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Interstitial Cystitis / Bladder Pain Syndrome

Interstitial cystitis or bladder pain syndrome (IC/BPS) is bladder-related pain, pressure, or discomfort with associated lower urinary tract symptoms lasting more than six weeks, in the absence of infection or other identifiable causes.[3][28] The 2022 AUA Guideline emphasizes an individualized, multimodal treatment approach rather than a tiered algorithm; treatments are grouped by modality (behavioral or non-pharmacologic, oral medications, intravesical, procedures, major surgery) and combined based on phenotype and response.[3]

For the procedural and surgical end of the pathway, see Pelvic Floor Physical Therapy, Intradetrusor onabotulinumtoxinA, Sacral Neuromodulation, and the major-surgery options (Bladder Augmentation, Supratrigonal Cystectomy, Simple Cystectomy and Urinary Diversion).

Definition and Classification​

Diagnostic criteria​

ESSIC definition: chronic pelvic pain, pressure, or discomfort perceived as bladder-related (ESSIC specified >6 months, versus AUA/CUA >6 weeks), with at least one other urinary symptom (persistent urge or frequency), after exclusion of confusable diseases. ESSIC's 2008 proposal described optional classification by cystoscopy with hydrodistension and biopsy findings; its 2026 expert proposal recommends specialist cystoscopy in the initial assessment to exclude confusable disease and identify Hunner lesions, while AUA 2022 does not require cystoscopy for uncomplicated presentations.[31][61][3]

Terminology (AUGS-IUGA 2025). A joint AUGS-IUGA report proposes replacing "interstitial cystitis/bladder pain syndrome" in women with female bladder pain syndrome (FBPS): a chronic, intermittent condition of at least 3 months' duration affecting women, with pain or discomfort localized to the bladder, often with bladder filling, that is not attributed to other pathology. Hunner lesion disease is kept as a phenotypic subtype.[33] The same report describes Hunner lesions in 5–10% of women with FBPS, advises cystoscopy for hematuria, suspected Hunner lesions or no relief with conservative care, and recommends against routine urodynamics for diagnosis (detrusor overactivity is found in about 15%, so the 1997 NIDDK urodynamic exclusion criteria do not separate FBPS from OAB).[33] An AUGS commentary clarifies that "IC/BPS" remains appropriate for research grants and ICD-10 billing, because men also develop the condition (often labeled chronic prostatitis/chronic pelvic pain syndrome) and the term is established in payer systems and treatment protocols.[34]

AUA Guideline basic diagnostic principles:[3]

  • Symptoms present ≥6 weeks with documented negative urine cultures
  • Document voiding frequency, urgency, pain location and severity
  • Baseline assessment using GUPI, ICSI/ICPI, or VAS
  • One-day voiding log to establish low-volume frequency pattern
  • Brief neurological exam; evaluate for incomplete bladder emptying
  • Cystoscopy and urodynamics not required for uncomplicated presentations; consider them when the diagnosis is in doubt

Phenotypic classification — Hunner vs non-Hunner​

IC/BPS is increasingly recognized as two distinct clinical entities.[2][5][6]

FeatureHunner-lesion IC/BPSNon-Hunner IC/BPS
AgeOlder (mean diff +6.7 years)[5]Younger
PathologyPancystitis, B-cell abnormalities, epithelial denudationMinimal histological changes
Bladder capacityReduced cystometric capacity (mean diff −113 mL)[5]Preserved
Urinary frequencyHigher (mean diff +3.2/day)[5]Lower
Urinary biomarkersElevated CXCL10, NGF, IL-6, IL-8, MIF, luminal NOLower inflammatory markers
Pain scores, symptom duration, sexNo significant difference in the meta-analysisNo significant difference
Comorbid pain syndromesSome studies report fewer; results conflictingSome studies report more (fibromyalgia, IBS); results conflicting
Treatment responseResponds to lesion-directed fulguration/triamcinolone; observational cyclosporine A series report higher response than in non-Hunner disease, but comparative evidence is limitedVariable; multimodal

Beyond the Hunner/non-Hunner split, a retrospective reanalysis suggests pain distribution may help guide treatment selection, pending prospective validation.[37] Pelvic floor muscle tenderness on exam is common (81% of participants with a urologic chronic pelvic pain syndrome diagnosis versus 9% of controls in the MAPP Symptom Patterns Study) and tracks with worse disease severity, supporting a pelvic floor-directed evaluation and referral to myofascial physical therapy when tenderness is prominent.[36] On baseline body maps from 424 MAPP participants (233 women, 191 men) with urologic chronic pelvic pain syndrome, 25% reported pain in the abdomen and pelvis only and 75% reported pain beyond the pelvis, 38% of whom had widespread pain (3 to 7 additional body regions); more pain locations were associated with worse nonpelvic pain, sleep disturbance, depression, anxiety and quality of life, but not with worse pelvic pain or urinary symptom severity.[54] Separately, a MAPP reanalysis of three prior negative IC/BPS treatment trials found that participants with predominantly local, pelvic pain responded better to therapy targeting local (bladder) symptoms, while participants with widespread pain beyond the pelvis responded better to centrally acting treatment.[37]

Epidemiology​

Prevalence:[1][7][8]

  • Women: 2.7–6.5% using symptom-survey definitions; 1.08% in a US population estimate derived from chart-validated Veterans Health Administration data and demographic adjustment[8][7]
  • Men: 0.66% in the same chart-validated, demographically adjusted estimate[7]
  • US overall: 0.87% (95% CI 0.32–1.42)[7]
  • Estimated 3.3–7.9 million US women with IC/BPS symptoms
  • Only 9.7% of women meeting survey symptom criteria reported an IC/BPS diagnosis.[8]

Demographics:[1]

  • Sex ratios vary substantially with case definition and ascertainment.[7]
  • In a single-clinic survey of 374 urologist-diagnosed patients meeting NIDDK criteria for interstitial cystitis, mean age at first symptoms was 42.5 years.[64]
  • Associated with depression, anxiety, sexual dysfunction, reduced QoL

Pathophysiology​

The etiology is incompletely understood; several mechanisms likely co-exist and interact.[10][11][12]

  1. Urothelial dysfunction or GAG layer deficiency. A proposed deficit in the glycosaminoglycan barrier could increase urothelial permeability to urinary solutes, including potassium.[10][11]
  2. Mast cell activation. Increased mast cell infiltration with histamine release[10]
  3. Chronic inflammation. Persistent inflammatory state with elevated cytokines[11][12]
  4. Oxidative stress. Reactive oxygen species impair bladder function through multiple pathways[11][12]
  5. Neurogenic inflammation. C-fiber activation, substance P release, peripheral neural upregulation[4][10]
  6. Autoimmune dysregulation. B-cell abnormalities, particularly in the Hunner-lesion phenotype[2][6]
  7. Central sensitization. Spinal cord changes producing chronic neuropathic pain[4]

Diagnosis​

Basic assessment :[3] careful history, physical exam, urinalysis and culture; exclude infections and confusable disorders; document symptoms characteristic of IC/BPS.

Ketamine use. Regular recreational ketamine use is associated with severe storage symptoms, pelvic pain and ulcerative cystitis on cystoscopy, and ketamine-associated uropathy belongs in the differential diagnosis of ulcerative cystitis. Ask young adults with these features about ketamine use. See Ketamine-Associated Uropathy (Ketamine Cystitis).[55]

In men, IC/BPS overlaps substantially with chronic prostatitis/chronic pelvic pain syndrome and is likely under-recognized because of it: more than half of men with CP/CPPS report pain that worsens with bladder filling, a pattern also characteristic of IC/BPS.[38][39] AUA 2025 advises considering IC/BPS in men with bladder-related pain, pressure or discomfort and lower urinary tract symptoms lasting more than six weeks, after excluding infection and other identifiable causes .[52] Evaluate for bladder outlet obstruction, urethral stricture, stones or malignancy when the presentation suggests them.

Cystoscopy indications:[3]

  • Should be performed when Hunner lesions are suspected
  • Consider in patients >50 years (higher odds of Hunner lesions)
  • Consider when the diagnosis is in doubt or conventional therapies fail
  • AUA: cystoscopy is not required for diagnosis in uncomplicated presentations ; the 2025 CUA authors advise routine flexible cystoscopy in suspected IC/BPS to identify Hunner lesions and exclude other pathology when indicated.[3][28]

Glomerulations. Hunner lesions typically involve the bladder dome, posterior wall and lateral walls, sparing the trigone.[41] Glomerulations, submucosal petechiae seen after bladder distension, are a separate and nonspecific finding: a systematic review of 29 studies found no consistent relationship between glomerulations and IC/BPS diagnosis, no correlation with symptom severity, and reports of glomerulations in people without bladder pain, including asymptomatic women undergoing tubal ligation and men undergoing TURP for BPH.[42][43][44] Glomerulations alone should not be used to confirm or exclude IC/BPS.

Urine markers. In 24-hour urine from 36 women with interstitial cystitis and 36 age-matched female controls, antiproliferative factor, epidermal growth factor, IGF binding protein-3 and IL-6 were increased and heparin-binding EGF-like growth factor and cyclic GMP were decreased in interstitial cystitis; only IL-6 correlated with a symptom (nocturia). Antiproliferative factor showed the least overlap between groups and was judged the most likely candidate for a diagnostic test.[53]

Validated assessment instruments:

  • O'Leary–Sant Interstitial Cystitis Symptom Index (ICSI)
  • O'Leary–Sant Interstitial Cystitis Problem Index (ICPI)
  • Genitourinary Pain Index (GUPI)
  • Visual Analog Scale (VAS) for pain
  • Voiding diary (minimum 1 day)

See the Assessment Tools & Questionnaires page for detail.

Behavioral and Non-Pharmacologic Treatment​

Self-care and lifestyle [3]​

  • Fluid management (restriction or additional hydration)
  • Individualized dietary modification based on reproducible symptom triggers
  • Heat or cold application to bladder or perineum
  • Stress management, meditation, imagery, and yoga. A 2025 randomized trial assigned 97 women to usual care with or without an app-based meditation program and standardized yoga video; 31/43 (72%) versus 10/39 (26%) with available 12-week data reported moderate or marked global improvement.[56]
  • Bladder training with urge suppression
  • Avoid tight-fitting clothing; manage constipation

Dietary triggers and supplements​

Commonly reported triggers include coffee, citrus, tomatoes, alcohol, carbonated drinks and spicy foods. Use a symptom diary and elimination and rechallenge to identify personal triggers; blanket exclusion of all these foods or all potassium-rich foods is not required.[3][14][15]

Evidence for supplements such as calcium glycerophosphate is limited.[15] Sodium bicarbonate adds sodium and alkali exposure.[15]

A small dietary-intervention study reported improved symptom and pain scores.[14]

Pelvic floor physical therapy — Statement 12 (Standard, Grade A)[3][16]​

Appropriate manual techniques should be offered to patients with pelvic floor tenderness when appropriately trained clinicians are available. Kegel-type pelvic floor strengthening should be avoided: the guideline finds no evidence that strengthening improves symptoms and notes it may worsen the condition. Where trained therapists are unavailable, it advises against routine strengthening-based pelvic floor therapy.

Appropriate techniques: myofascial release, trigger point therapy, soft tissue massage, connective tissue manipulation, muscle contracture lengthening.

RCT evidence: in 81 women with pelvic floor tenderness and symptoms for no more than three years, assignment to up to 10 myofascial PT sessions over 12 weeks yielded 59% versus 26% global response with massage (p = 0.0012). Pain, urgency and frequency improved in both groups without significant between-group differences in those individual secondary outcomes.[16]

Oral Medications​

AUA Guideline Statement 14 : these may be administered, listed alphabetically with no hierarchy implied.[3] Statement 15 requires counseling about macular risk before PPS.[3][17]

CUA 2025 conditionally recommends against oral PPS, weighing limited benefit against visual harm and cost; it notes that Health Canada contraindicates PPS in patients with any history of macular pathology.[28] It makes no recommendation for or against cyclosporine because evidence is insufficient, including for differential benefit by Hunner status.[28] For current doses, drug monitoring and reassessment, use the oral IC/BPS pharmacology hub.

AgentMechanismDosingEvidenceKey considerations
AmitriptylineTCA; anticholinergic, antihistamine, analgesicSee pharmacology hubBICSI reduction; anticholinergic side effects
Pentosan polysulfate (PPS)Proposed barrier protectionSee pharmacology hubAUA option (B)[3]; CUA 2025 conditional against[28]FDA-approved oral agent; retinal risk can be irreversible. Its weak anticoagulant effect warrants bleeding-risk evaluation before invasive procedures and with concurrent anticoagulants, high-dose aspirin or NSAIDs.[29]
HydroxyzineH1 antihistamineSee pharmacology hubAUA option (C)[3]A 121-patient randomized factorial pilot reported global response in 31% with hydroxyzine versus 20% without (p=0.26).[63] Sedation, anticholinergic burden and QT risk.
CimetidineH2 blockerSee pharmacology hubBLimited evidence; may reduce pain
Cyclosporine ACalcineurin inhibitorSpecialist-directedAUA option (C), Hunner lesions refractory to fulguration/triamcinolone[3]; off-label[60]Selected refractory cases; nephrotoxicity and monitoring burden

AUA permits cyclosporine, particularly for Hunner lesions refractory to fulguration and/or triamcinolone; this is an option requiring individualized toxicity assessment.[3]

PPS maculopathy — safety alert​

PPS is associated with a progressive, vision-threatening maculopathy.[3][18][19][20]

Clinical features:[18][20][21]

  • Prolonged dark adaptation; difficulty reading; blurred vision
  • Hyperpigmented macular clumps on fundus exam
  • Distinctive autofluorescence abnormalities on multimodal imaging
  • May progress even after drug cessation
  • Dose-dependent (cumulative exposure)

US prescribing-information warning (not boxed) and screening:[29]

  • Most reported cases followed three or more years of use, but shorter use has been associated with pigmentary changes
  • Detailed ophthalmologic history before initiation
  • Comprehensive retinal examination before starting in patients with preexisting eye disease
  • Baseline retinal exam including OCT and fundus autofluorescence is suggested for all patients within 6 months of starting[29]
  • Periodic retinal exams during treatment; no single annual interval is specified in the label
  • If pigmentary changes develop, reevaluate continuation and maintain retinal follow-up after stopping because changes may progress

Intravesical Instillations​

AUA 2022 : DMSO, heparin, and/or lidocaine may be administered.[3]

AgentMechanismProtocolEvidenceNotes
DMSO 50% w/w (Rimso-50)Multimodal local effectsLabel: 50 mL, 15-minute dwell, every 2 weeks until maximal relief, then longer intervalsGrade C[3]FDA-approved intravesical agent; garlic odor. The label states that intravesical use may harm patients with urinary-tract malignancy and recommends full eye examinations (including slit lamp) before and periodically during therapy, plus CBC and liver and renal tests about every six months.[30]
LidocaineLocal anestheticStudied regimens: 200 mg alkalinized lidocaine daily for 5 days with 1-hour retention (randomized trial)[57]; 1–2% lidocaine with heparin/bicarbonate (open-label study)[58]Grade B[3]Short-term relief; alkalinization increases penetration
HeparinGAG-layer restoration10,000–40,000 UGrade C; off-labelOften combined with lidocaine[3]
Hyaluronic acidProposed GAG-layer replenishmentIn an uncontrolled 25-patient refractory-IC study, 40 mg weekly for 4 weeks, then monthly[59]Off-labelEuropean use; limited US data
Chondroitin sulfateGAG-layer restorationVariableOff-labelOften combined with HA

The Cochrane review of intravesical therapy found a limited, mixed-quality randomized evidence base and very sparse DMSO data.[9] A 2025 DMSO meta-analysis included both randomized and observational evidence.[23] Separately, Moss 2023 compared DMSO plus triamcinolone with BTH (bupivacaine/triamcinolone/heparin). Of 83 women randomized, 70 completed six weekly instillations. Among patients with paired ICSI data, 19/30 (63%) receiving DMSO plus triamcinolone and 9/21 (43%) receiving BTH achieved a >29.5% ICSI reduction (p=0.15); pain scores favored DMSO plus triamcinolone at visits 5 and 6, while nocturia improved within that arm without a significant between-arm difference at visit 6.[22]

No single intravesical agent or cocktail is preferred by CUA 2025.[28] Use a pharmacy-validated formulation; see the intravesical pharmacology hub for the exact Moss study mixtures and evidence limitations.

DMSO enhances absorption of other substances, which creates potential for lidocaine toxicity when both are included in a cocktail.[3]

Procedures​

Hydrodistension (Statement 18, Option, Grade C)[3]​

Cystoscopy under anesthesia with low-pressure (60 to 80 cm H2O), short-duration (under 10 minutes) hydrodistension. Allows inspection for Hunner lesions, stones, tumors; mild distension makes Hunner lesions easier to identify. Can provide clinically significant relief. Temporary symptom flares can occur. Observational repeat-treatment studies give mixed results on capacity under anesthesia: a retrospective series of 76 patients reported no significant mean capacity change among the 51 who underwent multiple Hunner-lesion electrocautery procedures (438.6 versus 422.4 mL), with high satisfaction among questionnaire respondents,[49] while a separate retrospective series of 47 patients found that 23 needed repeated fulguration or resection with hydrodistension; among the nine who reached a fourth procedure, mean anesthetic capacity was 80% of baseline.[50] AUA Statement 25 (Recommendation, Grade C) advises against high-pressure, long-duration hydrodistension because of bladder rupture and sepsis risk.[3]

Performed with the patient positioned as for standard operative cystoscopy (dorsal lithotomy; see Endoscopy).[3] The guideline does not describe routine catheter placement after an uncomplicated distension; its literature review instead describes an isolated case of bladder perforation during hydrodistension managed with an indwelling catheter for one week.[3] As a brief anesthesia-based endoscopic procedure, it falls under the general low-risk ambulatory-procedure category in the VTE Prophylaxis framework rather than needing its own regimen.

Hunner lesion treatment (Statement 19, Recommendation, Grade C)[3]​

When Hunner lesions are identified:

  • Fulguration with laser or electrocautery
  • Intralesional triamcinolone, with concentration, aliquots and total dose determined by the specialist protocol; see intralesional corticosteroids
  • Combination

As chapter-author technique, Hunner lesions are usually visible on initial entry to the bladder before formal distension causes bleeding; location, number and size are recorded first, Hunner lesions themselves are biopsied to exclude malignancy[28]; other suspicious lesions and trigonal mucosa are biopsied (Hunner lesions rarely involve the trigone), and overdistension is avoided because it can obscure the field. Fulguration outlines the outer margin of each lesion and proceeds inward, because inflammatory change tends to spread outward from the lesion with electrocautery. One described submucosal triamcinolone technique injects 0.5 mL aliquots to a depth of 2–3 mm; the bladder is then emptied and instilled with 20 mL of 1% lidocaine and 20 mL of 0.25% bupivacaine for postoperative comfort.[48]

Benefit often lasts months and recurrence may require retreatment. Case series report symptom improvement in most Hunner-lesion patients (75–90%) after fulguration and/or triamcinolone injection, with mean time to retreatment of 7–12 months after triamcinolone injection and 11–29 months after fulguration.[5] When Hunner lesions recur after treatment, follow symptoms and bladder capacity over time.[50]

A single-center randomized trial of 126 patients with Hunner lesions found no significant difference between transurethral resection and transurethral coagulation in recurrence-free time or in secondary symptom outcomes (voiding-diary frequency, nocturia, urgency, ICSI/ICPI, the PUF scale and pain VAS); bladder injury was more frequent after resection (7.9%) than after coagulation (3.4%).[45] In a separate single-center retrospective series of 59 patients (106 fulguration procedures over 1993–2011), 13.1% required repeat fulguration within 1 year and 57.2% by 4 years, when the rate plateaued.[46]

Intradetrusor botulinum toxin A (Statement 20, Option, Grade C)[3]​

An off-label option for IC/BPS after inadequate improvement with other treatments.[28] CUA 2025 conditionally recommends intradetrusor botulinum toxin A, with or without hydrodistension, as an option for IC/BPS refractory to other treatments (very low-certainty evidence).[28] Benefit may last several months. Common adverse events: dysuria, straining to void, elevated PVR, CISC requirement. Patients must accept the possibility of intermittent self-catheterization. Injection sites vary (trigonal, lateral, posterior walls). In a small randomized trial (n=47) of women wanting procedural treatment, onabotulinumtoxinA gave lower O'Leary-Sant scores than bladder instillations at 2 months, but the difference did not persist at 6–9 months; 8% needed self-catheterization, and retreatment within 6–9 months was less frequent after toxin under a protocol that allowed retreatment 1 week after instillations versus 3 months after toxin.[32]

Sacral neuromodulation (Statement 21, Option, Grade C)[3][24][25][26]​

Not FDA-approved specifically for IC/BPS; many patients meet the frequency or urgency indication, and neuromodulation may help carefully selected patients.[3] Less effective for pain than for frequency or urgency.

Evidence: a meta-analysis of 583 patients reported improved pain, but predominantly uncontrolled, heterogeneous studies limit causal inference. A 2026 systematic review of 17 studies (1,087 adults with refractory IC/BPS entering SNM test stimulation) found that 64% (95% CI 55–72%) progressed to permanent implantation.[62] Longer-term cohorts report sustained improvement in selected recipients.[24][25][26]

Percutaneous tibial nerve stimulation (PTNS)​

The AUA 2022 IC/BPS guideline discusses a prospective study of 20 women with refractory IC/BPS treated with 12 weekly PTNS sessions; pain, symptom indices, global response and voiding did not change significantly. The study appears in the discussion of its neuromodulation Option (Statement 21, Grade C), whose conclusion names only sacral and pudendal stimulation.[3] Separately, an uncontrolled prospective chronic-pelvic-pain study in 33 adults reported subjective response in 14/33 (42%) after 12 weeks.[40]

Major Surgery​

AUA Statement 22 (Option, Grade C) allows major surgery (substitution cystoplasty, or urinary diversion with or without cystectomy) in carefully selected patients with bladder-centric symptoms, or in the rare end-stage small fibrotic bladder, after all other therapies have failed. Evidence consists of small retrospective series with variable selection and outcome reporting. The best-documented predictors of success are Hunner lesions and small bladder capacity under anesthesia; no single capacity cutoff is established, and this phenotype is uncommon among all patients with IC/BPS. Large capacity, absence of Hunner lesions, no relief from local-anesthetic instillation, pelvic muscle tenderness, pain beyond the pelvis and a polysymptomatic presentation point to an extravesical source and a higher risk of failure. Pain can persist after cystectomy, and a polysymptomatic presentation warrants evaluation for pain sources outside the bladder before major surgery.[3]

OptionEffect on capacityEffect on pain
Augmentation cystoplastyIncreasesNot reliably improved
Supratrigonal cystectomy with augmentationReservoir reconstructed; trigone preservedVariable: 39/170 (23%) failed across 11 guideline cohorts, and 27 later underwent cystectomy and diversion for persistent pain. In eight cohorts reporting voiding ability, 103/144 (72%) voided spontaneously without catheterization; pain or ulcers can recur in the trigone.[3]
Urinary diversion ± cystectomyDivertsMay or may not eliminate pain

A separate systematic review of 20 studies (450 patients identified; 448 underwent subtotal cystectomy with cystoplasty, cystectomy with orthotopic neobladder, cystectomy with ileal conduit, or urinary diversion alone) reported a 23% overall risk of failure to improve symptoms across these operations, with higher improvement rates after total cystectomy with orthotopic neobladder than after the other approaches.[47]

Major surgery is irreversible. A systematic review of 20 retrospective series (450 patients) reported a 26.5% complication rate in the 17 studies providing complication data and 1.3% overall mortality; complication reporting was incomplete.[47] Diversion without cystectomy can be complicated by pyocystis in the retained bladder.[47][35] Shared decision-making and multidisciplinary input (pain, psychiatry, PT) are needed.

Emerging Therapies​

Investigational approaches reported in the literature:[1][27]

TherapyMechanismStatus
Certolizumab pegolAnti-TNF monoclonal antibodyInvestigational; limited trial evidence
Hyperbaric oxygenIncreased tissue oxygenationLimited evidence
CannabinoidsAnalgesic, anti-inflammatoryInvestigational
Intravesical liposomesProtective coating against inflammationInvestigational
NGF inhibitorsAnalgesic (neural modulation)Investigational
Sustained intravesical release systemsExtended drug deliveryIn development
Intravesical platelet-rich plasma (PRP)Growth-factor delivery to the bladder wallInvestigational; see Platelet-Rich Plasma for the fuller evidence base

EAU 2026 Recommendations​

EAU classifies this condition as primary bladder pain syndrome (PBPS), defined as persistent or recurrent bladder-region pain with at least one other symptom, such as pain worsening with filling or frequency, and no proven infection or other obvious local pathology. EAU reports a prevalence range of 0.06% to 20% across studies, a female predominance of about 10 to 1, and a Hunner lesion proportion of 5% to 50%. It states that pain does not correlate with cystoscopic or histologic findings, and that type 3C disease can be confirmed only by cystoscopy and histology.[35]

Diagnosis and general care (all strong): perform rigid cystoscopy under general anesthesia to subtype the disease and exclude confusable disease, use a validated symptom and quality-of-life instrument, assess associated non-bladder conditions and psychological, sexual and behavioral effects, and offer subtype- and phenotype-oriented therapy. Always consider multimodal behavioral, physical and psychological techniques alongside oral or invasive treatment (strong). Offer dietary advice (weak).[35]

EAU 2026 recommendationStrengthEvidence level
AmitriptylineStrong1b
Oral pentosan polysulfateStrong1a
Oral pentosan polysulfate plus subcutaneous heparin in low responders to pentosan aloneWeak1b
Do not use oral corticosteroids long termStrong3
Intravesical hyaluronic acid or chondroitin sulfate, heparin, or lidocaine with sodium bicarbonate before more invasive measuresWeak2b, 3 and 1b respectively
Do not use bladder distension alone as treatmentWeak3
Submucosal bladder wall and trigonal onabotulinumtoxinA plus hydrodistension if instillations have failedStrong1b
Neuromodulation before more invasive interventionsWeak3 for sacral neuromodulation; pudendal nerve stimulation was superior to sacral neuromodulation (1b)
Transurethral resection, coagulation or laser of bladder lesions in type 3C onlyStrong3
Ablative or reconstructive surgery only as a last resort, by experienced surgeons after multidisciplinary assessment including pain managementStrong3

EAU rates intravesical BCG as not effective (1b), notes limited data for cimetidine (2b) and calls the outcome of cystectomy variable (3). For pentosan, EAU reports about half of patients responding at 32 weeks, a response related to treatment duration rather than dose, and a better effect in non-lesion disease than in type 3C for frequency.[35]

Treatment Algorithm Summary​

The AUA 2022 approach is modality-based:[3]

  • All patients. Provide education; discuss self-care and behavioral modifications and implement them as feasible.[3]
  • Pelvic floor tenderness. Manual physical therapy (avoid Kegels)
  • Suspected Hunner lesions. Cystoscopy, then fulguration and/or triamcinolone if present
  • Oral medications. Symptom-directed options; PPS requires the updated guideline and retinal-risk discussion above
  • Intravesical. DMSO, heparin, and/or lidocaine (alone or in combination)
  • Procedures. Hydrodistension, botulinum toxin A, sacral neuromodulation
  • Major surgery. augmentation cystoplasty, supratrigonal cystectomy, simple cystectomy and urinary diversion (carefully selected bladder-centric disease or an end-stage small fibrotic bladder after other feasible treatments have failed; Hunner lesions are not required).[3]

Core principles: treatment is individualized; shared decision-making is required; multimodal approaches are often required; phenotyping (Hunner versus non-Hunner) guides therapy.

Treatments Not to Offer​

The AUA 2022 guideline advises against:[3]

  • Long-term oral antibiotics (Statement 23, Standard, Grade B)
  • Intravesical BCG outside investigational settings (Statement 24, Standard, Grade B)
  • High-pressure, long-duration hydrodistension (Statement 25, Recommendation, Grade C)
  • Long-term oral glucocorticoids (Statement 26, Recommendation, Grade C)

As evidence context for the antibiotic recommendation, a 50-patient randomized, placebo-controlled trial of 18 weeks of sequential oral antibiotics (rifampin followed by 3-week courses of doxycycline, erythromycin, metronidazole, clindamycin, amoxicillin and ciprofloxacin) found no significant difference in intention-to-treat overall improvement (12/25 vs 6/25, p=0.14) or pain/urgency improvement (10/25 vs 5/25, p=0.22), with more adverse effects on antibiotics (80% vs 40%, p=0.009).[51]

Routine potassium sensitivity testing should not be used to diagnose IC/BPS: a positive result does not change management or treatment, false positives occur in other conditions on the differential (bacterial cystitis, radiation cystitis), and the test is painful and can trigger a severe symptom flare.[3]

Comorbidities​

IC/BPS frequently co-occurs with other chronic pain and functional conditions:[1][12][15]

  • Irritable bowel syndrome
  • Fibromyalgia
  • Chronic fatigue syndrome
  • Vulvodynia
  • Chronic headache / migraine
  • Temporomandibular disorder
  • Depression and anxiety

This overlap supports common mechanisms (central sensitization, chronic inflammation, oxidative stress) and a multidisciplinary treatment approach.[13]

See Also​

Podcasts​

Painful Bladder Syndrome
BackTable OBGYN, Ep. 38 (2023) · Jocelyn Fitzgerald, Amy Park
backtable.com
Breaking Down Interstitial Cystitis
BackTable Urology, Ep. 38 (2022) · Esther Han, Jose Silva
backtable.com
AUA Interstitial Cystitis/Bladder Pain Syndrome (2022) Guidelines ft. Dr. Philip Hanno
SUFU Podcast (2023)
podcasts.apple.com

References​

1. Imamura M, Scott NW, Wallace SA, et al. "Interventions for Treating People With Symptoms of Bladder Pain Syndrome: A Network Meta-Analysis." Cochrane Database Syst Rev. 2020;7:CD013325. doi:10.1002/14651858.CD013325.pub2

2. Akiyama Y, Homma Y, Maeda D. "Pathology and Terminology of Interstitial Cystitis/Bladder Pain Syndrome: A Review." Histol Histopathol. 2019;34(1):25-32. doi:10.14670/HH-18-028

3. Clemens JQ, Erickson DR, Varela NP, Lai HH. "Diagnosis and Treatment of Interstitial Cystitis/Bladder Pain Syndrome." J Urol. 2022;208(1):34-42. doi:10.1097/JU.0000000000002756

4. Nambiar AK, Eylert MF, 't Hoen LA, et al. "Bladder Disorder of Function." Chapter 23 in Campbell-Walsh-Wein Urology.

5. Lai HH, Pickersgill NA, Vetter JM. "Hunner Lesion Phenotype in Interstitial Cystitis/Bladder Pain Syndrome: A Systematic Review and Meta-Analysis." J Urol. 2020;204(3):518-523. doi:10.1097/JU.0000000000001031

6. Zhu L, Ke H, Wang Q, Xu K, Chen X. "Multi-Omics Profiling Reveals Distinct Pathogenic Mechanisms in Hunner and Non-Hunner Interstitial Cystitis Subtypes." Sci Rep. 2025;15(1):26536. doi:10.1038/s41598-025-12010-w

7. Anger JT, Dallas KB, Bresee C, et al. "National Prevalence of IC/BPS in Women and Men Utilizing Veterans Health Administration Data." Front Pain Res (Lausanne). 2022;3:925834. doi:10.3389/fpain.2022.925834

8. Berry SH, Elliott MN, Suttorp M, et al. "Prevalence of Symptoms of Bladder Pain Syndrome/Interstitial Cystitis Among Adult Females in the United States." J Urol. 2011;186(2):540-4. doi:10.1016/j.juro.2011.03.132

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