What Is Chronic Pelvic Pain Syndrome (CPPS)?

Chronic pelvic pain syndrome (CPPS) in women is defined as pain perceived to originate from pelvic organs or structures lasting more than 6 months, often associated with negative cognitive, behavioural, sexual, and emotional consequences, as well as symptoms of lower urinary tract, bowel, pelvic floor, myofascial, or gynaecological dysfunction.

From a pain medicine perspective, CPPS is best understood as a complex, multifactorial chronic pain condition rather than a single disease. In many women, symptoms arise from overlapping visceral, neuromusculoskeletal, and central sensitisation mechanisms. Several different pain generators may coexist, and symptoms often persist even after one apparent cause has been treated.

How Pain Develops in CPPS

Common Causes of CPPS

The most common causes include endometriosis, adenomyosis, bladder pain syndrome or interstitial cystitis, irritable bowel syndrome, myofascial pain, pelvic floor dysfunction, neuropathic pain, and psychosocial factors that amplify pain severity.

Clinical Presentation

The symptoms of CPPS are highly variable. Some women experience cyclical pain associated with menstruation, while others have constant daily pain that persists regardless of hormonal status. Pain may be described as aching, pressure, heaviness, cramping, sharp, burning, stabbing, pulling, or a sensation of “something being stuck” in the vagina or rectum.

Symptoms commonly worsen with sitting, exercise, prolonged standing, sexual intercourse, bladder filling, bowel movements, menstruation, or emotional stress. Pain may radiate to the lower abdomen, groin, buttocks, coccyx, hips, lower back, or legs.

Differentiating Pelvic Floor Hypertonicity and Hypotonicity

A critical clinical distinction is whether the pelvic floor is excessively tight (hypertonic) or weak and lax (hypotonic). These two states produce very different symptom patterns and require opposite treatment strategies.

Features Suggesting Neuropathic Pain

Burning, electric shock-like pain, tingling, numbness, hypersensitivity to touch, and pain radiating along the distribution of a nerve suggest a neuropathic component such as pudendal neuralgia or ilioinguinal nerve irritation.

Features Suggesting Central Sensitisation

Multiple pain sites, severe fatigue, poor sleep, fibromyalgia, migraine, irritable bowel syndrome, bladder pain syndrome, hypersensitivity to touch, and disproportionate pain severity suggest that the nervous system itself has become sensitised.

Evaluation Approach

A biopsychosocial evaluation is essential and should assess gynaecological, urological, gastrointestinal, musculoskeletal, neuropathic, and psychological contributors.

Pelvic imaging is important for identifying structural abnormalities, but a normal scan does not exclude significant pain mechanisms such as pelvic floor dysfunction, neuralgia, or central sensitisation.

Key Management Principles

In summary: Chronic pelvic pain syndrome is a complex disorder involving the interaction of pelvic organs, muscles, nerves, and the central nervous system. A comprehensive pain medicine approach is essential to identify all relevant contributors and guide effective treatment.

Causes of Chronic Pelvic Pain Syndrome (CPPS)

The causes of chronic pelvic pain syndrome in women are multifactorial and often coexist. CPPS should not be viewed as a single-organ diagnosis. In many women, pelvic pain reflects an interaction between visceral pathology, pelvic floor dysfunction, myofascial pain, neuropathic pain, central sensitisation, and psychosocial factors.

The most common causes include irritable bowel syndrome, bladder pain syndrome or interstitial cystitis, myofascial pain, and endometriosis. Among women with CPPS, approximately 60–70% have endometriosis or bladder pain syndrome, and nearly half may have both conditions simultaneously. At specialist centres where a structured musculoskeletal examination is performed, 50–90% of women have pain arising from musculoskeletal structures.

Visceral Causes

Visceral causes arise from pelvic organs, including gynaecological, gastrointestinal, and urological structures. Visceral pelvic pain is often deep, diffuse, cramping, pressure-like, or poorly localised. It may fluctuate with menstruation, bladder filling, bowel activity, inflammation, or hormonal changes. Importantly, visceral pain can also trigger secondary pelvic floor guarding and myofascial pain through viscerosomatic convergence.

Gynecologic Causes

Gastrointestinal Causes

Urologic Causes

Neuromusculoskeletal Causes

Neuromusculoskeletal causes are extremely common in CPPS and are often missed if the assessment focuses only on pelvic organs. Pain may arise from pelvic floor muscles, abdominal wall muscles, hip and pelvic girdle structures, peripheral nerves, or widespread pain-processing disorders. These causes are particularly important because they are often reproducible on examination and may respond to targeted physical therapy, myofascial treatment, or image-guided interventions.

Myofascial Syndromes

Neurologic Causes

Psychosocial Contributors

Psychosocial contributors are important in CPPS, but they must be framed carefully. Their presence does not mean the pain is imaginary or “all in the mind.” Rather, psychological distress, trauma, poor sleep, fear, stress, and adverse life experiences can amplify pain processing, increase muscle guarding, worsen central sensitisation, and reduce recovery.

Key Diagnostic Principles

A central principle in CPPS is that multiple conditions frequently coexist. The presence of one diagnosis should not prevent clinicians from looking for others. For example, endometriosis and bladder pain syndrome frequently overlap, and persistent visceral pain can drive pelvic floor hypertonicity, myofascial trigger points, and central sensitisation.

In summary: CPPS is best understood as an overlapping pain condition rather than a single diagnosis. Visceral, neuromusculoskeletal, neuropathic, central sensitisation, and psychosocial contributors frequently interact, and a comprehensive assessment is essential to identify the full pattern of pain drivers in each patient.

CPPS in Specific Patient Populations

The causes and clinical priorities in chronic pelvic pain syndrome vary according to age, hormonal status, reproductive stage, previous surgery, trauma history, and associated medical conditions. A structured approach helps avoid diagnostic bias and ensures that important causes are not missed.

For example, progressive dysmenorrhoea in an adolescent or premenopausal woman should raise suspicion for endometriosis, whereas new pelvic pain after menopause requires a different level of caution, particularly regarding malignancy, structural pathology, chronic inflammatory sequelae, and non-gynaecological causes.

Chronic Pelvic Pain in Adolescents

In adolescents, persistent pelvic pain is often first labelled as “period pain”, but clinically significant dysmenorrhoea that does not respond to NSAIDs and hormonal treatment should not be dismissed. Endometriosis is the leading cause of secondary dysmenorrhoea in adolescents and should be considered when pain is persistent, progressive, disabling, or associated with bowel, bladder, or sexual symptoms.

Adolescent endometriosis may be difficult to recognise because lesions can look different from the classic adult appearance. Lesions may be clear or red rather than the more typical dark lesions described in adults, and they can be missed if clinicians are not familiar with adolescent disease patterns.

Chronic Pelvic Pain in Premenopausal Women

Premenopausal women represent a large proportion of patients with CPPS. In this group, endometriosis, adenomyosis, bladder pain syndrome, irritable bowel syndrome, pelvic floor dysfunction, neuropathic pain, and pelvic congestion syndrome are particularly important considerations.

A cyclical pattern is an important diagnostic clue. Pain that worsens before or during menstruation, pain at ovulation, progressive dysmenorrhoea, deep dyspareunia, dyschezia, dysuria, cyclic bowel or bladder symptoms, and infertility should raise suspicion for endometriosis or adenomyosis. However, non-cyclical pain does not exclude endometriosis, especially when central sensitisation or pelvic floor dysfunction has developed.

A clinical diagnosis of endometriosis can often be made from symptoms and examination, and treatment may begin while imaging is arranged. Transvaginal ultrasound is commonly used as the first-line imaging test, particularly to identify endometriomas, adenomyosis, fibroids, adnexal masses, and signs of deep endometriosis. Where transvaginal ultrasound is not acceptable or appropriate, for example in some adolescents or survivors of sexual trauma, transabdominal ultrasound may be more appropriate.

Pelvic congestion syndrome is especially relevant in premenopausal, parous women because hormonal and venous factors can contribute to dilated, refluxing pelvic veins. Importantly, pelvic congestion syndrome and endometriosis may coexist, so the presence of one diagnosis should not prevent assessment for the other.

Chronic Pelvic Pain in Postmenopausal Women

In postmenopausal women, the differential diagnosis shifts away from oestrogen-dependent conditions and toward non-gynaecological, structural, inflammatory, post-surgical, vascular, myofascial, and neoplastic causes. Endometriosis usually regresses after menopause, although it may persist in women taking hormone replacement therapy or in selected complex cases.

Postmenopausal pelvic pain should be assessed carefully because malignancy must be excluded when symptoms include vaginal bleeding, palpable mass, bloating, unexplained weight loss, appetite change, early satiety, or new urinary frequency. Vaginal bleeding or a pelvic mass should take priority over general chronic pelvic pain assessment.

Chronic Pelvic Pain After Pelvic Surgery

Previous pelvic or abdominal surgery is an important risk factor for CPPS. In one prospective study, prior pelvic surgery was present in 72% of CPPS patients compared with 45% of controls. Surgery may contribute to pain through adhesions, nerve injury, scar sensitivity, mesh-related pain, pelvic floor guarding, myofascial dysfunction, or central sensitisation.

Neuropathic pain is particularly important after surgery. It should be suspected when pain follows a nerve distribution, is associated with allodynia or hyperalgesia, or is described as burning, pins and needles, razor blades, cutting pain, hot skin, raw skin, numbness, or electric shocks.

The value of adhesiolysis for chronic pelvic pain remains controversial. Current evidence does not support routine adhesiolysis, laparoscopic uterosacral nerve ablation, or presacral neurectomy as reliable pain treatments for CPPS. Persistent pain after surgery should therefore prompt a broader pain medicine assessment rather than repeated surgery alone.

Trauma and Abuse as Risk Factors

Psychosocial trauma is a significant risk factor for CPPS and can affect pain severity, pelvic floor tone, central sensitisation, emotional wellbeing, sexual function, and response to treatment. This does not mean the pain is psychological. It means that trauma can influence how the nervous system processes pain and how the pelvic floor responds to threat, stress, and previous experiences.

Women with CPPS are more likely to report childhood physical abuse, sexual abuse, verbal or emotional abuse, and prior trauma. Women with more generalised pelvic and abdominal pain may also have higher rates of trauma, poorer mental health, and poorer physical health.

Other Risk Factors

Several additional risk factors are associated with chronic pelvic pain and may help guide clinical assessment. For dysmenorrhoea, recognised risk factors include age under 30 years, low BMI, smoking, early menarche before the age of 12, longer menstrual cycles, heavy menstrual flow, nulliparity, premenstrual syndrome, and sterilisation.

For non-cyclical pelvic pain, risk factors include drug or alcohol misuse, miscarriage, heavy menstrual flow, pelvic inflammatory disease, previous caesarean section, pelvic pathology, and psychological comorbidity. Bowel constipation and a history of endometriosis are also significantly associated with CPPS.

In summary: CPPS must be interpreted in the context of the individual patient. Adolescents, premenopausal women, postmenopausal women, patients with prior pelvic surgery, and patients with a trauma history each require a tailored diagnostic approach that avoids both under-investigation and unnecessary repeated procedures.

Premenopausal versus Postmenopausal Chronic Pelvic Pain: A Comparative Overview

Chronic pelvic pain syndrome (CPPS) in premenopausal and postmenopausal women shares many core mechanisms, including viscerosomatic convergence, myofascial dysfunction, neuropathic pain, and central sensitisation. However, the hormonal changes associated with menopause fundamentally alter the dominant causes, symptom patterns, diagnostic priorities, and treatment approach.

In reproductive-age women, endometriosis, adenomyosis, and pelvic congestion syndrome are particularly important considerations. After menopause, the differential diagnosis shifts toward genitourinary syndrome of menopause (GSM), pelvic floor weakness and prolapse, post-surgical adhesions, vulvar dermatoses, chronic urinary tract problems, and the need to exclude malignancy.

Why Menopausal Status Matters

The menopausal transition is a major physiological turning point. Estrogen receptors are widely distributed throughout the pelvic floor, bladder, urethra, vagina, vulva, and connective tissues. Estrogen supports collagen synthesis, tissue elasticity, vascular health, lubrication, and neuromuscular function.

When estrogen levels decline, tissues become thinner and more fragile, the extracellular matrix weakens, lubrication decreases, and pelvic floor mechanics change. These changes contribute to dyspareunia, urinary symptoms, prolapse, recurrent infections, and altered pain processing.

Differential Diagnosis: How the Causes Shift

The Hormonal Pivot

Genitourinary syndrome of menopause (GSM) is the single most important new pain generator after menopause. It affects approximately 45–77% of postmenopausal women and causes vaginal dryness, burning, irritation, dyspareunia, urinary urgency, dysuria, and recurrent urinary tract infections.

The vulvar vestibule is particularly sensitive to estrogen deficiency. Many postmenopausal women have both GSM and vulvodynia. Correcting atrophy alone may improve tissue health, but neuropathic and myofascial pain components often require additional treatment.

Although endometriosis usually regresses after menopause, approximately 2–4% of women continue to experience symptomatic disease. In these patients, the absence of cyclical pain can make the diagnosis more challenging.

Symptom Profile Differences

Diagnostic Approach Differences

Treatment Priorities

What Remains the Same Across the Lifespan

Despite these differences, several principles apply equally to both groups. Myofascial pain is present in 50–90% of women with chronic pelvic pain and should be assessed routinely. Central sensitisation, cross-sensitisation, neuropathic pain, poor sleep, anxiety, and depression can occur at any age.

The most effective approach remains a comprehensive biopsychosocial assessment that evaluates pelvic organs, muscles, nerves, and pain-processing mechanisms rather than focusing on a single diagnosis.

In summary: Menopausal status profoundly changes the differential diagnosis and clinical priorities in chronic pelvic pain. Premenopausal women are more likely to have hormone-driven disorders such as endometriosis and pelvic congestion syndrome, whereas postmenopausal women are more likely to have GSM, prolapse, vulvar disorders, and structural conditions that require exclusion of malignancy. Nevertheless, the fundamental principles of comprehensive pain assessment and multimodal management remain the same.

Pelvic Congestion Syndrome (Pelvic Venous Disorder)

Pelvic congestion syndrome (PCS), now increasingly referred to as pelvic venous disorder (PeVD), is an important but often under-recognised cause of chronic pelvic pain. It refers to chronic pelvic pain associated with dilated, incompetent, and refluxing pelvic veins, most commonly involving the ovarian and internal iliac venous systems.

The condition is classically seen in premenopausal, multiparous women and may account for a significant proportion of chronic pelvic pain cases. However, its diagnosis can be challenging because symptoms overlap with endometriosis, bladder pain syndrome, irritable bowel syndrome, pelvic floor dysfunction, and myofascial pain.

Definition and Pathophysiology

PCS is defined as chronic pelvic pain related to incompetent pelvic veins. In healthy veins, valves help maintain one-way blood flow back toward the heart. In PCS, venous valves become incompetent or pelvic venous outflow becomes obstructed, causing venous dilatation, reflux, congestion, and raised venous pressure within the pelvis.

This venous congestion may irritate surrounding pelvic structures and contribute to chronic pelvic heaviness, deep pelvic aching, dyspareunia, urinary symptoms, and pain flares related to posture, menstruation, pregnancy, or sexual activity.

Nutcracker Syndrome

Nutcracker syndrome occurs when the left renal vein is compressed, classically between the aorta and superior mesenteric artery. This can increase venous pressure in the left renal vein and promote reflux through the left ovarian vein into pelvic venous plexuses.

When Nutcracker syndrome is clinically relevant, symptoms may include pelvic pain, flank pain, haematuria, or prominent pelvic and lower limb varicosities. In these cases, treating pelvic vein reflux alone may be insufficient if the upstream venous obstruction is not recognised.

May-Thurner Configuration

May-Thurner configuration refers to compression of the left common iliac vein by the right common iliac artery. This can obstruct venous drainage from the pelvis and lower limb, leading to venous hypertension and reflux into pelvic venous tributaries.

This matters clinically because PCS may be caused by reflux, obstruction, or both. When obstruction is the dominant driver, the obstruction often needs to be addressed before or alongside embolisation of refluxing veins.

Hormonal Factors

Hormonal factors help explain the typical patient profile. Estrogen promotes venous dilation, while progesterone relaxes smooth muscle within the venous wall. Together, these effects can increase venous capacitance and predispose to venous insufficiency.

This is why PCS is most often seen in premenopausal, parous women and why symptoms often worsen premenstrually, during menstruation, or during pregnancy. It also explains why PCS commonly improves after menopause, although venous abnormalities may still be seen on imaging.

Clinical Presentation

The typical pain of PCS is a dull, aching, heavy pelvic pain rather than a sharp or cramping pain. It is often worse later in the day and is strongly influenced by posture. Prolonged standing, walking, lifting, sexual intercourse, post-orgasm, menstruation, and pregnancy may worsen symptoms, while lying down often provides relief.

Associated symptoms may include pelvic heaviness, deep dyspareunia, post-coital pain, dysuria, urinary frequency, vulval or perivulval varicosities, buttock or perineal varicosities, and lower limb varicose veins. Some women also describe a dragging sensation or pressure in the pelvis that becomes more prominent with gravity and prolonged standing.

Distinguishing Pelvic Congestion Syndrome from Endometriosis

PCS and endometriosis can look similar clinically because both can cause chronic pelvic pain, dyspareunia, premenstrual worsening, and reduced quality of life. However, there are important distinguishing features. PCS tends to produce heaviness and postural pain, while endometriosis more often produces progressive dysmenorrhoea, cyclic bowel or bladder symptoms, and inflammatory pelvic pain.

Importantly, these two conditions may coexist. The diagnosis of endometriosis should not stop clinicians from considering PCS, and the diagnosis of PCS should not exclude assessment for endometriosis, pelvic floor dysfunction, bladder pain syndrome, or bowel-related pain.

Diagnostic Approach

PCS is a clinical and imaging diagnosis. The clinical history should specifically explore postural worsening, post-coital pain, pelvic heaviness, pregnancy-related worsening, varicosities, and overlap with bladder, bowel, and gynaecological symptoms.

Laparoscopy can miss PCS because carbon dioxide pneumoperitoneum compresses pelvic veins and the Trendelenburg position reduces venous congestion. Therefore, a normal laparoscopy does not exclude PCS.

Transvaginal Ultrasound Criteria

Transvaginal ultrasound with Doppler assessment is increasingly recognised as a useful first-line diagnostic tool. It allows assessment of pelvic varices, ovarian vein dilatation, myometrial venous enlargement, flow velocity, and reflux.

Recent work has supported ultrasound-based scoring systems that combine venous diameter, reflux duration, low flow velocity, Valsalva-evoked caudal flow, myometrial plexus enlargement, and bilaterality. In selected studies, ultrasound findings have shown strong agreement with venography.

MRI and Venography

MRI is increasingly used as a non-invasive method for assessing pelvic venous disorders. It can identify pelvic varices, ovarian vein reflux, venous anatomy, and possible compressive causes such as Nutcracker syndrome or May-Thurner configuration.

Post-contrast T1-weighted imaging and time-resolved vascular sequences can help evaluate venous conspicuity, flow direction, and reflux patterns. MRI is also useful when symptoms overlap with endometriosis, adenomyosis, adnexal pathology, or other pelvic conditions.

Catheter venography remains the traditional diagnostic gold standard, but it is now often reserved for patients in whom treatment may be performed at the same time. This avoids purely diagnostic invasive venography when non-invasive imaging and clinical findings are sufficient to guide referral.

Treatment Overview

Treatment depends on whether symptoms are driven primarily by venous reflux, venous obstruction, or a combination of both. It is also important to recognise coexisting pain generators such as endometriosis, pelvic floor hypertonicity, bladder pain syndrome, IBS, or central sensitisation.

Medical Management

Hormonal suppression has been used to reduce symptoms in selected patients. Medroxyprogesterone acetate has shown benefit compared with placebo in reducing pain, although side effects such as weight gain and bloating may limit acceptability. GnRH agonists such as goserelin have also shown improvements in symptoms and venographic findings in some studies.

However, pharmacological suppression is generally considered a short-term option. Long-term effectiveness is uncertain, and medical treatment does not correct the underlying venous reflux or obstruction.

Endovascular Treatment: Current Standard of Care

For confirmed symptomatic PCS, endovascular treatment has become the standard approach. This usually involves percutaneous transcatheter embolisation of refluxing ovarian veins and internal iliac vein tributaries using coils, plugs, sclerosants, or a combination technique.

Substantial pain relief has been reported in many women after embolisation, with improvement often increasing and being sustained over time. Reported complication rates are generally low, although patient selection and accurate identification of the venous mechanism are essential.

Key Clinical Pearls

In summary: Pelvic congestion syndrome is an important and underdiagnosed contributor to chronic pelvic pain, particularly in premenopausal, multiparous women. The classic pattern is dull pelvic heaviness, worse with standing and after intercourse, often relieved by lying down. Diagnosis requires careful clinical suspicion and appropriate venous imaging, and endovascular treatment is now the standard approach for confirmed symptomatic disease.

Diagnostic Approach to Chronic Pelvic Pain Syndrome

The diagnostic approach to chronic pelvic pain syndrome (CPPS) must be broad, structured, and clinically thoughtful. CPPS is rarely explained by a single abnormality. A woman may have endometriosis, bladder pain syndrome, irritable bowel syndrome, pelvic floor hypertonicity, neuropathic pain, central sensitisation, and psychosocial contributors at the same time.

The aim of assessment is therefore not simply to “find a lesion”, but to identify all relevant pain generators and understand how they interact. A normal scan, normal laparoscopy, or previous treatment of one condition does not exclude significant myofascial, neuropathic, visceral, or pain-processing mechanisms.

Clinical History and Pain Assessment

A detailed history remains the most important part of the assessment. The clinician should establish the onset, duration, location, radiation, severity, character, frequency, triggers, relieving factors, and functional impact of the pain. It is important to ask whether the pain is cyclical, constant, activity-related, bladder-related, bowel-related, posture-related, intercourse-related, or associated with previous surgery.

In premenopausal women, the history should explore menstrual pattern, progressive dysmenorrhoea, ovulation pain, premenstrual flares, deep dyspareunia, dyschezia, dysuria, fertility goals, contraceptive use, and symptoms suggestive of endometriosis or adenomyosis. In postmenopausal women, the history should specifically explore vaginal bleeding, bloating, weight loss, appetite change, hormone replacement therapy, previous malignancy, aromatase inhibitor use, urinary symptoms, vaginal dryness, prolapse symptoms, and surgical history.

The history should also screen for bladder pain syndrome, irritable bowel syndrome, fibromyalgia, chronic low back pain, migraine, fatigue, sleep disturbance, anxiety, depression, trauma history, and previous response to treatments. This broader approach reduces the risk of attributing all pain to a single gynaecological diagnosis.

Physical Examination

Physical examination should be targeted, respectful, and trauma-informed. Many women with CPPS have undergone repeated intimate examinations and may be anxious, guarded, or fearful. The examination should be explained carefully, consent should be obtained at each stage, and the patient should be able to pause or stop at any time.

The examination should assess the abdomen, pelvis, lumbar spine, sacroiliac joints, hips, abdominal wall, pelvic floor, and relevant peripheral nerves. A positive Carnett test, where abdominal tenderness worsens or fails to improve when the abdominal wall muscles are contracted, supports abdominal wall pain rather than visceral pain. Pelvic floor muscle tenderness and a positive FABER test may indicate neuromusculoskeletal contributors.

Laboratory Testing

Laboratory testing should be guided by symptoms rather than performed indiscriminately. In reproductive-age women, pregnancy should be excluded when clinically relevant. Vaginitis and sexually transmitted infection screening should be considered when there is abnormal discharge, pelvic inflammatory disease risk, dyspareunia, or cervicitis symptoms.

Urinalysis and urine culture are appropriate when urinary symptoms are present, although repeated negative cultures should prompt consideration of bladder pain syndrome, pelvic floor dysfunction, or myofascial urinary frequency syndrome. Endometrial biopsy should be considered for chronic abnormal bleeding, especially in women over 45, or where chronic endometritis or malignancy is suspected.

Imaging in Premenopausal Women

In premenopausal women, transvaginal ultrasonography is usually the initial imaging modality when chronic pelvic pain, suspected endometriosis, adenomyosis, fibroids, adnexal pathology, or pelvic venous disease is being evaluated. Where transvaginal ultrasound is not acceptable or appropriate, such as in some adolescents or survivors of sexual trauma, transabdominal ultrasound should be considered.

Clinical Diagnosis and Empiric Treatment

A clinical diagnosis of endometriosis may be made from symptoms, examination, or both. Symptoms such as chronic pelvic pain, progressive dysmenorrhoea, deep dyspareunia, dysuria, dyschezia, cyclic bowel or bladder pain, and infertility should raise suspicion. Empiric medical treatment can be initiated while imaging is arranged, so that treatment is not delayed unnecessarily.

Transvaginal Ultrasonography Technique

Ultrasound assessment in suspected endometriosis should go beyond a simple look at the uterus and ovaries. It should assess the uterus, ovaries, fallopian tubes, bladder, ureters, bowel, uterosacral ligaments, parametria, vagina, rectovaginal septum, and pouch of Douglas where clinically appropriate.

Dynamic assessment can be helpful. Loss of the uterine sliding sign may suggest deep endometriosis or adhesions in the pouch of Douglas. Other ultrasound clues include fixed retroversion, abnormal ovarian position, “kissing ovaries”, bowel tethering, site-specific tenderness, adenomyosis, hydrosalpinx, or hematosalpinx.

Limitations of Imaging

Ultrasound and MRI can detect endometriomas and deep endometriosis, but they cannot reliably exclude superficial peritoneal endometriosis. Imaging accuracy also depends heavily on the training and experience of the person performing and interpreting the scan.

A negative scan therefore does not eliminate the possibility of endometriosis, pelvic floor dysfunction, neuropathic pain, or central sensitisation. Treatment should still be considered in symptomatic patients when the clinical picture is convincing.

Role of Biomarkers

Blood, urine, endometrial, and other biomarkers are not recommended for diagnosing endometriosis. They should not replace careful clinical assessment, pelvic examination, and appropriate imaging.

Imaging in Postmenopausal Women

In postmenopausal women, imaging has a different priority. The first task is often to exclude important structural or malignant pathology, especially when there is vaginal bleeding, a palpable mass, bloating, unexplained weight loss, appetite change, early satiety, or new urinary symptoms.

Initial Imaging Strategy

Combined transabdominal and transvaginal pelvic ultrasound is the usual initial imaging approach when a gynaecological cause is suspected. Transabdominal ultrasound provides a wider overview of the pelvis, while transvaginal ultrasound provides higher-resolution assessment of the endometrium, ovaries, adnexa, pelvic fluid, and smaller pelvic structures.

Doppler ultrasound may be added when vascular pathology such as pelvic venous disorder is suspected. Ultrasound can also assess adnexal masses, endometrial thickening, hydrosalpinx, pyosalpinx, tubo-ovarian abscess, loculated fluid, and some post-inflammatory or post-surgical changes.

Follow-Up Imaging When Ultrasound Is Indeterminate

When ultrasound is inconclusive, MRI pelvis with and without contrast is often the preferred next step because it provides better soft-tissue characterisation. CT pelvis with contrast may be appropriate in selected cases, particularly where bowel, urinary tract, malignancy, inflammatory disease, or broader abdominal pathology is suspected.

Malignancy Exclusion

In postmenopausal women, vaginal bleeding and a palpable mass must take priority over the general complaint of pelvic pain. Endometrial and ovarian malignancy should be considered when there is bleeding, bloating, early satiety, weight loss, appetite change, abdominal distension, or suspicious adnexal findings.

For postmenopausal bleeding, transvaginal ultrasound is commonly used to assess endometrial thickness. An endometrial thickness of 4 mm or less has a very high negative predictive value for endometrial cancer, although clinical judgement remains essential where symptoms persist or risk factors are present.

Role of Ultrasound

Ultrasound is often the first-line imaging test in CPPS because it is accessible, non-invasive, and useful for identifying common gynaecological pathology. It can detect fibroids, adenomyosis, ovarian cysts, endometriomas, adnexal masses, hydrosalpinx, pelvic fluid, and features of deep endometriosis when performed with appropriate expertise.

For pelvic venous disorders, transvaginal Doppler ultrasound can assess ovarian vein diameter, pelvic varices, myometrial venous dilatation, low flow velocity, and reflux. However, standard pelvic ultrasound may miss functional pain generators such as pelvic floor hypertonicity, neuralgia, abdominal wall pain, or central sensitisation.

Role of MRI

MRI is useful when ultrasound is inconclusive, when deep infiltrating endometriosis needs mapping, when adenomyosis requires clarification, when complex adnexal pathology is present, or when postmenopausal pathology requires further characterisation.

MRI can also support assessment of pelvic inflammatory disease sequelae, adhesions, peritoneal inclusion cysts, vulval or vaginal lesions, pelvic venous disorders, and complex post-surgical anatomy. It does not, however, replace clinical assessment for pelvic floor pain, myofascial pain, or neuropathic pain.

When to Consider Laparoscopy

Laparoscopy has a role in selected patients, particularly when endometriosis is strongly suspected, symptoms are severe, imaging is inconclusive, or empiric treatment has failed. It can provide both diagnosis and treatment in the same procedure.

However, laparoscopy is not required before initiating empiric treatment for suspected endometriosis. Nearly 40% of laparoscopies performed for pelvic pain do not identify pathology, and many abnormalities found are early-stage endometriosis or adhesions. Some women continue to experience pain after surgery because myofascial pain, neuropathic pain, bladder pain syndrome, bowel dysfunction, or central sensitisation remain untreated.

Central Sensitisation and Cross-Sensitisation

Central sensitisation should be considered when pain is disproportionate, widespread, persistent despite treatment, associated with multiple pain syndromes, or accompanied by sleep disturbance, fatigue, anxiety, depression, hyperalgesia, or allodynia.

Viscero-viscero cross-sensitisation explains why one pelvic organ can sensitise another. For example, endometriosis may increase bladder or bowel sensitivity, and bladder pain may worsen pelvic floor guarding. Viscerosomatic convergence explains why visceral pain can produce muscle hypertonicity, abdominal wall pain, low back pain, and trigger points.

This is one of the main reasons why CPPS persists even after treatment of a visible lesion. The original trigger may no longer be the only driver of symptoms.

Key Diagnostic Principles

In summary: The diagnostic approach to CPPS should be systematic, trauma-informed, and mechanism-based. Imaging and laboratory tests are important, but they must be interpreted alongside the history, physical examination, pelvic floor assessment, bladder and bowel symptoms, neuropathic features, and central sensitisation markers.

Frequently Asked Questions

Chronic pelvic pain syndrome can be confusing and frustrating, particularly when symptoms persist despite normal scans, previous treatment, or surgery. The answers below address common questions patients often ask when trying to understand why pelvic pain continues and what may be contributing to it.

Key Take-Home Messages

Chronic pelvic pain syndrome is best understood as a complex, overlapping pain condition rather than a single diagnosis. The essential clinical messages are summarised below.

References

The following key guidelines, systematic reviews, and landmark studies informed the content of this article and provide an evidence-based framework for understanding chronic pelvic pain syndrome in women.