Interstitial Cystitis (Bladder Pain Syndrome)

Interstitial cystitis — also called bladder pain syndrome, and increasingly written as IC/BPS to reflect both names — is defined by the Society for Urodynamics, Female Pelvic Medicine and Urogenital Reconstruction (SUFU) as "an unpleasant sensation (pain, pressure, discomfort) perceived to be related to the urinary bladder, associated with lower urinary tract symptoms of more than six weeks duration, in the absence of infection or other identifiable causes." Both the current American Urological Association (AUA) guideline and the 2025 Canadian Urological Association (CUA) guideline adopt this same definition.^[1][2]

That final clause is the clinically important part: IC/BPS is fundamentally a diagnosis of exclusion. It is reached only after infection, bladder cancer, and other identifiable causes of the same pain-plus-urgency-plus-frequency picture have been actively ruled out — not applied the moment a patient reports pelvic pain and urinary frequency (see Assessment & Diagnosis and Red Flags/Refer).^[1]

How common is it?

Prevalence estimates vary widely, largely because there is no objective diagnostic marker and because different studies use self-report, symptom questionnaires, or clinician/billing diagnoses to define a case.^[1] A recent review combining individual chart abstraction with a national population-based data set review estimated IC/BPS prevalence at 1.08% in women and 0.66% in men.^[2] Earlier large United States self-report surveys (the National Health Interview Survey and NHANES III) estimated overall prevalence around 470-500 per 100,000, rising to roughly 850-865 per 100,000 among women — projecting to approximately 1.2 million American women and 83,000 American men.^[1]

The classically cited female-to-male ratio of about 10:1 likely overstates the true sex disparity. Uncontrolled clinical series over the past two decades, and the NIH-funded Multidisciplinary Approach to the Study of Chronic Pelvic Pain (MAPP) Research Network, suggest IC/BPS in men has been considerably under-recognized: about 3 in 4 men enrolled in MAPP with bladder pain/storage symptoms met IC/BPS-consistent criteria of "painful bladder filling" and/or "painful urgency."^[1] Men with IC/BPS are more likely to report suprapubic tenderness than perineal pain as their most bothersome symptom, and the diagnosis should be considered whenever a man's pain is perceived as bladder-related (see Recognize the Condition).^[1]

Delay, burden, and overlap

Patients often live with symptoms for years before a diagnosis is reached — CUA notes a typical interval of 4-7 years — and one study found a median of two years for the full frequency-urgency-pain symptom complex to develop.^[2][1] IC/BPS is most commonly diagnosed after age 40, though it can occur at any age.^[1] Its impact on health-related quality of life has been reported as comparable in severity to rheumatoid arthritis and end-stage renal disease, with significantly higher rates of depression, sleep dysfunction, and sexual dysfunction than in matched controls.^[1] In the MAPP cohort, 44% of IC/BPS patients had at least one additional chronic overlapping pain condition (COPC) such as fibromyalgia, irritable bowel syndrome, or chronic fatigue syndrome, and patients with this widespread-pain pattern had more severe urologic symptoms, worse psychosocial functioning, and a worsening symptom trajectory over time.^[1]

What drives it — leading, unconfirmed theories

The pathophysiology of IC/BPS remains incompletely understood, and no single mechanism has been proven to cause the syndrome; the following are leading candidate theories rather than settled fact.^[3] The most-cited theory is a defect in the bladder's protective glycosaminoglycan (GAG) layer — the mucous coating that normally shields the urothelium from urinary solutes. Biopsies in some patients show increased urothelial permeability with loss of tight-junction and adhesive-junction proteins, producing a "leaky" urothelium that may allow potassium and other irritants in urine to penetrate the bladder wall and trigger pain signaling.^[3] A second leading theory implicates mast cell activation: increased mast cell density has been observed in bladder tissue, particularly in patients with Hunner lesions, and mast cell mediators are thought to further stimulate afferent sensory nerve fibers.^[3] A third, related theory is neurogenic inflammation, in which sensitized nerve fibers release inflammatory neuropeptides that perpetuate a self-reinforcing cycle of nerve and mast-cell activation — a mechanism proposed to connect to the central pain-sensitization and altered pain-processing brain findings reported in some IC/BPS patients.^[3] None of these mechanisms is mutually exclusive, chronic activation of any of them can drive fibrosis and reduced bladder capacity over time in a subset of patients, and both national guideline panels treat IC/BPS as a genuinely heterogeneous clinical syndrome best approached by clinical phenotype rather than by a single presumed cause (see Recognize the Condition).^[3][2][1]

The hallmark symptom: pain

Pain — including sensations of pressure and discomfort — is the hallmark symptom of IC/BPS. Patients often use words other than "pain," such as "pressure," "burning," "sharp," or an "uncomfortable sensation of having to urinate," and some patients actively deny having pain while clearly endorsing these descriptors.^[1] Pain is usually felt in the suprapubic area but can be referred to any part of the pelvis, lower abdomen, back, urethra, vulva, vagina, or rectum.^[1][2] The single most clinically distinguishing feature is that pain characteristically worsens as the bladder fills and improves, at least transiently, with voiding — "painful bladder filling."^[1][2]

Urgency and frequency — and how to tell IC/BPS apart from overactive bladder

Frequency is the most prevalent lower urinary tract symptom in IC/BPS, present in over 90% of cases.^[2] Urgency is also very common, but on its own it cannot distinguish IC/BPS from overactive bladder (OAB) — the two conditions can coexist, and this is a genuinely important bedside distinction rather than a technicality. Key distinction OAB patients void out of fear of incontinence; IC/BPS patients void to relieve pain, pressure, or discomfort — "painful urgency."^[2][1] A positive response to antimuscarinic therapy suggests OAB, but be aware the two illnesses may coexist and complicate the picture.^[2]

Flares and comorbidities

Symptoms may appear gradually or with only one voiding symptom initially, with later progression to the full symptom complex.^[1] Individuals may talk about "flares," or times when symptoms suddenly and significantly intensify for hours, days, or weeks. Common flare triggers include stress, sexual activity, menstruation, and dietary factors — caffeine, alcohol, citrus fruits, tomatoes, carbonated beverages, and spicy foods are frequently reported (see Non-Pharmacologic Treatment for a practical, individualized approach to identifying a given patient's specific triggers).^[2] Gastrointestinal symptoms — constipation, diarrhea, abdominal pain — are common and should be explored directly.^[2] There is a strong relationship between past traumatic experience and post-traumatic stress disorder (PTSD) and IC/BPS; screening for a history of abuse, in a trauma-informed manner, is a genuinely essential part of the assessment.^[2] Beyond COPCs, sexual dysfunction is moderate-to-severe and occurs at high rates compared with controls, and in patients with treatment-refractory IC/BPS, poor sexual function is a primary predictor of poor mental quality of life.^[1]

Presentation in men

Historically considered rare in men, IC/BPS is now understood to be substantially under-recognized in the male population (see Clinical Snapshot). It overlaps significantly with chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS, or NIH Type III prostatitis) — pain in the perineum, suprapubic region, testicles, or tip of the penis, often exacerbated by urination or ejaculation, with voiding symptoms such as a sense of incomplete emptying and frequency also commonly reported.^[1] The diagnosis of IC/BPS should be strongly considered in men whose pain is perceived as bladder-related, or who have "painful urgency" and/or "painful bladder filling"; some men genuinely meet criteria for both conditions simultaneously, and treatment in that situation can combine established IC/BPS therapies with CP/CPPS-specific approaches.^[1]

Clinical phenotyping — an organizing framework for this chapter

IC/BPS is a genuinely heterogeneous clinical syndrome rather than a single disease, and recognizing which phenotype is in front of you may be one of the more impactful advances in IC/BPS management to date — it should be sought at every encounter and is the framework this chapter uses to organize treatment selection (see Choose Initial Treatment).^[2]

• Female sex — though IC/BPS in men is genuinely under-recognized, and the true sex disparity is likely smaller than the historically cited 10:1 ratio (see Clinical Snapshot).^[1]
• Age over 40 at typical diagnosis, though IC/BPS can occur at any age; older patients are considerably more likely to have Hunner lesions on cystoscopy — found in about 4% of patients under 50, in 20% of patients 50 to 70, and in as many as 55% of those over 70.^[2]
• Comorbid chronic pain conditions ("chronic overlapping pain conditions," or COPCs) — fibromyalgia, irritable bowel syndrome, chronic fatigue syndrome, vulvodynia, Sjögren's syndrome, and chronic headaches are all recognized associations, and 44% of IC/BPS patients in the MAPP cohort had at least one additional COPC.^[1]
• A history of psychological trauma or PTSD — there is a strong relationship between past traumatic experience and IC/BPS, and screening for a history of abuse in a trauma-informed manner is considered essential.^[2]
• A prior history of pelvic surgery, including hysterectomy — though the high incidence of such surgery in IC/BPS patients may partly reflect a missed diagnosis leading to unnecessary surgery for presumed gynecologic pain, rather than surgery itself being a true causal risk factor.^[1]
• Emerging evidence of a possible biologic-susceptibility or genetic component — genetic linkage studies have suggested a link between IC/BPS and panic disorder, though this remains an area of ongoing research rather than an established discrete risk factor.^[1]
• A history of exposures and conditions relevant to the broader differential rather than strict causal risk factors for IC/BPS itself — prior pelvic surgery or radiation, drugs that can cause cystitis (such as cyclophosphamide or ketamine), autoimmune disease, allergies, and other gynecologic conditions (vulvodynia, endometriosis, dyspareunia) — all worth asking about directly during history-taking.^[2]
• Smoking — not itself a specific risk factor for IC/BPS, but relevant because it materially raises bladder cancer risk and therefore lowers the threshold for cystoscopic exclusion in anyone being worked up for IC/BPS-like symptoms (see Assessment & Diagnosis and Red Flags/Refer).^[1]

History

Take a comprehensive history documenting symptom duration (the case definition requires more than six weeks), the location, character, and triggers of pain or discomfort, voiding pattern, prior urinary tract infection history, obstetric/pelvic surgical/radiation history, sexual dysfunction, gastrointestinal symptoms, and — in a trauma-informed manner — a history of past trauma or abuse.^[2][1] A prior culture-proven urinary tract infection can be identified on presentation in 18-36% of women, though subsequent cultures at the time of IC/BPS presentation are negative; up to 50% of patients report a past UTI, underscoring how much this history genuinely overlaps with IC/BPS and why a current urine culture remains essential (see below).^[1][2]

Physical examination

• Abdominal and pelvic examination, with attention to masses, bladder distension, hernias, and areas of tenderness.^[2]
• Suprapubic and bladder-neck point tenderness are frequently observed in both men and women, though not specific findings on their own.^[2]
• It is crucial to palpate the pelvic floor muscles in both sexes, feeling for trigger points, tight bands, and pain. In one cohort of 70 women, 87% with IC/BPS reported pelvic floor pain on examination.^[2]
• In men, palpate the perineal area between the scrotum and the anus, which may identify tenderness; in women, palpate the anterior vaginal wall along the urethra's path up to the bladder neck.^[2]
• A screening exam for vulvodynia, vaginitis, periurethral masses/diverticulum, atrophic changes, and prolapse should be part of the female pelvic exam.^[2]
• A focused neurologic and musculoskeletal exam may be contributory.^[1]

Bladder diary / frequency-volume chart

A frequency-volume chart helps distinguish polyuria from the small voided volumes typical of IC/BPS. In one study of 47 adult women with IC/BPS, the average volume voided was under 100 mL, compared with an average of roughly 289 mL in asymptomatic women; the average number of daytime voids was 17 to 25 in IC/BPS patients compared with about 6 in non-IC/BPS patients.^[2] A diary can be used both for positive reinforcement during behavioral and pharmaceutical interventions and to assess the severity of storage symptoms over time.^[2]

Laboratory testing

Urinalysis is the minimum laboratory testing needed. Leukocytes do not necessarily rule infection in or out. If a urinary tract infection is suspected, a urine culture and sensitivity test is necessary — this is genuinely the single most important exclusion step in the whole workup, given how much IC/BPS symptoms overlap with those of infection. If sterile pyuria continues, consider testing for mycoplasma, ureaplasma, Corynebacterium species, Candida species, and Mycobacterium tuberculosis.^[2] Measurement of a post-void residual is advised when there is a history of insufficient emptying and/or the bladder is palpable on examination.^[2]

Symptom questionnaires

The Interstitial Cystitis Symptom Index (ICSI), Interstitial Cystitis Problem Index (ICPI), and Genitourinary Pain Index (GUPI) are self-administered symptom questionnaires that can establish a baseline and monitor response to therapy, but none has been shown to have sufficient specificity to serve as a stand-alone diagnostic instrument.^[2][1]

Cystoscopy and Hunner lesions

Cystoscopy and/or urodynamics should be considered when the diagnosis is in doubt; these tests are not necessary for making the diagnosis in typical, uncomplicated presentations.^[1] That said, given how directly Hunner-lesion status changes the available treatment options, the authors of the 2025 CUA guideline recommend routine flexible cystoscopic evaluation in all patients suspected of IC/BPS — while emphasizing that treatment should not be delayed while awaiting cystoscopy.^[2] Cystoscopy should specifically be performed in patients for whom Hunner lesions are suspected, and it is reasonable to offer routinely to IC/BPS patients over age 50, given the much higher lesion prevalence in that group (see Risk Factors).^[1][2] Hunner lesions — originally described by Hunner in 1918 — appear as one or several inflammatory patches of red mucosa with small vessels radiating to a central pale scar, and may look acutely inflamed and friable or, in a more chronic phase, blanched and non-bleeding.^[1] Because formal identification requires direct visualization, biopsy should be performed where an ambiguous or suspicious lesion raises concern for malignancy.^[2]

Glomerulations (pinpoint petechial hemorrhages) seen on cystoscopy with hydrodistension are not diagnostic for IC/BPS — they are neither sensitive nor specific, and are also seen after radiation therapy, in active bladder cancer, with chemotherapeutic or toxic drug exposure, in defunctionalized bladders, and even in asymptomatic patients undergoing cystoscopy for unrelated reasons.^[1][2] There are no agreed-upon urodynamic criteria diagnostic for IC/BPS, and urodynamic testing is not required for the routine diagnosis; it may still have a selective role when outlet obstruction or poor detrusor contractility is suspected, or when a patient is unexpectedly refractory to first-line therapy. Detrusor overactivity coexists in roughly 12-20% of IC/BPS patients and can make it difficult to determine whether overactivity alone, or overactivity together with IC/BPS, best explains the picture.^[1]

Differential diagnosis

• Reduce bladder pain and pressure, and reduce urinary frequency, urgency, and nocturia.
• Improve quality of life and function, and directly address the psychosocial impact of the condition — depression, anxiety, and sexual dysfunction are common and genuinely significant given how disabling and often refractory this condition can be (see Non-Pharmacologic Treatment).^[1]
• Direct therapy according to clinical phenotype (bladder-centric/Hunner-lesion, pelvic-floor, or widespread-pain) rather than applying a single uniform protocol to every patient (see Recognize the Condition).^[2]
• Use an individualized, stepped approach — start with the lowest-risk, most reversible options and escalate only as needed; periodically reassess efficacy and stop treatments that are not working rather than layering therapies indefinitely.^[1]
• Pursue multimodal pain management (pharmacologic, physical, and psychological) when pain control is inadequate, and refer to a multidisciplinary team — gastroenterology, neurology, rheumatology, gynecology, or a pain clinic — when the presentation suggests a wider polysymptomatic, poly-syndromic pattern.^[1]
• Reconsider the IC/BPS diagnosis itself if no improvement occurs despite multiple adequately trialled treatment approaches, rather than continuing to escalate indefinitely against a diagnosis that may be wrong.^[1]
• Avoid treatments the evidence base does not support — see Choose Initial Treatment and Common Errors to Avoid.^[1]

First-line — education and self-care (essentially all patients)

Patients should be educated about normal bladder function, what is and is not known about IC/BPS, the benefits versus risks/burdens of the available treatment alternatives, the fact that no single treatment has been found effective for the majority of patients, and the fact that acceptable symptom control may require trials of multiple therapeutic options — including combination therapy — before it is achieved.^[1] Self-care practices and behavioral modifications that can improve symptoms should be discussed and implemented as feasible, and patients should be encouraged to implement stress-management practices to improve coping and manage stress-induced exacerbations (see Non-Pharmacologic Treatment for the specific dietary-trigger-identification approach).^[1] This first tier is genuinely the foundation of management for essentially all patients, regardless of phenotype.^[1][2]

Second-line — pelvic floor physical therapy and oral pharmacotherapy

Pentosan polysulfate — a genuinely current safety issue

Oral PPS is the only oral medication approved by both the FDA and Health Canada specifically for IC/BPS management, working through a mechanism similar to the glycosaminoglycan layer itself — buffering cellular permeability and protecting the urothelium from irritants.^[2] Based on a pooled analysis of randomized trials, the 2025 CUA panel judged the magnitude of symptom benefit to be trivial (an estimated 65 more patients per 1,000 would experience symptom improvement compared to placebo, with wide confidence intervals) while harms, though infrequent, were judged serious.^[2] On December 15, 2020, Health Canada issued a safety alert regarding long-term PPS use and the risk of a vision-threatening pigmentary maculopathy, now corroborated by larger studies showing a strong dose-response relationship — patients with cumulative exposure above roughly 1,500 g were found to be nearly five times as likely to have PPS maculopathy as those with 500-999 g of cumulative exposure.^[2] PPS is now contraindicated in patients with a personal history of any macular pathology, and prescribers are advised to obtain a baseline ophthalmologic history and retinal exam before starting therapy, with regular retinal exams thereafter.^[2] Importantly, PPS-induced maculopathy can continue to progress even after the drug is stopped — there is no evidence to support a specific weaning protocol for patients already established on long-term therapy, but the CUA panel suggests informing the patient of the observed risk, engaging in shared decision-making about continuing versus stopping, referring for a baseline ophthalmologic assessment if continuing, and — if a patient opts to discontinue — using a gradual taper (for example, a patient on 100 mg three times daily might step down to twice daily for four weeks, then once daily for four weeks, then discontinue) while watching closely for a symptom flare during the wean and being ready to offer an alternative, phenotype-directed treatment.^[2]

Third-line — intravesical instillation therapy

DMSO, heparin, and/or lidocaine may be administered as intravesical treatments, alone or combined into cocktails, typically by a urology specialist (AUA evidence Grades C, C, and B respectively, listed alphabetically with no hierarchy implied).^[1] Despite this being commonly done in practice, the 2025 CUA systematic review and network analysis found the evidence base too heterogeneous — small trials, inconsistent cocktail composition, and variable outcome measures — to recommend any one intravesical agent or combination of agents over another.^[2] Intravesical lidocaine may also be of therapeutic benefit for symptomatic flares specifically, and can help confirm that a patient's pelvic pain is genuinely bladder-centric.^[2] Should not be offered bacillus Calmette-Guérin (BCG) intravesical instillation outside of an investigational study setting — it lacks demonstrated efficacy for this indication.^[1]

Fourth-line and beyond — procedures

Cystoscopy under anesthesia with short-duration, low-pressure hydrodistension may be undertaken as a treatment option in its own right, not solely as a diagnostic step — though high-pressure, long-duration hydrodistension should not be offered, since it lacks efficacy and carries genuine harm.^[1] Intradetrusor onabotulinumtoxin-A (BTX-A), with or without hydrodistension, is conditionally recommended specifically for patients refractory to other treatments; patients must be counselled up front, before injection, that post-treatment intermittent self-catheterization may become necessary due to urinary retention risk.^[2][1] A trial of neuromodulation (sacral nerve stimulation) may be performed if other treatments have not provided adequate symptom control and quality-of-life improvement; if a trial of nerve stimulation succeeds, a permanent neurostimulation device may then be implanted.^[1]

Hunner-lesion-directed therapy — its own algorithm

Patients with Hunner lesions (HLs) tend to have more favourable treatment responses than those without, so identifying HL status via cystoscopy is genuinely treatment-changing and should be sought actively.^[2] If Hunner lesions are present, fulguration (laser or electrocautery), intralesional triamcinolone injection, and/or intradetrusor BTX-A ± hydrodistension are all conditionally recommended options; the 2025 CUA panel could not rank these against each other directly given the paucity of head-to-head comparative data, judging that all three achieve a similar improvement in pain and symptom scores with lower morbidity than transurethral resection (TUR).^[2] TUR of the entire lesion may still be preferred when the diagnosis is unclear or malignancy is suspected — in one randomized trial comparing TUR with fulguration, both achieved similar long-term improvement, but TUR carried roughly double the rate of bladder-injury complications (7.9% versus 3.4%).^[2]

Refractory disease and major surgery

Oral cyclosporin-A may be offered to patients with Hunner lesions refractory to fulguration and/or triamcinolone, though the 2025 CUA panel made no recommendation for or against its use, concluding there is insufficient evidence to determine whether cyclosporin-A has different efficacy or harms among patients with or without Hunner lesions.^[2][1] Major surgery (for example, substitution cystoplasty, or urinary diversion with or without cystectomy) may be undertaken in carefully selected patients with bladder-centric symptoms, or in the rare instance of an end-stage small fibrotic bladder, for whom all other therapies have failed to provide adequate symptom control and quality-of-life improvement.^[1]

Treatments that should not be offered

The following appear to lack efficacy and/or carry an unacceptable adverse-event profile: long-term oral antibiotic administration, intravesical bacillus Calmette-Guérin outside investigational study settings, high-pressure, long-duration hydrodistension, and systemic (oral) long-term glucocorticoid administration.^[1]

Dietary trigger identification — not a universal restrictive diet

Common bladder irritants reported by patients include caffeine, alcohol, acidic or spicy foods, citrus fruits, tomatoes, carbonated beverages, and artificial sweeteners.^[2] Because individual triggers vary considerably from patient to patient, frame this as a personal trigger-identification exercise — an elimination-and-reintroduction approach using a bladder diary to isolate a given patient's own triggers — rather than a blanket, rigid, universally restrictive diet, which risks unnecessary nutritional and quality-of-life harm without clear individual benefit.^[2]

Stress management and bladder training

Patients should be encouraged to implement stress-management practices to improve coping techniques and manage stress-induced symptom exacerbations, since stress and flares are closely linked (see Recognize the Condition).^[1] Bladder training — gradually extending voiding intervals within what the patient can tolerate — may help some patients, applied cautiously and only as tolerated given that, unlike in OAB, the goal here is pain relief rather than continence.

Manual pelvic floor physical therapy

Appropriate manual physical therapy techniques — maneuvers that resolve pelvic, abdominal, and/or hip muscular trigger points, lengthen muscle contractures, and release painful scars and other connective tissue restrictions — should be offered by an appropriately trained clinician to any patient presenting with pelvic floor tenderness on examination (see Recognize the Condition and Choose Initial Treatment). Avoid generic pelvic-floor-strengthening (Kegel) exercises, which can worsen symptoms in a hypertonic, painful pelvic floor.^[1]

General chronic-pain management principles

Pharmacologic pain-management agents (urinary analgesics, acetaminophen, NSAIDs, opioid and non-opioid medications) may be used after counseling patients on the risks and benefits; pain-management principles for IC/BPS should follow the same general approach used for other chronic pain conditions, rather than a bladder-specific protocol on their own.^[1]

Talk about it directly

The psychosocial burden of IC/BPS is genuinely significant and pervasive — depression, anxiety, sexual dysfunction, and a strong association with past trauma and PTSD are all common, and quality of life has been reported as comparable in severity to rheumatoid arthritis and end-stage renal disease.^[1][2] Screen for trauma history directly, in a trauma-informed manner, and normalize the conversation about pain, urgency, and their impact on daily life and relationships rather than treating the physical bladder symptoms as the entirety of the problem.^[2] When pain management is inadequate, give real consideration to a multidisciplinary approach — gastroenterology, neurology, rheumatology, gynecology, or a pain clinic — and refer appropriately, particularly for patients whose presentation suggests widespread pain across multiple organ systems.^[1]

Women of reproductive age

IC/BPS primarily affects working-age adults, and especially women aged 25-50, making its economic and quality-of-life impact particularly significant during the most productive years of life.^[1] Safety data for many IC/BPS-directed therapies in pregnancy and lactation are limited; individualize amitriptyline, pentosan polysulfate, and any intravesical or procedural therapy with obstetric input, and favour the lowest-risk, most reversible options — education, self-care, dietary-trigger identification, and pelvic floor physical therapy — during pregnancy where feasible.

Men

IC/BPS in men is likely under-diagnosed, given the considerable symptom overlap with CP/CPPS and the historically assumed rarity of IC/BPS in this population (see Clinical Snapshot and Recognize the Condition). Consider IC/BPS in men whose pain is perceived as bladder-related, or who report "painful urgency" and/or "painful bladder filling"; some men meet criteria for both IC/BPS and CP/CPPS and benefit from combining established therapies for each.^[1]

Older adults

Hunner lesions are substantially more common with age — found in about 4% of patients under 50, 20% of those 50 to 70, and up to 55% of those over 70 — which lowers the threshold for offering cystoscopy in this group.^[2] Polypharmacy and comorbidity can complicate oral pharmacotherapy choices; weigh the anticholinergic burden of amitriptyline carefully against alternatives such as hydroxyzine or cimetidine in frailer older adults.

Patients on long-term oral pentosan polysulfate ("legacy" patients)

Any patient already established on long-term oral PPS deserves the vision-risk conversation described in Choose Initial Treatment, even if they feel entirely well — PPS-associated maculopathy can continue to progress after the drug is stopped, and there is no evidence that stopping the drug reliably halts or reverses disease already present.^[2] Offer referral for baseline ophthalmologic assessment if the patient opts to continue therapy, and use a structured, gradual taper with close symptom monitoring if the patient opts to discontinue, being ready to offer an alternative phenotype-directed treatment during the wean.^[2]

Patients with significant psychiatric or trauma comorbidity

Given the strong, likely bidirectional relationship between IC/BPS and psychosocial functioning — including PTSD, depression, and anxiety — screen for trauma history in a trauma-informed manner and involve multidisciplinary psychological support alongside bladder-directed therapy rather than treating the physical symptoms in isolation.^[2][1]

Patients being considered for intradetrusor BTX-A

Must be willing to accept the possibility of needing post-treatment clean intermittent self-catheterization; this conversation should happen proactively before injection, and patients should be taught the technique in advance where feasible rather than only after retention has already occurred.^[2][1]

• Reassess baseline symptom and pain measures periodically using validated instruments (ICSI, ICPI, GUPI, or a simple 1-10 visual analog scale) to track treatment response objectively rather than relying on unprompted recall.^[1][2]
• Efficacy of any treatment should be periodically reassessed, and treatments that are not working should be stopped rather than layered indefinitely on top of one another.^[1]
• Patients continuing oral pentosan polysulfate: arrange baseline and then regular retinal exams per the Health Canada safety alert, and ask specifically at every visit about difficulty reading, slow adjustment to low or reduced light, and blurred or wavy vision — particularly near or in the centre of the visual field.^[2]
• Patients treated with intradetrusor BTX-A: monitor for urinary retention and check post-void residual; confirm the patient has been taught clean intermittent self-catheterization technique and knows when to use it.^[1][2]
• Patients with Hunner lesions treated by fulguration, intralesional triamcinolone, or BTX-A: response, while often more favourable than in non-Hunner-lesion phenotypes, may not be durable — plan for cystoscopic surveillance and re-treatment as needed rather than assuming a single treatment is curative.^[2]
• Reconsider the IC/BPS diagnosis itself if no meaningful improvement occurs despite multiple adequately trialled treatment approaches, rather than continuing to escalate therapy against a diagnosis that may need revisiting.^[1]

1. Education, self-care, and dietary-trigger identification not controlling symptoms after an adequate trial: add manual pelvic floor physical therapy if pelvic floor tenderness is present on exam, and/or start an oral agent — amitriptyline is typically favoured first in practice — matched to the patient's phenotype.^[1][2]
2. Oral pharmacotherapy alone insufficient: consider intravesical instillation therapy (DMSO, heparin, and/or lidocaine) administered by a specialist, recognizing that the evidence does not currently support ranking one agent or cocktail above another.^[2]
3. Intravesical therapy insufficient, or bladder-centric symptoms/Hunner-lesion phenotype not yet confirmed: proceed to cystoscopy under anesthesia with short-duration, low-pressure hydrodistension, specifically assessing for Hunner lesions.^[1][2]
4. Hunner lesions identified: fulguration, intralesional triamcinolone injection, or intradetrusor BTX-A ± hydrodistension — these cannot currently be ranked against one another directly. Transurethral resection is a reasonable alternative when the diagnosis is unclear or malignancy is suspected, but carries roughly double the bladder-injury complication rate compared with fulguration.^[2]
5. No Hunner lesions, refractory to instillation therapy: intradetrusor onabotulinumtoxinA is a reasonable next option after a thorough discussion of self-catheterization risk; a trial of neuromodulation is a parallel or subsequent option if symptom control and quality of life remain inadequate.^[1][2]
6. Refractory Hunner-lesion disease despite fulguration and/or triamcinolone: oral cyclosporin-A may be considered, with the clear understanding that current evidence is insufficient to support a firm recommendation either for or against it.^[2]
7. Severe, refractory, bladder-centric or end-stage disease despite all of the above: major reconstructive surgery (substitution cystoplasty, or urinary diversion with or without cystectomy) is a genuine option in carefully selected patients — reaching this point reflects thorough prior stepped management, not a failure of care.^[1]

• Diagnosing IC/BPS without first obtaining a urine culture to exclude infection — up to 50% of patients report a past UTI and symptoms overlap substantially; a positive culture means it is not, at that moment, an IC/BPS flare.^[2]
• Attributing new hematuria to IC/BPS rather than pursuing cystoscopy and upper tract imaging to exclude bladder cancer, especially in smokers or patients over 60.^[2][1]
• Recommending Kegel/pelvic-floor-strengthening exercises — essentially the opposite of what a hypertonic, painful pelvic floor typically needs, and specifically advised against.^[1]
• Relying on cystoscopic glomerulations as a diagnostic finding — they are neither sensitive nor specific and appear in many unrelated conditions, and even in asymptomatic patients.^[1][2]
• Ordering urodynamics or a potassium sensitivity test as routine diagnostic tools — neither is required, validated, or recommended for typical diagnosis, and the potassium sensitivity test in particular carries a real risk of triggering a severe symptom flare with minimal proven predictive value for treatment response.^[1]
• Starting or continuing long-term oral antibiotics, intravesical BCG outside a study setting, high-pressure/long-duration hydrodistension, or long-term oral glucocorticoids — all four are treatments the current AUA guideline specifically states should not be offered.^[1]
• Continuing a patient on oral pentosan polysulfate indefinitely without ever discussing the vision risk, obtaining a baseline ophthalmologic assessment, or considering a structured taper — a genuinely dated practice pattern given the 2020 Health Canada safety alert and the 2025 CUA guideline's recommendation against routine use.^[2]
• Proceeding to intradetrusor BTX-A without first counseling the patient about the real possibility of needing clean intermittent self-catheterization afterward.^[1][2]
• Treating every IC/BPS patient with the same protocol rather than identifying clinical phenotype (Hunner-lesion/bladder-centric, pelvic-floor, or widespread-pain) — arguably one of the most impactful, and most commonly skipped, steps in management.^[2]
• Framing dietary counseling as a rigid, universal restrictive diet rather than an individualized trigger-identification exercise.^[2]
• Missing the psychosocial and trauma dimension of the condition and treating only the physical bladder symptoms.^[2]

How to use this table: Doses are adult doses and require patient-specific confirmation (renal/hepatic function, weight, allergy history). Pediatric dosing is weight-based per the current product monograph unless stated. Drug pricing is intentionally omitted. Select any drug name to open its complete Pharmasist Drug Database page.

Second-Line Oral Pharmacotherapy

Listed alphabetically by the AUA guideline with no hierarchy implied; amitriptyline is typically favoured first in practice. Added after first-line education/self-care and, where relevant, pelvic floor physical therapy have been tried.

Third-Line Intravesical Instillation Therapy

Administered by a urology specialist. No single agent or combination cocktail has been shown superior to another in the current evidence base — this reflects a genuine limitation in the literature, not an oversight.

Hunner-Lesion-Directed Therapy

For patients with Hunner lesions confirmed on cystoscopy. These options cannot currently be ranked against one another directly given the paucity of head-to-head comparative data.

Refractory Disease — Oral Cyclosporin-A

For Hunner-lesion patients refractory to fulguration and/or triamcinolone. The 2025 CUA panel made no recommendation for or against use, citing insufficient evidence.

General Chronic Pain Management Adjuncts

Pharmacologic pain management for IC/BPS should follow the same principles used for other chronic pain conditions, used after counseling on risks and benefits — not a substitute for phenotype-directed, bladder-specific therapy.