Chronic pelvic pain

• Chronic pelvic pain is not a single diagnosis. It is a long-lasting symptom with many possible causes, often several at once, and it may be present even when no structural disease is found.
• Duration thresholds differ by guideline: the EAU defines chronic pelvic pain as pain perceived in pelvic structures for at least 3 months, while the RCOG defines it as intermittent or constant pelvic pain for at least 6 months that does not occur only with menstruation or intercourse and is not linked to pregnancy. ^[2]
• A UK study found a prevalence of chronic pelvic pain of 14.8 per cent in women aged 25, and the RCOG estimates it affects about 1 woman in 6.^{[2][1] [3]}
• The RCOG also notes that chronic pelvic pain presents in primary care about as often as migraine or low-back pain.^[2]
• In a third to a half of laparoscopies done to investigate chronic pelvic pain, no obvious cause is found.^[3]
• Good care is biopsychosocial and multidisciplinary: listen, validate, diagnose red flags, phenotype the pain, and combine self-management, physiotherapy, psychological care, appropriately chosen drugs, and targeted invasive treatment.^[1]

By the end of this page you should be able to:

1. Define chronic pelvic pain and separate chronic primary pelvic pain (no ongoing pathology) from chronic secondary pelvic pain (an identifiable cause).
2. List the common causes in the gynaecological, urological, gastrointestinal, musculoskeletal and neuropathic groups.
3. Take and interpret a targeted history and examination, including pelvic floor and pain-quality assessment.
4. Choose first-line, confirmatory and referral investigations without over-investigating.
5. Explain central sensitisation, referred pain and pelvic floor overactivity as mechanisms that keep pain going.
6. Outline multidisciplinary management, including the evidence for the main drugs and why some common drugs fail.
7. Recognise red flags that require urgent exclusion of malignancy, infection or other serious disease.
8. Counsel a patient using honest, realistic language about outlook and self-management.

The EAU defines chronic pelvic pain as chronic or persistent pain perceived in structures related to the pelvis of either men or women, often associated with negative cognitive, behavioural, sexual and emotional consequences and with symptoms suggestive of lower urinary tract, sexual, bowel, pelvic floor or gynaecological dysfunction.^[1] "Perceived" matters here: both patient and clinician localise the pain to a pelvic area using history, examination and appropriate investigation.^[1]

• Chronic primary pelvic pain (CPPPS): a pain syndrome lasting at least 3 months under EAU terminology, in which no ongoing pathology such as infection, cancer or primary anatomical disease is identified, even though neuropathic pain from nerve damage is a recognised exception. The diagnosis rests on the symptom cluster, not on a negative test.^[1]
• Chronic secondary pelvic pain: pain driven by an identifiable condition such as endometriosis, adenomyosis, pelvic inflammatory disease, bladder pain syndrome, irritable bowel syndrome or nerve injury. Treating that condition is the first step.
• Classification by system: EAU guidance organises causes and treatment by gynaecological, urological, gastrointestinal, musculoskeletal, sexual and psychological domains, because patients often have problems in several domains at once.^[1]

• A UK study found a prevalence of chronic pelvic pain of 14.8 per cent in women aged 25.^[1]
• RCOG estimates that about 1 woman in 6 is affected, and that chronic pelvic pain is seen in primary care about as often as migraine or low-back pain.^[2][3]
• Primary bladder pain syndrome (PBPS, interstitial cystitis) has a prevalence reported between 0.06 and 20 per cent, with a female predominance of about 10 to 1.^[1]
• Primary prostate pain syndrome (PPPS, formerly chronic prostatitis) has population-based symptom prevalence between 2.2 and 14.2 per cent, with risk rising about 3.1-fold in men aged 50 to 59 compared with men aged 20 to 39.^[1]
• Symptoms of primary bladder pain syndrome often start before age 18, so it cannot be dismissed on age alone.^[1]
• Chronic pelvic pain consumes large amounts of health care: a World Health Organization review of chronic pelvic pain in women found it responsible for a substantial share of gynaecology outpatient visits and laparoscopies. The EAU chapter cites this neglect of a common morbidity.^[1]
• No organic cause is found in a third to a half of laparoscopies performed for chronic pelvic pain.^[3]

Risk factors are largely non-specific, but the EAU has summarised consistent findings from a systematic review of risk factors for chronic non-cyclical pelvic pain in women:^[1]

• sexual or physical abuse, odds ratio 1.51 to 3.49; ^[1]
• anxiety, odds ratio 2.28 (95 per cent CI 1.41 to 3.70); ^[1]
• depression, odds ratio 2.69 (95 per cent CI 1.86 to 3.88); ^[1]
• multiple somatic symptoms ("hysteria"), odds ratio 4.83 (95 per cent CI 2.50 to 9.33); ^[1]
• psychosomatic symptoms, odds ratio 8.01 (95 per cent CI 5.16 to 12.44). ^[1]

These are associations. They do not prove that the pain is "in the mind".

Other risk factors or contributors include:

• early-life stress and adverse life events, which can sensitise the hypothalamic-pituitary-adrenal axis;
• central sensitisation, in which repeated pain input lowers the threshold for future pain and can spread across sites;
• genetic clustering of pain conditions in families;
• female sex hormones, which modulate nociception;
• pain comorbidities such as fibromyalgia, chronic fatigue, migraine and irritable bowel syndrome;
• prior episodes of acute pelvic infection, endometriosis with dysmenorrhoea or post-surgical pain.

Two practical points follow. First, ask about adverse life events, trauma and abuse in both women and men with suspected chronic primary pelvic pain syndrome, because the association is strong but the mechanisms are complex.^[1] Second, ask what the patient believes is the cause of the pain; many patients fear cancer or untreated infection, and explaining their illness reduces anxiety.^[1]

Chronic pelvic pain is best understood through the biopsychosocial model. Neither "all in the mind" nor "a single damaged organ" is adequate.

1. An initial event (infection, inflammation, surgery, endometriosis, trauma, urological disease) activates pelvic nociceptors and may itself damage nerves.
2. Acute afferent signalling travels through small unmyelinated C fibres and thinly myelinated A-delta fibres. Visceral afferents are sparse and many are "silent" until switched on.
3. Inflammation and cell injury lower transducer thresholds and increase receptor responsiveness, so that less stimulus produces more pain.
4. Central sensitisation in the spinal cord dorsal horn amplifies the signal, expands the receptive field, lowers threshold and increases response duration. After this, light touch or normal bladder or bowel filling may be perceived as pain (allodynia) and ordinary pain may be magnified (hyperalgesia).
5. Descending modulation from brain centres can inhibit or facilitate these signals; mood, attention, sleep and stress shift that balance.
6. Viscero-somatic convergence: afferent nerves from the bladder, bowel, uterus and somatic areas meet the same second-order neurons, so pain is felt at a distance from the true source (referred pain). Viscero-visceral cross-sensitisation explains why bladder and uterine, or uterine and colonic, afferents can amplify each other.
7. Pelvic floor overactivity and trigger points send ongoing input to the central nervous system, sustaining sensitisation and creating muscle tenderness distant from the original stimulus.

Pelvic organs produce visceral pain: poorly localised discomfort arising from stretch, distension, inflammation or ischaemia, often with autonomic symptoms such as nausea and sweating. Somatic structures (muscles, ligaments, fascia, skin) produce somatic pain: sharper, better localised pain arising from mechanical, thermal or chemical stimuli. In chronic pelvic pain the distinction blurs, because converging afferents and central sensitisation make somatic and visceral pains amplify each other.

Many of these red flags were framed around women by RCOG patient information based on Green-top Guideline No. 41. In men, add scrotal or testicular pain, haematuria and post-void symptoms that may point to urological disease.^[3]

Chronic pelvic pain is diagnosed clinically. History gives most of the answer; investigation is used to exclude specific disease and to phenotype.

• Pain diary: ask the patient to record for 2 to 3 cycles, or for 2 to 3 months if cycles are irregular, the site, duration, severity, triggers, relation to menses, intercourse, bladder, bowel, posture and medication. Apps such as menstrual trackers can help.^[3]
• Character and anatomy: site, radiation, quality (aching, cramping, burning, electric, pressure), steady or intermittent, first onset and progression.
• Cyclicity: relation to menstruation, ovulation, intercourse and defecation. Secondary dysmenorrhoea starting after previously painless periods suggests endometriosis or adenomyosis.
• Urological system: pain with bladder filling, relief after voiding, day and night frequency, urgency, dysuria, haematuria, stress or urgency incontinence, prior mesh or prolapse surgery.
• Gastrointestinal system: abdominal pain, stool form, frequency, bloating, straining, incomplete evacuation, bleeding, mucus and relation to food.
• Musculoskeletal system: posture, movement, lifting, prolonged sitting, cycling, hip pain, back pain and whether activity changes the pain.
• Nerves: burning, shooting pain, numbness, allodynia, relief by standing and worse by sitting, history of childbirth, pelvic or spinal surgery, trauma, cycling or prolonged sitting.
• Sexual and reproductive history: obstetric history, gynaecological surgery, sexually transmitted infection, contraception, fertility, dyspareunia, avoidance, anorgasmia and postcoital pain.
• Psychosocial domains: sleep, mood, anxiety, catastrophising, pain-related fear, work and roles, relationships, social support, early-life adversity, abuse and the patient's own explanation for the pain.
• Irritable bowel syndrome: Rome IV symptom-based criteria are used for IBS, with pain related to defecation and changed stool frequency or form.
• Anaemia and malignancy clues: weight loss, bleeding, appetite change, menopausal status, family history.

A full clinical examination of the abdomen, pelvis, musculoskeletal and nervous systems is needed, aimed at questions whose answers will change management. Explain every step and obtain consent; offer a chaperone; stop if pain becomes severe.

• General and abdominal examination: scars, masses, distension, herniae, cutaneous allodynia over the T11 to L1 dermatomes.
• External genitalia: lesions, discharge, vulval allodynia, scrotal components in men, urethral palpation.
• Pelvic examination: preferably single-finger, avoiding routine bimanual examination when pain is severe. Assess tenderness in the uterus, adnexae, lateral fornices, rectovaginal septum and pelvic floor muscles.
• Pelvic floor assessment: tone, ability to contract and relax, tenderness and trigger points in levator ani, puborectalis and obturator internus, and posterior traction on puborectalis for levator ani syndrome.
• Neurological examination: sensory changes in the perineum and lower limbs, reflexes, pelvic floor strength and allodynia in the S2 to S4 dermatomes.
• Rectal examination: anal tone, fissure, puborectalis tenderness, prostate in men, pain on palpation and pelvic floor trigger points.
• Musculoskeletal examination: hips, sacroiliac joints, lumbar spine, gait and tender points, including muscles outside the pelvis.

Examination often produces tenderness without a structural cause. That is useful phenotyping information, not proof of imaginary pain.

There is no single diagnostic test for chronic primary pelvic pain syndrome. Investigations should follow a positive clinical suspicion, not be a fishing exercise, because over-investigation can reinforce illness behaviour.

• Every patient: targeted infection screening including sexually transmitted infections, urinalysis, urine culture and, where bladder pain syndrome is suspected, urine cytology in risk groups.^[1]
• Imaging: transvaginal or transabdominal ultrasound is a common first test; MRI is used for nerve pathology, suspected mesh complications, rectal and pelvic floor dysfunction, and selected gynaecological conditions. MR defecography assesses complex anorectal dysfunction.
• Laparoscopy: the most useful invasive investigation to exclude gynaecological pathology in women. In a third to a half of laparoscopies for chronic pelvic pain, no obvious cause is found. It can reduce anxiety about serious disease but is not a treatment.^[1][3]
• Bladder pain syndrome: cystoscopy under general anaesthesia distinguishes Hunner lesions from non-Hunner disease, determines bladder capacity and allows biopsy to exclude carcinoma in situ and tuberculosis. Do not rely on cystoscopy alone; history and exclusion of confusable disease lead the diagnosis.^[1]
• Gastrointestinal evaluation: anorectal manometry, balloon expulsion testing and colonoscopy when red flags exist; Rome IV-based diagnosis for functional anorectal pain disorders.
• Nerve assessment: image-guided local anaesthetic block is preferred over electrophysiological tests; peripheral nerve damage can exist with normal nerve conduction studies.
• Psychological assessment: ideographic assessment of anxiety, depression, catastrophising and abuse; standard depression scores are poorly adapted to chronic pain patients.

EAU diagnostic criteria require pain, pressure or discomfort thought to be bladder in origin, plus at least one other symptom such as daytime or night-time increased urinary frequency, after exclusion of confusable diseases. Bladder pain classically worsens with filling, may radiate to groin, vagina, rectum or sacrum, is relieved by voiding, and returns quickly.^[1]

Management is based on the biopsychosocial model. Empathetic communication, validation and patient education are prerequisites. Single interventions from any discipline should sit inside a personalised, shared plan that includes self-management, not be offered one at a time by uncoordinated clinicians.^[1]

Set realistic goals with the patient: pain reduction to a meaningful but partial level, improved function, sleep, mood and sexual life, fewer emergency visits and a shared plan for flare-ups. Chronic primary pelvic pain is often a fluctuating long-term condition; cure should not be promised, but improvement is common.

• Explain how pain works, including central sensitisation and referred pain, in language the patient can use.
• Provide trusted written or audiovisual resources rather than leaving the patient to search alone.
• Agree which resources are reliable, tailored to language, culture and health literacy.
• Discuss worries, preferences, questions and what the patient believes is the cause of the pain.
• Build a flare-up plan, activity-pacing plan and medication review schedule.

Caution is appropriate, because evidence is limited and mixed. Still, pelvic floor overactivity and trigger points should be treated, ideally by physiotherapists trained in both pelvic musculoskeletal and pain neuroscience.

• Therapy: teach relaxation of pelvic floor muscles during pain, interrupt the pain-spasm-pain cycle, stretch shortened muscles, dry or wet needling of trigger points, manual therapy, posture and movement retraining.
• Evidence: pelvic floor-directed physical therapy benefits some patients, especially women with interstitial cystitis. In one randomised trial of chronic prostatitis, global response to global massage was 57 per cent versus 21 per cent for bladder-type pain; in the bladder pain group, myofascial therapy did significantly better than massage, whereas in the prostatitis group massage helped as much as myofascial therapy.^[1]
• Biofeedback: in chronic anal pain syndrome, biofeedback gave adequate relief in 87 per cent of patients with tenderness on puborectalis traction after 1 month and in 58 per cent of the whole group after 12 months, versus roughly half and one quarter with electrogalvanic stimulation or massage.^[1]
• Myofascial release: manual therapy of trigger points is commonly used, though evidence that manual techniques beat no treatment is weak. There is insufficient evidence to support botulinum toxin injections into pelvic floor trigger points over lidocaine: BTX-A costs more and reviews have found no advantage over the cheaper drug.^[1]
• Other modalities: extracorporeal shockwave therapy may improve symptoms in chronic prostatitis; acupuncture has positive randomised trial evidence against sham in chronic prostatitis. These should be considered adjuncts, not defaults.^[1]

Psychological interventions target pain, coping, mood, fear and function. Meta-analyses of the relatively few pelvic pain trials show benefits over a few months that are not always sustained. Exposure to pain-related fear is superior to manual therapy for pain-related fear and disability in women with chronic pelvic pain. Early referral for relationship and sexual counselling is valuable where sexual dysfunction is present. Remote delivery is appropriate for less disabled and distressed patients.^[1]

Use a dietician for irritable bowel syndrome and bladder pain syndrome. Scientific evidence for dietary restriction alone is limited, but avoidance of individual triggers and a modified diet trial are reasonable. Evidence for linaclotide at 290 micrograms once daily is specific to abdominal pain in IBS with constipation and did not assess pelvic pain. ^[1]

• Paracetamol (acetaminophen): commonly used, but review evidence questions routine first-line use because efficacy is inadequate in many pain conditions, including dysmenorrhoea. ^[1]
• NSAIDs: more effective than placebo and paracetamol for inflammatory pain such as dysmenorrhoea, but evidence in chronic pelvic pain overall is weak or absent and NSAIDs have more side effects. There is insufficient evidence to prefer one NSAID. Try for a short period and review both analgesia and function.^[1]
• Amitriptyline: the most used tricyclic antidepressant for neuropathic pain, at 10 to 75 milligrams per day, sometimes up to 150 milligrams per day, titrated at night against benefit and side effects. It is a candidate neuromodulator for chronic pelvic pain and is effective in PBPS. Nortriptyline or imipramine can be used instead. ^[1]
• Other antidepressants: duloxetine 60 milligrams per day has evidence in some neuropathic pain conditions and fibromyalgia, but did not significantly improve symptoms of PBPS. Side effects are common. ^[1]
• Anticonvulsants: gabapentin and pregabalin are used for neuropathic pain. Gabapentin showed no benefit and higher side effects in women with chronic pelvic pain without an obvious cause in one randomised trial. Pregabalin is dosed in the 300 to 600 milligram per day range for responders; evidence in chronic pelvic pain is weak and misuse risk is increasing, so review benefit, function and harm regularly. ^[1]
• Opioids: role is limited. They may help a small number of patients at low dose in a monitored setting, but there is evidence of harm including endocrine and immune effects, dependence and opioid-induced hyperalgesia. Follow local guidance on tapering.^[1]

Endometriosis or cyclical pelvic pain: Women with cyclical pain should be offered a therapeutic trial of hormonal treatment for 3 to 6 months before diagnostic laparoscopy. Hormonal options include combined oral contraceptive, progestogen-only pill, implant, depot progestogen injection or levonorgestrel intrauterine system. Hormonal treatment can also help some women whose pain is non-cyclical. A Cochrane review supports progestogens and identifies possible benefit from GnRH agonists such as goserelin, although evidence quality is generally low and adverse effects such as weight gain and bloating limit acceptability.^[2][3]

Primary bladder pain syndrome: Amitriptyline can help. Pentosan polysulphate is a semi-synthetic beechwood-derived drug with subjective improvement in pain and urinary symptoms, mainly in non-Hunner disease after 32 weeks. Intravesical treatments (alkalised lidocaine, heparin, hyaluronic acid, chondroitin sulphate) provide local effect with few systemic side effects. Antihistamines, cimetidine, misoprostol, L-arginine, oxybutynin and duloxetine have limited or no evidence of benefit. Hyperbaric oxygen has moderate effect in a small subgroup, at high cost and low availability.^[1]

Chronic anal pain syndrome (proctalgia fugax and levator ani syndrome): For chronic primary anal pain syndrome, biofeedback is superior to electrogalvanic stimulation or massage. Intermittent short attacks may respond to inhaled salbutamol; other options include topical diltiazem and botulinum toxin. Rome IV criteria require chronic or recurrent rectal pain lasting at least 30 minutes, excluding other anorectal pathology.^[1]

Pelvic floor muscle overactivity: Trigger-point injections of bupivacaine or lidocaine with triamcinolone improved pain in up to three-quarters of women with the first injection in one study. Botulinum toxin injection into pelvic floor trigger points is more expensive and not proven superior to lidocaine.^[1]

Primary prostate pain syndrome: Evidence-supported options include anti-inflammatory drugs, alpha-blockers, a six-week antibiotic course where uropathogens are suspected, and pollen extracts. Finasteride may help older men with PSA elevation; pregabalin can be offered according to neuropathic pain principles, though a large RCT did not show significant reduction in symptom score. Botulinum toxin and tanezumab are not recommended outside research. Antibiotics must not be repeated or used unnecessarily; local resistance patterns matter.^[1]

Neuropathic and pudendal pain: Identify the mechanism, then use amitriptyline or other tricyclic, gabapentinoids or SNRIs at the lowest effective dose, with patient review. Image-guided nerve block with local anaesthetic and corticosteroid is both diagnostic and, occasionally, therapeutic.

• Nerve blocks and neuromodulation: pudendal nerve block, posterior tibial nerve stimulation and transcutaneous electrical nerve stimulation are useful adjuncts for some patients.
• Surgery: surgery is rarely the main treatment. Laparoscopy is diagnostic more than therapeutic; lysis of severe adhesions may help selected women, but mild adhesions surgery does not appear to help. Removal of mesh may be necessary when mesh is identified as the pain source. Hysterectomy is not a treatment for unexplained pain.
• Adhesions: adhesions are a common cause of chronic abdominal pain after abdominal or pelvic surgery, but evidence for management is limited.
• Botulinum toxin: intravesical or urethral sphincter injection has been reported in niche indications, but routine trigger-point use is not supported.
• Escalation: refer to a specialised multidisciplinary pelvic pain clinic, pain management service or the appropriate specialist when first-line treatments fail, function declines, pain escalation is marked, or diagnosis remains uncertain.

Refer early to a gynaecologist after complete urological evaluation if a gynaecological cause is suspected; laparoscopy should follow gynaecological guidance. Refer to a pain specialist or urologist when PBPS is severe or Hunner disease is suspected, and to gastroenterology when inflammatory bowel disease or persistent anorectal pathology is present. A single coordinating clinician reduces fragmented care.

Reassess pain severity, physical and sexual function, mood and sleep at each visit. Use a five-point verbal scale, an 11-point numerical scale, a pain visual analogue scale or the Brief Pain Inventory to track change. Agree in advance what counts as clinically meaningful improvement. If treatment is ineffective, consider alternatives before saying nothing works; if effective, plan maintenance, relapse and self-management. Refer on when the next level of care is needed.^[1]

• Adolescents: pain often starts young in PBPS. Be alert for abuse, sexual health and school impact. Explain that normal investigation does not mean imaginary pain.
• Pregnancy and postpartum: hormonal therapy and many drugs are not appropriate. Focus on explanation, pelvic floor therapy, topical care and multidisciplinary planning; investigate new or severe postpartum pain because trauma and nerve injury can be overlooked.
• Men: primary prostate, urethral, scrotal and pudendal pain syndromes. Sexual dysfunction is common and should be asked about directly.
• Older adults: have a lower threshold for excluding malignancy, urological and gastrointestinal disease and post-surgical complications.
• Low-resource settings: history, examination and pelvic floor retraining carry most of the value. Basic urinalysis, transvaginal ultrasound where available and infection screening are sufficient first steps. Avoid repeated laparoscopy or expensive imaging when the result would not change care; use shared education, physiotherapy and simple analgesia first. Opioids are harder to monitor safely when follow-up is limited.

Chronic pelvic pain itself causes substantial burden even without organ damage: impaired quality of life, depression, fatigue, sleep disturbance, reduced work capacity, sexual dysfunction, strained relationships and high healthcare use. Central sensitisation and pain comorbidity may outlast treatment of a specific cause. This is not treatment failure; it is the chronic-pain diagnosis requiring ongoing multidisciplinary care.

• Chronic pelvic pain is common, disabling and a symptom rather than a diagnosis.^[2]
• Duration thresholds differ: the EAU uses at least 3 months and the RCOG at least 6 months.^[1][2]
• A UK study found 14.8 per cent prevalence in women aged 25, and RCOG estimates 1 in 6 women overall.^[1][2]
• No organic cause is found in a third to a half of laparoscopies.^[3]
• Causes span gynaecological, urological, gastrointestinal, musculoskeletal and neuropathic systems, and several may coexist.^[1]
• Central sensitisation, referred pain and pelvic floor overactivity can sustain pain after the original injury has resolved.^[1]
• Diagnosis is clinical; investigation excludes treatable disease and phenotypes rather than confirming a label.^[1]
• History, including bladder, bowel, sexual, musculoskeletal and psychosocial domains, gives most of the diagnosis.
• Red flags such as postmenopausal or postcoital bleeding, pelvic mass, weight loss, fever or suicidal ideation require urgent exclusion of serious disease.
• Management is biopsychosocial, multidisciplinary and goals based, combining self-management, physiotherapy, psychology, analgesia or neuromodulators, and targeted blocks or surgery.
• Hormonal treatment for 3 to 6 months is a reasonable first trial for cyclical pain before diagnostic laparoscopy.^[2]
• Chronic pelvic pain can cause major psychological and social consequences; these are part of the condition, not evidence that the pain is imaginary.^[1]

Endometriosis; Adenomyosis; Pelvic inflammatory disease; Irritable bowel syndrome; Interstitial cystitis and primary bladder pain syndrome; Dysmenorrhoea; Vulvodynia and vestibulodynia; Pudendal neuralgia; Pelvic floor disorders; Chronic pain and central sensitisation.

This page reflects the 2026 edition of the EAU Guidelines on Chronic Pelvic Pain and the 2012 second edition of RCOG Green-top Guideline No. 41. Write "DONE" only when this file and the claims file are saved.