinary incontinence

The most common problem is a sudden, compelling need to pass urine that may be difficult to postpone. Some patients leak before reaching the toilet.

This often results from detrusor overactivity, in which the bladder muscle contracts involuntarily during filling because the brain is no longer suppressing it normally.

Associated symptoms can include:

  • Passing urine frequently.
  • Waking several times at night to urinate.
  • Sudden urgency.
  • Leakage associated with urgency.
  • Bedwetting.
  • Reduced warning before urination.

Difficulty emptying the bladder

Some patients develop a weak or poorly coordinated bladder contraction and cannot empty effectively. This may cause:

  • Difficulty starting urination.
  • A slow or interrupted urinary stream.
  • Straining to pass urine.
  • A sensation of incomplete emptying.
  • Frequent passage of small amounts.
  • Overflow leakage from an overfilled bladder.
  • Recurrent urinary infections.

Urinary retention may be more likely during the acute phase of stroke because of reduced consciousness, immobility, constipation, medication effects, pain, infection or a pre-existing obstruction such as an enlarged prostate.

Functional incontinence

Not every episode of leakage is caused by abnormal bladder contractions. A patient may recognise the need to urinate but be unable to reach or use the toilet because of:

  • Weakness or paralysis.
  • Poor balance or slow mobility.
  • Visual impairment.
  • Difficulty removing clothing.
  • Communication problems.
  • Confusion, memory loss or reduced awareness.
  • An inaccessible toilet or lack of timely assistance.

This is called functional incontinence. Treating the bladder alone will not solve it; the physical and environmental barriers must also be addressed.

Loss of bladder awareness

A stroke can reduce awareness of bladder filling. The patient may not recognise the need to urinate until leakage occurs—or may remain unaware that the bladder is full.

Stress urinary incontinence

Leakage with coughing, sneezing, standing or exertion is not usually caused directly by stroke, but pre-existing pelvic-floor weakness may become more noticeable when mobility and general muscle function decline.

Nocturia and nighttime incontinence

Nighttime urination may be caused by an overactive bladder, sleep disturbance, leg swelling, obstructive sleep apnoea, medication timing or increased nighttime urine production. It is important because repeated attempts to reach the bathroom can significantly increase the risk of falls.

Does the site of the stroke predict the bladder problem?

There are broad associations between the area of brain injury and the type of bladder dysfunction, but the relationship is not exact enough to base treatment on the brain scan alone.

Frontal and subcortical strokes are frequently associated with urgency and detrusor overactivity. Brainstem strokes can interfere with coordination between the bladder and urinary sphincter, while larger strokes may impair bladder sensation, mobility and awareness.

The bladder pattern can also change during recovery. This is why treatment should be based on the patient’s current symptoms and objective bladder assessment rather than the location of the stroke alone.

How is bladder dysfunction assessed?

Assessment should consider the bladder, the patient’s neurological recovery and the practical circumstances surrounding each episode of leakage.

Medical and medication history

Important questions include:

  • Was urgency, nocturia or poor urinary flow present before the stroke?
  • When did the symptoms begin?
  • Is the patient aware of bladder filling?
  • Can the patient reach and use the toilet independently?
  • Is there constipation, pain, visible blood in the urine or fever?
  • What fluids, caffeine and alcohol are being consumed?
  • Could medication be contributing?

Diuretics, sedatives, opioids and some medications with anticholinergic effects can aggravate urinary symptoms, confusion or retention.

Bladder diary

A bladder diary records fluid intake, the time and volume of each urination, urgency and leakage episodes. It can help distinguish reduced bladder capacity from excessive urine production or predominantly functional incontinence.

Physical examination

The assessment may include examination of the abdomen, genital area, prostate where appropriate, pelvic floor, mobility, cognition, sensation and neurological function.

Urine testing

Urinalysis and urine culture when clinically indicated, can identify infection or blood in the urine. Bacteria in the urine without urinary symptoms do not automatically require antibiotics.

Bladder scan and post-void residual

A painless ultrasound bladder scan measures the urine remaining after urination. This is particularly useful when there is a weak stream, retention, recurrent infection, overflow leakage or before treatments that could make emptying more difficult.

Additional investigations

Depending on the circumstances, evaluation may include:

  • Kidney function blood tests.
  • Urinary flow testing.
  • Ultrasound of the kidneys and bladder.
  • Cystoscopy when there is haematuria, suspected obstruction or another appropriate indication.
  • Urodynamic studies.

Are urodynamic studies always necessary?

No. Many patients with straightforward urgency or functional incontinence can begin conservative treatment after clinical assessment, urine testing and measurement of the post-void residual.

Urodynamic studies may be helpful when:

  • The symptoms and clinical findings do not agree.
  • Both urgency and poor emptying are present.
  • There is persistent or unexplained urinary retention.
  • Initial treatment has failed.
  • An invasive treatment such as bladder Botox is being considered.
  • There is concern about obstruction, weak bladder contraction or poor bladder compliance.
  • Previous prostate, bladder or continence surgery complicates the diagnosis.

Urodynamics can distinguish an overactive bladder from impaired bladder contractility, obstruction or sphincter discoordination. This helps avoid giving treatment that reduces bladder contractions to someone who already empties poorly.

Treatment options

Treatment should be based on the bladder abnormality, the patient’s functional ability and their personal goals. Family members, continence nurses, physiotherapists, occupational therapists, rehabilitation physicians and urologists may all contribute.

Treat reversible factors

The first step is to identify problems that may be aggravating bladder control, including:

  • Urinary infection.
  • Constipation or faecal impaction.
  • Excessive caffeine or alcohol.
  • Excessive or poorly timed fluid intake.
  • Uncontrolled diabetes.
  • Leg swelling and nighttime fluid redistribution.
  • Medication side effects.
  • Prostate obstruction.
  • Reduced access to the toilet.

Adequate hydration remains important. Simply restricting fluid can produce concentrated urine, constipation and bladder irritation.

Prompted or timed toileting

Scheduled toileting can be very effective, particularly when memory, mobility or awareness is impaired.

Options include:

  • Timed voiding: visiting the toilet at regular planned intervals.
  • Prompted voiding: a carer reminds and assists the patient to use the toilet.
  • Habit retraining: the schedule is matched to the patient’s usual bladder pattern.
  • Bladder training: gradually increasing the interval between toilet visits when the patient can recognise and suppress urgency.

Easy-to-remove clothing, a bedside commode, urinal, improved lighting and a clear path to the toilet can make a considerable difference.

Pelvic-floor rehabilitation

Pelvic-floor muscle training may improve urinary control in appropriately selected patients who can identify and contract these muscles. A continence or pelvic-floor physiotherapist can adapt the program for weakness, impaired coordination or cognitive limitations following stroke.

Medication for urgency and overactive bladder

Medication may be considered when conservative measures are insufficient.

Antimuscarinic medication

Medicines such as solifenacin, darifenacin, oxybutynin or trospium can reduce involuntary bladder contractions. Possible adverse effects include:

  • Dry mouth.
  • Constipation.
  • Blurred vision.
  • Difficulty emptying the bladder.
  • Confusion or cognitive deterioration.

These medicines should be selected cautiously after stroke, particularly in older patients, those with cognitive impairment, constipation, glaucoma or an elevated post-void residual. The total anticholinergic burden from all medications should be reviewed.

Beta-3 agonists

Mirabegron relaxes the bladder during filling and may have fewer dry-mouth and cognitive adverse effects than antimuscarinic treatment. Blood pressure should be checked because mirabegron may worsen hypertension. Residual urine should also be monitored when there is concern about poor emptying.

Vibegron is another beta-3 agonist, although availability and funding can vary.

Management of incomplete emptying or retention

Treatment depends on the cause and severity.

Options may include:

  • Reviewing medicines that impair bladder contraction.
  • Treating constipation and infection.
  • Managing prostate or urethral obstruction when present.
  • Double voiding.
  • Intermittent catheterisation.

Clean intermittent catheterisation is generally preferred when the bladder cannot empty safely and the patient or carer can perform it. An indwelling urethral catheter may sometimes be necessary during the acute phase, but prolonged unnecessary use should be avoided because of infection, urethral trauma and bladder-stone risks.

A suprapubic catheter may be considered when long-term catheter drainage is unavoidable and urethral catheterisation is unsuitable.

Botulinum toxin injections into the bladder

Botulinum toxin A, commonly called bladder Botox, can reduce severe detrusor overactivity when medication has been ineffective or poorly tolerated.

It may significantly improve urgency and leakage, but it can also weaken bladder emptying. The patient must understand that intermittent catheterisation may be required, sometimes for several months. Careful selection, measurement of residual urine and appropriate follow-up are essential.

Neuromodulation

Posterior tibial nerve stimulation may help some patients with urgency and overactive bladder symptoms. It is minimally invasive but usually requires repeated treatment sessions.

Sacral neuromodulation can be effective in selected people with refractory urinary urgency, urge incontinence or non-obstructive retention. Evidence specifically in post-stroke patients is more limited than in the general overactive-bladder population. The patient’s neurological stability, cognition, mobility, ability to operate the device and need for future MRI examinations should be considered.

Continence products and skin care

Pads, absorbent underwear, mattress protection and external collecting devices can preserve dignity while recovery and treatment continue. They should support, not replace, proper assessment and rehabilitation.

Regular skin care is important, particularly when mobility is limited. Condom drainage systems may help selected men, but correct fitting and skin monitoring are essential.

Can bladder control improve after a stroke?

Yes. Many patients experience substantial improvement during the first weeks and months as consciousness, mobility, communication and neurological control recover.

Persistent urinary incontinence, however, can be a marker of a more severe stroke and may be associated with greater disability. It should not be dismissed as an inevitable consequence of ageing or brain injury. Early assessment and an active continence program can improve independence, participation in rehabilitation and quality of life.

When should medical help be sought urgently?

Prompt medical assessment is required for:

  • Complete inability to pass urine.
  • A painful or visibly swollen lower abdomen.
  • Fever, chills, confusion or suspected urinary infection.
  • Visible blood in the urine.
  • New flank pain.
  • Recurrent infections.
  • Increasing residual urine.
  • New leg weakness, numbness or loss of bowel control.
  • Sudden new neurological symptoms, which may represent another stroke.

In Australia, sudden facial weakness, arm weakness or speech disturbance should be treated as an emergency—call 000 immediately.

The key message

Bladder problems following a stroke are common, but they are not all the same. Leakage may result from an overactive bladder, impaired awareness, poor mobility, urinary retention, obstruction or several factors acting together.

Successful management begins by determining why the problem is occurring. A combination of bladder rehabilitation, environmental assistance, pelvic-floor therapy, carefully selected medication, catheterisation or specialist intervention can then be tailored to the individual patient.

References

  1. Agapiou E, et al. Lower urinary tract dysfunction following stroke. Bladder. 2024. PubMed Central
  2. Agapiou E, et al. Bladder dysfunction following stroke: an updated review on diagnosis and management. Bladder. 2024. PubMed Central
  3. European Association of Urology. EAU Guidelines on Neuro-Urology. 2026. EAU Neuro-Urology Guideline
  4. Stroke Foundation Australia. Incontinence after stroke. Stroke Foundation patient fact sheet
  5. Stroke Foundation Australia. Urinary continence and stroke—resources for health professionals. InformMe
  6. Canadian Stroke Best Practices. Bladder and Bowel Function Following Stroke. Heart & Stroke Foundation of Canada
  7. National Institute for Health and Care Excellence. Stroke rehabilitation in adults (NG236). Updated 2023. NICE recommendations
  8. National Institute for Health and Care Excellence. Urinary incontinence in neurological disease: assessment and management (CG148). NICE guideline
  9. American Urological Association and Society of Urodynamics, Female Pelvic Medicine & Urogenital Reconstruction. Adult Neurogenic Lower Urinary Tract Dysfunction Guideline. AUA/SUFU guideline
  10. Intercollegiate Stroke Working Party. National Clinical Guideline for Stroke: Rehabilitation and recovery—activity and participation. National Clinical Guideline for Stroke

This article provides general educational information and does not replace individual medical assessment. Treatment should be tailored to the type of bladder dysfunction, other medical conditions, current medications and the patient’s rehabilitation goals.

Parkinson’s Disease and the Bladder: When the Brain–Bladder Signal Misbehaves

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Parkinson’s disease is best known for tremor, stiffness and slowed movement, but it can also affect many automatic body functions: including bladder control. Urinary symptoms may disturb sleep, restrict social activities and increase the risk of falls when someone rushes to the toilet.

The reassuring message is that bladder symptoms can usually be improved. The important first step is to identify what the bladder is doing, because not every urinary problem in a person with Parkinson’s is caused by Parkinson’s itself.

How does Parkinson’s affect the bladder?

The bladder normally stores urine quietly and empties only when the brain decides that the time and place are appropriate. Dopamine-dependent circuits in the brain help suppress unwanted bladder contractions during filling.

Parkinson’s can weaken this “hold on” signal. The bladder muscle may contract before it is full, a condition called detrusor overactivity. This produces the familiar overactive-bladder symptoms of urgency, frequency and urge incontinence.

This is a form of neurogenic lower urinary tract dysfunction; bladder or sphincter function altered by disease of the nervous system. However, Parkinson’s does not create one single bladder pattern. Age-related bladder changes, prostate enlargement, pelvic-floor problems, constipation, diabetes, mobility limitations and medications may all contribute.

Common urinary symptoms

People may experience:

  • a sudden, difficult-to-defer need to pass urine;
  • frequent urination during the day;
  • waking several times at night to urinate (nocturia);
  • leakage before reaching the toilet (urge incontinence);
  • bedwetting;
  • hesitancy, a slow stream or straining;
  • a feeling that the bladder has not emptied; or
  • recurrent urinary infections.

Some apparent bladder leakage is partly functional: the person recognises the urge but rigidity, slow movement, poor balance or difficulty managing clothing prevents timely access to the toilet.

Difficulty emptying can occur, but substantial urinary retention is less typical of uncomplicated Parkinson’s disease. It may indicate prostate or urethral obstruction, an underactive bladder, medication effects, severe constipation, pelvic-organ prolapse, or another neurological disorder. Prominent retention, erectile dysfunction or severe postural blood-pressure problems early in a parkinsonian illness may warrant neurological review for conditions such as multiple system atrophy.

How is the bladder evaluated?

A careful assessment is more useful than assuming that every symptom is “just the Parkinson’s”. It may include:

  1. History and medication review: urinary symptoms, fluid intake, bowel function, mobility, cognition, falls and all prescribed and non-prescribed medicines.
  2. Bladder diary: usually recording drinks, voided volumes, urgency and leakage for three days. This is particularly helpful for nocturia.
  3. Examination: abdominal, neurological and, when appropriate, prostate or pelvic assessment.
  4. Urine test: to look for infection or blood.
  5. Post-void residual measurement: a bladder ultrasound after urination shows whether emptying is adequate.
  6. Uroflowmetry: measures the strength and pattern of the urinary stream.
  7. Further tests when indicated: renal function, ultrasound, cystoscopy or prostate assessment according to the clinical findings.

Blood in the urine, pain, fever, recurrent infection or a sudden major change in bladder function needs separate investigation and should not automatically be attributed to Parkinson’s.

Are urodynamic studies always necessary?

No. A patient with straightforward urgency and urge leakage, a normal urine test and a low residual volume can often begin conservative treatment without invasive testing.

Urodynamics may be particularly useful when:

  • symptoms and initial test results do not agree;
  • there is a high or rising post-void residual;
  • weak flow, retention or obstruction is suspected;
  • symptoms persist despite appropriate treatment;
  • the diagnosis is uncertain, for example, overactivity versus poor bladder contraction;
  • previous prostate, bladder or continence surgery complicates the picture; or
  • Botox or another invasive treatment is being considered and the result would alter management.

During urodynamics, thin catheters measure bladder and abdominal pressure while the bladder fills and empties. The test may demonstrate detrusor overactivity, impaired contraction, obstruction or, less commonly, unsafe storage pressure. It should answer a specific clinical question not simply be performed because Parkinson’s is present.

First steps: practical and behavioural treatment

Management should be individualised and, where helpful, involve the urologist, neurologist, Parkinson’s nurse, continence physiotherapist, occupational therapist and carer.

Useful measures include:

  • treating urinary infection and constipation;
  • reviewing diuretics and other medicines with the prescribing doctor;
  • spreading fluid intake through the day while avoiding dehydration;
  • reducing late-evening fluids, caffeine and alcohol when nocturia is troublesome;
  • timed or prompted voiding;
  • bladder training when cognition and mobility permit;
  • pelvic-floor physiotherapy where appropriate;
  • improving toilet access, lighting, clothing and mobility aids; and
  • using a bedside urinal or commode when falls are a concern.

Nocturia is not always caused solely by an overactive bladder. Leg swelling, sleep apnoea, excessive urine production overnight and disturbed sleep may require different treatment.

Medication options

Antimuscarinic medicines

Medicines such as solifenacin, darifenacin, tolterodine, fesoterodine, oxybutynin or trospium can reduce involuntary bladder contractions. They may improve urgency, frequency and urge leakage.

The trade-off is important in Parkinson’s disease. Anticholinergic burden may worsen dry mouth, constipation, blurred vision, urinary retention, confusion or memory. Older people, those with cognitive impairment, glaucoma or poor bladder emptying need particular caution. Oxybutynin can be especially troublesome cognitively in susceptible patients. Drug choice should consider the person’s complete medication list and residual urine.

Beta-3 agonists

Mirabegron relaxes the bladder during filling without adding the same anticholinergic burden and has shown benefit in people with Parkinson’s and overactive-bladder symptoms. Blood pressure should be checked because it can rise, and interactions and cardiac history should be reviewed. Vibegron is another beta-3 agonist available for overactive bladder in Australia; Parkinson-specific evidence is more limited.

Combination treatment may be considered in selected patients when one medicine provides incomplete relief, with monitoring of blood pressure, side effects and bladder emptying.

If emptying is the main problem

Treatment depends on the cause. Prostate medication or surgery will help only if genuine bladder-outlet obstruction is present. An alpha-blocker may worsen dizziness or postural hypotension, already common in Parkinson’s. If significant residual urine persists, clean intermittent self-catheterisation, performed by the patient or a carer where feasible, is generally preferable to a long-term urethral catheter. A suprapubic catheter may be considered when intermittent catheterisation is not practical.

Botox injections into the bladder

Botulinum toxin A (Botox) can be effective for troublesome detrusor overactivity or overactive-bladder symptoms that have not responded to, or cannot tolerate, tablets. It is injected through a cystoscope into multiple areas of the bladder wall, usually as a day procedure.

Benefits may include fewer urgency episodes, fewer leaks and better sleep and quality of life. The effect is temporary, commonly lasting several months, so repeat treatment may be required.

Important risks include:

  • urinary infection;
  • blood in the urine or short-lived discomfort;
  • incomplete bladder emptying or urinary retention; and
  • the possible need for temporary or occasionally ongoing intermittent catheterisation.

Before treatment, the patient’s hand function, cognition and support network matter: could the patient or carer perform catheterisation if retention occurred? Measuring residual urine before and after treatment is essential. Urodynamics is often helpful if the underlying bladder behaviour or emptying ability is uncertain, although it is not mandatory in every otherwise clear case.

Can sacral neuromodulation be used in Parkinson’s disease?

Yes, in carefully selected patients. Sacral neuromodulation (SNM) sends mild electrical impulses to the sacral nerves involved in bladder control. It can be considered for refractory urgency, frequency, urge incontinence and, in selected circumstances, non-obstructive urinary retention.

Treatment begins with a test or staged phase. A temporary or tined lead is used to assess whether symptoms improve meaningfully, commonly by at least 50%, before a permanent battery is implanted. This trial is particularly valuable because Parkinson’s symptoms and bladder patterns differ between patients.

Small observational studies and systematic reviews suggest that some people with Parkinson’s achieve worthwhile improvement. However, the Parkinson-specific evidence is less extensive than the evidence for non-neurogenic overactive bladder, and response cannot be guaranteed.

Points to consider include:

  • confirming that infection, obstruction and severe retention have been addressed;
  • whether symptoms are likely to be modulated by SNM;
  • the person’s ability, or carer support, to operate and attend follow-up for the device;
  • falls, mobility and future disease progression;
  • possible lead movement, pain, infection, device revision or battery replacement; and
  • future MRI requirements. Modern systems may be MRI-conditional, but the exact device and scanning conditions must always be checked.

SNM is therefore not automatically excluded because a person has Parkinson’s. It is best considered through shared decision-making after appropriate evaluation and failure or intolerance of simpler measures.

Botox or sacral neuromodulation?

Feature Bladder Botox Sacral neuromodulation
How it works Temporarily reduces bladder-muscle overactivity Modulates sacral nerve signalling
Treatment pathway Cystoscopic injections, repeated when effect wears off Test phase followed by an implant if successful
Main advantage No permanent implant; established effect on detrusor overactivity Testable before permanent implantation; no routine bladder injections
Main limitation UTI and retention; intermittent catheterisation may be required Implant surgery, programming, revisions and battery management
Parkinson-specific evidence Supportive but based mainly on relatively small studies Promising but still limited; careful selection is essential
Particularly important question Could the patient or carer catheterise if necessary? Can the patient manage the device and follow-up as Parkinson’s progresses?

Neither option is universally “better”. The choice depends on bladder-emptying ability, infection history, dexterity, cognition, mobility, MRI needs, willingness to have repeat procedures or an implant, and the individual’s priorities.

When should you seek prompt medical attention?

Contact a doctor urgently for inability to pass urine, fever with urinary symptoms, flank pain, visible blood in the urine or a sudden neurological or bladder deterioration. New persistent incontinence also deserves assessment rather than simply adding pads.

The take-home message

Bladder symptoms are common and often overlooked in Parkinson’s disease. Urgency, frequency, nocturia and urge leakage are the usual pattern, but obstruction and poor emptying must not be missed. Most patients do not require urodynamics at the outset; it becomes valuable when the diagnosis is uncertain, emptying is impaired, treatment has failed or an invasive procedure is being planned.

Treatment progresses from practical measures and medication to Botox or sacral neuromodulation in suitable patients. The best plan balances symptom control with cognition, blood pressure, constipation, mobility, manual dexterity and the likely course of Parkinson’s disease.

Patient information: This article provides general education and is not a substitute for an individual medical assessment. Do not stop Parkinson’s, blood-pressure or bladder medication without discussing it with your treating doctor.

References and further reading

  1. European Association of Urology. EAU Guidelines on Neuro-Urology. 2026.
  2. Ginsberg DA, et al. AUA/SUFU Guideline on Adult Neurogenic Lower Urinary Tract Dysfunction. J Urol. 2021; amendment 2024.
  3. Li FF, et al. Prevalence of lower urinary tract symptoms, urinary incontinence and retention in Parkinson’s disease: a systematic review and meta-analysis. Front Aging Neurosci. 2022;14:977572.
  4. Sakakibara R, et al. A guideline for the management of bladder dysfunction in Parkinson’s disease and other gait disorders. Neurourol Urodyn. 2016;35:551–563.
  5. Cho SY, et al. Mirabegron for treatment of overactive bladder symptoms in patients with Parkinson’s disease: a randomised, placebo-controlled trial. Neurourol Urodyn. 2021.
  6. Greenberg DR, et al. Sacral nerve stimulation in Parkinson’s disease patients with overactive bladder symptoms. Urology. 2020;144:99–105.
  7. Smith MD, et al. Neuromodulation for storage lower urinary tract symptoms in Parkinson disease: a systematic review. Neuromodulation. 2022.

 

Multiple Sclerosis and the Bladder: Symptoms, Tests and Treatment Options

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Multiple sclerosis (MS) affects the brain and spinal cord, the same nervous system pathways that coordinate bladder storage, bladder emptying and urinary sphincter control. As a result, bladder symptoms are common and may change as MS changes.

The important message is that “an MS bladder” is not one single condition. Some people develop an overactive bladder, some cannot empty properly, and others have a mixture of both. Treatment should therefore be based on the individual bladder pattern, not simply on the diagnosis of MS.

How does MS affect bladder control?

Normally, the bladder stores urine at low pressure while the urinary sphincter stays closed. When it is convenient to urinate, the brain allows the bladder muscle (detrusor) to contract while the sphincter relaxes.

MS plaques can interrupt these signals in different places. This may cause:

  • Neurogenic detrusor overactivity: the bladder contracts unexpectedly during filling, causing urgency, frequency, nocturia and urge incontinence.
  • Detrusor sphincter dyssynergia: the bladder contracts while the sphincter fails to relax properly, rather like pressing the accelerator and brake together. This may produce poor flow, straining, incomplete emptying, high bladder pressure and recurrent urinary infection.
  • Detrusor underactivity: the bladder contraction is too weak or does not last long enough, causing slow emptying or retention.
  • A mixed pattern: urgency and leakage can coexist with a significant residual urine volume.

The European Association of Urology (EAU) reports that approximately 75% of people develop voiding dysfunction within ten years of MS. Reported urodynamic patterns include neurogenic detrusor overactivity in 43–65%, detrusor sphincter dyssynergia in about 35%, and detrusor underactivity in about 25%. These patterns can overlap and can change over time.

Symptoms that deserve assessment

Bladder symptoms may include:

  • sudden urgency and difficulty postponing urination;
  • frequent urination by day or night;
  • leakage before reaching the toilet;
  • hesitancy, interrupted or weak urinary flow;
  • straining to urinate;
  • a feeling of incomplete emptying;
  • recurrent urinary tract infections (UTIs);
  • new bedwetting or unexpected leakage; and
  • an inability to pass urine.

Seek prompt medical review for fever, flank pain, visible blood in the urine, severe bladder pain, inability to urinate, or a sudden major change in bladder function. A UTI can temporarily worsen neurological MS symptoms (a pseudo-relapse), while a true neurological relapse can also alter bladder function.

How is the bladder assessed?

Assessment is tailored to symptoms, disability, MS course and previous treatment. It may include:

  1. A detailed urinary, neurological, bowel, medication and mobility history.
  2. A three-day bladder diary recording fluid intake, voids, urgency, leakage and catheter volumes.
  3. Urinalysis and urine culture when infection is suspected.
  4. Measurement of post-void residual urine with a bladder scan.
  5. Kidney-function blood tests where appropriate.
  6. Urinary tract ultrasound in selected patients, particularly where retention, recurrent infection, stones or upper-tract risk is suspected.
  7. Uroflowmetry, which measures the strength and pattern of the urinary stream.
  8. Urodynamic studies when the result is likely to clarify the diagnosis or change treatment.

Urodynamic studies: useful, but used selectively

Urodynamics measures bladder pressure, abdominal pressure, urine flow and sphincter activity during filling and emptying. It can distinguish urgency caused by detrusor overactivity from poor emptying caused by detrusor weakness, outlet obstruction or detrusor–sphincter dyssynergia. Video urodynamics can additionally show the bladder outlet, reflux and anatomical changes.

Urodynamics is especially useful when:

  • symptoms and residual urine measurements do not tell the same story;
  • both storage and emptying symptoms are present;
  • recurrent UTIs, retention or raised bladder pressures are suspected;
  • invasive treatment such as bladder Botox is being considered;
  • previous treatment has failed or produced unexpected problems;
  • there is concern about kidney or upper urinary tract safety; or
  • bladder function has changed significantly.

Precautions before and during urodynamics

  • Active symptomatic UTI should be treated before an elective invasive study.
  • The team should know about antibiotics, anticoagulants, allergies, pregnancy possibility and previous difficulty with catheterisation.
  • Mobility, spasms, fatigue, cognition, hand function and transfer needs should be planned for in advance.
  • Catheter placement and rapid filling can alter the result; artefacts must be recognised and the study interpreted alongside the person’s normal symptoms and bladder diary.
  • A single study is a snapshot. Results may vary, and repeat testing may be appropriate when findings are inconsistent or the clinical situation changes.
  • Autonomic dysreflexia is mainly a concern in susceptible people with high spinal cord lesions rather than typical MS, but blood pressure and heart rate must be monitored whenever an individual is considered at risk.
  • Preventive antibiotics are not automatically required for every patient; use should be individualised according to urine findings and infection risk.

Treatment: matching the solution to the bladder problem

The aims are to improve continence and quality of life, empty the bladder safely, reduce infections, protect the kidneys and preserve independence.

Everyday measures

Useful first steps may include:

  • timed voiding or bladder training;
  • adjusting excessive, poorly timed fluid intake without becoming dehydrated;
  • reducing caffeine, alcohol or other individual bladder irritants;
  • treating constipation;
  • improving toilet access, clothing and mobility support;
  • pelvic-floor physiotherapy where muscle control and the bladder pattern make this appropriate; and
  • continence pads, sheaths or other products as support, not as a substitute for investigating retention.

Medication for urgency and neurogenic overactive bladder

Antimuscarinic medicines can reduce involuntary bladder contractions and improve capacity. Possible side effects include dry mouth, constipation, blurred vision and impaired bladder emptying. Cognitive burden is relevant, particularly where fatigue, memory concerns or multiple anticholinergic medicines are already present.

Beta-3 agonists, may improve urgency and frequency with less dry mouth and constipation. Blood pressure and drug interactions require consideration. In neurogenic detrusor overactivity, symptom improvement does not necessarily mean that bladder pressures have normalised.

Before and after starting storage medication, the residual urine may need checking because suppressing bladder contractions can reveal or worsen incomplete emptying. Combination therapy is sometimes used under specialist supervision.

An alpha-blocker may occasionally be used to reduce outlet resistance in selected patients with voiding difficulty, although it will not correct every cause of neurogenic retention.

Catheterisation and intermittent self-catheterisation (ISC)

If the bladder cannot empty safely, intermittent catheterisation is often preferred to leaving a catheter in continuously. A small catheter is passed at planned intervals and removed once the bladder is empty.

ISC may:

  • reduce residual urine and overflow leakage;
  • improve bladder-pressure control;
  • make storage medicines or Botox safer; and
  • protect the upper urinary tract in selected patients.

However, it must be practical. Hand dexterity, tremor, spasticity, vision, fatigue, cognition, body position, urethral anatomy, bathroom access and carer support all matter. Training by an experienced continence nurse is valuable, and adaptive equipment or a different catheter may make a major difference.

Possible difficulties include discomfort, urethral trauma, bleeding, false passage and UTI. Bacteria in the urine without symptoms do not always require antibiotics. The EAU emphasises shared decision-making because ISC can increase treatment burden; one cited MS study found a higher UTI rate after starting intermittent catheterisation without a corresponding improvement in quality of life or symptom score.

If ISC is impossible and drainage is essential, an indwelling urethral or suprapubic catheter may be considered. Long-term catheters carry risks including infection, blockage, encrustation, leakage, bladder stones and urethral damage. When long-term drainage is necessary, a suprapubic catheter may offer practical advantages for selected patients, but it is not complication-free.

Bladder Botulinum Toxin injections

Botulinum toxin type A is injected through a cystoscope into multiple areas of the bladder wall. It reduces the nerve signals that trigger involuntary detrusor contractions and is well supported for MS-related neurogenic detrusor overactivity when tablets are ineffective or poorly tolerated.

Benefits may include fewer urgency-incontinence episodes, improved bladder capacity and lower storage pressure. The effect is temporary, commonly lasting several months, so successful treatment usually requires repeat injections.

The main precautions are:

  • UTI must be excluded or treated around the procedure according to local protocol.
  • Botox may weaken bladder emptying and cause urinary retention.
  • A patient who does not already catheterise must be willing and physically able to perform ISC, or have reliable help, if retention develops.
  • UTIs, temporary blood in the urine and discomfort can occur; generalised muscle weakness is rare.
  • Residual urine and symptoms require follow-up, and urodynamics may occasionally be repeated to confirm safe bladder pressures.

Dose and injection technique are individualised. In MS patients who still void spontaneously, a lower dose may reduce—but does not eliminate—the likelihood of needing catheterisation.

Sacral neuromodulation (SNM)

SNM delivers mild electrical stimulation to the sacral nerves, usually via a lead placed near the S3 nerve root and connected to a small implanted pulse generator. It can be considered in carefully selected patients with refractory urgency, urgency incontinence, frequency or non-obstructive urinary retention.

A major advantage is that treatment can be tested first. During a trial phase, symptom diaries help determine whether stimulation produces a meaningful improvement before the permanent battery is implanted.

Important considerations in MS include:

  • the evidence base is smaller and less disease-specific than the evidence supporting Botox for neurogenic detrusor overactivity;
  • results may be less predictable if neurological disease progresses or the bladder pattern changes;
  • implantation requires a procedure and ongoing programming;
  • pain, infection, lead movement, loss of effect, device malfunction and future revision or replacement can occur; and
  • people with MS commonly require future MRI scans. Modern systems may be MRI-conditional, but the exact lead and generator combination and the scanner conditions must be verified before implantation and before every MRI.

SNM does not remove the need to monitor residual urine, infection risk or upper-tract safety when clinically indicated.

Botox versus sacral neuromodulation in MS

Feature Bladder Botox Sacral neuromodulation
Main role Neurogenic detrusor overactivity with urgency and urge incontinence after medication is inadequate or poorly tolerated Selected refractory urgency, urge incontinence, frequency or non-obstructive retention
MS-specific evidence Stronger; supported by randomised trials in neurogenic detrusor overactivity Promising, but fewer MS-specific studies and less certainty about ideal candidates
How it works Temporarily reduces detrusor nerve activity and contractions Modulates sacral nerve signalling to the bladder and pelvic floor
Procedure Cystoscopic injections into the bladder Trial lead followed by permanent implant if successful
Reversibility Effect wears off over months Stimulation can be adjusted or switched off; device can be removed
Repeat treatment Usually repeat injections are required Programming and eventual battery/device revision or replacement may be required
Retention/ISC risk Important; new ISC may become necessary Generally less likely to cause retention; may also treat selected non-obstructive retention
Infection considerations UTI is a common adverse event; urinary infection should be addressed before treatment Surgical-site or device infection can require antibiotics or device removal
MRI considerations No implanted device restriction Confirm that the complete implanted system is MRI-conditional and follow device-specific conditions
Best fit Proven high-pressure or overactive bladder where reducing contractions is the priority and catheterisation is feasible if needed A carefully selected patient who values a test phase, has suitable symptoms and accepts an implant and follow-up
Key limitation Temporary effect and possible urinary retention Implant-related complications and less certain outcomes as MS evolves

Which is better?

Neither treatment is universally “better.” Botulinum Toxin is often favoured when urodynamics demonstrates neurogenic detrusor overactivity and the main goal is to suppress involuntary bladder contractions or unsafe storage pressure. SNM may be attractive in a carefully selected patient with refractory urgency or non-obstructive retention who wants a testable, adjustable treatment and wishes to avoid the higher catheterisation risk associated with Botox.

The decision should consider urodynamic findings, current residual urine, ability to perform ISC, recurrent UTIs, hand function, mobility, expected MRI needs, disease stability, patient preference and access to long-term follow-up.

Other interventional and surgical options

For selected patients, posterior tibial nerve stimulation may improve overactive bladder symptoms without an implant, although evidence in MS is less robust. When severe high-pressure bladder dysfunction remains unsafe despite medication, catheterisation and minimally invasive treatment, reconstructive options such as augmentation cystoplasty or urinary diversion may be considered in a specialist neuro-urology service. These are major procedures reserved for carefully selected cases and require lifelong follow-up.

Follow-up matters

MS and bladder function can both evolve. Review may include symptom assessment, bladder diary, urinalysis when symptomatic, residual urine measurement, renal function, urinary tract imaging and repeat urodynamics according to risk and clinical change.

A useful treatment plan is therefore not simply “stop the leakage.” It should answer four questions:

  1. Is the bladder storing urine at a safe pressure?
  2. Is it emptying adequately?
  3. Is the treatment practical and sustainable for this patient?
  4. Are the kidneys and quality of life being protected over time?

Take-home message

Bladder problems in MS are common, treatable and often more complex than the symptoms suggest. Urgency does not exclude retention, and leakage does not prove that the bladder empties well. A structured assessment, including a residual urine measurement and selective use of urodynamics, allows treatment to be matched to the actual dysfunction.

Medication, ISC, Botox and sacral neuromodulation all have valuable roles. The best choice is the one that safely addresses the individual bladder pattern while fitting the person’s abilities, priorities, MS course and future care needs.

This article provides general information and does not replace individual medical assessment. Treatment availability, indications and funding vary. Patients should discuss their symptoms with their GP, neurologist, continence clinician or urologist.

References and further reading

  1. European Association of Urology. EAU Guidelines on Neuro-urology. Current online guideline: https://uroweb.org/guidelines/neuro-urology/chapter/the-guideline
  2. National Institute for Health and Care Excellence. Urinary incontinence in neurological disease: assessment and management (CG148). https://www.nice.org.uk/guidance/cg148
  3. Gajewski JB, Schurch B, Hamid R, et al. An International Continence Society report on the terminology for adult neurogenic lower urinary tract dysfunction. Neurourology and Urodynamics. 2018;37(3):1152–1161.
  4. Ginsberg D, Gousse A, Keppenne V, et al. Phase 3 efficacy and tolerability study of onabotulinumtoxinA for urinary incontinence from neurogenic detrusor overactivity. Journal of Urology. 2012;187(6):2131–2139.
  5. Cruz F, Herschorn S, Aliotta P, et al. Efficacy and safety of onabotulinumtoxinA in patients with urinary incontinence due to neurogenic detrusor overactivity. European Urology. 2011;60(4):742–750.
  6. American Urological Association/Society of Urodynamics, Female Pelvic Medicine & Urogenital Reconstruction. Adult Neurogenic Lower Urinary Tract Dysfunction Guideline. https://www.auanet.org/guidelines-and-quality/guidelines/adult-neurogenic-lower-urinary-tract-dysfunction