Radical Prostatectomy After Radiation Therapy for Prostate Cancer

When prostate cancer returns after radiotherapy

Radiotherapy, whether external-beam radiation or brachytherapy can provide excellent long-term control of localised prostate cancer. However, a rising prostate-specific antigen (PSA) after treatment may indicate that the cancer has returned.

This does not automatically mean that the cancer is still in the prostate, nor does every PSA rise require immediate treatment. Recurrence may be confined to the prostate, present in lymph nodes or bones, or involve more than one site. Some recurrences also progress slowly enough that surveillance may be appropriate.

When clinically significant cancer is proven to have returned within the irradiated prostate, with no evidence of spread elsewhere, removal of the prostate may still offer a chance of cure. This operation is called a salvage radical prostatectomy.

What is a salvage radical prostatectomy?

A salvage radical prostatectomy removes the entire prostate and seminal vesicles after previous prostate radiotherapy. Depending on the cancer and imaging findings, pelvic lymph nodes may also be removed.

The operation may be performed using robotic-assisted or open surgery. A robotic approach can improve magnification and access, but it does not remove the biological effects of previous radiation. Surgeon and centre experience are therefore more important than the label attached to the surgical technique.

Salvage surgery is technically more difficult than a prostatectomy performed before radiotherapy. Radiation can cause:

  • scarring and fibrosis around the prostate;
  • loss of the normal tissue planes between the prostate, bladder and rectum;
  • reduced tissue blood supply;
  • poorer tissue healing; and
  • pre-existing damage to urinary, erectile or bowel function.

For these reasons, salvage prostatectomy should generally be undertaken in a centre with specific experience in complex prostate cancer surgery and access to multidisciplinary care.

When might salvage surgery be considered?

The aim is to identify a man who has a meaningful risk from his recurrent cancer, but whose disease still appears curable with local treatment. Possible indications include:

  • a rising PSA after radiotherapy, commonly assessed using the Phoenix definition: a PSA rise of at least 2 ng/mL above the lowest PSA reached after treatment;
  • prostate cancer confirmed on biopsy after radiotherapy;
  • imaging suggesting that the recurrence is confined to the prostate or immediate surrounding tissues;
  • no evidence of distant metastatic disease;
  • a life expectancy long enough to benefit from curative treatment, often more than 10 years;
  • good general health and fitness for major surgery;
  • acceptable baseline bladder function; and
  • willingness to accept a higher risk of urinary and sexual side effects than with a primary prostatectomy.

Factors such as the PSA level, PSA doubling time, interval since radiotherapy, biopsy Grade Group, clinical stage and the original cancer characteristics help estimate whether salvage treatment is likely to be worthwhile.

Assessment before considering surgery

A rising PSA is the beginning of the assessment—not the final diagnosis. Investigations commonly include:

Review of the original treatment

The radiation dose and field, use of brachytherapy, previous androgen-deprivation therapy, original biopsy grade and pre-treatment imaging should all be reviewed.

Multiparametric MRI

MRI can help identify the site and extent of a local recurrence, assess the seminal vesicles, bladder neck and rectal interface, and guide biopsy. Interpretation after radiation can be challenging and benefits from specialist radiological expertise.

PSMA PET/CT

PSMA PET/CT is used to look for disease in lymph nodes, bones or other organs. Finding metastatic disease usually changes the treatment plan and may mean that removing the prostate would not provide the expected benefit. Very small-volume disease can still be below the resolution of any scan.

Prostate biopsy

Major guidelines recommend pathological confirmation before potentially morbid local salvage therapy. Biopsy can confirm viable cancer, determine its grade and help distinguish clinically important recurrence from post-radiation change. Both targeted and systematic sampling may be considered.

Urinary-function assessment

Assessment may include symptom scores, urine testing, urinary-flow measurement, residual urine ultrasound and cystoscopy. Urodynamic testing may be helpful when there is significant urgency, leakage, poor flow, retention or uncertainty about bladder function.

Who may not be a good candidate?

Salvage prostatectomy is less likely to be appropriate when:

  • metastatic or extensive nodal disease is present;
  • the cancer is unlikely to be completely removable;
  • life expectancy is limited by age, frailty or other illness;
  • the recurrence is low risk and unlikely to threaten health;
  • severe urinary or bowel damage already exists after radiation; or
  • the anticipated harms of surgery outweigh the probability of cancer control.

These are not absolute rules. Individual circumstances should be reviewed by a multidisciplinary team involving urology, radiation oncology, medical oncology, radiology and pathology.

What are the potential benefits?

For carefully selected men, salvage prostatectomy can:

  • remove the recurrent cancer and provide complete pathological staging;
  • provide durable PSA control without immediately committing the patient to lifelong hormonal therapy; and
  • offer a possibility of cure when disease is truly confined to the prostate.

Published results vary considerably because most evidence comes from retrospective series involving highly selected patients. The European Association of Urology reports five-year biochemical recurrence-free estimates broadly around 41–52% in a large contemporary systematic review, while older selected series have reported ranges of approximately 47–82%. A broader meta-analysis of all local salvage approaches found roughly 50–60% five-year recurrence-free survival, without clear evidence that one approach was oncologically superior. These figures should not be interpreted as a personal prediction.

Cancer control is generally more favourable when the PSA is lower, the recurrent tumour is organ-confined, the cancer grade is lower, the PSA doubling time is longer and there is no nodal or distant disease.

Side effects and complications

Complication rates vary with baseline function, radiation type and dose, disease extent, surgical technique, definitions used in studies and surgeon experience. Results from specialist centres may not apply everywhere.

Urinary incontinence

Loss of urinary control is one of the most important risks. Radiation may already have affected the sphincter, bladder and urethral tissues, and surgery removes the prostate through which the urethra passes.

Leakage may range from mild stress incontinence to severe continuous leakage. Pelvic-floor rehabilitation can help, but some men may later require a male sling or artificial urinary sphincter. Continence outcomes reported in the literature vary widely because studies use different definitions; the risk of significant or persistent leakage is clearly higher than after primary prostatectomy.

Erectile dysfunction

Erectile function is often already impaired by radiotherapy, age, vascular disease or hormonal treatment. Preservation of the erectile nerves may be unsafe or technically impossible because of tumour location and radiation fibrosis. Consequently, erectile dysfunction after salvage prostatectomy is very common and recovery of unassisted erections is uncommon.

Rehabilitation and treatment options include tablets, vacuum devices, penile injections and penile prosthesis surgery. As with any radical prostatectomy, ejaculation and natural fertility are lost because the prostate and seminal vesicles are removed.

Bladder-neck contracture or urethral narrowing

Scar tissue may develop where the bladder is reconnected to the urethra. This can cause a weak stream, straining, incomplete emptying, retention or recurrent infection. Treatment may require endoscopic incision or dilatation, sometimes more than once. Repeated procedures can worsen incontinence.

Urine leak and delayed healing

The new bladder-to-urethra join may heal slowly because irradiated tissues have reduced blood supply. A urinary catheter may need to remain in place longer, and imaging may be required before its removal. Persistent leakage can require drainage or further intervention.

Rectal injury and urinary fistula

The rectum can be densely adherent to the prostate after radiotherapy. Rectal injury is uncommon in expert contemporary practice but occurs more often than during primary prostatectomy and can be serious. It may require repair, temporary bowel diversion or, rarely, more extensive surgery. An abnormal connection between the urinary tract and rectum—a rectourinary fistula—is rare but particularly difficult to treat.

Other surgical risks

Other possible complications include bleeding or transfusion, infection, blood clots, lymphocele after lymph-node dissection, injury to nearby structures, anaesthetic complications, chronic pelvic pain and the need for further procedures.

Cancer may still recur

Even when preoperative imaging suggests local disease, microscopic cancer may already exist outside the prostate. PSA may therefore remain detectable or rise again after surgery. Further treatment—such as hormonal therapy, systemic therapy or selected metastasis-directed treatment—may still be required.

Are there alternatives?

Depending on the cancer, previous treatment, anatomy, urinary function and patient priorities, alternatives may include:

  • active monitoring for a slow or low-risk recurrence;
  • androgen-deprivation therapy, sometimes with additional systemic treatment;
  • salvage brachytherapy or stereotactic re-irradiation;
  • cryotherapy;
  • high-intensity focused ultrasound (HIFU); or
  • focal salvage treatment in carefully selected cases.

No single salvage treatment is best for every patient. Available studies are mostly non-randomised and use differing definitions. A large meta-analysis found broadly similar five-year cancer control among local salvage methods, but severe urinary toxicity was higher after salvage prostatectomy than after modern re-irradiation approaches. Treatment should therefore be selected through shared decision-making rather than on cancer-control figures alone.

The bottom line

Radical prostatectomy after prostate radiotherapy is possible and can be curative, but it is not a routine operation. The best candidate is generally a fit man with biopsy-proven, clinically significant recurrence confined to the prostate, no metastatic disease on appropriate staging, a meaningful life expectancy and a clear understanding of the potential functional consequences.

Accurate staging, confirmation by biopsy, assessment of baseline urinary function and review by an experienced multidisciplinary team are essential. The decision must balance the chance of durable cancer control against the higher risks of urinary incontinence, erectile dysfunction, urinary narrowing, poor healing and rectal complications.

This article provides general information and does not replace individual medical advice. Recommendations should be tailored to the pathology, imaging, previous radiation treatment, general health and preferences of each patient.

References

  1. European Association of Urology. EAU Guidelines on Prostate Cancer: Treatment—management of PSA failure after radiation therapy and salvage radical prostatectomy. Current online edition. https://uroweb.org/guidelines/prostate-cancer/chapter/treatment
  2. Morgan TM, et al. Salvage Therapy for Prostate Cancer: AUA/ASTRO/SUO Guideline. Journal of Urology. 2024. https://www.auanet.org/guidelines-and-quality/guidelines/salvage-therapy-for-prostate-cancer
  3. Valle LF, et al. A systematic review and meta-analysis of local salvage therapies after radiotherapy for prostate cancer (MASTER). European Urology. 2021;80(3):280–292. doi:10.1016/j.eururo.2020.11.010.
  4. Grubmüller B, et al. Salvage radical prostatectomy for radio-recurrent prostate cancer: an updated systematic review of oncological, histopathological and functional outcomes and predictors. European Urology Focus. 2021;7(5):967–978.
  5. Perera M, et al. Morbidity of salvage radical prostatectomy: limited impact of the minimally invasive approach. European Urology Open Science. 2022;39:64–72.
  6. Zumsteg ZS, et al. The natural history and predictors of outcome following biochemical relapse in the dose-escalation era for prostate cancer patients undergoing definitive external beam radiotherapy. European Urology. 2015;67(6):1009–1016.

 

Focal Laser Therapy for Localised Prostate Cancer: What Do We Know?

Focal therapy is an evolving approach to treating selected prostate cancers. Instead of treating or removing the entire prostate, it aims to destroy the identified cancer while preserving as much surrounding prostate tissue as possible.

One technique under investigation uses laser energy delivered through a fine fibre placed into the prostate. Early clinical reports are encouraging, but focal laser therapy is not suitable for every cancer and long-term evidence remains limited compared with established treatments such as radical prostatectomy and radiotherapy.

This article explains the disease, the principle of focal laser ablation, the early Guy’s Hospital pilot and the questions patients should consider before choosing treatment. It does not recommend a particular product, device or provider.

Understanding localised prostate cancer

Localised prostate cancer appears confined to the prostate on the available investigations. However, cancers vary greatly in their grade, size, position and biological behaviour.

Assessment commonly considers:

  • PSA level and PSA density
  • digital rectal examination findings
  • multiparametric prostate MRI
  • prostate-biopsy grade, often reported using Grade Group
  • number, position and extent of positive biopsy cores
  • whether clinically significant cancer is present in one or several parts of the prostate
  • the patient’s age, health, life expectancy and preferences
  • staging investigations where indicated

Some low-risk cancers may be monitored safely with active surveillance. Other cancers require treatment because their features suggest a meaningful risk of growth or spread.

What is focal therapy?

Focal therapy treats the known area of clinically significant cancer rather than the whole prostate. Depending on the extent and location of disease, treatment may target a small focus, a larger region or one side of the gland.

Energy sources used or investigated for focal therapy include:

  • high-intensity focused ultrasound
  • cryotherapy
  • irreversible electroporation
  • focal laser ablation
  • other thermal or energy-based techniques

These methods are not interchangeable. Each has different equipment, treatment planning, evidence, limitations and regulatory status.

How does focal laser ablation work?

Focal laser ablation delivers laser energy through a thin fibre positioned within the planned treatment area. The energy heats and destroys targeted tissue.

Placement may be performed through the perineum, the area between the scrotum and anus, with MRI and ultrasound information used to guide treatment planning and positioning. Temperature monitoring, cooling systems or other safeguards may be used according to the particular technique.

The intended advantage is to treat the cancer focus while reducing injury to structures involved in urinary continence, erections and bowel function. This is a treatment aim, not a guarantee. Damage to surrounding tissue and functional side effects remain possible.

What did the Guy’s Hospital pilot report?

Guy’s Hospital in London began a pilot involving 30 patients with localised prostate cancer. According to the hospital information reported by the BBC, assessment of the first 10 treated patients found no remaining cancer in the treated area in eight, while two had a small amount of residual cancer.

These figures should be interpreted cautiously:

  • they concern only the first 10 patients of a small pilot
  • they describe early findings in the treated area, not long-term cure
  • cancer may be present elsewhere in the prostate
  • follow-up was not long enough to establish durability, metastasis prevention or survival benefit
  • results from carefully selected research participants may not apply to all patients

The pilot includes ongoing follow-up, including imaging. Larger studies, longer observation and peer-reviewed comparative evidence are needed before firm conclusions can be drawn about long-term cancer control and functional outcomes.

Who might be considered for focal therapy?

Focal therapy may be discussed for carefully selected patients whose clinically significant cancer can be identified and targeted while untreated areas can be monitored reliably.

Selection may take account of:

  • MRI-visible disease
  • biopsy confirmation and cancer grade
  • location, volume and number of cancer foci
  • proximity to the urethra, urinary sphincter, rectum and neurovascular structures
  • prostate size and anatomy
  • previous prostate treatment
  • ability and willingness to undergo close follow-up and repeat biopsy
  • availability of appropriate expertise and governance

Multifocal, poorly defined, extensive or higher-risk cancer may make a focal approach unsuitable. An apparently single MRI lesion does not prove that no important cancer exists elsewhere in the gland.

What assessment is needed beforehand?

Accurate mapping of the cancer is essential. Depending on the patient, assessment may include:

  • review of PSA history
  • high-quality multiparametric MRI
  • targeted and systematic transperineal biopsy
  • expert radiology and pathology review
  • staging imaging when indicated by risk
  • baseline urinary, erectile and bowel function assessment
  • discussion by a multidisciplinary prostate-cancer team

A treatment decision should not be based on MRI alone. Biopsy remains important for confirming the grade and distribution of cancer.

Potential advantages

Possible advantages for appropriately selected patients include:

  • treatment directed at the known cancer rather than the entire prostate
  • usually a shorter procedure and recovery than radical prostatectomy
  • potential for same-day discharge
  • a lower treatment burden for some patients
  • the possibility of preserving urinary and sexual function more often than with whole-gland treatment
  • retention of other treatment options if further cancer is later detected

These are potential advantages, not assured outcomes. Comparisons with surgery or radiotherapy are difficult because patient selection, outcome definitions and follow-up periods differ across studies.

Risks and limitations

Possible complications include:

  • blood in the urine or semen
  • discomfort, bruising or swelling
  • urinary infection
  • difficulty passing urine or temporary catheterisation
  • urinary retention
  • urethral narrowing
  • urinary urgency or leakage
  • erectile or ejaculatory changes
  • injury to tissue surrounding the prostate
  • residual cancer within the treated area
  • clinically significant cancer elsewhere in the prostate
  • need for repeat focal treatment or conversion to surgery or radiotherapy

Rare but serious complications may occur. The specific risk profile depends on the technology, treatment location, operator experience and individual anatomy.

Focal therapy does not remove the need for surveillance

Unlike radical prostatectomy, focal therapy leaves prostate tissue behind. PSA therefore remains detectable and cannot be interpreted in the same way as after complete prostate removal.

Follow-up may include:

  • regular PSA testing
  • clinical review
  • repeat MRI
  • targeted and systematic repeat biopsy
  • assessment of urinary and sexual function

Imaging alone may not exclude residual or recurrent cancer. Patients need to be willing to undergo structured, long-term surveillance and possible further biopsy or treatment.

How does it compare with established options?

Active surveillance

Active surveillance avoids or delays treatment in suitable patients with lower-risk disease. It involves scheduled PSA tests, MRI, examination and repeat biopsy. It avoids immediate treatment side effects but carries the burden of monitoring and the possibility that treatment will later be required.

Radical prostatectomy

Surgery removes the prostate and seminal vesicles and provides complete pathological assessment of the removed gland. It has extensive long-term evidence for selected patients but may cause urinary incontinence, erectile dysfunction, loss of ejaculation and other surgical complications.

Radiotherapy

External-beam radiotherapy and brachytherapy are established treatments for localised prostate cancer. Risks may include urinary, bowel and sexual effects, which can develop during treatment or later. Some patients also require androgen-deprivation therapy.

Focal therapy

Focal therapy attempts to balance cancer control with preservation of function. Its principal uncertainties are the selection of suitable patients, untreated cancer elsewhere in the prostate, definitions of treatment success and the lack of mature comparative and long-term cancer-control data.

What happens if cancer remains or returns?

Further management depends on the location and risk of the cancer, previous treatment and patient preference. Options may include:

  • continued surveillance in selected circumstances
  • repeat focal treatment
  • radical prostatectomy
  • radiotherapy
  • another appropriate cancer treatment

Salvage treatment after focal therapy may be technically more complex and can have different side-effect rates from primary treatment. Patients should discuss the available rescue options before choosing focal therapy, not only after treatment failure.

Australian regulatory status and access

Regulatory status, approved indications, availability, reimbursement and participation in clinical trials can change. A device being used in research overseas does not automatically mean that the same system is approved, routinely available or publicly funded in Australia.

Patients considering a particular technology should ask:

  • Is the exact device included in the Australian Register of Therapeutic Goods for the proposed use?
  • Is treatment being offered as standard care, through a clinical trial or under another access pathway?
  • What evidence supports this technique for my particular cancer?
  • What costs and follow-up procedures are involved?
  • Who will manage surveillance and any residual or recurrent cancer?

Current regulatory information should be confirmed directly through the Therapeutic Goods Administration and the treating institution. This article does not make a claim that any named focal-laser system is TGA approved.

Questions to ask your prostate-cancer team

  • What is my Grade Group and clinical risk category?
  • Is the cancer confined to one clearly targetable area?
  • How confident are we that significant cancer is not present elsewhere?
  • Is active surveillance a safe option for me?
  • What are the established alternatives and their long-term outcomes?
  • What evidence is available for this focal technique?
  • How will success be measured?
  • Will I need another biopsy?
  • What are the urinary, sexual and bowel risks?
  • What happens if the cancer is not completely treated or later recurs?
  • Is this standard treatment or part of a research study?

The bottom line

The early Guy’s Hospital experience adds to growing interest in focal laser treatment for localised prostate cancer. The reported initial findings are encouraging, but 10 early cases cannot establish long-term cure, comparative effectiveness or safety.

Focal therapy may be reasonable to discuss for carefully selected patients who understand the uncertainties and accept close surveillance. It should be considered alongside active surveillance, surgery and radiotherapy through shared decision-making with an experienced multidisciplinary team.

This article provides general disease education. It does not recommend or promote a particular therapeutic device, treatment system, clinician or health service and does not replace individual medical advice. Regulatory status and clinical evidence should be checked at the time treatment is considered.

References and further reading

Publication note

This is an original educational article, not a republication of the BBC report.

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

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.

Spinal Cord Injury and the Bladder: Upper Motor Neuron versus Lower Motor Neuron Injury

Meta description: Spinal cord injury can cause urgency, leakage, urinary retention and dangerous bladder pressures. Learn how upper and lower motor neuron injuries differ, how neurogenic bladder is investigated, and which treatments may protect the kidneys and improve continence.

Best treated in an organised spinal unit.

Why can a spinal cord injury affect the bladder?

Passing urine is not simply a bladder reflex. It requires communication between the brain, the spinal cord, the sacral nerves and the urinary sphincter. During normal bladder filling, the bladder muscle, called the detrusor, remains relaxed while the outlet stays closed. When it is appropriate to urinate, the detrusor contracts and the sphincter relaxes in a coordinated fashion.

A spinal cord injury (SCI) can interrupt these pathways. The resulting problem is called neurogenic lower urinary tract dysfunction, often shortened to neurogenic bladder. A person may develop urgency, leakage, difficulty emptying, urinary retention, or a combination of these.

The most important issue is not always the symptom that is most noticeable. A bladder may feel relatively quiet yet store urine at a pressure high enough to threaten the kidneys. Conversely, severe urgency may occur without dangerous pressure. Assessment therefore aims to answer two separate questions:

  1. Is urine being stored and emptied at a pressure that is safe for the kidneys?
  2. Does the bladder routine provide acceptable continence, independence and quality of life?

The early phase: spinal shock

Immediately after an acute SCI, the bladder commonly becomes temporarily areflexic or acontractile. It fills but does not contract effectively, causing urinary retention. Bladder sensation may also be absent. Catheter drainage is usually required in this acute phase.

This phase may last days, weeks or sometimes longer. Reflex activity can then return below a suprasacral injury and the eventual bladder pattern may be very different from the early one. For this reason, the bladder should be reassessed as the neurological situation evolves.

Upper motor neuron versus lower motor neuron bladder

The traditional distinction is useful, but it is a guide—not a substitute for urodynamic testing.

Feature Upper motor neuron pattern Lower motor neuron pattern
Typical injury site Above the sacral micturition centre, often a suprasacral spinal cord lesion Sacral cord, conus medullaris, cauda equina or sacral/peripheral nerve injury
Bladder contraction Often involuntary detrusor contractions during filling—neurogenic detrusor overactivity Weak or absent detrusor contraction—detrusor underactivity or acontractility
Outlet behaviour The sphincter may contract instead of relaxing during a bladder contraction—detrusor-sphincter dyssynergia (DSD) Outlet resistance may be reduced if sacral innervation is damaged, although obstruction from other causes can coexist
Common symptoms Urgency, frequency, reflex voiding, urge leakage, interrupted emptying and residual urine Reduced bladder sensation, infrequent voiding, straining, retention, overflow leakage and recurrent infection
Main safety concern High storage or voiding pressure, poor compliance, reflux, hydronephrosis and renal damage Chronic retention, over-distension, infection, stones and overflow incontinence
Typical emptying strategy Often clean intermittent catheterisation, sometimes combined with bladder-relaxing treatment Clean intermittent catheterisation is commonly required when detrusor contraction is inadequate

Upper motor neuron injury: the overactive but poorly coordinated bladder

With an injury above the sacral spinal cord, the local sacral reflex circuit may remain intact but lose normal coordination from the brain. After spinal shock resolves, the bladder may contract unexpectedly during filling. At the same time, the external urinary sphincter may fail to relax or may tighten when the bladder contracts.

This combination of detrusor overactivity and DSD can produce:

  • urgency and reflex urinary leakage;
  • a stop–start urinary stream or incomplete emptying;
  • high bladder pressure;
  • urinary tract infection and bladder stones;
  • vesicoureteric reflux, hydronephrosis and, if not controlled, renal impairment.

People with SCI at or above approximately T6 can also develop autonomic dysreflexia. Bladder distension, a blocked catheter, infection or urological procedures may trigger sudden severe hypertension, a pounding headache, sweating or flushing above the injury, anxiety, nasal congestion and a slow or irregular pulse. This is a medical emergency: sit the person upright, check the catheter and drainage system promptly, and seek urgent medical assistance if symptoms or elevated blood pressure persist.

Lower motor neuron injury: the bladder that cannot squeeze effectively

Damage involving the sacral cord, conus medullaris, cauda equina or sacral nerves can interrupt the reflex pathway to the bladder. The detrusor may contract weakly or not at all. Sensation of filling may be reduced, so the bladder can become very full without the usual warning.

Possible features include:

  • difficulty starting or inability to pass urine;
  • infrequent voiding and a weak stream;
  • abdominal straining to empty;
  • a large post-void residual;
  • overflow leakage;
  • recurrent infection, stones or bladder over-distension.

If outlet innervation is also impaired, stress leakage can coexist with retention. A lower motor neuron lesion is therefore not automatically a “low-pressure and harmless” bladder.

Why the neurological level does not tell the whole story

Real-life bladder dysfunction does not always fit neatly into one box. An incomplete lesion can preserve some sensation or voluntary control. Injuries around the conus may affect upper and lower motor neuron pathways together. Pre-existing prostate enlargement, urethral stricture, pelvic floor dysfunction, medications, constipation and infection can further change bladder behaviour.

Most importantly, neurological examination and lesion level do not reliably predict bladder pressure or sphincter coordination. Symptoms can also change over time. Urodynamic findings, not the label alone, should guide risk assessment and treatment.

How is bladder function investigated after SCI?

Clinical assessment

Assessment usually includes:

  • the level, completeness, timing and cause of the SCI;
  • bladder sensation, urgency, leakage, voiding method and catheter routine;
  • recurrent infections, visible blood, stones, catheter blockage and episodes of autonomic dysreflexia;
  • fluid intake, urine output and a bladder diary where practical;
  • bowel function and constipation;
  • mobility, hand function, cognition, carer support and personal goals;
  • medicines that may affect storage or emptying;
  • abdominal, genital, perineal and focused neurological examination.

Basic tests

Depending on the clinical situation, these may include:

  • urinalysis and urine culture when infection is suspected;
  • measurement of the post-void residual by ultrasound or catheter;
  • kidney function blood tests, while recognising that serum creatinine may underestimate renal impairment in people with low muscle mass;
  • renal and bladder ultrasound to look for hydronephrosis, stones, bladder wall changes and residual urine;
  • other renal function assessment when clinically indicated.

A urine culture should not be used to screen for and repeatedly treat bacteria in an otherwise well catheter user. Asymptomatic bacteriuria is common and generally should not be treated, apart from recognised exceptions such as pregnancy or before selected urological procedures that breach the urinary mucosa.

Urodynamic studies

Multichannel urodynamics, sometimes combined with X-ray imaging as video-urodynamics, is central when the risk is unknown or potentially significant. It can determine:

  • bladder sensation and capacity;
  • detrusor overactivity;
  • bladder compliance and storage pressure;
  • detrusor strength during attempted voiding;
  • sphincter coordination or DSD;
  • leakage pressure, residual urine and, with video, reflux or outlet anatomy.

The test is not merely to explain incontinence. Its crucial role is to identify a hostile, high-pressure bladder before silent upper urinary tract damage develops. Repeat testing may be required after treatment, when symptoms change, after recurrent complications, or when renal imaging deteriorates.

Other tests

Cystoscopy is not a routine screening test for every person with SCI. It is used for a specific indication, such as visible blood in the urine, recurrent catheter blockage, suspected stones, difficult catheterisation, urethral injury or another anatomical concern. CT, MRI or nuclear renal imaging may be added when ultrasound or the clinical picture warrants it.

Management: protecting the kidneys while fitting treatment to the person

Treatment should be individualised with a urologist, rehabilitation physician, continence nurse and allied health team. The aim is low-pressure storage, reliable emptying, continence where achievable, fewer complications and a routine the person can realistically manage.

1. Reliable bladder emptying

Clean intermittent catheterisation (CIC/ISC) is often the preferred method when the bladder does not empty adequately. It avoids a continuously indwelling tube and can provide predictable, low-pressure drainage. Frequency is tailored to fluid intake, catheterised volumes, bladder pressure and the treatment plan. Hand function, access to the urethra, cognition, carer assistance, work and travel must all be considered.

If intermittent catheterisation is not feasible, an indwelling catheter may be required. When long-term indwelling drainage is necessary, a suprapubic catheter is often favoured over a urethral catheter because it avoids chronic urethral pressure and erosion, although it still carries risks of infection, blockage, leakage and stones.

Reflex voiding into a sheath system may suit selected men, but only after confirming that bladder pressures and emptying are safe. Regular reliance on abdominal straining or the Credé manoeuvre is generally discouraged because it can generate high pressure and may not empty the bladder adequately.

2. Reducing overactivity and unsafe storage pressure

Options include:

  • antimuscarinic medicines, which reduce involuntary bladder contractions but can cause dry mouth, constipation, blurred vision and cognitive adverse effects;
  • a beta-3 agonist, which may improve storage with a different side-effect profile but requires attention to blood pressure and other contraindications;
  • carefully selected combination therapy;
  • intradetrusor botulinum toxin A (Botox) when tablets are ineffective or poorly tolerated. This can markedly reduce detrusor overactivity and pressure but may increase urinary retention; the person must be willing and able to catheterise if required.

Alpha-blockers may reduce outlet resistance in selected people who void spontaneously, but they do not correct every form of DSD and may cause dizziness or low blood pressure.

3. Managing sphincter dyssynergia or outlet resistance

Where DSD prevents safe emptying, management may include intermittent catheterisation, bladder-relaxing therapy, selected alpha-blocker use, sphincter botulinum toxin, or less commonly, an outlet procedure such as sphincterotomy in carefully selected men using sheath drainage. Any procedure that lowers outlet resistance may improve emptying but can trade obstruction for incontinence.

4. Treating an acontractile lower motor neuron bladder

For a bladder that cannot contract effectively, CIC is usually the mainstay. There is no consistently effective oral medicine that restores a truly acontractile detrusor. Correcting reversible contributors: constipation, medicines, infection or mechanical obstruction remains important. Outlet surgery should only be considered when a proven obstruction is present and the likely effect on continence and catheterisation has been discussed.

5. Reconstructive surgery and urinary diversion

If conservative and minimally invasive measures cannot produce safe storage or practical drainage, options may include:

  • augmentation cystoplasty to increase capacity and reduce pressure;
  • creation of a continent catheterisable channel, such as a Mitrofanoff-type channel;
  • selected outlet continence surgery when sphincter weakness is the main problem;
  • urinary diversion, with or without bladder removal, in complex or refractory cases.

These are major procedures with long-term surveillance requirements and should be undertaken in an experienced neuro-urology service.

What about sacral neuromodulation?

Sacral neuromodulation is not a routine treatment for a complete spinal cord injury with established DSD or an acontractile bladder. It may be considered in carefully selected people with an incomplete, stable neurological lesion and suitable bladder function, but evidence in SCI is more limited than it is for non-neurogenic overactive bladder or non-obstructive retention. A test phase and specialist assessment are essential.

Follow-up is lifelong

Neurogenic bladder can change even when the spinal injury itself appears stable. Follow-up intensity is based on risk, bladder management method and previous complications. It may include review of symptoms and catheter volumes, renal function assessment, upper urinary tract imaging and repeat urodynamics in moderate- or high-risk patients.

Seek earlier review for:

  • new or worsening leakage;
  • difficulty catheterising or repeated catheter blockage;
  • recurrent symptomatic infection or fever;
  • visible blood in the urine;
  • flank pain, stones or hydronephrosis;
  • increasing residual urine;
  • new autonomic dysreflexia;
  • deterioration in kidney function.

The take-home message

An upper motor neuron injury often produces an overactive bladder that may fight against a closed sphincter. A lower motor neuron injury more often produces a poorly contracting bladder with retention. Both patterns can cause leakage, infection and kidney damage, and mixed patterns are common.

The safest plan is not based on the injury label alone. It combines symptoms, neurological assessment, kidney surveillance and where indicated, urodynamic testing. With an individualised catheter, medication, Botox or surgical plan, most people can achieve safer bladder pressures and a more predictable routine.

Medical disclaimer: This article provides general education and does not replace individual medical assessment. Sudden severe headache, sweating or flushing with high blood pressure in a person with SCI—particularly with an injury at or above T6—may represent autonomic dysreflexia and requires urgent attention.

References

  1. European Association of Urology. EAU Guidelines on Neuro-Urology. Current guideline edition. EAU Neuro-Urology Guidelines.
  2. Ginsberg DA, Boone TB, Cameron AP, et al. The AUA/SUFU Guideline on Adult Neurogenic Lower Urinary Tract Dysfunction: Diagnosis and Evaluation. J Urol. 2021;206(5):1097–1105. PubMed.
  3. Ginsberg DA, Boone TB, Cameron AP, et al. The AUA/SUFU Guideline on Adult Neurogenic Lower Urinary Tract Dysfunction: Treatment and Follow-up. J Urol. 2021;206(5):1106–1113. PubMed.
  4. American Urological Association; Society of Urodynamics, Female Pelvic Medicine & Urogenital Reconstruction. Adult Neurogenic Lower Urinary Tract Dysfunction Guideline. 2021; amended 2024. AUA/SUFU guideline.
  5. NSW Agency for Clinical Innovation. Management of the Neurogenic Bladder for Adults with Spinal Cord Injuries. State Spinal Cord Injury Service. NSW ACI spinal cord injury resources.
  6. Consortium for Spinal Cord Medicine. Bladder Management for Adults with Spinal Cord Injury: A Clinical Practice Guideline for Health-Care Providers. J Spinal Cord Med. 2006;29(5):527–573. Full text on PubMed Central.
  7. Pannek J, Blok B, Castro-Diaz D, et al. Guidelines on Neuro-Urology. European Association of Urology; updated annually. EAU Guidelines.
  8. Pannek J, Kennelly M, Kessler TM, et al. International spinal cord injury urodynamic basic data set (version 2.0). Spinal Cord Ser Cases. 2018;4:98. DOI.
  9. Hooton TM, Bradley SF, Cardenas DD, et al. Diagnosis, prevention, and treatment of catheter-associated urinary tract infection in adults: 2009 International Clinical Practice Guidelines from the Infectious Diseases Society of America. Clin Infect Dis. 2010;50(5):625–663. DOI.

 

How a Stroke Can Affect Bladder Function

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.

To My Bundaberg Patients: An Apology and an Explanation

I am sorry that I have had to cancel some of your procedures and appointments

Providing urological care to patients in Bundaberg and the surrounding region has been important to me, and I have greatly valued the relationships I have developed with my patients, their families, local doctors, nurses and hospital staff.

That is why having to cancel a consultation or surgical procedure at short notice is something I find particularly difficult.

Recently, however, I have had to make these decisions because of repeated last-minute changes and cancellations affecting flights I have booked with Qantas and Link Airways between Brisbane and Bundaberg.

To every patient who has been affected, I am sincerely sorry.

A cancelled operation is not simply a cancelled appointment

I know how much preparation goes into coming to hospital.

You may have taken time off work. Your partner may have taken leave to look after you. Someone may have driven several hours to be with you. You may have organised childcare, stopped medications, completed tests and fasted from the night before.

Most importantly, you may have spent days or weeks preparing yourself mentally for an operation.

Then, sometimes on the morning of your procedure, you are told that your surgeon cannot get to Bundaberg because the flight has been cancelled.

I can only imagine how frustrating, disappointing and, at times, distressing that must be.

You deserve better than that.

Regional patients deserve reliable transport too

Specialist medical care in regional Australia already comes with challenges that patients living in major cities often do not experience.

Visiting specialists are one way of bringing care closer to patients rather than expecting every patient to travel to Brisbane.

But that model depends upon something very basic:

The aeroplane actually needs to fly.

When an airline cancels or materially changes a regional flight at the last minute, the consequences extend well beyond inconvenience for an individual passenger.

In my circumstances, one cancelled seat can mean an entire operating list or clinic is disrupted.

Behind that operating list are real people.

Patients have prepared for surgery. Theatre staff and anaesthetists have been rostered. Hospital beds and equipment have been organised. Families have changed their plans. General practitioners have referred patients expecting them to receive specialist care.

A last-minute flight cancellation can unravel all of that remarkably quickly.

My frustration with Qantas and Link Airways

I appreciate that airlines sometimes need to cancel flights. Weather, aircraft safety, operational problems and other circumstances can make cancellation unavoidable.

However, the frequency and particularly the last-minute nature of the disruptions I have personally experienced with Qantas and Link Airways have made maintaining a dependable visiting surgical service to Bundaberg increasingly difficult.

This is not simply about the inconvenience caused to me as a traveller.

It is about the patients waiting at the other end of the flight.

Regional air services are part of the infrastructure that allows professionals, businesses and healthcare services to function outside Australia’s major cities.

I believe airlines operating regional routes need to recognise the broader consequences when those services become unreliable, particularly when cancellations occur with little notice and there is no realistic alternative that allows a specialist to reach the region in time.

Why can’t I simply take the next flight?

I wish it were that easy.

An operating theatre is not something that can simply be shifted several hours down the timetable.

An operation requires an anaesthetist, nursing staff, theatre personnel, specialised equipment, hospital beds and sufficient postoperative support. Other patients are also scheduled for procedures throughout the day.

Most importantly, surgery should never be rushed.

If a cancelled flight means I cannot arrive with enough time to safely complete an operating list, I will cancel or postpone the procedure rather than compromise patient care.

That decision is deeply frustrating, but patient safety will always win that argument.

To the patients I have disappointed

This is the part that matters most to me.

If you have been sitting at home fasting since midnight, or already travelled to hospital, only to discover that your operation cannot proceed, I am very sorry.

If your consultation has been postponed after you arranged work, travel or family commitments around it, I am sorry.

And if you have wondered whether your appointment or procedure was somehow unimportant, please know that it was not.

I know there is a person behind every name on my operating list.

I know that you have a family, responsibilities, anxieties and plans. I also know that being told “we will need to reschedule” does not magically undo everything you have already organised.

I remain committed to regional patients

I strongly believe that Australians living in regional communities should have reasonable access to specialist healthcare.

Whenever it is practical and safe to do so, I want to continue supporting patients outside Brisbane and reducing the need for people to make long journeys simply to see a specialist.

But regional specialist medicine cannot function in isolation.

It requires hospitals, doctors, nurses, allied health professionals and transport services to work together. Reliable regional aviation is part of that chain.

When that link repeatedly fails, patients ultimately carry the consequences.

Thank you

To my Bundaberg patients, their families, the local doctors who refer to me, and the wonderful nursing, administrative and theatre staff who have had to deal with the consequences of these disruptions:

Thank you for your patience, understanding and support.

And once again, to any patient whose care I have had to postpone because I could not get to Bundaberg:

I am genuinely sorry.

I will continue to do everything reasonably within my control to provide you with reliable, safe and compassionate urological care.

Perhaps there is also a broader conversation that needs to occur about the reliability of regional aviation and the people who depend upon it.

Because when a regional flight is cancelled, sometimes much more than a flight is cancelled.

Dr Jo Schoeman
Urological Surgeon

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

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

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

Hydronephrosis and Urinary Stones in Pregnancy What expectant mothers should know about flank pain, infection, premature labour and safe imaging

Pregnancy changes the urinary tract. The kidneys filter more blood, the hormone progesterone relaxes the ureters, and the enlarging uterus can compress them. As a result, the kidney drainage system and ureters often become dilated, a finding called hydronephrosis or hydroureter.

In most women this is a normal, temporary effect of pregnancy. However, hydronephrosis can also be caused by a kidney or ureteric stone, infection or, less commonly, another obstruction. The challenge is deciding whether the dilatation is physiological or whether the kidney is genuinely blocked and needs treatment.

Seek urgent medical assessment for flank pain accompanied by fever, chills, feeling faint or very unwell, persistent vomiting, difficulty passing urine, reduced fetal movement, contractions, vaginal bleeding or fluid loss. An infected, obstructed kidney is a urological emergency.

Why does hydronephrosis occur during pregnancy?

Physiological hydronephrosis usually develops during the second trimester, becomes most marked around 24–28 weeks and is often greater on the right. It results from:

  • progesterone-related relaxation of ureteric smooth muscle;
  • compression of the ureters by the growing uterus at the pelvic brim;
  • rotation of the uterus, which tends to place more pressure on the right ureter; and
  • increased urine production during pregnancy.

This dilatation commonly settles within several weeks after delivery. Physiological hydronephrosis is not itself a stone and does not automatically require a stent or operation.

Features that make pathological obstruction more likely include severe colicky flank pain, blood in the urine, a visible stone, dilatation extending below the pelvic brim, an absent or reduced ureteric jet on the symptomatic side, impaired kidney function, infection or worsening hydronephrosis. No single ultrasound sign is perfect; the symptoms, blood and urine tests, imaging and obstetric assessment must be considered together.

Kidney and ureteric calculi in pregnancy

Urinary calculi are stones located in the kidney or ureter. They are an important cause of non-obstetric abdominal or flank pain during pregnancy and occur most often in the second or third trimester. Typical symptoms include:

  • sudden pain in the loin, flank, abdomen or groin, which may come in waves;
  • nausea and vomiting;
  • visible or microscopic blood in the urine;
  • urinary frequency, urgency or burning; and
  • fever or rigors if infection is present.

Pregnancy increases urinary calcium and urate excretion, while other natural protective factors also rise. For this reason, pregnancy does not necessarily increase the overall number of stones, although the stone pattern may differ and calcium-phosphate stones are relatively more common.

Why infection matters

Pregnancy-related ureteric dilatation and slower urinary drainage encourage urinary stasis. A stone can worsen this by partly or completely blocking the ureter. Bacteria trapped above an obstruction may cause pyelonephritis, pyonephrosis, bacteraemia or sepsis.

All women with suspected renal colic should therefore have urinalysis and a urine culture. Blood tests commonly include a full blood count, kidney function, electrolytes and inflammatory markers. Antibiotics are selected according to pregnancy safety, local resistance patterns and culture results.

Antibiotics alone are not sufficient when infection is trapped behind an obstructed kidney. Urgent decompression with a ureteric stent or percutaneous nephrostomy is required, together with intravenous antibiotics and coordinated obstetric care. Definitive stone treatment is usually delayed until sepsis has resolved.

Is there a risk of premature labour?

Observational studies associate symptomatic stones and renal obstruction in pregnancy with higher rates of urinary infection, hospital admission, preterm contractions and preterm delivery. Severe pain, dehydration, inflammation and infection may all contribute. However, the absolute risk for an individual woman varies, and an association does not mean that every renal colic episode will trigger premature labour.

The condition requiring intervention may itself be responsible for some of the reported risk. For this reason, treatment decisions should not be based on procedure statistics alone. The balance is between allowing a stable stone time to pass and promptly treating uncontrolled pain, infection or threatened kidney function. Depending on gestational age and clinical circumstances, fetal monitoring and assessment for contractions may be appropriate.

How is it investigated?

1. Ultrasound first

Renal and bladder ultrasound is the preferred first-line test because it uses sound waves rather than ionising radiation. It can show hydronephrosis, some kidney or ureteric stones, ureteric jets and alternative diagnoses. Transvaginal ultrasound may help identify a distal ureteric stone.

Ultrasound has limitations: physiological hydronephrosis can resemble obstruction, and a small ureteric stone may not be visible. A normal or inconclusive scan does not always exclude a stone.

2. MRI or MR urography when uncertainty remains

MRI without gadolinium can identify the level and pattern of obstruction without ionising radiation. Stones usually appear as signal voids rather than being seen as clearly as on CT. MRI is therefore a useful second-line test, particularly when ultrasound is inconclusive and the patient is clinically stable. Gadolinium contrast is not routinely used during pregnancy.

3. Low-dose non-contrast CT only when clinically necessary

Low-dose CT is the most accurate test for a urinary stone, but it uses ionising radiation. European Association of Urology guidance places low-dose CT as a last-line option in pregnancy, after ultrasound and usually MRI, when diagnostic uncertainty could change urgent management.

The practical radiation principles are:

  • use imaging only when it will answer an important clinical question;
  • prefer ultrasound, followed by MRI without contrast, when suitable;
  • if CT is necessary, use a pregnancy-adapted low-dose protocol and limit the scanned area;
  • avoid repeated or multiphase CT examinations unless clearly justified; and
  • involve an experienced radiologist and document the risk–benefit discussion.

Diagnostic imaging should not be withheld when delay or uncertainty poses a greater risk to the mother or baby. The EAU notes that deterministic fetal effects require substantially higher exposure than most diagnostic studies and considers doses below 50 mGy safe in this context; nevertheless, any ionising-radiation examination must be justified and kept as low as reasonably achievable. Ultrasound and MRI do not use ionising radiation.

Management options

Treatment is individualised by symptoms, infection status, stone size and location, kidney function, gestational age, obstetric factors and local expertise. Close collaboration between urology, obstetrics, radiology, anaesthesia and neonatology may be needed.

Conservative management

Most uncomplicated cases are initially managed without surgery. This may include:

  • oral or intravenous fluids sufficient to correct dehydration, forced overhydration does not “flush out” a stone;
  • anti-nausea medication;
  • analgesia suitable for the stage of pregnancy;
  • urine culture and pregnancy-compatible antibiotics when infection is confirmed; and
  • follow-up to ensure symptoms resolve and kidney drainage and function remain satisfactory.

Paracetamol is commonly used first-line. Opioids may be used for severe pain under medical supervision. Non-steroidal anti-inflammatory drugs such as ibuprofen and diclofenac should not be self-administered in pregnancy; their fetal renal, amniotic-fluid and ductus arteriosus risks depend on gestation, dose and duration. The evidence for medical expulsive therapy with alpha-blockers during pregnancy is limited, and such treatment should only be considered after specialist discussion.

Conservative treatment is unsuitable when there is sepsis, deteriorating kidney function, a solitary obstructed kidney, bilateral obstruction, persistent vomiting, uncontrolled pain, severe or progressive hydronephrosis, renal forniceal rupture, threatened premature labour or failure of the stone to pass with ongoing clinically important obstruction.

Ureteric stent

A JJ stent bypasses the obstruction and drains urine from the kidney to the bladder. It can be inserted with minimal or no fluoroscopy, using ultrasound guidance where appropriate. Stents can cause urinary frequency, urgency, discomfort, blood in the urine, infection and encrustation. Encrustation develops faster in pregnancy, so regular review and sometimes exchange every 4–6 weeks are required. A stent must not be forgotten after delivery.

Percutaneous nephrostomy

A nephrostomy tube drains the kidney through the back and can often be placed with ultrasound guidance. It is particularly useful when retrograde stenting is not possible or when urgent drainage is required in selected circumstances. Disadvantages include an external bag, discomfort, blockage, displacement, infection and rapid encrustation, with possible repeat exchanges.

Ureteroscopy and laser treatment

Ureteroscopy allows a surgeon to pass a fine telescope through the bladder into the ureter, remove the stone or fragment it with a laser, often without fluoroscopy. It provides definitive treatment and avoids prolonged drainage in selected patients. If a non-urgent procedure is required, the second trimester is generally preferred, and it should be performed by an experienced team with obstetric and neonatal support available. Ureteroscopy is not the first step in an untreated septic obstruction; drainage and infection control come first.

Treatments generally avoided

Shock-wave lithotripsy is contraindicated during pregnancy. Percutaneous stone removal is rarely required and is reserved for carefully selected cases in highly experienced centres. Routine definitive treatment can often wait until after delivery when symptoms and kidney function permit.

After delivery

Follow-up should confirm that hydronephrosis has resolved, any stent or nephrostomy has been removed, the stone has passed or been treated, and kidney function is normal. A retrieved stone should be analysed. Women with recurrent stones, a strong family history, infection stones or other risk factors may benefit from a metabolic evaluation after pregnancy, when physiology and diet have stabilised.

The important message

Most hydronephrosis in pregnancy is physiological, and many stones pass with careful conservative management. The dangerous combination is obstruction plus infection. Fever, rigors or systemic illness with flank pain requires urgent assessment because prompt antibiotics and drainage can protect the mother, kidney and pregnancy. Imaging should follow a stepwise approach, ultrasound first, MRI second and low-dose CT only when the clinical benefit justifies it.


References

  1. European Association of Urology. EAU Guidelines on Urolithiasis: Diagnostic imaging during pregnancy; management of urinary stones during pregnancy. Current online guideline. https://uroweb.org/guidelines/urolithiasis/chapter/guidelines
  2. Lee MS, Fenstermaker MA, Naoum EE, et al. Management of nephrolithiasis in pregnancy: multi-disciplinary guidelines from an academic medical center. Front Surg. 2021;8:796876. https://doi.org/10.3389/fsurg.2021.796876
  3. Chan K, Shakir T, El-Taji O, et al. Management of urolithiasis in pregnancy. Curr Urol. 2023;17(1):1–6. https://doi.org/10.1097/CU9.0000000000000181
  4. American College of Obstetricians and Gynecologists. Guidelines for diagnostic imaging during pregnancy and lactation. Committee Opinion No. 723. Obstet Gynecol. 2017;130–e216. https://www.acog.org/clinical/clinical-guidance/committee-opinion/articles/2017/10/guidelines-for-diagnostic-imaging-during-pregnancy-and-lactation
  5. Drescher M, Blackwell RH, Patel PM, et al. Antepartum nephrolithiasis and the risk of preterm delivery. Urolithiasis. 2019;47:441–448. https://doi.org/10.1007/s00240-018-1085-3

This information is general education and does not replace individual medical or obstetric advice. Medication and imaging decisions in pregnancy should be made with the treating obstetric, urology and radiology teams.

Vesico-ureteric reflux: when urine travels in the wrong direction

Vesico-ureteric reflux, also called vesicoureteral reflux or VUR, occurs when urine flows backwards from the bladder into one or both ureters and sometimes as far as the kidneys.

Normally, each ureter enters the bladder through a short tunnel in the bladder wall. As the bladder fills and contracts, this tunnel is compressed, acting like a one-way valve. In VUR, the valve does not close effectively.

VUR itself does not always cause symptoms. Its importance is that infected urine may travel towards the kidneys, increasing the risk of pyelonephritis, renal scarring and, in a small number of higher-risk patients, long-term kidney damage.

Primary and secondary reflux

Primary VUR

Primary VUR is usually a developmental condition. The ureter’s tunnel through the bladder wall is too short or positioned in a way that prevents reliable closure. It is most commonly diagnosed in infancy or childhood.

As a child grows, the bladder and ureteric junction mature. For this reason, many cases particularly lower-grade reflux, improve or resolve without surgery.

Secondary VUR

Secondary reflux develops because pressure within the bladder is abnormally high or because the bladder does not empty properly. Causes may include:

  • posterior urethral valves or another bladder-outlet obstruction
  • dysfunctional voiding
  • constipation and bladder–bowel dysfunction
  • neurogenic bladder, including spina bifida or spinal cord disease
  • urethral stricture or an enlarged prostate in adults
  • previous bladder or ureteric surgery
  • a poorly compliant, high-pressure bladder.

Treating the underlying bladder or outlet problem is essential. Correcting the reflux alone may fail if the bladder remains unsafe or under excessive pressure.

How does VUR present in children?

Most children do not feel the reflux itself. It is commonly discovered while investigating a urinary tract infection.

Possible presentations include:

  • a fever without an obvious cause, particularly in an infant
  • recurrent urinary tract infections
  • febrile UTIs or kidney infections
  • vomiting, lethargy, irritability or poor feeding in babies
  • abdominal, loin or back pain
  • painful or frequent urination
  • urinary urgency or wetting
  • poor urinary stream or straining
  • antenatal ultrasound showing hydronephrosis or an abnormal urinary tract
  • poor growth
  • high blood pressure or impaired kidney function in more advanced reflux nephropathy.

A child with fever, vomiting, flank pain or marked lethargy may have pyelonephritis and should receive prompt medical assessment.

How does VUR present in adults?

VUR is much less commonly diagnosed for the first time in adulthood. Some adults have persistent congenital reflux that was never detected in childhood, while others develop secondary reflux due to bladder dysfunction or obstruction.

Adults may present with:

  • recurrent febrile UTIs
  • repeated kidney infections
  • loin or flank pain
  • renal scarring found on imaging
  • high blood pressure
  • protein or blood detected in the urine
  • reduced kidney function
  • pregnancy-associated urinary infections
  • lower urinary tract symptoms or incomplete bladder emptying.

Adult VUR should prompt assessment for an underlying cause such as bladder-outlet obstruction, neurogenic bladder, poor bladder compliance or dysfunctional voiding. The evidence guiding adult treatment is less extensive than the paediatric literature, so management is individualised.

How is VUR investigated?

Not every child who has one uncomplicated UTI requires an invasive reflux study. Imaging is selected according to age, clinical presentation, ultrasound findings and whether the infection is atypical or recurrent.

Urine testing

Urinalysis and urine culture confirm infection and help guide antibiotic treatment. A properly collected urine specimen is particularly important in babies and young children.

Kidney and bladder ultrasound

Ultrasound is painless and does not use radiation. It can assess:

  • kidney size and development
  • hydronephrosis or ureteric dilatation
  • bladder-wall appearance
  • congenital urinary abnormalities
  • residual urine after voiding.

A normal ultrasound does not completely exclude VUR.

Micturating cystourethrogram

A micturating cystourethrogram, also called an MCUG or VCUG, is the standard test for confirming and grading reflux.

A small catheter is placed into the bladder, contrast is introduced, and X-ray images are taken while the bladder fills and during urination. The test shows whether contrast travels backwards into the ureters or kidneys and also provides information about the bladder and urethra.

Because catheterisation and a small radiation exposure are involved, MCUG is generally reserved for children in whom the result is likely to influence management.

Contrast-enhanced voiding urosonography

In centres where it is available, contrast-enhanced ultrasound can identify reflux without ionising radiation. Availability and local expertise vary, and conventional MCUG may still be required when detailed urethral anatomy needs assessment.

DMSA renal scan

A DMSA scan assesses the functioning renal cortex and can identify established renal scars. It is not required for every child but may be considered after recurrent febrile infections, in higher-grade reflux, when ultrasound is abnormal or when renal damage is suspected.

Additional assessment

Depending on the circumstances, investigation may also include:

  • blood pressure measurement
  • serum creatinine and estimated kidney function
  • urine protein assessment
  • a bladder and bowel history
  • uroflowmetry and measurement of residual urine
  • a bladder diary
  • urodynamic studies when a high-pressure, neurogenic or poorly emptying bladder is suspected
  • CT or other upper-tract imaging in selected adults.

The five grades of reflux

VUR is graded from I to V according to the international grading system.

Grade Imaging appearance General interpretation
Grade I Reflux reaches the ureter but not the kidney Mild
Grade II Reflux reaches the renal pelvis without dilatation Mild
Grade III Mild to moderate dilatation of the ureter and renal collecting system Moderate
Grade IV Moderate ureteric and collecting-system dilatation with some twisting of the ureter High-grade
Grade V Severe dilatation and tortuosity with loss of normal calyceal detail Severe

The grade is important, but it is not the only factor determining treatment. Age, recurrent infections, kidney scarring, bladder and bowel function, whether reflux affects one or both sides, and family preferences all matter.

What is the aim of treatment?

Treatment aims to:

  • prevent febrile UTIs and pyelonephritis
  • reduce the risk of further renal scarring
  • preserve kidney function
  • treat bladder, bowel or outlet dysfunction
  • avoid unnecessary medication, radiation and surgery.

It is important to understand that repairing reflux cannot reverse established renal scars. Treatment is intended to prevent further infection and injury.

Observation and conservative management

Observation is appropriate for many children, particularly those with lower-grade reflux, healthy kidneys and no recurrent febrile infections.

Conservative care may include:

  • prompt urine testing when fever or urinary symptoms occur
  • regular and complete bladder emptying
  • adequate fluid intake
  • avoiding prolonged holding of urine
  • treating constipation
  • timed voiding
  • management of daytime wetting or dysfunctional voiding
  • periodic clinical and ultrasound review.

Lower-grade reflux is more likely to resolve as the child grows. Higher grades, bilateral reflux and reflux associated with renal abnormalities are less likely to resolve spontaneously.

Continuous low-dose antibiotic prophylaxis

A low dose of antibiotic may be prescribed daily to reduce recurrent infections while waiting for reflux to improve or while deciding whether intervention is required.

Prophylaxis is more likely to be considered in:

  • infants with VUR following a febrile UTI
  • recurrent febrile UTIs
  • higher-grade reflux
  • bladder–bowel dysfunction
  • renal cortical abnormalities
  • children considered at increased risk of another kidney infection.

Antibiotics can reduce recurrent UTIs in appropriately selected children, but they do not mechanically correct the reflux. Disadvantages include medication side effects, adherence difficulties and antibiotic resistance. The need for ongoing prophylaxis should therefore be reviewed rather than continued automatically.

Treating bladder and bowel dysfunction

Constipation, urinary urgency, wetting, infrequent voiding and incomplete bladder emptying increase the risk of recurrent infection and may reduce the success of reflux treatment.

Management can include:

  • regular timed voiding
  • relaxed toilet posture
  • treatment of constipation
  • pelvic-floor or continence physiotherapy
  • medication for selected bladder conditions
  • intermittent self-catheterisation when emptying is inadequate.

In secondary reflux, treating the bladder or outlet disorder may reduce or occasionally eliminate the reflux.

When is a procedure considered?

Intervention may be discussed when there is:

  • a febrile breakthrough UTI despite appropriate prophylaxis
  • recurrent pyelonephritis
  • new or progressive renal scarring
  • persistent high-grade reflux
  • reflux unlikely to resolve spontaneously
  • difficulty tolerating or adhering to antibiotic prophylaxis
  • an anatomical abnormality requiring correction
  • significant family preference after discussion of the alternatives
  • persistent symptomatic reflux in a carefully selected adult.

The two main corrective options are endoscopic injection and ureteric reimplantation.

The STING procedure

STING stands for subureteric transurethral injection. A small telescope is passed through the urethra into the bladder under anaesthesia. A bulking material is injected beneath or within the lower end of the ureter to support and lengthen the valve mechanism.

Dextranomer/hyaluronic-acid copolymer, commonly known by the brand name Deflux, is the best-known injection material. Modified techniques such as HIT or double-HIT place the material within the intramural ureter rather than only beneath its opening.

Advantages

  • minimally invasive
  • no abdominal incision
  • usually performed as day surgery
  • relatively short anaesthetic and recovery
  • low risk of major complications
  • can be repeated if reflux persists.

Limitations and risks

  • success is lower and less predictable than formal reimplantation
  • results are generally better for lower grades of reflux
  • more than one injection may be required
  • reflux may persist or recur
  • temporary blood in the urine, discomfort or infection can occur
  • ureteric obstruction is uncommon but important
  • reflux may occasionally appear on the opposite side
  • long-term durability is not as certain as with successful reimplantation.

Published cure rates vary considerably because they depend on reflux grade, anatomy, injection technique, material used and how success is defined. A single injection commonly corrects approximately 70–80% of refluxing ureters overall, with lower success in grades IV–V. Additional injections can increase the cumulative success rate.

Ureteric reimplantation

Ureteric reimplantation is reconstructive surgery that creates a longer tunnel for the ureter through the bladder wall, restoring the one-way valve mechanism.

The operation may be performed using:

  • an open extravesical approach
  • an open intravesical approach
  • laparoscopic surgery
  • robot-assisted surgery in selected centres and patients.

Open reimplantation has a long-established success rate of approximately 95–98% for primary VUR when performed in suitable patients.

Advantages

  • highest and most durable anatomical correction rate
  • effective for high-grade reflux
  • allows correction of some associated ureteric abnormalities
  • usually requires only one definitive operation.

Limitations and risks

  • more invasive than injection
  • longer anaesthetic and recovery
  • temporary bladder spasms, pain or blood in the urine
  • urinary infection
  • transient urinary retention, particularly after some bilateral extravesical repairs
  • ureteric obstruction
  • persistent reflux or reflux on the opposite side
  • rare need for further surgery.

Robotic or laparoscopic reimplantation can reduce incision size, but it is still major reconstructive surgery and has not made open surgery obsolete. The best approach depends on the child’s anatomy, age, surgeon’s expertise and the reason for intervention.

STING versus reimplantation

Consideration Endoscopic injection Ureteric reimplantation
Invasiveness Minimally invasive Reconstructive surgery
Typical stay Usually day surgery Often one or more nights
Recovery Generally quicker Longer
Success after one procedure Lower and grade-dependent Approximately 95–98%
Repeat treatment Sometimes required Uncommon after successful repair
Best suited to Selected low- or moderate-grade reflux and families prioritising minimal invasiveness High-grade, persistent or complicated reflux; failed injection; selected anatomical abnormalities
Main trade-off Easier recovery but less predictable cure More invasive but more reliable correction

Neither operation is automatically “best.” STING may be attractive when a minimally invasive approach is preferred and its probability of success is acceptable. Reimplantation may be more appropriate when the highest likelihood of definitive correction is important.

VUR in adults

Adults with incidentally detected reflux and no infections, renal deterioration or high-pressure bladder may not require corrective surgery.

Treatment is more likely to be considered when there is:

  • recurrent febrile UTI or pyelonephritis
  • progressive kidney damage
  • troublesome reflux-associated flank pain
  • an untreated bladder-outlet or functional abnormality
  • pregnancy planning in a patient with recurrent infections or reflux nephropathy.

The underlying bladder problem must be identified before anti-reflux surgery. Endoscopic injection can be effective in selected adults, although the supporting evidence is mainly from smaller observational studies. Ureteric reimplantation remains an option when a durable anatomical repair is required.

Women with previous VUR or reflux nephropathy who are considering pregnancy may benefit from pre-pregnancy assessment of blood pressure, kidney function, urine protein and infection risk.

Follow-up

Follow-up should be tailored to reflux grade, renal findings, treatment and infection history.

During observation

Review may include:

  • interval history of UTIs or unexplained fevers
  • height, weight and growth in children
  • blood pressure
  • urine testing when symptoms occur
  • assessment of constipation and bladder symptoms
  • renal and bladder ultrasound
  • serum creatinine and urine protein testing when renal damage is present or suspected
  • selective repeat MCUG, contrast-enhanced urosonography or radionuclide cystography
  • DMSA scanning when new scarring is suspected.

Routine repeated invasive imaging is not necessary for every child. The timing and type of imaging should be chosen only when the result is likely to alter management.

After STING

Follow-up commonly includes an ultrasound to exclude obstruction and clinical monitoring for further UTIs. A repeat reflux study may be recommended after several months, particularly in high-grade reflux, recurrent febrile infection or when confirmation of cure will affect treatment.

Any fever or urinary symptoms after injection should prompt urine testing. Flank pain, vomiting, reduced urine output or significant hydronephrosis requires assessment for the uncommon complication of ureteric obstruction.

After reimplantation

Ultrasound is commonly performed after surgery to check drainage. Routine postoperative MCUG may not be necessary after an uncomplicated reimplantation with a reassuring recovery, but it may be appropriate after breakthrough infection, persistent hydronephrosis or an atypical clinical course.

Long-term surveillance

Patients with renal scarring, bilateral severe reflux, a solitary functioning kidney, proteinuria, hypertension or impaired renal function may require long-term follow-up into adulthood.

Monitoring can include:

  • blood pressure
  • kidney function
  • urine protein
  • recurrent infection
  • pregnancy counselling when relevant.

Even when reflux has resolved, established reflux nephropathy can remain clinically important.

When should urgent medical advice be sought?

Seek prompt medical assessment for:

  • fever with loin or back pain
  • vomiting or marked lethargy
  • reduced urine output
  • a very unwell infant
  • urinary symptoms during pregnancy
  • fever or flank pain after a reflux procedure.

Early diagnosis and treatment of pyelonephritis are particularly important in patients with known VUR.

The key message

Vesico-ureteric reflux ranges from a mild childhood condition that resolves with growth to high-grade reflux associated with recurrent kidney infections and renal scarring.

Treatment should not be based on grade alone. The safest plan considers infection history, kidney health, age, bladder and bowel function, likelihood of spontaneous resolution and the advantages and disadvantages of observation, antibiotic prophylaxis, endoscopic injection and ureteric reimplantation.

References and further reading

  1. European Association of Urology. EAU Guidelines on Paediatric Urology: Vesicoureteric reflux. EAU Paediatric Urology Guidelines
  2. American Urological Association. Management and Screening of Primary Vesicoureteral Reflux in Children. AUA Vesicoureteral Reflux Guideline
  3. National Institute for Health and Care Excellence. Urinary tract infection in under 16s: diagnosis and management (NG224). NICE guideline NG224
  4. RIVUR Trial Investigators. Antimicrobial prophylaxis for children with vesicoureteral reflux. New England Journal of Medicine. 2014;370:2367–2376. PubMed
  5. Mattoo TK, Chesney RW, Greenfield SP, et al. Renal scarring in the Randomized Intervention for Children with Vesicoureteral Reflux trial. Clinical Journal of the American Society of Nephrology. 2016;11:54–61. PubMed
  6. Läckgren G, Cooper CS, Neveus T, Kirsch AJ. Management of vesicoureteral reflux: what have we learned over the last 20 years? Frontiers in Pediatrics. 2021;9:650326. Full text
  7. Salib A, Pizzi M, Landman J, et al. Vesicoureteral reflux in adults with urinary tract infections: is there a role for treatment? Current Urology Reports. 2020. PubMed record

This article provides general education and does not replace individual medical advice. Decisions about imaging, antibiotic prophylaxis or surgery should be made with an appropriately experienced urologist or paediatric urologist.